Wound Care A Collaborative Practice Manual for Physical Therapists and Nurses
Edited by Carrie Sussman, PT Sussman Phys ical Therapy Inc. Torrance, California
Barbara M. Bates-Jensen, MN, RN, CETN Assistant Professor of Clinical Nursing Department of N ursing University of Southern California Los Angeles, California
AN ASPEN PUBLICATION'" Aspen Publishers, In c.
Gaithersburg, Maryland 1998
The au thors have made every effort to ensure the accuracy of the infonnation herem. Ilowever. appropriate information sources should be consulted, especially for new or unfamiliar procedures. It is the responsibility of every practitioner to evaluate the appropriateness of a particular opinion 111 the context of actual clinical situations and with due considerallons to new developments. Authors. editors. and the publisher cannot be held rc!:>ponsible for any Iypogmphical or other errors found in this book library of Congress Catalogmg-In-Publication Data Wound care: a collaborative practice manual for physical therapists and nurses edited by Carrie Sussman. Barbara M. Oates-Jensen p cm. Includes bib liograplucnl references and mdex. ISBN 0-8342-0748-6 1. Wounds and injures Treatment 2. Physical therapy, 3. Nursing. I. Sussman. Carrie, II. Bates-Jensen, Barbara M [DNLM: 1. Wounds and Injuries rehabilitation. 2. Wounds and Injuries nursing, 3. Wounds and Inluries diagnosis. 4. PhYSical therapy methods, WO 700 W93H4 1998] R093 .W683 1998 617.1 dc21 ONLM OLe for Library of Congress 97-40496 CIP Copyright c 1998 by Aspen Ilubllshcrs. Inc All nghts reserved Aspen Publishers. Inc., grants permission for photocopying for limited personal or Internal usc. ThiS consent docs not extend to other kinds of copying. such as copying for general distribution, for advertising or promotional purposes. for ercatlllg new collec tive works, or for resa le. For IIlformation. address Aspen Publishers. Inc .. Permissions Department. 200 Orchard Ridge Onve. SUite 200, Gaithersburg. Maryland 20K78 Orders: (800) 638-8437 Customer Service: (800) 234- 1660
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Printed III tlte U"ited SllIf('.\· or.·lmerlcCl
I 234 5
Table of Contents
Color Plates .. . . . . . . . . . . . . . . . . . . • . . . . . . . . . . . . . . • . . . . . . . . . . . . . . . . • . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Contributors
xi
xiii
Foreword
xv
Prerace ........ .... .... . ......................................................................
xvii
Acknowledgments. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . • . . . . . . . . . . . . . . . . . . . . . . . . . . . .
xix
Introduction:
xxi
The Need for Collaborative Practice. . ...... . . . . ...• . • .•.. ..... . •. . . .. . . . . . . . . . . . . .. Carrie Sussman and Barbara M. BllIes-Jel/sell
PART I- INTRODUCTION TO WOUND DIAGNOSIS Carrie Sussman C hapter I- The Diagnostic Process .......................................... ...................
3
Carrie Sussman, Barbara M. Bmes-Jensen. alld Melisa TljJallY Step I: Assessment Process .... . .......................................... . . ... .... Case Study: Cognitively Impaired Patient with Leg Ulcers ................. . .......... . . . ... Case Study: Example of Patient History Influencing Wound Care Management .... . •. . .... . . . . . Step II : Diagnosis . . .. . . . . . .. .. . . . . .. . . . . . .. .. . . . . . . .. . . . . . . .. .. . . . . . . . .. .. .. . . . . . . .. Step III : Progress and Goals ............ . ........ . ........... . ..... ... . . .............. The Functional Outcome Report ... ..... . ............ . . . . . ......... • . . . , .. . ......... . . . Conclusion ............................................ .. ...... .. . . . . ........ .. .... Appendix I- A: Patient History Form . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. Appendix I- B: Focused Assessment for Wounds .................................. . ..• . .. Appendix 1- : Form HCFA·700 ......................... .. ......... .. ................ Appendix 1- 0 : HCFA·700 Form with FOR Template To Guide Documentation in Italics ......... Appendix I E: Sample Case Report Using HCFA· 700 . . ............................. . .• . . .
111
3 II 14 15 17 22 24 26 27 28 29 30
IV
WOUND CARl
31
Chapter 2- Wound Healing Biology and Chronic Wound Healing Carrie Sussman Wound Healing Models .............................................................. Acute Wound Healing Biology ........................................................ Fetal Wound Healing ................................................................ Chronic Wound Healing. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Conclusion ....... . . . . . .. . . . . .. . . .. . . . . .. . . . . .. . .. . . . .. . . . . .. . . .. . . .. . . .. .. . .
31
32 40 40 45
49
Chapter 3-- Assessment of the Skin and Wound Carrie Sussman
The Assessment Process ............................................................. Assessment of Wound StalUs ......................................................... Case Study: Dangers of Differing Clinical Procedure and Facility Policy ...................... Assessment of the Peri wound and Wound Tissues .............. . ................... Wound Hca ling Phase Diagnosis and Prognosis .................................. . ...... Referral Criteria ......................................................... . ......... Conclusion .......... , ............................................................
. . . . . . .
49 55
56 66 67 81 81
83
C hapter 4- Wound Measurements Carrie Sussman
Baseline Assessment Accepted Measurements ..... Measurement Assessment Forms ...................................................... . Location ......................................................................... .
Wound Size Measurement Accuracy and Reliability ...................................... . Linear Wound Size Measurements . .................................................... .
Wound Photography ................................................................ . Referral Criteria ............................................................. . Referral Sources .... Sci f·Care Teaching Guidelines ........................................................ . Conclusion ....................................................................... .
Resources ........................................................................ .
83 83 83 87 87 88 99 101
101 101
102 102
C hapter 5-- Tools To Measure Wound Healing ....... .. .. .... ............... ......•. ......... ...... Carrie Sussman Gnd Barbara A1. Bates-Jensen
103
Inlroduction .............. ,.... . .................................... . Sussman Wound Healing Tool ....... . ........................................ . The Pressurc Sore Status Tool ............................ . ....................... . Appendix 5- A: Instructions for Pressure Sore Status Tool ................................. .
103 105
C hapter 6-Noninvasive Vascular Testing .. .... . .... .....• ..............•......................•. . Aline Siegel
114 122 125
. .......... .
125
Chief Complaint ............................................................... . Past Medical History ............................................................... . . ............................................. .
125 125 125
. .......•.•..........•..........•............
127
Introduction
............... , . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Physical Examination. . . . . . . . . . . . . .
Pu Isc
EX31TI . . . . . . . . . . . . . . . . . . • . • .
Table a/Colllell/,
Noninvasive Va scular Testing . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Case Study: Ankle-Brachial Index. . . . . . . . . . . . . . . . . • . . . . . . . . . . . . . . . . . . . . . . . . . . . Addilional Vascu lar Studies ................. . ............................ . . . . . . . . . . . . . Noninvasive Venous Testing. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Conclusion ........................... . ............................................ Referral Criteria ............... . ...... . .... _ .................... _ . . . . . . . . . . . . . . . . . . Self-Care Teaching Guidelines ........................... .
v
129 132 133 133 133 133 135
PART II- MANAGEMENT BY WOUND CHARACTERISTICS Barbara At!. Bales-Jensell
137
Chapter 7- Managemcnt of Necrotic Tissue .............. _. _ ................ _. _ .. _....... _. _ ...... _ Barhara A1. Bates-Jensen
139
Significance of Necrotic Tissue. . . . . . . . . .
. .............. , ....................... .
Interventions . .................................................................... , .
Mechanical Debridement Procedures ......... , .......... . Entymatic Debridement Procedures .....................
. ..................... .
Sharp Debridement Procedure . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ..................... . AUio lylic Dcbridement Procedures ...... .. . .............................. _ . _ ..... . OutconlC M easurcs . . . . . . . . . . . . . . . . . . . . . . . ..... .. ........... . ............... . Referral Criteria .........................................................•....... Self-Care Teaching Guidelines .............. _ . ........ .. ......... . .................... . Appendix 7 A: Debridemem Choices for Chronic Wounds ....................... .. ...... . . Appendix 7 B: Enzymatic Preparalions ......... ... .................................... . Chapter 8- Management of Exudale and Infection Barbara M. Bates-JenseJ/
139 140 140 143 144 146 148 148 148 151 157 159
Significance of Exudate ..................... . .............................. _ ... _... _. Significance of Infection .......................................................... _ . . Procedures for Quantitative Wound Cullure .....................................•...... Management of Exudale and Infeelion ...................•.... . ............... _ . _ . _. . . Outcome Measures. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. ............. Referral Criteria .............. . ....... _. . . . . . . . . . . . . . • . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Self-Care Teac hing Guidelines. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
159 162 165 166 174 176 176
Chapter 9- Management of Edema .. _.......•. • ......... _.... _ ...... _. . . . . . . • . . • • . . . . . • . • . . . . . . Laurel A. Wier.'lema-B,:vol1l
179
Introduction ...................... . Overview of Ihe Problem ............ . Tests and Measurement ............................................... . Modes of Intcrvention and Procedures for Intervention. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Procedures for Managemelll of Edema ................ _ .......................... _ . . Leg Elevation and Exercise ...................... . ...... _ . • . . . . . . . . . . . . . . . . . Compression Wraps (Elastic Bandages) ................. _ . . . . . . . . . . . . . . . . . . . . . . Paste Bandage ................................................................... Four-Layer Bandage . . . . . . . . . . . . . .. ... _ . _ . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Compressio n Stockings ......... . ..... _ ......... . ...... _ . . . . . . . . . . . . . . . . . . . . . . . . . Sequential Compression Pump .. .. .. . . . .. . . . . . . . . .. . . . . . .. .. . . . . . . .. . . . . . . .. . .. .. Referral Cri teria ....... . ..... . ..... . ..... _ ............ _ . _ ...................... _ ... _ Self-Care Teaching Guidelines ... _ .......... _ ................ _ . _ ...................... .
179 179 179 180 185 185 186 187 188 193 195 197 198
VI
W OU, D CARE
Case Study I: A Case for Elastic Bandages. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Case Study 2: Combination Therapy with Sequential Pump and Class I Stockings............... C hapt er 10- Manage m ent of th e Wound Enviro nment Geoffrey Sussmall
199 199 20 1
Introducti on ........ .. ........ . ....... . ...... . .......... . ................. . . .. ..... Inert Wound Dressings.................................. . ............................ Ideal Dressing . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Modern Wound Dressings ............................................................ Dressing hoiee ....................... . ................ ................. . .......... Secondary Dressings ................................... . ......... . .... ....... ....... The Usc of Antiseptics in Wounds . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Antiseptics and Acute Wounds. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Antibiotics ............. .. ................. . . . . ... . . ... .. . . . .. ..................... Wou nd Cleansi ng ............................... . ...................................
201 201 20 I 202 209 211 211 2 12 212 2 12
PA RT Ill- MA AGEMENT BYWOU ' D ET IOLOGy.... . ... .... ..... .. .. .... ........ .. .... .. .... . Barbara 1.1. Bates-Jensen
2 15
C hapt er II - Ac ut e Surgical Wound Ma na ge ment ........ . • . • . •.• .. ... . • .• . ..• . ...•. . ..... . • . ...... Barbara M. Bates-Jensen al/d James Wethe
21 9
Acute Surgical Wound Definition .......................... . ... ... ..................... Factors Aflecting Healing in Acute Wounds .... . ...... . .... . .... .. ............ Assessment of the Acute Surgical Wound .. ....... . ................................... Manage ment of the Acute Surgical Wound ......... . . . . ... . . .. . .......................... Secondary and Tertiary Intention Wound Healing . . . . . . . . . . . . . . . . . . . . •. . . . . . . . . . . . . . . . . . . . . Outcome Measures . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Case Study: Lack of Innammatory Response Postoperatively ................................ Conclusion ... ... ........ .. ............ _ . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Referral Criteria .................................................................... Self-Care Teaching Guidelines. . . . . . . . . . . .. . . . .... . .. . . . .. . .... . .. . ... ... . . . . ... . .... . . Case tud y: Incisio nal Wound Healing ........ . ..... . ................ . . . .. . ... . . ..• ... ..
219 2 19 224 226 226 227 227 228 228 230 231
C hapt er 12- Press ure Ulcers: Pathophys iology a nd Prevention Barbara /\11. 8t1les-Jel/sell Press ure Ulcer Definition ............................................................ Pressure Ulcer Pathophysiology .... . . . .............. .. ............... . .... . ........... Clinical Prese ntat ion of Press ure Ulccrs ................................................. Press ure Ulcer Staging . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Pressure Ulcer Prediction: Risk Factor Assessment ..................•..................... Press ure Ulcer Prevention: Early Interventions. . . . . . . . . . . • . . . . . . . . . . • . . . . . . . . • . • . . . . . . . . . . Outcome Measures . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Referral Criteria .. . ...... . ...... . ....... ...........•.......... ... .. ....... . ....... . . Self-Care Teaching Guidelines . . . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . ... . . . . . .. . Cha pter 13- Ma nage ment of Pressure by T hera peuti c Positionin g Laurie M. Rapp/ Introduction .............................................•......................... The Diagnostic Process Applied 10 Therapeutic Positioning ........... . ..................... Functional Diagnostic Process. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Rationa le for Intervention in the Sitting Position .............................. : : ..........
235 235 235 238 239 241 252 266 266 266 27 1 27 1 271 274 276
Table oj COli/ellis
VII
Rationale for Intervention in the Recumbent Position ... . . ... .... . . .... ...•.•.... .... ......
290
Case Study: Therapeutic Positioning for Press ure Ulcer Healing. . . . . . . . . . . . . . . • . • . . . • . • . • . . . . Resources . .................................................................•.•....
295 298
C hapter I4-Diagnosis and Management of Vascular Vlcers
Car/os E.
301
D Ollllyre
Introducti on ......................................................•.•....... . ...... Vascular Anatomy of the Lower Ext remities .. . . . . . . . . . . . . . . . . . . . . . . . • . • . • . . . • . • . . . . . . . . . . Occlusive Peripheral Vascular Disease- Signs and Symptoms ..........................•.•.. Diabetes and Foot Ulceratio n . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . • . . . . . . . . . . . . . . . . . . . . • . • . • . . Venous Stasis Ulcers ............................ . ..... . ... .. . . . . ...•.... . •... . ...... Chapt er IS- 1anagcment o f th e Ne uropathic Foot
30 I 30 I 303 305 308 315
Nan(v EI{lman Introduction ................................. . ... • ..... . ........................... Pathogenesis ........................ . ........• . . . ...............•.... . ..... . ....... Medical History .. . ........................... . ... • . • .•. . .......... . . . ...•.•...•....
Systems Review and Examination .. . ..... .... ...... .... ....... ..... ....... ... ......... . Further Visual and Physical Assessments ...•• . ......•...•.•..............•.•...•.•.. . ... Case Study: Charcot Arthropathy .........•..............•.•.•.................. • .•.•.. Inter ventions . ................. . ...... .. ...... .. . . ..•.... ... ....... ... ..... ..... .... Doculncntation ................ , .. , ... . .. .. ... ... . .. , ...................•.•...... , .. .
Self·Care Teaching Guidelines ............•.• . ....... .. ....•. •.•...... .. ..... .•.• .•.. .. Resources ... . ..... . ...................................................... • ........
PART IV- MANAGEMENT OFWOVND HEALI NG WITH PHYSICA L THERAPY TECHNOLOGIES ......... . ........................................................ . Carrie Sussma" Case tudy: Choosing the Appropriate Treatment Intervention .....•.•.• . .. . .......... . . .. ...
315 316 316 318 324
331 332 340 340 343 347 352
Chapter I6--Eloctrical Stimulation for Wound Healing .... ................•......................... Carrie Sussman lIlIll NlIlley Byl
357
Introduction ............................... . ........... . .......... . .....•...•...... Definitions and Terminology . .. .... .... ....... . ........ .. .....•..... .. ................ Theory and Science of Electrica l Stimulation ...... . ........ . ........... ..... ......... . .. .
357 357 361 366 368 374
Clin ical Studies ........................................ . . . . . . .. ................... . Choosing an Intervention : Cl inical Reasoning ................ . . ... . . .................... .
Wound Healing Protocol Selection for Electrica l Stimulation ..........•. •. .................. Protocol for Wound Healing ............................• ..... • . • • .. .• ... • ....... . . . Protocol for Treatment of Ede ma .................................................... . Protocol for Infection Control and Disinfection Protocol for Treatment of Chronic Vcnous InsufTiciency or Chronic Deep Vein Thrombosis .... . . Doculnclltation ......... .. ..... .. .... .... ..... ..... ..... .... ......... .. ............ .
Case Study I: Pressure Ulcer Treated with ES ...•. .. ...........•.•....... . ........ ... .... Case Study 2: Vasc ular Ulcer Treated with ES ... . ...... . ...• .. . . ... . ............•.• . ..•.. Chapter 17- Pulsatile La"age with Co ncurrent Suction
378
380 380 381 382 383 385 389
Itardeff Baugh Loe/m e
Definition .. . .................................•.•................•.•.• .. ......... .. Theory and Science of the Therapy . . . . . . . . . . . . •.• . . . . . . . . . . . . . . • .• . . . . . . . . . . . . . . . . . . • . .
389 389
viii
W OUN D C ARE
Indications for Therapy ...•. .... ...........•................... . .... . ... . .... . ... . ... Precautions ............... . . . ...... . . .. .. . .. . .. . . ..... •.. .. ... ... .. ... ... . ...... . .. Outcome Measures . . . . . . . . . . . . . . . . . . . . . . • . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Frequency and Duration . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Cautions .......................... . ........ .. . . . .. .. . .. . .......... . ............... Vacuum Assisted Closure. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Performance of Pulsati le Lavage with Suction ....•............................ . ... . .... . . How To Use Different Equipment Models .. ....... . .... . ... . ................... . ........ Davo l Simpu lse Plus Procedure . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Davol Simpulse Solo/Simpu lse VariCare Procedure . ..................................... Stryker SurgiLav Plus Procedure . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Zimmer Pulsavac Procedure .............. . ............ . ......... . ........... . ...... Zimmer Pulsavac III Procedure . . . . . . . . . . . . . .• . . . . . . . . . . . .. . . . . . . . . . . . .. . . . . . .. . . . .•. Zimmer Var-A-Pulse Procedure . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ... ... .. . . . ... . . .. . Documentation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ... . . . . . .. . . . . . . Case Study: Gunshot Wound Treated with Pulsatile Lavage with Suction . . . . . . . . . • . . . . . . . . . . . . .
C hapter IS- Pulsed Short Wave Diath ermy a nd Pulsed Radi o Frequ ency Stimulati on Carrie Sussman Introduction .. ... .......................................................... . ....... Definitions and Terminology . . . ... . . .. ..... . ..... . ......... . .......................... T heory and Science of the Therapy ..................... . ... .. .... .. ... . .. . .. . . .. .. . .... Choosing an Intervention: Cli nical Reaso ning ............... . ............ . ..... . ...... . .. Equipment ... ..... .......................... . ...................•............... . . Procedures ...... . .. .... . . .... ... . . . .... .... .. . ..............•...... . ...• .. ....•... Protocols for PSWD ..... . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Magnatherm'" PSWD Protocol . . . .. .... . ...... . ... . ...................•.......... PSWD (Magnatherm"') for Venous Disease ..... . ... . .... . .. ... .. .. . .... .. .. . .. .. . .. Pulsed Radio Frequency Stimulation Protocol ......•. . ......•.................•........ Self-Care Teaching Guidelines . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Documentation ..... . .......................................... . ... . ... .. .. .. . .. ... . Case Study I: Pressure Ulcer Treated with Pulscd Short Wave Diathermy ............. . ........ Case Study 2: Surgical Wound Treated with Pulsed Radio Frequency Stimulation ..... • .......... C hapter 19- Ther apeuti c a nd Diagnostic Ultrasound Carrie Sussman and Mmy Dyson
390 392 393 393 393 394 394 397 397 399 399 400 400 401 401 401
405 405 405 409 414 417 41 8 419 419 42 1 421 422 422 423 424 427
Introductio n ....... . ..... . . . ....... . ..... .. ... .. . . ..... . ........... . ....•.......... Definitions and Terminology ... . .............................. .... .. . ... . .. .. ..... . . .. High-Reso lution Diagnostic Ultrasound .. . . . ........... ..... ..... . . .. .• . ... . ...... . ..... Theory and Science of Ultrasound on Wound I-Iealing ... . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . .. . Choosing an Intervention: Clinical Reasoning ............ . .... . ............. . . .. ..... . ... Procedures ...................................... . .... . .......... . . .. ... .... ... . . .. Self-Care Teaching Guidelines.... .. ..... . ................................... . .. . ..... . Documentation ................ .. ..... . ..... .. . . ..... . ..... . ...•..........•......... Case Study I: Venous Ulcer Treated with US .................... . .... . . .. .. . .... . .. . ... . . Case Study 2: Blood Blister on the Heel Treated with US . ........... . .......... . ...........
427 427 429 432 436 437 442 442 443 444
Chapter 20- Whirlpool ....... .... .... . . . . ....•.... . ....... . .... ... .... . .... ..... ...... .... .... Carrie Sussman
447
Introduction ....... . .................... . ....... .. . . ..... .. ...... . .................
447
Table oj COllle lllS
IX
Theory and Science oflhe Therapy............... ......... ...................... . ...... Therm al EfTects ........... .. ............. .. ........................................ Phys ical and Mechani cal EfTects ........................ .. ..... .•.• . ..•................
44 7 449 450
Choosing an Intervention: Clinica l Reasoning ..................... .. .......... . ..........
45 1
Equ ipment .... . ............. . ................. • ................................... Procedure ............................................................... . .. .. . . ... Ex pected Out comes .. . ...... . ...... . ...... . ........ .. ............................... elf-Ca re Teaching Guidelines. . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . •. . . . . . . . . . . . . . . . Case Study: Patient with Esc hars on Both Heels. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
454 454 456 457 457
Appe ndi x A-C uid e to To pical Anlise ptics, Anlifungals, a nd Antibacterials. . . . . . . . . . . . . . . • . • . . . . . . . . . . . .
461
Appe ndi x B-A Quick Reference G uid e 10 Wound Ca re Producl Ca lego ri es . . . ..... • . • . . . . . . . . . . . . . . . . . . Diane Krasner
477
Index ............. .. ... . ..... ... . ... ... ... .. .... . .. .. ...... . ... .... . ....•....................
483
Abo ul lhe Edilors ............. . .................... .. .. .. •.... .. • . • .• .•.. . • . .......... . • . • . • . •.
493
Color Plates
Plates 1-6
Progression through Three Phases of Wound Healing
Pla tes 7-9
Progression through Proliferation Phase
Plates 10- 11
Abnormal Proliferation Phase
Plat e 12
Wound in Remodeling Phase
I' la te 13
Anatomyof
Pla tes 14- 18
Wounding of the Skin
Pla tes 19- 22
Assessment or Darkly Pigmented Skin
Plat es 23- 24
Abnormal Wound Attributes
I' la tes 25-30
Necrotic Tissue Types
Plates 3 1-34
Wound Edges
Plates 35-36
Surgical Dissection for Tunneling
Plates 37- 39
Undermining and Tunneling
Pla tes 40-45
Reading the Dressing: Wound Exudate Assessment
Pla tes 46-48
Arterial Ischemic Wound s
Pl ates 49- 54
Venous Disease
Pl ates 55-56
Wound Healing with Electrical Stimu lation- Chapter 16
Plates 57- 59
Wound Ilcaling with Pulsatile Lavage with
Plates 60-62
Wound I-Iealing with Pulsed Short Wave Diathermy- Case Study I- Chapter 18
Plates 63-64
Wound I-Ieali ng with Pulsed Rad io Frequency Stimulation- Case Study 2
Pla tes 65-67
Wound Hea ling with Ultrasound- Case Study I- Chapter 19
Pla tes 68- 7 1
Wound Ilealing with Ultrasound- Case Study 2-Chapter 19
on Tisslie
L1ction
xi
haptcr 17
Chapter 18
Contributors
Barbara M. Bates-Jensen, MN, RN, CETN
Evonne Fowler, MN, RN, CETN
Assistant Professor of Cli nical Nursing
Wound/Ostomy/Skin Care Specia list
Department of Nursi ng Un iversity of Southern Ca lifornia
Be ll flower Kaiser Hospital
Bell nower, Ca li fornia
Los Angeles. Ca lifornia
Nancy Byl, PhD, PT
Diane Krasner, PhD, RN, CETN
Director Program in Physical Therapy
Consultan t Nursing Care of Patients Wound Care, Ostomies. Incontinence Baltimore. Maryland
University of Cali fornia at San Francisco
Oak land. California
Carlos E, Donayre, M D
Harriett Baugh Loehne, PT
Assistant Professor of Surgery Un iversity of California. Los Angeles School of Medicine Harbor/UCLA Medical Center
Staff Physica l Therapi st The orth Caro lina Baptist Hospital s, Inc. Winston-Sa lem, North Caro lina
Department of Vascular and Genera l Surgery Torrance. Ca li fornia
Laurie M. Rappl, PT Clinica l Support Manager Span-America Medical Systems, Inc.
Mary Dyso n, BSc, PhD, C Biol, M I Bioi Division of Anatomy and ell Bio logy UM DS Medical School Guys Hospital London England
Greenville. SOllih Caroli na
Ann e Siegel, RN, RVT, CVN Vascular
Nancy Elftman, CO, C.Ped.
urgery N urse Coordi nator
University Hospital Los Angeles, Ca lifornia
Certified Orthotist. Certified Pedorthi st Cosmos Extremity Hands on Foot
Carrie Suss man , PT
LaVerne, Ca lifornia
Rancho Los Amigos Medical Center (Reti red)
Sussman Physica l Therapy, Inc.
Downey, Ca li fo rni a
Torrance, Ca li fornia
xiii
xiv
W OUND CARE
Geoffrey Sussman, PhC, MPS, MSHPA, AFAIPM, MSMA,JP Director, Wound Dressing Ed ucatio n and Research Department of Pharmacy Pract ice Victorian Co llege or Pharm acy Monash Uni versi ty Park ville, Victoria, Austra li a
Melisa Tiffany, BSN, RN, CETN Graduate Student ET Nursing Uni versit y of South ern Califo rni a Los Angeles, Ca liforni a
James WeIhe, MD South Bay Plasti c Surge ry Torra nce, Ca lifornia
Laurel A. Wiersema-Bryant, MSN, RN, CS C linica l Nurse Specialist Barnes-Jewish Hos pita l at Washington Uni versity Medica l CCllI cr St. Louis, Missouri
Foreword
Bates-Jensen, MN, CETN, a nu rsc wound care specialist. Both are recognized throughout th e co untry for th eir clin ical knowledge, practical expertise, and unwavering dedi cati on to wou nd care. Both have national reputations HS superb . teachers who emphasize critica l thinkin g/deduct ive reasoning in deci sion making. Their purpose for writing th e book is to provide basic and advanced informati on on wou nd healing and wound ca re therapies, to promote co llabo ra ti ve wound management between nurses and phys ica l therapists by providing a better understanding of the similarities and differences between di sciplines, and to promote an understanding of wound manage ment by challenging the thinking process. The chapters are wrinen by wound ca re specialists from many disciplines, who arc on the fore front of wound healing practice and research. They have joined toge ther to sharc thei r accu mulated knowledge base, wisdom, and divcrse experiences and expertise in wound manage ment. Wound manage ment is multifaceted : th e causes and consequences of non-hcal ing wounds afC complex and multidimensional and resolutions rcquire an agg ressive interdisc iplinary approach to management. The best approach for handling chronic wo unds is management by a multidisciplinary team working in a collaborat ing. support ing manner and using a science-based practice. This wound care manual provides a beginning for a li vi ng reso urce for excellence in wound management .
I was delighted to be given the opportunit y to write a forewo rd to this unique manual about wound care. As a strong support er of collaboration and comm un ity and deep ly embedded in wo und management, I commend the authors for giving us this excellent wound care resource manual. An environmenllhal supports a collaborative spirit allows clinicians from both disciplines to provide their unique perspecti ve to best meet the needs for each individual patient with a wound problem. Chronic wounds are a major problem for the person who has one, for th e significant olhers involved with them, and th e health care providers who care for them . \Vound manage ment is carried out in all cafe settin gs: aClIte and long-term care faciliti es, in the home. and in olltpat ient clinics. In most sett ings, the care is otten provided by health care professional s not formall y educated in wound healing. Howeve r. when wound healin g has not been achieved, the wound is diffi cult to treat, or time consllming and cosIly. onen the patient wi ll be seen by a wound care speciali st. Usually first called is the nu rse wound care specialist or physical therapist wound care specialist. The specia li st may assess the si tuation, and recommend a manage ment plan lIsing advanced care products and techniques or alternati ve methods of managc ment or provide the care. Having a wound care resource manual on hand wo uld be a direct aid to practice. WOllnd Care: II Collaborative Practice Malllla/jor Physical Therapists Gnd Nurses is a much nceded resource for the health care providers who work dai Iy to manage these troublesome wounds. It is a use r-fri endly reso urce vo lume, formatted for quick reference as a guide in any clini cal se ning. The procedures and guidelines included in the chapters provide the clinician with a too l box for dail y practice in wound manage ment . This resource manual is a collaborati ve effo rt . wri tten by Carrie Sussman. PT, a physical therapist, and Barbara M.
El'ol/l/e FOII'Iel; liN. MN. CErN Wound/Ostomy/Skin Care Specialis( Bellflower Kaiser Hospital Belliloll'el; Calijomia
xv
Preface
TI-I E MULTID ISCI PLINA RY TEAM
ca l therapists have used the medical diagnosis of the paricnt to describe the focus of their practice. There is better nu rs-
Writing this book has been a collaborative effort between the two editors and the I J contributors. Early on in the writillg it was recogni zed thaI. just as in the rC ~11 world. the skills and expertise ora multidisciplinary team were needed to provide the scope of information needed for wound management. The writing tcam represents the disciplines usually
ing and physical therapy- re lated termino logy to describe the
found on the wound management team. Our authors include two surgeons. two researchers (one is a physical therapist) ,
five nurses, one certified pcdorthisl. one pharmacist, and three physicallhcmpi sls. What's more, a number of the chapters arc coauthored by representatives ofdifTcrent disc iplines. Two authors arc from outside the United States. Wound l11anagcl11cnI is a global problcm and a multidisciplinary challenge, and collaboration across all borders must be encouraged . Yes. at timcs collaborating was challenging, but it has been very rewarding. Yct it scemed very logical that we should prepare this work as a collaborative effort and thus set the stage for collaborative practice.
impairments, risk factors, and functional deficits for which nurses and physical therapists intervene. As it turns out, terminologics used by nurses and physical therapists arc very similar- all the bCller to foster communication and co llaboration between the two groups. The rest of Part I reviews implementation of the diagnostic process and includes chapters on review of wound healing biology. chronic wound healing, asscssmcnt of the wound and surrounding skin, specific examinations and tes ts for wounds, and the complication factors of vascular disease. These chapters form the assessment foundation for the patient with a wound. Part II describes management of the wound by specific wound characteristics. Recently, the American Physical Therapy Association convened a panel of five integumentary subject matter expert physical therapists to develop pro-
active patterns for management of integumentary impairl11elllS and disabilities. It was the consensus of the panel tha t wounds and burns are managed similarly, and that the factors that affect management of the wound are the depth of the injury (partial versus fu ll thickness and extending into deep tissues) and the wound-associated characteristics ofnecrosis, edema. and infection. Everything else rcvolves around management of the wound environment or the factors influencing healing. Chapters inc lude Management of Necro tic Tissue, Management of Exudate and Infection , Management of Edema, and Management of the Wound Environ ment. Threc wound characteristics. necrotic tissue, exudate and infection. and edema, are the wound characteristics that most often drive interventions and cause concerns for clinicians. Each chapter begins with a definition of the characteristic,
O RGAN IZATION OFTH E BOO K
The book is organized into four parts. Part I reviews the diagnostic process used by both nurses and physical thera-
pists when cva luating thc patient with a wound. Why start with diagnosi s? Nurses and phys ical therapists have exten-
sive education with unique bodies of knowledge and as professionals, have a level of autonomy and self-regulation. The usc ofa process to arrive at a diagnosis for the patient with a wound provides clarity in communication and collaborativc practice. Clear coml11unication assists with accountability and greater professional autonomy. 1-1 istorically. nurses and physixvii
xviii
W OUND CAR l·
the significance oftilc findings, assessment for the characteri sti c. and basic interventions appropriate for the wound characteri sti c. Each chapter ends with outcome measures, self-care teaching guide lines, and referral criteria for th e specific wound characteristic. Where appropriate. procedures and protocol s for interventions arc inc luded. Part III focu ses on management orthe wound by etiology. This sec tion includes chapters on management of acute surgical wou nds, management and prevention of pressure ulccrs, managcment of pressure with thcrapeutic positioning. and management and diagnosis of vascular and neuropathic ulcers. The chapters focus on pathophys iology, prevention, classification. and intervention. Part IV, Management of Wounds with Physical Therapy Technologies. app lies the diagnos tic process to se lec tion of
wound treatment intervention s with ph ys ical th erapy technologies including electrica l stimulation, pul sed shortwave diathermy, pul sed radiofrequcncy stimulation. ultrasOllnd, pul sa til e lavagc with suction, and whirlpool. Each physical therapy technology chap ter begins with a defini tion of the intervention, the science and theory of the intervcntion as it relates to wound healing. and application ofthc diagnostic process to appropriate se lection of candidates for trea tment. Each chapter includes protoco ls and expected outcome re suits for the thera py described, as well as case studi es.
Carrie Sussman Barbara At!. Bares-Jensen
Acknowledgments
We would like to express our apprec iat ion to the many individuals who hm c made this book possible including:
-
- The individua ls who have contribu ted their c1inicHI and academic knowledge, - Mary Anne Langdon. Ruth Bloom, Laura Sm ith , Jan Kortkamp a nd th e rest ort he stall'at Aspen Publi shers fo r their help and support in production, The reviewers and consu ltants whose suggesti ons were invaluable during development: Michelle Cameron, PT, OCS, Linda Frankenberger, MS. PT. Deborth lI ag ler, PT, Robert Kellogg. PhD. PT, Marko Markov, PhD, Gretchc n Swanson. MPII. PT. Eleanor Price, PhD, Nancy A. Stons, EdD, R •
-
Kris Johnson and Erin McEntyre who took care of many or the details associated wi th preparation of th e Inanuscript , The authors, publishers. companies, and colleagues who have allowed us to publish th e ir art work, photographs. and tables 10 illustrate the informat ion.
Our JIlIS/}(IIU/s (llId childrell- Robert Sussman and Ronald Ho lly, and Thomas Jense n, who have swea ted the big and sma ll stufTwith us during the years of development and preparation of th e manuscript and without whom complcti on of thi s projcct wou ld not have been possible.
Carrie Sussma n Barbara NI. Bates-Jensell
XIX
Introduction: The Need for Collaborative Practice Carrie Sussmall and Barbara M. Bales-Jensen
as a team 10 solve patient problems. Payers and hcalth carc settings benefit from fewer duplicated services and better patient outcomes at lower costs. Patients benefit from improved wound healing management. including better wound healing outcomes as a result of hcalth care service intcgration. To practice in a collaborat ive spirit. each discipline must undcrstand the process of wo un d hea ling. chronic wound difficulties, and the skills and services ofTered by e;.ch di scipli ne. Each practitioner has areas ofknowlcdge that by definition are not shared by others. Vet both physical therapy and nursing practice have many similarities. The main purpose of this book is to provide basic information on wound healing and wound care therapies to nurses and physical therapists in a user-fricndly resource volume for clinicians who deal with wounds on a daily basis and who do not have access to a "wound cnre expert." A secondary purpose of this manual is to promote collaborative wound managemcnt berween nurses and physical therapists by providing a better understanding of the similarities and differences between disciplines. This book is for nurses and physical therapists in acu te care, long-term care. outpatient care. and home health care sett ings. The book is forma tted for lise as a quick reference guide in any clinical setting. The book is designed to appea l to severa l groups of Ilurscs . EnteroSlOmal therapy (ET) nurses are ofien consulted on wound care and have additional education in wound care. ET nurses may find the book a direct aid 10 their practice and a va luable educational tool for use with other clinicians involvcd in wound care. Home health care nurses and nurses in long-term care settings in conjunction with physical therapists provide direct wound care in the home and long-term care selling with minimal support or education in new technologies for wound care diagnosis or management. Rehabilitation nurses work with spinal cord- injured patients: these
COLLA BORATION Physical therapy and nursing arc the two health care disciplines Illost often involved in providing care for the patient with a wound. We believe onc key to providing optimal wound care management to individuals with chronic wounds is collaborative practice between the health care disciplines of' nursing and physicallhcrapy. It has been our experience that in clinical practice, true coll aboration is not the standard, and in many instances there exists some level of conflict between nursing and physical therapy. Conflicts may arise from misconceptions about the "other" discipline's ability. education level, or experience with wounds, from interpersonal difTerenccs, or from "turf battles" wherein one discipline is fighting with the other for greater control over the wound care segment of health care. Much of the connict may be related to simple misunderstanding about the true nature of collaborative practice. True interdisciplinary collaboration does not require that one disciplinc "give up control" of wound care. nor does it require that clinicians always agree upon management options for patients. An environment that supports a collaborative spirit allows clinicians frolll both disciplines to provide their unique perspectives to best meet the needs for each individual patienl with a wo un d problem . Collaboration is challenging. The challenges to collaboration include the wide variety of clinical settings in which patients with wounds are managed, the variety of education and experience of clinicians, and the struggles of each discipline to clarify and beller define professional roles. Vet when collaboration is implemcnted successfully, the rewards to clinicians. payers. health care agencies, and patients are numerous. Clinicians benefit from the free exchange of ideas from differing perspectives and the excitement of working xxi
xxii
WOl "'IU CARl
paricnts arc a high-risk group for pressure ulcer wounds, and treatment of pressure ulcers is one of the main points in thc book. Physical therapists will find the text valuable as a refercnce for therapy and also as an educational tool for usc with other health care professiona ls. Physical therapists arc bcing asked to do more in the wound care arena, and many fcclthc need for additional education in this dynamic area.
EDUCATI ON OF NU IlSESAND PHYSICAL HI ERAPI STS Nurses nre licensed health care professionals who diagnose and treat human responses to health and illness.· The nursing profession is committed to the care and nurturing of both healthy and ill people, individually or in groups and communities. There arc four essential features ofcontcmporary nursing practice as defined by the American Nurses' Association Social Policy Statement: " ... Attention to the full range of human experiences and responses to health and illness without restriction to a problem-focused orientation. integration of objective data with knowledgc gained from an understanding of the patient or group's subjective cxperience, application of sc icnti ric know ledge to the processes of diagnosis ~lI1d treatment, and provision ofa caring rela tionship that facilitates health and healing."""") The difference between professional and technica l nurses is the depth and breadth of clinical nursing practice based on the knowledge foundation of the nurse, the nurse's role, and the type ofpatient service. 1 urses study biologic, physical. and social sciences in addition to nursing theory and the science of nursing practice. Nurses acquire knowledge in anatomy. physiology, pathophysiology, pharmacology, microbiology, chemistry, and statistics, as well as nursing science. ursing education includes the traditional focus on illness and acute care clinical practice and the more pressing current focus on health promotion and community nursing. Nurses practice at a variety of educational levels. The vocational or practical nurse education programs arc located in technical or vocational schools. The vocational nurse education program is typically I year in length and leads to a certificate of completion and eligibility to take the state licensure examination to be designated as a licensed vocational nurse (LVN) or a licensed practical nurse (LPN). LPNs and LV s are prepared to work with registered nurses (RNs) and to be supervised by RNs. The purpose of the vocational nurse programs is to prepare assistant licensed nurse workers:' These programs generally do not articulate well with collegiate nursing programs, although LP slLVNs may receive advanced placement in collegiate programs. The first formal nursi ng education in thc Unitcd States was in diploma programs. Diploma programs are typically
hospi tal based and were the predominant model for nursing education in this country. Diploma programs are usually 2 to 3 years in length, and many include summer sessions. Graduates of diploma programs arc eligible to take the RN licensure examination. The purposc of the diploma programs is to prepare clinically competent bedside nurses.' Some diploma programs have now aligned with other academic institutions, and many now offer an assoc iate degree in nursing, ADN or AA.j Associate deg ree programs are community or junior college base~ and the nursing portion is 2 years in length. The purpose of the associate degree nursing programs is to prepare compctent technical bedside nurses for secondary care settings:' Many nurses enter associate degree programs with future intentions of continuing theireducation in nursing at the baccalaureate level. s Some 4-year university programs also otTer combination degree programs to allow flexibility. Baccalaureate programs in nursing are 4 years in length, with the nursing curriculum concentrated at the upper division. Graduates of baccalaureate programs are prepared as nurse generalists to practice nursing in beginning leadership positions in a variety of scttings. In 1965, the Amcrican Nurses' Association designated the bacca laureate degree as the en try level for professiona l nursing prac tice. The majority of programs admit both pre lice nsure st udents and RNs who arc graduates of diploma or associatc degree programs. The general education requirements are the same for all students, and those with prior nursing education or experience arc allowed to progress through the nursing curriculum by designs that capitalize on prior learning. Master's degree education in nursing is typically 2 years in length and builds on the baccalaureate nursing major. Program content usually includes a group of core graduate·level courses. research course work, and specialty nursing courses. Mastcr's-prepared nurses function at an advanced practice level and include nurse anesthetists, nurse midwives, nurse practitioners, and clinical nurse specialists. The degree most often awarded on completion of a master's program is the MSN (master of science in nursing) or the MN (master of nurs ing) degree. The purpose of master's education in nursing is to prepare advanced practice nurses in a specialty area such as psychiatric mental health nursing or nursing management. ~ In addition, advanced practice nurses serve as mentors, consultants. and educators of nurses in basic practice. They conduct research to expand the knowledge base of nursing practice, provide leadership for practice changes, and contribute to the advancement of the profession. health care, and society in general. 1 Doctoral programs in nursing range from 3 to 5 years of full-time study. Doctoral programs include advanced content in concept development, theoretical analysis, research, advanced nursing, and supporting cognates. Doctoral pro-
/IIl1vdll Clioll
grams prepare leaders for programs in education. administration, clinical practice. and resea rch . In addition to formal education programs. many nurses are specialty certified. The necd for specia lizeuion in nursing developed as technologic advances in health care occurred over the last 10 yea rs. Specialty programs arc varied in scope, length of timc. and requirements. Most specialty programs prcpare RNs to take a certification examination as a part of credential ing in th e specialty area. Certifi cation requirements va ry, depending on th e specialt y area, and may inc ludc completion of an education or training program, as wcll as c linical ex perience requirements. National certification examinations arc offe red through professional organizations in a variety of specialties. including wound ca re and ET nursin g. In most states, RN s are required to maintain currency in their practice by co mpletin g specified amounts of continuing educa ti on. Physical th erapi sts (PTs) are licensed health ca re professionals who eva luate and treat people with health problems resulting from disease or injury. The American Phys ical Therapy Association (APTA) is the national organization represe nting the phys ical therapy profession, which accredits education program s for PTs and PT assistants (PTAs). Professional education req uired for PTs includes a minimum 4 yea rs of college or universi ty level training resulting in a baccalaureate degree in physica l therapy from an accredited professional education program. The information explosion in the health-related scie nces has led to current requirements that most therapi ts enter th e profession as master's levelprepared clinicians. and now so me are entering with a professional docto ral degree. FolJowing graduation, PTs mu st pass a national licensi ng examination to qualify for state licensure. Like nurses, PTs may be specialty certified in a variety of areas of practice. Although there is no current spec ialt y certification for wound care, instruction in wound management skills is a requirement for accreditation of phys ical therapist and phys ical therapist assistant programs. The requirements for continuing education for relicensure by PTs varies by state. The fact is that 1110st PTs seek co ntinuing education so as to be at the cutting edge of practice. even though it may not be a mandated requirement. Specialty certifi ca tion in wound manage ment is a targeted goal of the Wound Management Special Interest Group within the Section on Clinical Electrophysiology of theA PTA . The speci al interest group was formed to bring together PTs and PTAs from many practice settings who have special interest in wound management. PTAs arc trained and licensed paraprofessionals with 2 years of educational training in an approved PTA program or who have worked as a phys ical therapy aide for a specific period of time and then passed a qualifying examination. The PTA provides se rvices under the supervi sion of a PT.
XX III
The PTA can perform various tests and measures for which the assistant is trained, such as wound meas urements. tisslle attribute recording. and provision of treatment services with physical agents and electrotherapeutic moda lities. In so me states, the PTA may also perform sharp debridemellt. Both PTs and PTAs are qualified to apply topical agents and dressings to wounds. Many individual s are surpri sed that the PT is included in the wound management team . Re ports of wound management, including burn and wound interventions. by PTs appeared in the physical therapy literature for more than three decades. By education and training, PTs learn anatomy. physiology, and pathophysiology related to body sys tems respo nsible for repair and rege neration of soft tisslie. For example. human cadaver dissection is part of the basic anatomy education o f the PT and provides a foundation for the skills needed in sharp debrideme lll of nonviable ti sslle. Courses in cardiopulmonary and vascular system physiology are required. These two system s are critical to wound healing. Neuropathy plays an important part in development of chronic wounds. PTs take courses in neurology and learn neurologic te sting and eflccts of inse nsitivity on the integumentary system. The PT is expected to examine the integument as part of an overall evaluation . Postsurgical wounds are routinely seen and evaluated by the PT as part of the rehabilitation se rvice. For example, dehi sce nce of a wound on an amputated limb requires wound managemcnt before prosthetic training is initiated . PTs a lso are ski lled in the use of physical agcnts (heal, I ight, so und. and water), electrotherapeutic modalities. and therapelltic exercise, a ll of which are used in wound healing strategies. The PT can manage the wound as well as the prostheti c training and an exercise program to achieve the desired outcomes. PTs are interested in evidence-based hea lth care choices. and many research studies by PTs on wound healing that demonstrate treatment efficacy arc cited in this book. Phys ical therapy is the ca re and services provided by or under the direct supervi sio n of a PT.6 Services provided by others using technologies generically referred to as physica l therapy should not be co nfu sed with the se rvices of a PT. Outcomes research studies show that expected outcomes may not be equivalent. 7 PTs arc important players in the provision of primary care. defined as ''' integratcd accessi ble health care services by clinicians who are accollntable for addressing a large majority ofpersonai health care need, developing a sustained partnership with patients and practicing in the contcxt of family and community." f!\P11.1 1 In 30 states, direct access to physical therapy se rvices from a liccnsed PT is part of the practice acts. PTs play major ro les in seco ndary and tertiary care as well. For example, patients with wounds are often seen initia ll y by another health care practitioner and then referred to the PT. PTs provide tertiary care in highly
XXIV
W OUI\O CARE
specia li zed co mplex . and tec hn ological ly adva nced se tti ngs. In such situatio ns, a patient may have a traumati c wound, surgica l wo und, or burn plus compl icat in g medica l problems, and the PT is ca lled upon to manage th e wound as well as the oth er as pec ts of patient rehabilitation.
3.
Ameri can Nurscs' Associ:l1ion. FacH abouf N/lrsing. Kansas City,
MO; 1987. 4.
lIart SE. Path wuys of nursing educ:nion. In: Crcasia JL. Parkcr B. cds. CfJncepwlll Fowu/mio n5 of Profl'.uionll/ Nllrsing Practice. 2nd cd. 51. Louis. MO: Mosby: 1996:26-45 .
5.
Kozicr Il Erb G. I3111is K. PmfessiOlwl NII":"i,,!: PraClice: Co" cep/~ alltl Perspeclil'f!s. 3rd cd, Men lo Park. CA : Add ison-Wesley: 1997 :
2 27. 6.
America n Physical Therapy Association. A guide to physical therapist practice. I : a descri ption of patient managemenl. Phys Tiler.
1995 ;75:707 764. I.
American urscs' A!isoc iation. Nllnil/g A Social Policy SUlfemenr. K an!>a~ Ci ty. MO : 1980.
7.
American Physical Therapy Association . Olilcomes EffeC/il'e"f!H of Physical Therapy : All Allllou/led IlibUegmp"y, Alex.andria, VA: 1994.
2.
Amcrican Nur!>e~' A!>sociation. Nllr.H·ng ...· Social Wash ington. DC: 1995.
8.
Donaldson M, Yordy K. Vanse low N. Defillillg Primary Care: AIII,,lerim Report. Washington. DC : National Academy Press; 1994.
Poli£~l t
SrMemenl.
P A RT
I
Introduction to Wound Diagnosis Carrie Sussman
Dc\clopmcllt of diagnoses to direct and guide treatment by nurses and physical thcrapi!'lls has been growing over the
last 15 to 20 years. Both disciplines recognize that use or a diagnostic proccss applies the skills and knowledge or the proressional nurse and physical therapist to the appropriatc treatment of client situations they can and shou ld treat lega lly and independently. The role or diagnostician is unramiliar to many. and practice experience in the area of diagnosis varies frol11l1oncxistcnt to full-practice integration for many years. Because the incorporation of diagnosis into the health care professions is still in its infancy, there is much \-ariance in l1nder~landing of the process. Therefore. there arc a number of questions that need to be clarified as the process begins : • What docs a diagnosis really mean? • What kinds of information need to be collected to yield a diagnosis'! • lIow are diagnoses differcntiated from each other? • lIow is a diagnosis tailored to the patient's functional problem or human response to health or illness? • How does diagnosis relate to prognosis and outcOines? • J low docs the nursing or physicalthcrapy diagnosis direct interventions? Ad\anced clinicians who arc more familiar with classification systems and diagnostic methods will ha\c othcr typcs of questions: • Can and should the medical diagnosis be part or the physical therapy diagnostic statement? • What kind of functional diagnostic statement should be \Hittcn for a person at risk for wounds? • What is the dilTcrence between diagnosis and classification'!
Part I begins with an introduction to the diagnostic process. It seeks to answer these questions. including specifics about wound diagnosis. Guidelines for writing functional diagnoses that are meaningful and related to the prognosis and treatment interventions arc included for both disciplines. One of the things that became clear to the authors as Chaptcr I was craned is thai the diagnostic process and the terms of the diagnosis of the nurse and physical therapist arc ve ry simi lar. Both incorporate functional impairment and disability into the diagnostic process. For example. the nurse determines the clients response to health or illness as positive functioning. altered functioning. or at risk for altered functioning. 1 Nurses use a diagnosis that incorportnes risk that could \\ork equally well ror the physicaltherapisl. Nursing diagnosis specifically identiries collaborati, e problems and then the health care practitioner needed for joint management. The most appropriate joint manager for wounds may be the dietitian. the physician. or the physical therapist. Nurses already hm e taxomony for impaired tisslle integ,.ity and impaired skin imegrit): Physical therapists use disablement terminology. including the terms impai,.ment. disahility. and halldicap in their management modcl.;! FUllctional diagnosis requires understanding offu llctional impairment. Functional impairment dilTcrs from the pathogenesis or etiology of the problem and describcs a functional change as physiologic. anatomic. structural, or functional at the tissue. organ. or body system levcl. 1 Functional impairments are the system or organ impairments that prevent normal function :' In impaired wound healing there is a functional impairment of wound healing that occurs at a system, organ. or tissue levcl in the body. Chapter 2 is devoted to understanding the system functions related to wound healing biology and chronic wound healing. Assessment, examinations. tests, and measuremcnts are an integral part of cs-
tabli shing a di ag nosis. Chapte rs 3, 4 ,5, and 6 descri be techniqu es to pe rform th e procedu res and how to interpret the find ings. At the conclusion o f Part I. clinicia ns will bc abl e to pcrform th e tes ts and measures necessary to determ ine functi onal wo und di ag nosis. deve lop a prognosis, a nd stale the expected ourcomc. Thcy wi ll bc able to doc ume nt the diagnosti c process and th e findings with a fun cti onal out comes report. The clinicia n will then be rcady to go to Parts II. III , a nd IV to Ica rn th e man age me nt sk ills fo r diffe rent wound related proble ms and interve nti ons.
I{EFEI{ENCES I.
Carpenito LJ. Nllnillg Dillg1l0.\ /\ Applicatioll 10 Omical Pmclict!. 6th cd. Philadelphia : l B. Lippincott: 1994.
2.
Amcrican Physical Therapy i\:,:,ociaiion . A guidc to phY:'lcal thcmpy p racticc. I : a dcscriptioll of p:ltlcnt munagclllcnt. Pil.\'I Tiler.
3.
World Ilclllth Organization . /lIll!rmlliu1IlIl c/{/\\·i/icalill1l of Impai,.· mell1;" f)imbiIiNe.I', und II{/I/dic(lp~ . Geneva, S'A il7crlnnd: 1980.
4.
kttcAM. Physical disablement concepts lor physica lthcrapy rcsc:lrch and pracllee. Pill"> 711t!r 1994:74:380 ·386.
1995:75:707 764.
CHAPTER
1
The Diagnostic Process Carrie SusslIlan, Barbara M. Bales-Jensen. and Melisa TiffcJIIY
didacy or noncandidacy for serv ices; for nurses. the hi story and systems review determine the direction for the treatment plan. Many physica l therapists retai n the belie f that all referrals automaticall y show candidacy for wo und care. The realit y is that not all patients arc appropriately re re rred ror phys ica l therapy. To some physical therapi sts thi s will sound li ke heresy, but proper ut iliza tion management is mandatory in today's hea lth earc environmcnt. Utili zati on managemcnt is part ofthc process ofpros pccti ve managc ment and is designed to ensure that only medi ca lly necessary, reasonable, and appropriatc services arc providcd. Utili zatiol1managcl11cnt attempts to influencc the treatmcnt path way to cnsure optimal clinical outcomes.' For nurscs. the assessment process provides the framework for planning comprehensive wo und care incorporating uti lization manage ment. and may include making a referral for physical therapy. Utili zation management for the patient with the wound and for comorbidit ies and coimpairment are separate but re lat ed. Co ll aborati ve intcrdi sc iplinary manage mcnt o f comorbid iti cs and coi mpairmcJ1t s will redu ce iatroge ni c cffccts from in appropriate selectio n of intcrve nti ons or handling of thc wound, and will Icsscn extrinsic and intrinsic complications. Chapte r 2 cx plains and di scusses comorbiditi es and co impairments as well as the iat rogenic extrinsic and int rin sic fa ctO rs thai a ffcct wound hcaling. The interdiscipl inary nature inherent in cari ng for the patient with a wound requires clinic ians to carefull y determine candidacy for services be fore initiating rcfcrral or treatment. The assessmcnt process assists in clinica l decision makin g by avoiding undirected care and inappropriate treatment. Assessment with attcntion to utili zation managcmcnt allows selcction of a path for rcferral for another intcrvcnti on or to other hea lth care disc iplines and practitioners. For ex-
Thi s chapter descri bes th e di ag nosti c process for mana gement o f pati ents wit h chronic wounds. N urses and phys ica l therapi sts usc essenti ally th e sam e decision-makin g process in diagnosing pati ent probl ems, although the term s used to
describe the process may differ slightly. Nurses lise the nursing process and nursing diagnosis as the framework for planning and eva luating palient carc. The nursing process includes the following steps: assess ment. diag nosis, goals. interventions. and evaluation. Physical therapy uses a process that inc ludes the steps o f assess ment. cx aminari on. di agnosis.
prognosis, and Olltcomes, To simplify and guide the reader, the diag nost ic process has been broken into four steps, each with two or th ree parts. Step I, assessment. includes review of the reason for re ferral, history, systems rev iew/physical assessment, and wound assess ment. Step II. diagnosis. includes examination strategy, evaluation, and diag nosis. Step III , goals, includes prognosis, goa ls, and outcomes. Step IV, intervent ion. is described in subsequent chapters. Examinations and specific measurements plus special test procedures are found in Chapters 6 and 8. as wcll as in others. STEP I:ASSESSMENT PROCESS The assessment process is the first stcp in wo und care manage mcnt. Assessment is done ror all patients berore determ ining the need fo r special testing examinations and interven tions. For nurses. th is process begins when the patient is admitted to the age ncy. For phys ica l therapi sts. thi s process begins wi th the reason for referral. which is part of the patient hi story. The assessment process involves gathering data from the patie nt history and physica l exam ination. The pati ent hi story determines which relevant systems reviews are needed in the physica l examination. For physical therapists. the history and systems review determine the can-
3
4
WOUND CARr
amp le, the physical th erapist may determine that the patient is not a candidate for whirlpool therapy as ordered by the physician, and sends the findings with an alternative recol11-
mendation to the referring physician . An addi tional example is provided when the history and phys ica l examination of th e wound suggest to th e nurse th at vascular examination
and testing procedures arc needed. The usc of standardi zed fo rm s is the best method of collect ing assessment data quickly and efficiently. thus ensur-
ing that important information is not losl. Use ora form that the c linicia n completes and a form that the patient comp letes e ns ures da ta maintenance from the interview. A sc lf-adm inisrcred patient hislOry form helps the clinician to focu s the interview and can save time. Samples of an assessmen t form for a se lf-administered hi story and an illlcrview form for physical thcnlpi sts and nurses are prcse nted in Appendixes I- A and I B. The forms inc lude reason for admission/ referral, past medical history. physical examina tion findings. and a place to list suggestcd examinations to follow based on the int ake information. Forms may be completed by both the cli ni cian and the patient or significant other. Some informalio n w ill be fo un d in the patient's medical record but many times the paticnt or s ignificant ot her can prov ide additional ins ights ~1I1d informHtionnot o th erw ise avai lab le. Partncring or e ngagi ng th e patient in hi s or her own care from the beginning is esscntial to achieving mutually sati sfactory outcomes.
Itc\'icw ofAdmission/ Rcfcrrul It is essen tial for a physical therapist to know the reason why a patient is referred. This referral is the first step in documen ting patient hi story. The initial referral for wound ca re management is us ually to the nurse; if the nurse determines a need for physical therapy services, the physica l therapist is brought into th e team . It is cri tical for nurses to know ex pec tati ons and projected outcomes from a physical therapy referral in order to refer appropriate ly. In so me health care settings, a wound care team decides the serv ices nece ssa ry for wound management and makes the appropriate referral s. T he patient referred to th e physica l therapist for wo un d healing is usua ll y an individual who has not shown signs of normal wo und repair. Most often other treatment interventions arc in use or have been tried with limited or no success. Phys ica l therapy services usually involve an additional fee. The referra l to physica l therapy is regarded as an attempt to ma xim ize and en hance wound repair. However, expectati o ns of rcfe rra lm
ca l capacity necessary for healing because of multiple comorbidities that impair wound healing, such as chronic pulmonary di sease or end-stage cancer. For the patient who presents with factors th at impair wound healing. the rea so n for referral is to achieve a clean. stable wound thai can be managed easi Iy by the nurse or caregive r at homc. Pain management may be the underlying reaso n for referra l, with physical agen ts and electrotherapeutic modalities prescribed to help contro l pain . Thus, for both the nurse and the physical therapist, wound c losure may not be th e highest priority. Both nurses and physical therapists mu st understand the rca so n for the rcfc rral and the expected ou tco mes. There !lllist be a match between se lected intervention and cxpec ted outcomes to meet the referral objecti ves. For examp le. Ih e palient with a foot ulcer secondmy to pressure and insensitivity is fearful of ampu tation and loss of ability to walk. The patient's main concern is limb salvage. and expectations are high. In con trast, the fami ly of a debilitated nurs ing home patient may on ly desire comfort for the ir family member with no expectations of wound closurc. Fami ly and caregiver perceptions of va ri ous intervention s may differ from the c li nician's view. What is perceived by one to be heroic and painful mea sures may in truth bc normal procedures. The nurse mu st add ress these issues before a referral to phys ical thcrapy is madc.
Patient History Patient history informa tion is co mmonly collected by an in terv iew process w ith the patient, fami ly. signifi can t o th ers. and carcgivers; by consu lt ati on with other health care practitioners; and by rev iewing the medical reco rd . Idea ll y, in the continuum of care, the information about the patient hi story will be transmi tt ed with th e patient. Unfortunately, this is not always the case. The c lin ician may have to piece together the h istory from the many so urces listed above. If a limited amount of medical and soc ia l information is available. the clinician may havc to choose diagnosti c options based on available data. It is easie r to plan appropriate care with a co mplete hi story.
Clinical Wisdom: Patient History Needed To Determine Care Direction
• Reason for admission or referral • Expectations and perceptions about wound healing • Psychosocial-cultural-economic history • Present medical comorbidities • Current wound status
The Dillgnm;tic PlVce.\'s
Remember that one of the primary goa ls during the patient interview is to begin to develop a th erape uti c relationship wi th th e patient and family. The hi story taking allows the clinician to assess and diagnose patient problems and place the problcm wit hin the contex t of the individual patient 's life. The sk ills used by cli ni cians during the patient hi sto ry are th ose of Iistenin g, observing. a nd asking questions. Severa l types of questions are useful to the clinician condu cti ng the patient hi story. C losed-ended questions require a brief response, usually yes or no. and a re useful when speci fi c informat ion is req uired such as age. ma rital status. o r presence ofa specific healt h risk such as smo kin g. Open-ended questions aimlo el icit more information in patient respo nses. An example of an open-ended question is "Can YO ll tell me about your wound?" Questions can be directive, to lead th e patient to focus on a s pecific area, and arc most useful during the systems review portion of the hi story. An exampl e of a directive question is " Have you ex perie nced any problems with veno us disease in the pasl, such as lower leg edema or swell ing, previous ulcers. o r skin color chan ges on the lowe r Icg?"The last type of question is the permission-giving question. Permi ssio n-giving questions arc especia ll y Llseful when dealing with difficult topi cs. An exa mpl e of a permissiongivi ng question is "Ma ny patients I see have questions or concerns abou t sex ual ac ti vi ty wi th a wound. What are you r questions?" The clinician also uses act ive listenin g and obse rvati on skills during the interview. For exa mpl e. when questioning a patient about alco hol or tobacco lise the clinician also observes for sig ns of alcoho l o r tobacco usc suc h as an odor of alcohol or smoking. Chie/Complaint ali(I !-Iealth !-I;"'ilOry
Begin the patient history by finding out th e patient's c hief cOlnplaint or major reason for seek ing care and the duration of the problem. Find out why th e patient is seeki ng he lp at Ihi s tim e. It may be simp le convenience or it may be Ih at the wound problem was wo rsenin g and the patient felt Ihat treatment was needcd at this time. Investigate ot her agendas the patient may have other than the obv iolls problcm by asking a question s uch as ·'How did yo u hope I coul d he lp yo u todayT' Exp lo re the mcaning of the wound with the paticnt. Questions sll ch as "What do you think ca used your wound?" and "Why do yo u think it started when it did?"' and " What do you think your wound does to you and how long do you think the wound wi ll last?" help reveal the patient's level of unde rslanding of the hea lth problem. Based on answers obtained ca re can be planned that is se nsi ti ve to Ihe patient's needs and level of understanding. The clinician seeks a complete understanding of th e patient'S symptoms (symptoms are the subjective feelings of th e patient) during th e interview. Seven cri teria can be lIsed to describe symptoms: location. c hara cter, scve rit y, timing. sett ing in which the symp-
5
tom occ urs, antecedents and co nseq uences of the symptom, and other associated symp toms.
Clinical Wi sdom: Questions To Ask To Elicit Extent of Wound Symptoms Location:
Character: Severity:
Timing:
Setting:
Anteceden ts and consequences: Other associated symptoms:
Where do you feel the wound? Do you feel it anywhere else? Show me where it hurts. What does it feel like? On a scale of to 10, with 10 being the worst pain you co uld imagine, how would you rate the discomfort you have now? How does the wound interfere with your usual acti vities? How bad is it? When did you first notice the wound? How often have you had wounds? Does the wound occur in a certain place or under certain circumstances? Is it associated with any specific activity? What makes it better? What makes it worse? Have you noticed any other changes?
°
During Ihe patient inte rvi ew, answers to these questions should provide a thoro ugh understanding of the paticnts wound symptoms. Review the patient'S present health and present illness status. This provides info rmati on relevant to the patient's reasons for seek in g care. Describe th e pati en ts usual hea lth and then foclls o n the present problem, investigatin g the chi ef complain t thoroughly as described above. For interpretation and a na lysis of the patient's proble m, it is helpful to document the ch ief complai nt data in chrono logie orde r. Next, review th e patient's past health hi story. The purpose of the past health history is to identify major past hca lth proble ms that may have some effect on the patient's current problem. Information abou tm anagcme nt of and rcsponse to past problems provides an indication of the patient's potential response to curre nt trcatmcnt of th e problcm. Much of this information may be available in the patient'S medical record. Ifnot available, the following infonnation shou ld be obtained : past ge neral health, childhood illnesses. accidents or injuri es with any associated disabilities. hospita lizations. s urge ries, maj o r acute or chro ni c illnesses, immuni zat ions, medica tions and transfusions, and allerg ies. Curren t healt h info rmati on inc ludes al lergies. hab its, medications. and sleep and
6
WOUND CARl
exercise patterns, all of which provide information on the patient's health habits. Investigate environmental, food drug. animal, or other al lergies. Specific allergies may have a bear-
sig ns of the disease as yet undiagnosed and is at hi gher risk of eventual disease development.
ing on interventions chosen for lhe patient 's wound care regi-
Sociologic lIistory
men. Allergic reactions usually affect the gastrointestinal tract, the respiratory tract, and the sk in. Allergic reactions invo lve the release of histamine from the !nast cells. The cli-
nician should be aware of signs and symptoms of an allergic reac lion. which is a type of inflammatory response. The allergic inflammatory respon se can be erroneously interpreted
as celluliti s or infection. It can also cause a contact dermatitis or pruritus and scratching with res ultant excoriation of th e sk in. The excoriarion lesio ns can become infected and may be the pathogenesis of the wound. Some products used for wound carc can contributc 10 an allergic reaction . One is latex that is found in dressings. g loves. and plastic tubing. Tape is ano th er notorious culprit often associated with skin al lergies. The cli nicia n should be aware of warning signs and ta ke necessary measures 10 control the offending allergen . Sulfonamide is a coml11on drug alle rgen. and Silvadene is a common topical therapy for wound care Ihal contains sulfonamide. so the clinician would need to choose another topica l agent to accomplish the goa ls for that patient. Eval uate current and past habits relevant to th e health of the palienl inc lud ing alcohol. tobacco. substance. drug. and caffeine use. A !coho!. tobacco. and substance use in particular prese nt significant problems with tissue perfusion and nutrition for wound healing. Complete a full medication profile, including both prescription and over-the-counter medicati ons. names. dosages. frequency. intended effect. and compliance with the regimen . Many medications interfere with wound hea ling or may interact with wound therapy. Evaluate the patient's uSLIal routine for patterns ofphysical and sedentary activities. Ask the patient to describe a usual day's activities. Exercise patterns influence healing in severa l wound types, such as ve nous di sease ulcers. Finally, describe the patient's s lecp pattern and whether the patient perceives the s leep to be adequate and sat isfactory. Ask the patient where he or she usually sleeps. Patients with severe arterial insufficiency may sleep sitting up in recliner chairs because of th e pain associa ted with the disease. Likewise, patients wit h chronic obstructive pulmonary disease may s lee p s ilt ing up because of difficulty breath ing in the supine position. The ramily heallh history provides inrormalion abollt Ihc gcnera l health of the patient's relatives and family. Family health informatio n is helpful in identification of genetic. familial , or environmenta l illnesses. Specific areas to target are diabetes mellitlls, heart di sease. and stroke. Each of these diseases can impair wound healing in an existing wound and arc ri sk factors for further wounding. If the patient has a ramil y hislory or th ese diseases. he or she may have early
Diagnosis and management of the patient's wou nd problem is best accomp lished within the context of the whole persoll . It is important to gather information abo ut the patient's sociologic. psyc hologic. and nutritional status. Many patients are unaccustomed to questions about nonphysical matters. and it may be necessary to explain the purpose of gathering th is information to the patient. For example, the clinician can simply Slate, ''To be effect ive in cari ng for yo ur wound, it is important for me to know something about you as a person." Sociologic data fall into seven areas: relationships with fami ly and significant others, environment. occupational history. economic status and resources, educational level. daily li re. and pallerns orheallh care. Relationships with family and significant others includes gathering information on the patient 'S position and ro le in the fami ly, the perso ns li ving with the patient. the persons to whom the patient relates. and any recent fami ly changes or cris is. The role of the patient within the fami ly may dictate treatment decisions. For examp le, the g randmot her wit h venous di sease ulcers may also be thc primc caregiver of young grandchild ren. thus it is unrealistic to expect compli· ance with a therapeutic regimen that includes frequent peri· ods of elevating lower ex tremities. The famil y support system may be a critical component whe n determining wound care management programs and answe rs to questioPls such as "Who will change the wound dressi ng and perform procedures?" "Who prepares meals?" and ';Who will transport the patient to the clinic?" may influence treatment options. Personal relationship information gathering can extend to discussion of how the wound affects the patient's sex uality. Sexua lly active patients arc going to need treatment considerat ions that will not interfere wi th th eir sexual functio ns. Forexample, a paraplegic patient with a sacral ulcer is going to need press ure relief and a dress ing that will not impede sexual activity, cause trauma to the wound or leak. The environment plays a significant ro le in hea lth and illness of individuals. Ask questions abou t the home, comm unity, and work environments. Home care patients present chal lenging environments for wound repair. For example, the elderly woman li ving alone with four cats in a two-room trailer with minimal bathroom faci liti es wi ll require different management strategies than the middle-aged man living wit h a spo use and family in a three-bedroom house in the suburbs. The community environment may provide additional resources for the patient. such as senior citizens' cente rs, health fairs, or the neighborhood grocery store that delivers to the home. The work environment along wi th the occupa-
The Diagnostic
tio nal hi story provides info rmat io n o n th e abil ity of th e patien t to e li mi nate ce rt a in ri sk fac to rs fo r impai red healing. For exa mp le, the groce ry clerk w ith a ve no us disease ulcer will need he lp wi th work adj ustm ent o f a job when standing for long peri ods of tim e is req uired. Occ upati o na l hi sto ry ca n pi npo int hea lth-ri sk jobs stich as th ose that require prolo nged sta ndi ng. Eco nomi c stat us and reso urces are impo rtant to determine adeq uacy for thera py co mplia nce. It is not necessa ry to know the palient's exact inco me; instead, as k whether the pati ent feels the inco me is adequ ate and e li c it the source o f the income. It is impo rt ant to ide nti fy pa tie nt s w ith inadequ ate reso urces and make ap propria te re fer ra ls fo r f inanc ia l ass ista nce. Be s ure to inc lude an assessment o f the pat ient'S health insurance reso urces. If th e ex pectat io n is prolo nged wound hea ling, a disc ussio n of f inanc ia l reserves may be des ira ble. The economic histo ry needs to include no t o nly the pa tient 's payer so urce for ins ura nce cove rage, but also th e reso urces the pat ient has avai lable to obta in necessary d ress in g supplies. Some patie nts have insurance coverage that pays fo r all d ressi ng supp li es, ot her pati ent s have insurance coverage that pays for o nly ce rt ain types o f suppli es (ga uze, bu t no t tape), and yet o th er pati ent s have no coveragc fo r supplies at a ll. The econo mic hi story is a lso needed to determ ine whether th e pat ient has adequ ate reso urces ava ilable to pay fo r a ca regiver. if o ne is needed to co me in to help w ith caregivin g or changing d ress ings. The ed uca tional leve l of th e pat ient and judgme nt of ageappropriateness of intell ect is he lpful in pla nnin g future educati o n o n self-care o f th e wo und . Ask the pat ient to desc ribe a typ ica l day and to identify any d ifTere nces o n the wee kend. The da ily profile a ll ows th e cli ni cia n to perceive the who le patie nt. Q ues tions abo ut th e socia l and recrea tio na l activ ities of the pa tie nt as we ll as ty pical da il y ro utines provide va luab le insights into th e patient 's li fes tyle and poss ible hea lth ri sks. Eval uati o n of prev io us hea lth care access and use assists wit h c li nica l judg mcl1l o f past hca lth pro moti o n and prevent ion act ivit ies and wheth er th e pati e nt 's care has had continu ity. P~ycllOlogic
HisrOlT
The psyc ho logic histo ry inc ludes a n assessme nt of the patient's cogniti ve abi lilies ( including lea rn ing style, memo ry, com prehensio n), respo nses to illness (coping patte rns, reactio n to illness), res po nse to care (co mpli ance), and cultura l implica ti o ns fo r care. Us ua lly at th is poi nt th e clinicia n has some idea of th e patient'S co mprehensio n, memo ry, and ove rall cogni ti ve stat us. If menta l fun cti o n is still unc lea r, the clini c ian Illay wan t to admin iste r a menta l status examina tio n such as the mini- men ta l status exa m. Prev ious coping patterns and react io ns to illness provide insight to possi ble
P1Vces~
7
reactio ns to the currcnt si tuat io n. I-las th e patie nt had diffi culti es w ith wound healing in the past? Is there a histo ry o f chro ni c wo und s? How has the pat ie nt respo nded to prev io us chro ni c wo unds? A ll are import ant q uesti o ns to ask the patie nt. Respo nse to prev io us ca re and co mpl iance w ith o ther th erapy reg imens may indica te pote nti a l adhe re nce diffi c ulties w ith the current treatm ent pla n. Cullllrctillisfory
People co me fro m di ffe re nt wa lks of li fe, a nd often have beli e f systems sig nifica ntly dinerent fro m those o f the c lini cia n. It is th ere fore ve ry impo rta nt to take nothing for g ranted and to assess the pat ie nt's a nd ca reg ivers va lues and be lie fs abou t hea lth and we llness. Fo r example, Hinduism espo uses the be lief that if something was w rong in a past li fe, the n ka rm a is bad and th e pat ie nt dese rves th e wo und. Asia n cul tu res may be li eve that th e body sho uld go bac k to whe re it ca me from whole, and th e wo und cau ses the body to be not whole. Hispani cs ofte n be lieve th at if pat ient s are un able to make the ir own dec isio ns regarding the ir care, the n the e ldest so n sho ul d direct the care, even if a middl e da ug ht er has been pe rforming direct hands-o n ca re for 6 mo nth s. Patie nts fro m Swede n o ft en be li eve tha t if a problem is ig no red it does n't ex ist. and thu s they may de lay seeking app ropriate care. These examples arc not prov ided so th at the c linic ia n ca n j ump to concl usions abo ut a pati e nt o r family be li e f systern , but ra th er as a re mi nde r th at we all have different va lues and beliefs about healt h ca re, hea lin g. and we ll ness. As c lin ic ia ns. we need to be parti c ul arly sensi ti ve in o ur assessment of th e pa ticnI 's culture and va lues.
NUfI'itiollalllistOlY Nut rition plays a majo r ro le in wo und hea ling. During th e patie nt interview, dete rm ine th e pa ti ent 's us ua l da il y food inta ke, ris k fo r ma lnut rit ion. a nd speci fi c nutriti ona l deficiencies, Eva lu ate th e pat ie nt 's weig ht in compa ri so n to th e usual weig ht of th e pa ti enl.A sk th e pati e nt to recall a ll foods eaten in th e past 24 ho urs a nd de termine whether th is is a norma l patte rn fo r the patie nt. Eva lu ate inta kc of fruits, vegetables, meat s, da iry prod ucts, and breads and cereals. Look fo r hi gh-ri sk food behav iors such as hi g h int ake of red mea t; low amo unt s o f fi be r, fru its, and vegetables; o r hi g h intake of ca lo ries.
Mel/iciltioll Hi.'itory An acc urate and complete medica ti o n hi story is an impo rt ant cleme nt of a co mple te pat ient hi story. Medi ca tio ns ca n have a signifi ca nt impact o n wound prog ress. Dctermine a ll prescri pti on a nd ove r-the-co unt cr medi ca tio ns in usc by th e pati ent. Clari fy th e dose, frequen cy, and reaso n fo r the medi ca ti on. Is the patie nt compliant with the medi cati on regi-
8
W OUND
CARl
men? Why o r why no t? What over-the-counter medi cati ons
does the patient take and for what reasons? Is there ev idence o f po lypharmacy, overmedi ca ti o n, drug-drug interactions, o r drug-co ndi tio n intcracti o ns?Th c phys ical th erapist wi ll need
to work with the nurse to belief understand the medicati on reg imen and the e ffects of drugs in usc o n potenti a l wo und hea ling. T hi s is a wo nde rful o ppo rtunit y for coll abo rati o n. Syste ms Rev iew a nd Phys ical Assess me nt
The systems review portion of the patient hi story and the physical assess ment o f each system prov ide info rm ati o n on cO lll o rbidil ics th a I may impa ir wo und hea lin g. Th e
individual's capac ity to heal may be lim ited by specific di sease effects on tissue integrit y and perfusion. patient mobility, compl iance, nut rition, and ri sk for wo und infection. Throughout the patient history, systems review, and physical assess ment the clinician considers host factors that affect wo und healing. The physical assessment of relevant systems otTers the clinician insight into fac tors that determine patient candidacy, se lection of appropriate tests, and ultimately wound prognosis. Ge nerall y, physica l therapists rcview the medica l record and query the patient durin g the systems review. Nurses usually gather the pertinent history from the patient and perform a physica l assess ment of each system. The pertinent factors for each body system arc presentcd below, along wi th guidelines fo r history takin g, followed by a brie f discussion of physical assessment parameters to look for in each system. Respirll llJry System
The respiratory system is critica l for de li very of oxygen and nutri ents to the ti ssues to promote wo und healing and control infection. Pulmonary disease may be progressive in conditions such as cystic fib ros is, chronic obstructi ve pu lmonary disease (CO PD). and lung cancer. No np rogressive di sease states to consider arc pneumonia, postcardiac or postthoracic surge ry. and tra umatic injury. Specific res piratory diseases affect wound healing. Considerations related to major pulmonary pathology are presented. Ch r(}nic Obstr rt ctil'e Pulm olla ry Disellse. Patients with
ca po have probl ems of pulmonary secretion retenti on, which fill s alveolar sacks and reduces the surface area for transference of oxygcn th rough the alveolar membrane into the blood stream. Assessment includes eva luation of pu lse oxi metry, pulmonary fun ction tests, and mode and amount of oxygen delivery. Transcutaneous oxygen transport measurement s are also helpful (see Chapter 6). If noninvasive vascular test results arc not availabl e. they should be considered as part of the examination strategy for patients with ca po. It is critical for clinicians to kn ow the status of avail -
able oxygen for wound healing and infection cont ro l. Oxyge n deli very is even more compromised fo r COPD patients on bed rest. Oxygen deli very is severely reduced when the body is in rhe hori zontal position. In the supine position the diaphragm has reduced excurs ion space that decreases the thoracic ex pansion and tidal volume of air into the lungs. Elevating the head of the bed and placi ng the patient in semiFowler's position may improve ai r fl ow into the lungs. However, skin over the sacrococcygeal area wi ll be at risk for pressure ulcer formation because of shearin g and friction forces present in the typical semi- Fowler's positi on. Decreased mobility is often an add itional complication of CO PO because of poor endurance. dcconditioning, and di tTiculty of breathing during activity. Decreased mobility is an indicator for positioning and risk reduction examinations. Pll eulIloll ill. The patient with pneumonia should be assessed for etiologic factors and pulmonary status. The patient most at ri sk for pneumonia is the elderl y, frail. insti tutionalized patient with multi ple health deficits. Check chesl radiograph rcports to determ ine onset date and location of the infiltrate. Patients with swa llowing di sorders and those with nasogastric tu be feedings are at high risk for aspiration pneumonia. and radiographic studies may demonstrate as piration into the lungs. The patient may ha ve a hi story of recurrclll pneumonia. P;:uiellls wi th pneumonia have elevated temperatures. chest congestion. and decreased lung sounds. and appear acu tely ill. The stress of the illness and the related signs and symptoms lead to impaired wound hea ling. Wounds will ge nera lly plateau. fail to continue heali ng, or deteriorate until the pneumonia is reso lved. Wound repair may not be an option for thi s patient un til the underlyi ng di sease is under cont ro l. Maintaining current wound staws and preparing the wo und for hea ling may be goals for th is time frame. Prevention of wound trauma and furth er skin breakdown wo uld be ex pected outcomcs fro m thcrapeutic positioning. Asthma. Asthma is a collection of res piratory symptoms caused by infections, hypersensit ivity to irritants (poll utants. allergens) psychologic stress. cold air, exercise. or drug usc. Asthma may be symptom-cont ro lled with medications incl uding steroids sllch as predni sone. Inqu ire about the timc of onset of the asthma and the start of steriod therapy. Some individuals have a long hi story of steroid use and th is wi ll affect ability to heal. Steroids repress the inflammatory response, and without inflammation wound healing will not progress. The e tTects of steroids can be mitigated by usc of oral or topical vitamin A. The physician should bc contacted with recommendations for vitamin A adm inistra tion as soon as possibl e. Re."ipi rfltory System Physiclll Asse.\·smellf. As previously di scussed, the p3l ielll hi story determines the physical assess-
The Diagl1osfh.: Pmcess
ment needed. A respi ratory physical examination includes a thorough assessment using observation. pa lpation, percussion. and auscultation. The findings will help determine etiology and plan of care. The clinician needs to pay particular atten tion to overall clinical statu s. Is the patient having labored respirations at rest. talking. or ambul ating short distances? This indicates potential for decreased oxyge nati on to the wound bed. C lin icians shou ld evaluate laboratory val ues such as arteria l blood gascs (ABGs). The clini cian palpates for crepitus. uses percllssion for areas of dullness, and auscultates for adventit ious breath so unds such as crackles or ra les. rhonchi. or wheezes. Document abnorma l findings and monitor for adeq uate breath sou nd s.
CardiOilascu/ar System Patients wi th cardiac disease have poor pump function. There may be dysfunction of the coronary arteries, the valves, or the cardiac e lec trica l conducti on system. In gene ral. any dysfunction of the cardiac system poses significant difficulties related to wound healing. The heart is responsib le for pumping oxygenated blood throug h the circu latory system to all body tissues. Thus, if the heart is not fu nctio na l. all body tissues suITer. Specific pathology with concerns for wound patients include coronary artery disease and congestive heart failure.
Clinical Wis dom: Pacemaker Caution for Physical Therapists Some patients have pacemaker implants to support
or replace the dysfunction of the cardiac system. This is important information for physical therapists when
9
of both right- and left-sided failure re late to fluid overload. Diuretic therapy is common ly prescribed to assis t in fluid balance, decrease the burden on the heart. and thus improve heart pumping action. Is diuretic therapy sllccessfu l? Information on severity of heart failure and effectiveness of therapeutic management gu ides th e clinician's exa minat ion strategy. For example, in evaluation of the patient with C HF and concomitant lower leg ulcers and lower extremity edema, it is esse nti a l to differentiate the edema assoc iated wit h C HF from edema assoc iated with venous disease. Treatme nt for the edema in the patient wi th both C I-I F and venous disease may differ from treatment for the patient with edema re lated to venous disease only.
CardiOllas{:ular System Phy.\·ical Asse,\'smellt. Ca rdiac system physical assessment includes palpation of pulses and auscu ltation of the heart. Physical assessment inc ludes eva luation for dependent edema (i n lower ex tre miti es if ambulatory or in a c hair. and in sac ral area if patient is supi ne), pi tting edema of the lower extremi ties, weight gain from fluid retenti on. muscle weakness, and fatigue. The effects of edell1a o n wou nd healing include s lowed o r impaired wo und . hea li ng response. Interven ti ons must incorporate management of blood fl ow wit hin the body's capacity to hand le fluid movement. For instance, a patient with C I-I F and a necrotic hee l u lce r is re ferred to physica l th crapy for whirlpoo l therapy. The c linician should know that placing a leg in a dependent position in a warm whirlpool wi ll aggravate an already overloaded vascu lar and interstitial fluid sys tem, and a lternative therapy shou ld be recommend ed. The patient wi th C I-IF and a wound will need sign ifi ca nt help to progress, and the outcome may be limited to a c lean stable wound.
selecting a treatment intervention with electrothera-
peutic agents.
Corollflry A rtery Disease. In co ronary artery disease, blood vesse ls may become clogged, producing signs and symptoms of angina pectoris or myocardial infarction. In either case, the effect is to shunt blood flow away from the periphery of the body. This impedes circulation to the tissues. Impaired blood flow reduces oxygen and nutri ents. A questioning guideline is to determine whether the pa tient is a candidate for cardiac bypass surgery or va lvu lar surgery. If surgery is indicated, it should precede aggressive intervention by the clinician. The wound should be managed conse rvative ly during the presurgical phase.
Congestive Heart Failure. Congestive heart failure (C HF) is the heart's inabi lit y to pump enough blood for body functioning. In CHF th e right or left side of the heart can fa il. Either case generally involves the other side, and symptoms
Ga.\·troilltesti"al System The anatomy of the gastrointestinal (GI) tract inc ludes the esop hagus. stomach, sma ll intestine. and large intes tine. The G I syste m is responsible for digestion a nd absorp ti on of nutrients and nuids. Specific disorders of concern for patients with wo und s include GI bleeding or problems with digestion and absorption of nutri ents. Gastrointestina l bleeding weakens the patient and decreases blood supply. Any disease causing G I malfunctioning leads to poor absorpti on of nutrients and nuids for the patient. Patients with gastrostomy tubes receive enteral nutrition directly into th e stomach, bypassing the mouth. Tube feedings may be accompanied by loose stools. which can irritate skin and seep into wounds in the pe lvic area, resulting in wound contamination. A dietary co nsult ati on may be helpful in the optimal manageme nt of patients with G I tube feedings or malnu trit io n rela ted to G I patho logy.
Clinical Wisdom: Diarrhea with GI Tube Feedings Diarrhea associated with tube feedings requires investigation. Sometimes slowing the rate of the feeding infusion, diluting the formula. or using a formula containing fiber may help decrease or eliminate the
diarrhea. Wound therapy choices for patients with diarrhea from tube feedings include attention to dressings that protect the wound area from fecal contamination.
wound prognosis and wound recurrence as well as the aggressiveness of treatment interventions. Ilydration status can be determined by interpreting intake and output sheets. Intake and output sheets are onen kept in the patient's room and may be completed by nurses or nursing assistants. depending on the hec:tlth care selling. Signs of dehydration include thirst, tongue dryness in non mouth breathers. and decreased skin turgor.
Clinical Wisdom: Skin Turgor Assessment GlISl ro illlestillll1 System Phy.',; ital Asse,,,·sm elll. Physical
assessmenl oflhe GI syslem uses skills of palpation, percussion. and auscultution. Palpate the abdomen with attention to areas causing pain or tenderness and any masses or lumps palpaled. I'ercuss Ihe abdominal fields and. finally. auscullate for bowel sounds and arterial bruils. Check Ihe medical record for the pattern of stool evacuation and interpret the stool data for diarrhea or constipation patterns.
Nutritio/l 1IIllll-ly dratioll. Nutritional screening is an imporlant component of assessment because of the relationship among malnutrition, pressure ulcer development. and impa ired wound healing. Nutritiona l data may be found in the mcdica l rccord as a single assessment or as pieces of information that need to be brought together by thc clinician.A sample nutritional assessment guide and diagram can be found in Chapler 2. I f no slandardized nutrilion assessment form exi!>ts within the agency or selling. the following should be evaluated by the clinician: current weight. prior weight, weight change. and percentage change in weight. height, and body mass index. Body weight is a commonly used indicalor of nutrition. An involuntary increase or decrease in wcight of5°0 is prcdictive ofa drop in scrum albumin .~ Serum albumin is a measure of protein available for heal ing: a 110rmal levcl is greater than 3.5 mgldL. Other laboratory tests to evaluate include prealbumin levels and total Iymphocyle counl. Malnutrition may be a consequence of sevcral factors, including chronic disease. cognitive impairment , or social isolation. EHch requires a separate assessment. Some individuals arc unable or unwilling to take nutrition by mouth and refusc other mcan s of obtaining nutrition such as tube feedings . Somc individuals have difficulty obtaining healthful food or preparing meals, or are socially isolated for meals wi th resultant poor intake. Likewi se, the cogniti\cly impaired individual may bc unable to prepare meals or si mply forget 10 eal available food . It is essenlial Ihal palienls and family caregivers receive education on nutritional needs and the effects of malnutrition on wound healing. The patient and caregiver response to nutrition information has an impact on
Assess skin turgor by evaluating for tenting of the skin. Gently pinch the skin and release; observe tissues for the speed of return to normal contours. It is best to check for tenting of the skin on the patient's forehead or sternal (chest) areas.
Dehydralion afTecls wound healing by reducing Ihe blood volume available to transport oxygen and nutrients to healing lissues. The slale of hydralion afTecls weighl and albumin levels. Jugular vein distention may indicate overhydratioll, The thirst reflex is diminished in older adults. placing them at higher risk of dehydration . Nutrition and hydration intake history that indicates inadequate dietary or nuid inlake should trigger assessmenl of Ihe physical and psychosocial barriers to good nutrition . Ask questions such as: Is Ihe gUI funclioning properly'! Can Ihe palient swallow? Is the patient depressed? Is the patient at an end-stage of life? Unlillhese mailers arc addressed Ihe palienl may nol respond positively to aggressive wound healing interventions. and palliative or preventive therapy may be most appropriate.
Case Study: Malnutrition and Wound Management in End-Stage fllness A malnourished patient with a pressure ulcer on the coccyx is in the end-stage of life. The patient and family refuse tube feedings and understand the consequences of the minimally nourished and dehydrated condition. In this case, palliative and prevention treatment is indicated. The wound can be kept clean and dressed to control drainage and odor. Yet the patient is also a candidate for a pressure-relief mattress replacement or specialty bed for prevention of additional skin breakdown. A turning schedule and training of the caregivers is also part of the prevention intervention strategy.
The Diagnostic Process
Case Study: Cognitively Impaired Patient with Leg Ulcers A patient who was cognitively impaired with a history of venous disease and recurrent ulceration of her legs can demonstrate how the change in nutritional status affected her recurrent ulcers. Emma was an
elderly nursing home patient with a diagnosis of Alzheimer's disease and was confined for her safety to a secure medical unit. She was labeled " Mrs . Houdini" because she could undo any restraint, in-
cluding climbing the bedraHs. Emma walked all day long with negative consequences on her venous disease. Compression stockings were out of the ques-
tion. She would not tolerate putting them on or wearing them. Emma was hyperactive and a very poer eater. The director of nurses decided to investigate her
nutritional status. She reviewed Emma's weight status and found progressive loss of weight over the previous 3 to 4 months. Consultation with the physician led to further evaluation and revealed a low albumin level of 2.5 mg/dL. Evaluation by the speech pathologist demonstrated delayed swallowing response and resulted in a recommendation for a videofluoroscopic examination. The nutritional assessment with the resultant rec-
ommendation for gastrostomy tube placement was shared with the family. Emma tolerated the procedure well. A benefit of the gastrostomy tube placement for Emma was that it could be covered by her clothing and was out of sight and therefore out of mind for this individual, so she left it alone. In a couple of weeks the added nutrition to her diet made her much less irritable and hyperactive. Emma
could be placed in a gerichair with a restraint tray and her legs were elevated part of the day. She walked with assistance a couple of times a day. She was transferred from the secure unit to the long-term care custodial area of the facility and had more social interaction. She gained weight and had no further episodes of venous dermatitis or ulceration during the next year.
Gellitourillary System The genitourinary system is divided into the upper tract (kidneys and ureters) and th e lower tract (bladder, sphincters. and urethra). Patients with kidney failure may require treatment involving some form of dialysis and a special diet that may impair wound healing. The patient with kidney failure often has multiple system failure. Evaluation for other diseases such as diabetes and hyperten sion is warranted, as they often coincide with kidncy dysfunction.
II
Urinary I" colltillell(·e. Bladder dysfunction. outlet problems, or sphincter dysfunction can cause urinary incontinence. Urinary incontinence has implications for skin damage. including macera tion from moisture on the sk in, softening and separating the epiderma l layers. and irritation related to increased friction and shearing. Wound contamination is also an issue for patients with sacrococcygea l wounds and concomitant incontinence. There are several types of urinary incontinence. The most prevalent type of incont inence in institutionali zed older adults is urge incontinence. Urge incontinence involves involuntary bladder contractions with loss of large amounts of urine with or withou t a strong urge to void. Stress incontinence occurs predominant ly in women and involves loss of a small volume of urine associated with increased intra-abdominal pressures slich as laughing, coughing, or sneezing. Overflow incontinence is associated wilh out lei obstruction sllch as an enlarged pros tate in men and manifests with constant dribbling and fee li ngs of incomplete bladder emptying after voiding. Functional incontinence is urine loss due to cognitive impairment . physical functioning, environmental barriers (no access to toilcting facilities), or psychologic unwillingness (depression). The type of incontinence influences the treatment. Some incontinence may be reversible, such as incontinence caused by a mcdication side effect or infcction. In reversible incontinence, when the causative factor is removed the incontinence resolves. Persistent incontinence can often be managed or cured by behavioral interventions. Il'lcdications, and sometimes surgery. It is important to remember that incontinence is not a normal response to aging; il is a symptom of an underlyi ng pathologic condition and as such should be investigated . Urillury TrtlCt Illfectio". Bladder or urinary tract infection is an additional stressor to the body and may slow wound repai r. Management of urinary tract infections usually involves systemic antibiotic therapy. Treatment of a urinary tract infection will influence the amount of timc prcdicted for the wound to respond to therapy. For example, if a urinary tract infection is present , the clinician may add a week to progress through the initial phase of wound hea ling. Gellitollrillary System PilysiclllAssessmellt. Physica l examina ti on of the urinary systcm occurs in tandem with assessment of the gastrointestinal systcm. During the abdominal exami nation, the clinician is attun ed to location of the bladder and the presence of any abnormalities. Specific assessment of the perineal area involves primarily observation, and the focus is on the external sk in . Look for indications of urinary incontinence- related ski n damage. Specific assessments for determining type of urinary incontinence are usually indicated, and laboratory values should also be evaluated. Standard urine ana lysis and culture and sensit ivity re-
12
WOUND CARl
ports may indicate the pathogen involved in a urinary Iract
infection and d irect the appropriate treatment. Periph eral Vascular System The peripheral vascular system includes the venOllS. arterial, and lymphatic circulatory systems. Chapter 14 describes the pathogenesis and differential diagnosis of peripheral vascu lar disease (PVD). The clinician should pay particular attention to all medical chart notations or comments by and questions asked of the patient or family about vascular disorders, including hi story of hypertension , dccp vein thrombosis. claudicatio n. cold feel, and chronic swe ll ing of the
lower extremities. Patients with PVD arc at high risk for development of chronic wounds and resultant impaired wound healing. The diagnosis of PVD guides the c1inician's examination strategy for observational and noninvas ive vascular testing. The important observations and testing procedures for patients with PVD are outlined in Chapter 6. NoninV'dsive Vascular Testing Procedures. Perip heral VUH:ll lar System Physical Assessment. Physica l exami nation invo lvcs assessmcnt of temperature, co lor. capillary refill , and cdema of both lower cxtremities. ol11pare one side with the other with attention to detection of deficits th at are bi lateral or unilateral in nature. Note nail growth . Are the nails hypertrophic or discolorcd? Note sk in color of both extremities. Is there evidence of hemosiderin staining or dependent rubor present (see Chapter 3)'1 Is the cxtrcmity shiny, naky, moist. dry. odorous, or dcformcd? Eva luate range of motion and strength in the 100\'cr extremiti es. Check lowcr ext remity pulses and renexes. The presence of lower extremity symptoms may be clinica l indicators of peripheral vascular disease and necessitate a more focused assessment. Neurologic a"d Mu.\·c:uloskeletal S),Mem An imbalance or insufficient movemcnt of body segmcnts, limbs. or th e whole body due to impairment or di sabi lity of the neurologic or musc uloskeletal system arc known factors for predicting cCfla in wound development such as prcss urc ul cers and neuropathic ulcers. Ncuro logic disorders and dysfunction ofthc musculoskelctal system includc a broad range of mcdical diagnoses sllch as spinal cord injury. cerebrovascular accidents. Parkinson's diseasc. arthritis. and multiple sclerosis. See Chapters 12. 13. and 15 for more information about the impact ofmovemcnt disability on pathogencsis of pressurc ulcers, pressure ulcer prevention. therapeutic positi oning, and problems of the nellroparhic fool. The neurologic or musculoskeletal dcficit guides examination strategies for the c linician. For examp le, the Ilurse caring for a patient with lim ited bod y movements and neurologic deficits performs a pressu re ulcer risk assessment to evaluate
risk factors for pressure ulcer development , which may trigger referral s for therapcutic positioning evaluation by a physical therapist and a nutritional consu ltati on. In another example. patients who have had a cerebrovascular acc ident or stroke may have decreased activity and mobility, increasing their risk for pressure ulcer development or reducing the healing capacity of current wounds. Cerebr0l1asclliar Accidell'. Cerebrovascular accidents (CVAs) or strokes are caused by disruption in blood now to the brain. CVAs usually affect one hemisphcre of the brain, causing deficits 011 the contralatera l side oflhe body. Stroke can resu lt in impaired abi lity to walk, impaired abi lit y 10 lise an upper limb, and inability to communicate, think. or see adequately. The patient's limited ability to move body parts places the patient at risk of developing pressure ulcers, skin tears, or friction and shearing injury.
A rthritis. Arthritic disorders affect the joints of the body. The two main types are rheumatoid arthritis and osteoarthritis. Osteoarthritis affects older adults and is associated with painful joints, particularly knees, ankles, and hips (weightbearing joint s). Evaluation of the wound patient with arthritis may be more difficult because of pain 011 positioning for adequate view of the wound. Treatment ofarthritis commonly includes non steroidal anti-innammatory drugs and steroids. both of which can impair or slow wound healing . Rheumatoid arthritis affects the joints of the hands and fingers. making self-care of wounds difficult or imposs ible. Neurologic: (wd ft111 .\·(·u l oskeletal System Phy.'i ic(1 1 Assessmellt. The clinician assesses cranial nerves I to XII and renexes to determine the level of in volvement of the stroke. The clinician needs to assess gait. balance. tremors. ataxia. one-sided weakness. and cognition. Joints involved in arthritis should be evaluated for pain and range of 1110tion . Assessment of the patient with a stroke includes examination of the affected side of the body for strength and range of motion . naccidity or spasticity, and hemineglect syndrome. Hemineglect can cause a patient to bump into objects on the neglected side of the body or fail to attcnd to one side of the bod y. resulting in injury. Assessment should also incl ude eva luation of the patient's gait. mobility. and ba lance. Assessment of lhe neurologic and musc uloskeletal systems includes completion of a functional assessment. It is important to evaluate the patient's abi lit y to perform activities of daily living and instrumental activities of dail y living. Hemutologic Sy.'item Disease processes such as anemia. tluid and electro lyte imbalance, or o th cr blood dyscras ias assoc iated wi th medication side effects or disease pathology affcct wound healing ca pacity. Evaluation of laboratory values to rule out
The Diagllostic PlVces.'i
anemi a, el ec tro lyte imbalance, o r infecti o ns is th e key to hematologic sys tem assess me nt. The pat ient may require iro n su pple ments o r blood tra nsfusio ns to correc t th e def ici t. Hematologic Sy~·te", Phy.';ical A~'seH",ellt. Assess fo r skin co lo r. Is it pa le? Docs the pati ent have mult iple brui ses? Docs th e skin see m " th in"? Loo k at the mucous mcmbranes. Arc th ey pa lc? Docs th e pati ent repo rt bleedin g gum s o r frequcn t nosebleeds? Docs th c pati ent co mplain of fa ti g ue? Eva luate laboralO ry data fo r ev idcncc o f ancmi a such as low hemoglo bin. he matoc rit. o r iro n. Ellt/OL'rille S),,\·tem
T he e ndocr ine syste m inc ludes num ero us gland s th at secrete body-regul at in g horm o nes. One of those gla nds is the pa nc reas. whic h co ntrol s ins ulin levels in the body. Diabetes me ll itus is the disease of most co nce rn in th e endocrin e syste m, Diabetes impa irs wo und healing and poses signi fican t ri sk fo r wo und devc lo pment. G lucose levels a lter wo un d healing and iml11un e syste m fun cti o ning to control infecti o n. Chec k for a di agnos is o f di abetes mellitus. Is it type I insu lin dependent o r type II no n- ins ul in dependent '? The type of di abetes sig na ls whethe r th e patie nt w ill use ins uli n or d iet and exe rc ise to co nt ro l glu cose. Type I di abctics requi re insulin fo r gl ucose ma nage ment. Type II di abet ics manage glucose co ntrol ini tia ll y w ith d iet and exe rc ise, th en if unsuccessful , w ith ora l hypogl ycc mi c agc nt s o r insulin.
ElllloCl'illeSY.'ilem PhysiclIfAs,'iessmellt. This is th e time to rev iew the record fo r glu cose levels. No rmal g lucose leve ls arc 80 mgld L. Leve ls o f 180 to 250 mg/dL or g rea ter arc indicato rs th at glucose levels are o ut of co nt ro l. Leve ls of grea ter th an 200 mg/dL are know n to have a n impac t o n wou nd healing. ] Rev iew of laborato ry valu es is prude nt to determin e leve l o f dia bet ic co nt rol. Loo k spec ifi call y fo r a fas tin g blood glucose level < 140 mgldL and a glycosy lated hemoglob in ( HbA ,, ) o f less th an 7%. T he HbA" he lps dete rmine the level of glu cose co nt ro l the patient ha s had ove r the las t 2 to 3 mon ths. The diabeti c pati e nt w ill need both medi cal and nursi ng management to bring glu cose levels w ithin no rma l limi ts. Many diabeti cs mo nit o r Ihe ir blood sugar at home with a blood sliga r monito r such as One-To uch or Acc uChec k, o r th ey perfo rm self- mo ni torin g with si mpl e finge rstic k glu cose testing. T he c linicia n will wa nt to know abo ut the method o fm anage mcnt and success of th e cOlltroimeasures. Thi s will hclp predi ct the success o f wo und therapy int crven tions. Addi ti o na l informa ti o n ca n be used to g uide therapy. Answers to key questi o ns. Is th e palient e lderl y'?" and "' Is diabetes of recent o nset?"' provide a hi story of the di abetes. Co mplica tio ns fro m diabe tes gene rall y occ ur th e lo nger the pa-
13
ti e nt has th e disease. Pati ents w ith re lati ve ly new o nset o f di abetes may not ex hibit neuropathi c o r vasc ular compli cati o ns related to di abetes. Pati e nts w ith di abetes ovcr lo ngcr peri ods o f time and those wi th type I diabetes are more at ri sk fo r co mpli ca ti o ns assoc iated w ith the di sease, slich as neuropathy, retin opathy, and vasc ul ar changes. T he diabeti c wi th a wound sho uld trigge r exa minati on o f se nsa ti o n in the feet a nd vision testin g. Pati ent s wi th diabeti c neuro pathy may prese nt w ith ul cers o n th e soles o f th e feet, a nd ca re sho uld be ta ken to examin e the planta r surfaces for ca llus fo rma ti on. crac king, and bo ny deformi ties. Additi onal info rma ti o n o n ma nage me nt o f th e pat ie nt with va sc ular a nd neuropathi c d isab ilities re lated to di a betes is di scllssed in Chaplers 14 and 15. A ltho ug h thi s rev iew of systellls with phys ica l assessme nt g uide lines is no t incl usive, it prov ides a framewo rk of those areas o f most co ncern to the clini cian manag ing pati ent s w ith wo und s. A compl ete hi sto ry and phys ical examinati o n provides the co ntex t for the wo und itself. After co mpl ctin g the hi story and phys ical exa min ati o n th e cl inicia n can turn attenti o n to pl anning imer ve nl io ns. If the info rmatio n is very limited th e c linicia n w ill have to make a c linical decisio n . abo ut th e a ppro priateness of th e re ferra l from th e reaso n for re ferral , ex pec ted o ut co mes. and perso na l o bse rva ti o ns of th e pati ent . C linicia ns ca n co mpl ete th e gene ral hi sto ry. systems rcv iew, and phys ica l assess ment in abo ut 30 to 40 minut es for a si ngle wound. A n expe ri e nced clinic ian can pe rform the basic phys ical assessme nt in 10 to 15 minut es. Typi ca lly all info rmati o n is no t gath ered at the sa mc time. Po rli o ns o f the hi story and physica l assessme nt Illay be gath e red ove r a peri od o f seve ra l days after severa l c lini c visits o r hOin e visits. By the end o f a I-ho ur evalu ati o n the c linic ian sho uld be able to compl ete th e hi story a nd phys ica l assessmc nt, cvaluate the wound, dctermin e ca ndidacy o f th e pati ent fo r service (i f clinic ian is phys ical the rapist) , a nd deve lo p a strategy fo r spec ific exam inati o ns or refe rral s. (Sec the Case Study in th e foll owi ng secti o n fo r an exa mpl e o f pati ent hi story innuenc ing wo und ca re manageme l1c)An expe ri enced nurse sho uld be able to eva luate the hi sto ry fo r ri sk fa cto rs fo r impaired hea lin g, perform the necessa ry phys ica l assess ment and wo und evaluatio n. a nd develop a strategy fo r inte rvent io n in abo ut 40 minutes.
Wound Assessment Wo und assessment invo lves eva luatio n o f a composite o f wo und c haracteristi cs, includin g locati on, shape, size, depth, edges, undermining and tunn e ling. necrot ic ti sslie cha racteri stics, ex ud ate c ha ra cte ri sti cs, sur rounding skin co lo r. periph eral ti ss ue ede ma and induratio n, and the prese nce o f granul ation ti ss ue and epithe li a li za ti o n (sec Chapter 3 o n wo und assessme nt , Chapter 4 o n wo und measureme nt. and Chapter 5 on tools).
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'VolI/ullli.'itory The next que stions arc directed toward acquiring information abou t the hi story of the wound. How long has the
wound been present'! Is there a hi story of previous wounds? What intervention s have been used and have they been suc-
cessfu l? What discipli nes have been involved in the management of the wound? For instance, if the paliclll has been seen by many disciplines and has had multiple interventions without success ful progress toward hea ling, the patient 's candidacy for morc aggressive intervention is questionable. What factors have impaired the wound response so far? Previous therapy and response to therapy must be carefully examined to avoid repeating unsuccessful intervention. Some patients may not heal . Howcver, evaluation of past interventions with altention to appropriateness of topica l wound care, prevention strategies, risk factor and comorbidity management. and use of adjunct therapy such as a whirlpool or electrical stimulation may revca l inconsistenci es in treatment approach.
the candidacy of the patient for services: with nursing. the option of dctermining candidacy for nursi ng services does not exist. The nurse usua lly has no choice in determining whether or not to provide nursi ng services to th e patient. However, the nurse docs have the option of assisting in detennination of nppropriatc therapy for the patient involving other di sciplines. The medical hi story and system s review findings may suggest to the clinician that the patient 's problem req uire s co nsultati on; is outside the scope of the clinician's knowledge. experience. or ex perti se; or the intervention originally suggested is inappropriate. In physical therapy. th e patient is thcn identified as a noncandidate for the referred physical therapy service. It then becomes th e re spon sibility of the clinician to rcfer to another practitioner who is more sk illed, more knowledgeable, or beller able to manage thc identified problem or recommend an alternative treatment and management strategy. Below are examples of SOine criteria that would trigger a referral:
• Vascular testing shou ld be considered ifassessll1ent findPati ent Ca ndidacy for Physical T herapy Se r vices During the assessment process, the clinician focli ses on how the medical history and systems review will affect th e candidacy of the patient . Physical therapi sts may determine
ings include hair loss. skin pallor or cyanosis, and cold temperature of the feet. • CalJus and hemorrhagic spots on the ca llus are indicators of deeper ti ssue damage and a need for further assessment.
Case Study: Example of Patient History Influencing Wound Care Management An 83-year-Old Spanish-speaking illiterate gentleman was referred by the vascular department to the leg ulcer clinic of the county hospital for healing the ulcer on his leg. The patient presented with a large, full-thickness ulcer on his left leg due to underlying venous disease. He lived alone, had no family to help, was on county welfare, and had no regular transportation to the clinic except for a monthly clinic visit. He was embarrassed about having the ulcer on his leg and did not want to involve neighbors in his care. During the interview it was observed that he was ambulatory, alert, and able to learn. The clinician performed the evaluation following the diagnostic process and decided that the patient was not a candidate for the leg ulcer clinic because he lacked transportation to the clinic. There were no caregivers available other than the patient himself. Therefore, the patient would have to be taught self-care. Financial resources were very limited. He was eligible to receive wound care supplies and he could come in to the clinic monthly for supplies and to have the ulcer evaluated. He was alert and motivated and demonstrated the ability to learn selfcare if he was given simple instruction in Spanish. The teaching plan involved demonstration and return demonstration, and the patient returned home to self-man-
age the wound with monthly follow-up apPointments at the clinic. The medical history guided the wound examination. It was examined for drainage, size, status of surrounding skin, and healing status of the wound. Since he had had a prior vascular examination determining the presence of venous disease, further vascular testing was ruled out. A treatment intervention that he could safely perform and that was appropriate for his wound problem and underlying pathology needed to be selected. Since his underlying disease was venous insufficiency, compression of the venous system was needed. Since the wound was draining he needed a dressing to control exudate and keep the wound and surrounding skin clean. The clinician elected to clean the wound with normal saline and apply a hydrocollOid dressing under an Unna's boot treatment to be changed every 4 days. The patient demonstrated that he understood wound care instructions and dressing techniques. He required support in case he developed problems. Instructions about potential problems he might encounter and the phone number of the Spanish-speaking nurse assigned to his case were given to him with instructions to call with any questions or to report problems with the ulcer. With this approach to wound care, ulcer healing progressed.
The Diagnostic PlVcess
• Toenail abnormalities: ifnot an area ofcxpcrtise of the examiner. should be referred . • Assessment of an abscess in a tunnel or sinus tract requires immediate referral for surgical managemcnt. • Undermining or tunneling that is a black hole without a boltom should be immediate ly referred for surgical management . • Signs of granulation tissuc infection (superficial bridging. friable tissuc. bleeding on cont3ct. pain in the wOllncL or rcgression of hCHling) need mcdical intervcntion. STE P II : DIAGNOSIS
15
skills of a physical therapist. The physical therapist prognoses an expected functional outcome of risk reduction following interventions of pressure elimination and stimulation leading to healing. In both cases, the ulcerations are re lated to underlying medical pathology. In the former case the ulcer would not be expected to respond unless the underlying pathology was addressed. In the second casc, the ulccr management was appropriate along with risk reduction management. The interpretation of the data from the histo ry and physical examinations sets the stage for the functional diagnosis and allows triage of cases that should be referred or managed conscrvat ively.
Exa mina tio n Stra tegy
EXflIlI;Illll;OIl : Par I II
Utilization management requires close attention to the management of factors that prolong healing. The risk factors for impaired healing arc identified at this point in the examination based on data collccted during the history and systems review. Because the infonnation about the patient determines the examination strategy. all patients will nO! receive the samc examination.
Pan II of the examination strategy is 10 look at four key features of the wound assessment. The four key fcaturcs are evaluation of the surrounding skin, assessment of the wound tissue, observation of wound drainage. and size measurements.A II four characteristics have several aspects to include in the assessment. Surrounding skin examination includes cvaluation of color. texture, temperature. edema, and pain in the ti ssues around the wound site. Assessment of wound tissue includes color, tissue stalUs. and visible structures. Observation of wound drainage includes odor, color, and quantity. Size measuremcnts taken include open surface area , depth, and undcrmining. Methods of performing wound assessment are described in Chapters 3,4, and 5. For example a wound with an open surface area, depth. and undermining present should have all three characteristics measured. A partial-thickness wound will require only measurement of the open surface area. Sequencing the examination will depend on visual obscrvation and palpation of the impaired tissucs. The examiner chooses those tests and measures specific to the wound situation . For example, temperature testing may be the best way to distinguish the presence of inflammatory processes in a pressure ulcer in persons with dark ly pigmented skin. A wound traci ng may be best method to measure the irregular shape of a venous ulcer. If signs or redness, heat , edema, pain, and loss of function are observed, the wound is in an inflammatory phase. The wound history provides information about wound etiology, duration of the wound status, and recent wound change in status. If the wound status has not changed significantly in 28 days it is in a chronic phase of repair and needs help to restart the biologic cascade. A fter completing the exarninalion part of the diagnos tic process, the clinician intcrprets the physiologic and anatomic systems information and wound assessment data. The clinician brings all the data together like the pieces ofa puzzle to develop functional diagnosis. 4
Examilllll ;Oll : PlIrl l
There are two parts to thc examination. Part I includes testing for factors related to the physiologic or anatomic status of the cOl11orbidities thai impair healing. such as vascular impairment or sensory impairment. For example, the patient is a candidate for noninvasive vasc ular testing if there is an ulcer on the ankle wilh the following characteristics: slow heal ing. cold foot. symptoms of claudication. pallor of the limb. and no report of an ankle-brachial index in the medical record . Sensory testing should have a high priority in the testing schcme ifthc patient has a history of long-term type I insulin-dependent diabetes. history of ulceration of the foot, or
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WOUND CARl
Evalu a ti o n a nd I)iag nosis The eva luation aspect of lhe diagnostic process includes eva luation and analysis of findings collected during the ex-
amination and leads to clinical judgments based
011
the data
co llected. Diagnosis includes the process and is also the conclusion reached aflcr the eva luation data has been organizcd. ~
Phys ical therapists arc expected to lise the diagnostic process to establish a diagnosis for the specific conditions requiring attention. I r the findings of the diagnostic process arc slIch that the management of the patient is outside the physical therapist's knowledge, experience, or expertise, the
patient should be referred to the appropriate practilioner. 5 The nurse may reach a diagnostic conclusion that a referra l to another practitioner is needed, but as mentioned previollsly, the nurse usually cannot bow out while waiting for a referral and is required to provide a plan of care for the patient in the interim. The purpose of data analysis is to draw conclusions about a patient's specific problems or needs so that effecti ve interventions can be implemented. Problem identification is a process of diagnostic reasoning in which judgments, decisions. and conclusions are madc nbout the meaning of the data co llected, in order to determine whethe r or not intervention is needcd. lI Diagnosis involves forming a clinical judgment identifying a disease/conditi on or human response through scientific evaluation of signs and symptoms. history, and diagnostic studies. In many respects a diagnosis is analogous to a research hypothesis. For example. a research hYPolhesis direcls the research study and a diagnosis directs the patiel1l's care plan. Both a research hypo thesis and a diagnosis arc chosen based 011 available data and information, and both research hypotheses and diagnoses may be proven correct or incorrect as the study or care plan progresses. Physical therapy diagnosis is defined as " ... a label encompass ing a cluster of signs, symptoms, syndromes, or categories." ~l r7 1 ~) The purpose of a diagnosis is to guide the clinician in determining the most appropriate intervention strategy for the individual. In the event thai Ihe diagnostic process docs not provide adequate information. intervention may be based on alleviation of symptoms and remediation of deficits. Nursing diagnosis can be defined as both a noun and a verb. As a ve rb. nursing diagnosis is the process of identifying spec ific patient problems or needs in the second step of the nursing process. As a noun. nursing diagnosis rcfers to labe ls or terminology that identify spccific palient problcms or needs or the means of describing health problems amenable to treatment by nurses. Health problems may be physical, socio logic, or psychologic. Nursing diagnosis is typica lly stated in three parls: the problem, the etiology. and the signs and symptoms. Problem statements arc drawn from the North American Nursing Diagnosis Association
(NANDA) approved lisl of nursing diagnoses. BOlh nurses and physical therap ists make diagnoses based on Ihe symptoms or the sequelae of the injurious process such as impaired wound healing. Physical therapi sts eval uate the functional implications of impairments and disabilities leading to a functional diagnosis. Impairment is loss or abnormality of psychological, physiological. or anatomical structure or function. 7 Impairmen t describes the loss of function of a body system or organ due to illness or injury.s An example is loss of function of the sk in and underlying soft tissue due to wounding or due to underlying pathology. Additional impairment characteristics include the effect of pathology/disease withoul attributing cause or Ihe loss ofa body part sllch as by amputation. Underlying pathology creates the susceptibi lity to loss offunction. eg. "undue susceptibility to pressure ulcers" and " undue insensitivity to pain."K The definition of a disability is any reslriction or lack (resuiting from an impairment) of ability to perform an activity in the manner or within the range considered normal for a human being. Disability may result from impairment or be caused by the person's response to the impairment. Disability may be permanent. reversible. or irreversible. Disability reOccts a deviation in performance or behavior within a task or acti vity. ~ Examples arc the disabled person who has musculoskeleta l disablement leading to di friculty wa lk ing or di fficulty moving or integumentary dis~lblel11ent related to the inability of the body to progress from the inOammalory phase of healing 10 Ihe proliferative phase. F Ullctiollal DiagllO.'iis
Functional diagnosis is defined as an assessment of the re lated impairments and associated disabilities that affect wound status and its abili ty to heal. Examples of functional diagnosis arc Ihe following: • Impaired sensat ion (unable to detect pressure or light touch) • Impaired circu lation (Ank le-Brachial Index below 0.8) of lower extremities • Impaired lower extremity strength and joint range of motion (i ncl ud ing malll13lmllscle test and range ormotion) resulting in persistent pressure to buttocks • Impaired healing associated with chronic inflammation phase. Physical therapists lise functional diagnosis to describe the consequence of disease a nd as a justification of medical necessily requiring the ski ll s of Ihe physical therapist. With respect to wounds. the wound healing phase can be lIsed as a func tional diagnosis to describe the status of wound healing (sec wou nd hea ling phases described in Chapler 2).
The Diagnostic PlVcess
Each phase of healing can be impaired. Impaired wound healing can be described as prolonged chronic or failure to occur, mcaning abscnt. Forexample. a wound wit h prolonged or chronic innal11l11ation has impaired functioning of the body system(s) needed to progrcss to the next phase of repair. The parlicu lar phase of wound heal in g lhat is dysfunctiona l he lps predict the interventions needed to restart the repair process.1.! The impairments in wound healing ca n be labe led with a diagnosis. The ",mOld healing phase diagnosis is a diagnosis of impaired statu s regarding the biologic phase of wound healing. There are 12 pos~ible wou"d b eldillg pllllse diagJloses: I. 2. 3. 4. 5. 6. 7. 8. 9.
Chronic innammatioJ1 Inflal11llH1I;011 Absence ofinflal11mation Chronic proliferation Proliferation Abscnce of proliferation Chronic epi th elializat ion Epitheli a lization Absence of epitheli a li zation 10. Chronic remodeling II . Rcmodcling 12 . Absence of remodeling The wound hea lin g phase diagnosis describes the biologic phase of repair observed by examination of the wound. Wounds become chronic and lacking in th e function necessary to progress to th e next phase of repair. This can occur in any of the phases of healing. Fo r example, when wound edges curl in and become fibrotic the wound demonstrates absence of epitheli a lization due to impairment in the epi thelia li zation process. Wounds ca n become "stuck" in the proliferation phase when infection is prese nt and impairs the proliferative process, thus demon strating chronic proliferation. Wounds can become chronically innamed when tissue trauma is prolonged. The wound healing phase diagnosi s describes the current status of the wound and can be used to predict how the wound hea ling shou ld progress. This is logical because wound hea lin g is an orderly series of even ts. A wound in onc phase should progress to and through each success ive phase. (See Chapter 2 for information about biologic cascade of healing.) A question frequent ly asked is how to stare the wo und healing phase diagnosis of a wound in transition from one phase 10 anolher. The transition is usually gradual and because phHses overlap it is appropriate to describe the change by using a ratio ofthedomi"al1l phase to the recessive phase. Domin1l11l refers to the 1110st ac tive phase observed. Recessive refers to the Icss active phase. A ratio is simply a re lationship between two variab les, in this case the relationship between two phases of hea ling. The way it ca n be used to
17
describe a wou nd w ith the dominate phase active innammcltion and the recessive phase active proliferation is to write the description as in the following sample: The wou nd hea ling phase di agnosis is INFLAMMAT IO N/proliferation. The use of capital lette rs for the dominant phase emphasizes its dom inance. Small lett ers show Ihe re lations hip of th e recessive phase. If the two phascs are equal they can both be capitalized (eg. INFLAMMAT IO N/ PROLIFERATION). The prognos is is Ih al Ihe wound healin g phase wou ld progress from inflammation to proliferation . A last example is th e newly reep ithe li alized wound. This can be written: EP ITH ELlALIZATION/absence of remodeling. It will gradua lly progress through the remodeling phase to deve lop a mature scar.
ST E P III : PROGNOS IS AND GOALS Once the diagnosis is establishecl the clinician predicts or prognoses the expected outcome goals and selects an in terve nti on. Pred icti on is a useful tool for goal setti ng. Prediction of the maximal improvement expected from an interye nti on and how long it will take is the prognosis. Prognosis may inc lude prediction ofimpro\'emelll at different interva ls during trea tl11ent. ~ For example, the biologic model us ing phases to monitor acute wound healing de scribed in Chapter 2, is organized and predictable. The phases of repair are benchmarks that can be used to determine the effec ti veness of treatment interventions. Many clinicians are intimidated by the idea of predicting outco mes. The c linician must be familiar wi th treatment effccts of interventions they prescribe and administer. If th e cli nician canno t predict the effects of an intervention, who ea n? Why would a patient want to expose himse lf or herself to the interven ti on with unpredictable results? Why shou ld a payer reimburse for services wi th unexpected benefit and indefinitc cost? The successfu l c linician is able to predict the patient outcomes. In the current health care e nvironment, familiarity with prognosis and outcomes is important for both nurses and physical therapists.
Wound Prognosis Options For wou nds, th e prognosis options are lim ited. One system for evaluat ing secondary intention wound healing defines healin g as minimally. acceptably, or ideally healed. An idea lly healed wound resuit s in return of the fully restorcd dermis and epidermis with intact barrier function . The prognosi s is ideally healed c loscd wound. An acceptab ly healcd wound has a resu rfaced epithelium capable of susta ined func~ tional integrity during activities of daily li ving. The prognosis is acceptably hea led c losed wou nd . A minimally hea led
18
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wound is characterized by recpitheliali zation but does not establish a sustained functional result and may recur. The prognosis is minimally healed wound. In all of these definitions of healing. complete closure of the wound is expectcd. 10 For some individuals and some wounds, closu re is not an option. The best prognosis that can be made is for a change in the wound healing phase from an impai red or early phase of repai r to a more advanced phase of repair. For example, a wound that is chronica lly inflamed is impaired frol11 progressing to more advanccd phases of healing. A predicted outcome can be that the chroni c in fl ammati on wi ll progress to acute inflamma ti on. An acutely inflamed wound progno-
sis is to progress to a proliferation phase. Olne wounds progress to the proliferation phase. and it is not expected nor is it preferred for the wound to c10sc by secondary intcllIion; the prognosis is a clean and stable wound or prepared for surgical closure. A change in phase is a functiona l outcome prediction. This method monitors a real change in the organ function of the ski n and soft tissues, wh ich is a measure of reduced functional impairment. A prognosis that the wound is not expected to improve based on the results orthe diagnostic process may determine referral for other management. Nursi ng may be expected to care for the wou nd but this patielll may not be a cand idate for physical therapy intervention. Prognosis is not an option for physical therapists; it is a requirement. Medicare has mandated that a functional outcome prediction be established by the physical therapist at the start of carc. This is part of utili za tion management of medical services. Goa ls
Nurses' Goals In determining goa ls for the patient , the nurse must set pri orities, establish the goa ls. and identify the desired outcomes. Goals arc determined in thc planning stage of the nursing process. Goa ls arc important because they assist in determining outcomes of care and effectiveness of intervention. To set goals, the nurse must first determine the priority of needs. Priorities are !luid and dynamic. The priorities for a patient can change day to day and even hour to hour in the course ofa day. Certain essential survival needs overshadow lesser needs. For example, a patient presents with an ulcer on the lower extrem it y and severe pain from the lesion. The priori ty will be management ofacutc pain , and wound managcmcnt becomcs a secondary priority. Basic survival necds and safety needs must be met before dealing wi th higherlevel nceds such as sc lf-cstecm or social intcraction. Once the needs are prioritized. the nurse can establish patient goals. A goa l is a broad guideline indicating the overall dircction ofmovcmcnt as a rcsult ofintervcntion. Goals can
be short term or long term. Short-term goals are usually actions that must be mct before the patient is discharged or moved to another level of care. Long-tcrm goa ls may require continued attention by the paticnt and the caregiver long after discharge. Short-term goals should move the patient toward the long-term goa l. Short term-goals arc small steps to the long-term goal.
Physicfli Therapist.',; ' Goals Physical therapists also have a historical requirement to document short- and long-term goa ls, Physical therapists' goa ls are expected to be measurable, objccti ve, and functional. Unlike nursing goals that arc broad guide lines indicating the overall direction of progress. goa ls used by physical thcrapists must be very specific. Traditionally, a shortterm goal has been one that is expected to bc achicved in 30 days or less and usually corresponds to the end of the billing period or length of stay. Long-tcrm goals arc those predictcd to be attainable by thc time of discharge. With the shifl to short lengths of stay in different care settings, the time framcs have also changed to corrcspond to the setting. Today there is a tcrminology shin away from using thc tcrm goal and replacing it wi th expected outcome. A goal is a desired or cxpected rcsu lt of an intervcntion. An outcome is the result or status aftcr the intcrvention . Completing thc diagnostic process wi th recommendations is one outcome of the serviccs of the physical therapist. The physical therap ist is able to targc t spccific measurablc outcomes for spccific interventions. To makc them functional outcomes. thcy must meet the criteria described below. Target outcomcs arc short-term spccific expectations of change in impairment status. Prognosis is the expected outcome after a course of care and is the long-term goal. Examples of wound healing prognosis are the following: I. Ideally healed closure 2. Acceptably healed closure 3. Minimally healed closure 4. Clean and stable open wound 5. Ready for surgical closure 6. Not expectcd to improvc Outcomes
Outcomes are now well-establishcd quality managcment tools, yet there is considerable confusion about the term outco me and how to report it. An olifcome is the rcsult of what is done. The intervention or activity that is done to achievc the result is the process to gct an outcome. How are outcomes measured? Performance indicators are objective measuremcnts that arc uscd to benchmark change as a result of an
The Diaglloslic Pmcess
intervention. Providers. payers. regulators. and clin icians are all working toward establishing reliable performance indicators that are useful for reporting clinical outcomes. Exhibit I- I lists examples of some wound-related performance indicators, wound outcomes, and functiona l outcomes for each. Methods and procedures for test ing and re levance of the performance ind icators arc presented th roughout the text. Assessing patient olltcomcs provides the nurse and physical therapist with a means for assessing how the intervention altered the problem . There are several types of outcomes, two types of which will be desc ribed: behavioral and functional. Payer groups have an interest in both th e behavioral and func tiona l outcomes. II The purpose of thi s section is to help the clin ician begin to formulate documentation for reporting outcomcs.
Reportillg Outcome.Ii The reponing of outcomes is frequentl y confused with proccss. There has been much discussion abollt outcomes, but what is being reported is mainl y process. This section will discuss some common ly m isused terms and the appropriate way to report the outcomc. Terms that wil l be di sc ussed include: • • • • • • • • •
Prevention Reduccd Maintained Co ntro lled Maximiled Minimizcd Im proved Provided Promoted
Pre\'ell,ioll is ofte n the target of a intervention . Prevention is the process to reduce or buffer ri sk. Risk factors usually exist prior to or at the onsct ofa problem (eg. immobilit y. deformities, smoki ng). Buffers are those attempts to reduce or intervene so as to alter the progression of an impairment. disability. or handicap (cg, take pressure offa d iabetic ul ce r).7Therc arc many reliable performance indicators that measure risk and intervcntion-related changes used by both nurses and physica l therapists. As part of the initial assessment, apply instrumcnts with performance indicators to test the current status and then retest status after applying the chosen intervcntion to mcasure achi evement of the predicted outcomc. Instead ofsayi ll g the prognosis is '''prevention of pressure ulcers" or "minimized risk of pressure ulcers," it wou ld be more appropriate to say " risk of pressure ulcers will be reduced from high to moderate based on the Braden scale."
19
For examp le, the Braden scale (see C hapter 12) is used to measure ri sk for development of pressure ulccrs. Mobility is one portion of the Braden sca le. If a patient on admission has a low mobility score on the Braden scale, indicating complete immobility, the patient is judged at high ri sk for development ofa pressure ulcer. The patient receives an intervent ion for mobility train ing. and the mobility sco re improves. Now the patient is slightly lim ited in mobility and makes frequent changes in body position . There has been a functional change in the mobility of the patient. The functional outcome is improved mobility status, whi ch leads to the conseq uence of reduced risk of pressure ul ce ration. Another topic of confusion is abollt reduced risk of infectioll. This is also not an outcome. Infection free or reduced by assessment of the exudate, odor, or cu ltu re results arc measurable outcomes. However, in order for any of these outcomes to be functional outcomes, they must cha nge the way the body system functio ns. Infection frce may be an outcome of wound cleansing, and it becomes a functional outcome if the wound healing progresses to the next phase of repair. The written functional outcome shou ld be stated as "the wound is infection free and the wound healing has progressed from the innamm3tory phase to the proliferative phase." A troublesome word in health care is mailllailled. Maintained is a process that implies no change. COil/roiled shou ld not be mistaken for mainwil1ed. If the edema is nuctuating. for instance, from treatment to treatment and then stabilizes as a result of intervention, the outcome is edema con tro lled. A functiona l outcome for edema controlled wo ul d be stat ed as "the edema in the ti ssues surrounding the wound is controlled and the wound is epithelializing."The functional outcome of contro l of the edema is that th e wound progresses to thc nex t phase ofhca ling. A1aximi=ed and minimi=e(/ is si milarly con fu sed with ou tcomes. For example. '"maximi zed participation in activi ti es of daily li ving" is not about the functiona l out comc of an intervention with an orthotic device. A functional outcome rcport s the result of the intervention , slich as "'the patient performs ADL wea ring/using orth otic equ ipme nt , has returned to work and/or resumed leisure acti vities." An exa mp le of mi suse ofminimi=ed as an outcome is "minimized stresses precipitating or perpetuating injury:' Correct use is: Functional outcome-pat ient/carcgiver identified stress-reduction methods to minimize ri sk or injury. /mprO\ 'ed is defined as to make better or enhance in val ue. Improved is a subjective measure, not a measurable ou tcome. An outcome report s the objecti ve result of improvement. For examplc. increased vital capacity measured in liters (performance indicator) is a measurable c hange in the pulmonary system wi th a result of increased oxyge nati on of
20
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tissues for wound healing. The functional outcome is "wound progresses to nex t phase of healin g." Provided is a sometimes confused with an outcome. This is an action by the clini cian. not the outcome orth e intervention. An exa mple of improper usc is "prov ided electri cal stimulation to enhance circulation." This describes the rationale for the interve ntion. not the outcome. A predicted fun cti onal out co me addresses the changes ex pected in the wound
from the interve nt io n, such as change of wound phase fro m innallll11<1lion to proliferation. Promoted is another inappropriately lIsed wo rd . " Promoted angiogenesis" is a process. Ang ioge nesis is an ex pected out come fro m treatm ent and
represents an attribute of wo und healing. The performance indicators of angioge nesis are change in wound attributes. phase. or size. The outcome is wound progression throu gh proliferat io n phase. Belta,,;ortlIOUfl:omes
Behavioral outcomes are written by listing behav iors. Outcomes must be spec ific, realistic. time o ri e nte~ obj ecti ve. patient centered. and measurable. Write outcomes by listing behaviors or items that can be observed or monitored to determine whether an acceptable or positive outcome is achieved within the desired time fram e. The outcome then serves as the eva luation too l. Use measura ble action ve rbs to describe behavioral outcomes. For example. the ve rb under.\'/{lIId is not measurabl e; we cannot measure a person's understanding. But the verb iden fijil is measurable; the patie nt can be tested to determine whether or not he or she can identify. Other action ve rbs include list. record. nllme. slOle. descrihe. explaill. demollstrate. use. schedule. dijJerellliate. compare. relate. design. prepare.lormlllllle. select. choose. increase. decrease. s/{Jnd. walk. and participate. Contrast these action ve rbs with the verbs lImlerstl/nd. feel. learn. kllou: and accept, all of which are not measurable. Examples of ex pected behav ioral outcomes for a wo und patient are the following: The patient will describe the signs of wo und infectio n and identify correct actio n within 24 hours, the patient will demonstrate wound dressing appl ication within 2 days. Documenting that the target outcome was met would include a statement : Palicnt is able to describc the signs of infectio n and li sts the steps for correcti ve action. Patient is abl e to dcmonstrate correct wound dressing appli cati on. These are behavioral outcomes. What implication do they ha ve for the patient 's fun ction? To become functi onal outcomes these behavioral outcomes need to include the implicat io ns for the pat ie nt. FlIllc/;OIl11l
Oll/come~'
What is " j ullctional olllcome? A functio nal outcomes helps to communi cate the change in functi on to thc pati ent.
caregiver. or paye r. Physical thera pists us uall y dea l with patients who have loss offunctional abilities and use fun ctional tests that measure physical att ributes to predict the fun cti on the patient is ex pected to achieve after a course of treatment. What is f unctioll? Function in this contex t refers to those acti vities or actions that arc meaningful to the patient or care· giver. Meaningful function is determined while completing the reason for referral portion of the assessment. To be a fun ctional olltcome, the results must meet th ree test sl ~: 1. Is the result meaningful ? 2. Is the res ult practica l? 3. Will the res ult be sustained outside Ihe treatment setting?
Meaningful is defined as of value to the patient. carcgivc r. or both. Functi on is achieved by the patient th rough the services of the physical therapist or nurse so that the patient can perform acti vit ies effect ively at home or work {ego wo und ex udate is cont ro lled or eliminated so the patient can rcturn to work }. Pracl iclli mea ns that the outcome is applicable to the patie nt's life situation. Sustainable Ol'er lime refers to functional abilities ac hieved th ro ugh the interve ntion maintained by the patient or ca regive r outside the cli nical setting (eg, patient-demonstrated ab il ity to apply dressing and stocking durin g two fo llow-up visits}.1 \ Standa rdi zed tests and measurement 100 is arc quite useful to monitor and trac k change over timc. The Pressure Sorc Status Tool (PSST) and the Sussman Wound Healing Tool (SWHT) arc described in Chapter 5 and can be used to document outcomes of change in wound attributes by change in test scores. Although these tools report outcomes as they affect wound attributes. to be functional outcomes the dots need to be connected between the items on the test and the meaningful . the practi ca l. and the sustainable implications. In the example described above, if the PSST is used 10 moni to r ex udate amounts. there wo uld be a change in score on that test item from 4 (moderate ex udate) 10 2 (sca nt ex udate) indi cating reduced drainage. This outcome is measurable. objecti ve, and meets all the criteria li sted fo r a valid outcomc. but th is information alone is not a fun ctional outcome. To interpret this score as a functional outcomc. a statement is needed that connects the findings with meaning to the patient, practica l effect. and sustainable result. A resulting statement of functio nal outcomcs is: Wound exudate PSST score has reduced fro m 4 (moderale) to 2 (scant ) ex udate. patient demonstrates ability to monitor for signs of infection and action to take, patient is now able to rcturn to work and will be scen for intermittent fo llow-up. Functional outcomcs should be documented th roughout the course of care. not j ust at di scharge. Statements that can be used to demonstrate intermittent functional change in-
The Dhlglloslic PlVcess
elude change in patient lifcsty lc. changc in paticnt safety. adaptation to th e impairment or disability. These statcments should be patieill-ccillcred and measurable. For instance. a functional outcome statemclll would be: II/ilial statemenf : Pati e nt is unable to s it in wheelchair without trauma to integument. Illifiti/larget outcome: s ilting for two hours in adaptivc scating sys tem in 2 wceks . IlIIerim outcome ajier I
lI'eek : paricnt sits for I hour in adaptive seating system. Discha rge stalemelll : s its in adaptive sca ting systcm for 2 hou rs wi th out di sruption of integumentary integri ty. Change in wou nd tissue a llri butcs and size can al so bc used as functional outcome: Necrosis free. reduced ri sk of ill feet ion. and size reduced 50%, wound is e lcan and stable. decreased frequency of visits requircd.
Exhibit 1- 1 Examples of Performance Indi cators. Wound Outcomes. and Functional Wound Outcomes
Performan ce /I/(I;ca lol's
ll 'rJlllul Outcomes
Fllnclional Olilcome
I. Change of wound and surrounding skin attributes 2. Reduced sevcrity of wound: depth. size 3. Change in wound ex udate characteristi cs. or undcrmining 4. Closure
Progressio n through the phases o f wound healin g (inflammation. proliferation. ep it hel ia lization)
I. Clean stable wound ready for su rgica l closure 2. Dressing cha nges needed biweekly in stead of daily 3. Exudate managed: patient returns to work 4. Rcturn to work/lei sure activities
I. Temperature comparison
Oxygcna ti on or perfusion of tissue
I. Progress 10 next wound healing phase 2. P:.lin level no longer interferes with
2. Transc lIlalleous partial pressure of oxygen level 3. Lase r do ppler I. Girth measurements
ADL Edema reduction o r controll ed
I. Patient abl e to don compress ion hosc 2. Leg ulcers arc smaller. require less frequent dressing changes
Infection controlled
I. Wound CXlldate odor controlled able to return to co mmunity 2. Pain alleviatcd pa tient resumes walking
Clcan stab le wound
I. Frequency of vis its reduced 2. Physical thcmpy interve ntion no longer required 3. Pati ent can now manage wound dressing changcs
Reduced risk of pressure ulccnltion
I. Pati ent performing self-care activities wh il e lip in whee lchair 2. I>atient demonstrates use of hand mirror to monitor skin
Acceptably healed sca r
I. I>atient idcnti fies ri sk fac to rs for reulceration 2. Patient uscs protectivc cquipment correct ly under scar tiss ue 10 perform functional activities in wheelchair
2. Volul1lc meter measurements 3. I)alpa tion grading system
I. Wound exudate characteristics
2. Wound and surrounding skin attributes 3. Culture I. Necrosis free
2. Prolifera tion phase ti sslle attributes 3. Change in depth or si7c
I. Braden Scale score.:
2. Functional activities performance 3. Comprehension testing
I. Wound closure
2. Functional activities pcrformed relatcd to lise of scar ti ssue
21
22
W OUND CARl
S ummary : N ow To JVr;te Olllcome S tlllem ent. When rcporting outcome. use th e following gu idel ines:
or
• An ou tco me expresses the result an intervention. not the int er ve ntion or the process to reach an outcome (eg.
wound resurfac ing/c losure). • A behavio ral out come may be learned information (eg. demonstrates application of wo und dressing). This out-
come would follow an interve nti on of instruction. • Coordin ation, com munica ti on. and documentation arc
behaviora l out comes lIsed to ensure proper utilization managcl11cl1I .
Functi onal out comes arc written to describe fun ct ion result s o f trca me n!. A functional ou tcome includes three pa rt s: 1. A functional outcome statement describes a meaningful functi onal change to a body system (eg. progres-
It is not unusua l that foll owing a co urse of therapy there wiil be rcsidual impairments and disabilities in conjunction wi th a meaningful functional outcome th at is important to the patient (eg, a clean. edema-free wound). This may be th e most important goal and the reaso n for the referral because it is mean ingful to th e patient. Part II is an analysis of/llllcriolloilimiroliolls. Function implies many different activities or actions. With respect to wounds. this includes identification and analys is of th e functional limits of th e loca l tiss ues to perform th e acti vi ti es necessa ry to initiate repair. Function also implies that the body systems have th e ability to perform the repair. For instance, the current status of th e ti ssue assessmcnt iden tifies tissue act ivit y (eg. innammati on phase) and the circul atory system res ponse to injury (eg. eryth ema. edema. pain, and heat). An impaired circul atory system functi on will impair thc healing process. The clin ician writes the report wi th the following leads:
sion th rough th e phases of heali ng).
2. A fun cti onal out come statement describes a practical result of the change in the body system (eg. wound is minimall y ex udative), 3. A functional outcome statement describes th e susla innblc result or change in th e impairment sta tus or dis-
ability res ultin g from the interve nt io n (eg, pressure elim ination allows the patient to situI' in wheelchair 2 hours twice a day) .
T H E FUNCTIONAL OUTCOME R E I'OIH
This chapter has described three of the four steps needed to complete the diagnostic process. The functional outcome report (FOR) deve lopcd by Swanson, described below. is a written report describing the diagnostic process," Swanson's
FOR he lps the therapist project cli nical reason in g that is c lea r. and understandab le to the reader. As previollsly explained paye rs walll to know about functional outcomes, not wound meas uremen ts and ti ss ue co lor. The FOR process helps communi cate treatment strateg ies to justify Ihe interve ntion and lead to a predictable functiona l outcome. 11 Exhibit I 2 is a completed example of th e report. There are additi onal exa mpl es of th e FO R in C hapter 14 a nd th e case studi es in Part IV. The FOR docum ent has six parts. Part I begins with th e reason jbr re.ferral. Ilere th e clin ician estab li shes patient needs. The repo rt will read in one of the following manners: l og i c~lI .
• Patie nt/fam il y seek se rvices for . . . • The patient/family re ports ... • The fo llowi ng medica l problcms arc associated with this req uest for se rvice . . .
• The spec ifi c fUll ctional ilems th at are ca using thc patient's need for se rvice arc (eg, impaired hea ling respo nse) • Pat ient's fUllctionalloss of hC~lling is due to (eg, impairmen t of the circulatory system ) • The loss of function causes th e following (eg. inability to progress th ro ugh th e phases of repair without interve ntio n) • Pati ent has improvemcn t potential (eg. patien t has improvement potential but rcm~lin s at risk for isc hemic ulceration) In Pa rt III , clinical {ISSessmellt or diagnO!;is is the clinica l impress ion based on the resu lts of the tests and meas ures selected by the clini cian. The clinician chooses tests and measures th at have performan ce indi cators for wo unds. This is defined diffcrently from thc medi ca l di ag nosis because it focuses on th e functional conseq ucnce of the disease rather than the eti o logy. See the sectio n on fun ctiona l di agnosis described earli er. Pa rt IV is th e justification of need/hI' ."killed service or (lte therapy prohlem . Ut il izat ion managcmc ill requires thai there be an identification of the specific elemen ts that will be changed as a result of th e intervention and once changed will improve the patient's functional status. An example ofa wound problcm th at can be expected to change as a result of an intervention is a chan ge in th e phase of wo und healing as a result of an intervention (eg. whirlpool). Change can also be expected in th e wo und symptoms (eg, erythema free. pain free), which wi ll demonstrate improved fun ctional status of the tissues. In Part V, prediction of a jUllctiollal ollfcome is expected because clini cians have a responsib ilit y to know the effect of the selected treatmcnt interventions. Patien ts and referral
The Diagnostic Pmct..'s\'
23
E\hibit 1-2 Sample FOR
ACE: 59
Patient 10: J.J
Palienl lIi slOr): Reu,\ollfor Referral: Patie"t/fiw,ily .\ et!k\ .\en'it:e,\for: Return to social acti\ Itles and concern abolll a pres~urc ulcer 011 a heel. CtlreJ.:il't!r\ reJl'Jrt: Less tllne IS nO\\ spenl out of bed and palIent has qmiodcs nfconfusion. Pl.Itient is usually alert and oricnted and hils adequate communication skills to make nceds. \\ants. and dlscomrort~ ~nown.
l\ledical HislOr): Medic'tlllmptl;rme"h. Ttlke" from Medi('tlllli,-wry.' • LIIll11cd respiratory capacily due 10 chronic obslructlve pulmonary dbea~e . • Rcqlllre!'i contllluou", oxygen from a concenlralor
1. SpeCIfic functlOnallos~es cau~lIlg the patient's need for ser\ ice arc: loss of wound hcallllg capacity. 2. Pallent's functional loss IS due to • Rcsplnllory Impairment and Circulatory ImpaIrment. • Mechanical Illlpalflncnts of the lower C\lrelllltlcs (conlraclures of hips and knecs). • Motor impalrll1Cnl (unable 10 reposition III bed and unable 10 transrer to \... heclch~lIf) Fu nctiona l Diagnosis: The loss of funcllon causes the follOWing : • Undue suscepllbllity for pressure wound on lower fecI. • In ab ilit y to heal withollt integumcntary IIllcrvcnllon
Prognosh: Pallent has Improvement potentml: will heal lollowlIlg Illtcr\ent lon but will eontinuc to he at risk for pressure ulceration
S) stems Rc\ ie\\ :
Tire Followi,,/.: SyMem, Are Impllired: (cmIiOpIIIII/OI/(//T S\',\1('/II
• Pulse oXlllletry' 9}l°o good o\ygcn saturallon achlc\ed wllh slIppkmcntal oxygen \ fll,\("/I/O,\'kl'l( ' wl S1".\/('1I/
• COlltracted to 90 al hIps blilly
~lIld ~nccs
and has I!Ill lied bed 1110-
J(I\ut/",. .S:\".\I('1II
• Impaired circulation ofthc 100vcr c\ln.!lllll les: coldness. pallor. absence of hour. and poor pulses. 11I1t'gUIllt!lIll11T
•
.S:n/('",
S~1I1 mtacI but Il11pillfed by eschar ()\,cr a pressure ulcer on the right heel
sources have a right to thIS information when they expose themselves to an episode of care. Prediction is not new. Previously. prc.::dictJOn \liaS klllWill as short- and long-term goals. A short-term goal usually refers to a 2- to 4-weck period of care and a long-term goal is what wi ll be achieved at discharge. The functional outcomes goal section of the report has three components rclatcd to the predicted functional outcome: the aCllvity that" 111 occur. the performance expected and the due date. For example. with respect to wounds the "acti\lly" may be erythema free. the "performance" change
to proliferatIOn phase. and the "due date" 2 to 4 weeks. This segment of the report promotes continuity of care when difTerent or multiple clinicians are involved in the patient's care. In Part VI . the final step in the FOR is to present the trelltment plan lI'j,1t rafional£'. Subscqucnt chapters Will provide the rationale for many difTcrent interventions based on established theory and science. Th,s IS the place \\ here the clJnician reveals the clinical judgment used to select a treatment plan. For examp le. the clinician "files thai Ihe wound
24
WO UND CARE
is in a chronic inflammatory phase related to a large amount of necrotic tissue. has fai led to respond to prior treatment interventions. and requires debridclllcIH to initiate the healing process. This becomes the rationale for selecting the treatment strategy (eg, pulsatile lavage with suction) to clean up the necrotic debri s. A I>pl ying FO R to Form H CFA-700 To become familiar with the diagnostic process and
the FOR method, review the samp le case in Exhibit 1- 2. Physica l therapists arc accustomed to using the Form 1-1 FA-700 (I 1-91) for documentation (see Appendix I-C). The HCFA-700 and the FOR method of reporting were designed to work together. A template added to the I-ICFA-700 (Appendix I -D) guides the physical therapi st through documentation of the diagnostic process and FOR methodology. Appendix I-E is a sample ease report on the I-I CFA-700 using FOR methodology.
I
Clinical Wi sdom Some faci lities have the HCFA-700 form on computer. If a template can be added to the form with the items as listed formatled to fit the computer field, it would help the physical therapist complete the documentation in an orderly and consistent manner. For those using a hard copy of HCFA-700, a template can still be useful to ensure that all items are recorded following the format.
Reevalu ati on Once the target outcomes and goals have been determined the reeva luation process is really quite simple. The clinician uses performance indicators to mcasurc the patient'S progress toward the outcome within the desired time frame. For example, if the target outcome is patielll .'s wOllnd will demollstrate 25% reduction ill si;e lI'ithill 2 lI'eeks. then the clinician simp ly monitors wound size over the 2-wcek period of time and then determines whether the wound has reduced surface area size by 25% at the end of week 2. I f the wound has decreased in size more than 25%, the outcome has been exceeded. I f the wOllnd has just decreased in size by 25%. the outcome has been acceptably met . If the wound has fai led to decrease in size by 25%. the outcome has not been met
and the goals must be adjusted and interventions reviewed. Reevaluation is an ongoing dynamic process that will recur on a regular basis following reexamination of the effects of treatmenLAt that time, goa ls and outcomes may be adjusted, new goals developed, and interventions modified . The PSST and SWI-IT tools described in Chapter 5 are validated methods for monitoring wound hea ling outcomes that are used throughout the evaluation and reevaluation process.The tools provide a quick checkup at regular intervals to determine efficacy of treatment or to alert the clinician to deviations from the expected course. Since utilization management attempts to innuence the clinical path from the beginning so as to reduce devia tion from an expected course and to produce optima l outcomes. th e adjustment of goals and expected outcomes should be minimal. The clinician must make accurate predictions at baseline. Multiple approximations to reach the target outcome will not be tolerated by patients or third-party payers. For example. the APTA Guide to PT Practice l4 lists wound management guidel ines regarding range of visits and length of episode of care by physical therapist s for patients with wounds. This range represents the lower and upper limits of services that it is anticipated that 80% of tile patients/client s with such wounds will need to achieve the predicted goals and outcomes (prognosis) listed. Multiple factors may modify the duration of the episode of care, frequency. and number of visi ts. Wounds extending into fascia. muscle. or bone (integumentary pattern E). for instance, will require 4 to 16 weeks (12-112 visi ts) for an episode of care (all types of etiologies included). The prognosis for wounds of thi s severity is that over the course of 4 to 16 weeks of care by the PT that one of the followin g will occur: o o • •
Wound will be clean and stable. Wound will be prepared for ciosure. Wound will be closed . Immature scar will be cvidcnt.14Ip'6l1~)
CONCLUS ION The diagnostic process described in thi s chapter is intended as a framework for clinicians working with patients with wounds. The information mayor may not be new. but there are limes when review ofmalcrial may be helpful. This chapter is meant to assis t those clinicians new to the diagnostic process or unfamiliar with its usc. Use of clinical judgment with diagnostic reasoning is one oflhe essential prac tice tool s that nurses and physical therapi sts use with the patients they serve.
The Diagnostic Process
REFE RENCES
25
7.
Jette AM . 1lhysical disablement concepts for physical therapy research and practice. Ph),s Ther. 1994;74:380 ·386.
I.
Clifton. Ow, Utilization management: whose Job is it? Rehab Man· age. June/July 1996;38:44.
8.
Swanson G. The IDH Guidebook/or Physica/Therapy. Long Beach. CA: Swanson and Company ; 1995.
2.
Bergstrom N. BcnnclI MA. Carlson C. ct al. Treatment of pressure ulcers. C/imca/ Practice Guideline. No. 15. Rockville. MD: US Department of Health and Human Services, AHCPR Pu blication No. 95-0652. December 1994.
9.
Sussman C. Case presentation: patient with a pressure ulcer on the coccyx . Paper presented at APTA Scientific Meeting and Exposilion, Minneapolis. MN . June 1996.
10.
3.
lI isen lB. White 1)1:: Medical nmnagcmcnt of su rgical patients wilh diabetes, In: Levin ME. O'Neal LW. Bowker JH . cds. 71Ie Diabetic Fool. Chicago: CV Mosby: 1993.
Lazarus GS. Cooper OM. Knigh ton DR . ct al . Definitions and guidelines for assessment of wounds and cvaluation of healing. Arch Dan/lIfOl. 1994; 130:489-493.
I I.
4.
Swanson G. The Guide to Phy.\ ical ThE-rapi!)1 Practice. vol I. Presentation at California cll:I ptcr. APTA. S:1Il Di ego. CA. October 1995 .
Swanson G. What is an outcome? And what docs it mean to you? VI/rohol/lltls. (Ca lifornia Private Practice Spcciallntercst Group Cali/omit! APTA). 1995; 94-51 :7.
12.
Swanson G. Functional outcomc report: The ncxt generation in physical Iherapy reporting in docume nting physica l thcrapy Qutcomes. In : Stuart D. Ablen S. cds. Docume"'ing I'hysical Therapy Outcomes. C hicago: CV Mosby: 1993:101 134.
13.
Staley M, Richard R. et a!. Functional outcomes for the patient wilh burn injuries. J Bllrn Care Rehab. 1996: 17(4):362367.
14.
Guide to physical therapi st pmctice. Phys Ther. 1997;77: 1593 1605.
5.
6.
Amcnc:m Physical Therapy Associalion. A guide to physicallhcrapy practice. I : a description of patient management. Phys Ther, 1995:75 :707 764 Oocnges MD. Moorhouse MF. Burley JT. Applicatioll of Nursillg Process (tnd Vurslllg Diagnosis. 2nd cd. Phil ade lphia: EA . Davis: 1995.
26
WOUND (",\It!
Appendix 1- A: Patient History Form
#___________
Medical Record Name' _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ __ Street Addrcss, _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ __ City, State, l1p _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ __ Telephone Number (-,-,-,--,---_ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _-,-,,---,---_ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ __ Sex: M f ___ lIeight ' _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ Wetghl. _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ __ Religiolls Preference: _____________________________________________
What is your primary reason ror seeking woulld care today'! ______________ Ilow long has your ""''QUlld existed'! ________________________________________
Who referred yOll hcre? _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ __ Who has bl!clllreating you hefore today? _ _ _ _ _ _-,--,---______________________________ Can you describe what you hu\c heen using on your wound'! _______________________________ Who has been helpmg you \.. l1h your wound care? __________________________________ 110\\ have yOll been paYlIlg for your supplies'! ____________________________________ Ilave you l!\cr had surgery'! Type: -,_ _",._________ Other? _ _ _ _ _ _ _ _ _ _ _ _ _ _ __ Do you have rilly allcrgies'! Medications (Sulf'l. PCllIcillin) _________ Packs per day: # of years: _________________ Do YOli smoke" Ilowoflt.,'1l do yOll u~e recreational or illicit drugs? ____________ 110\\ oOen do yOll drink alcohol'! _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ __ Do yOll ha\'l~ any palll? ______________________________________- - - - - - - On a scale oro 10 (0 No P;:lin, 10 Sc\"t!fC Pain). what is your p
!lavc you ever bcen told you had or do you currently have any of the following:
Stroke: _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ __ (j'.II1grene: ProbJcm~
\\ nh clrculallon:
Arterial: Venous: Diabetes:
Parkinson's: ____________________ AI£heIl11ers: _-,_ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ __
Congestlvc hearl lllilurc: ________________ l>roblel11s sleeping: __________________ 1 ' l1lphyscm~1
Bronchitis: _____________________ Chronic obstructl\c pulmonary disease: Problems controlllllg unne: Problcl1l:-; controlling bowels: ______________ AtherosclerosIS,;'ilrleriosc!crosls _ _ _ _ _ _ _ _ _ _ _ __ Malnutrition Dehydrallon Thyroid tlisurdcr: ___________________
S(I///'('('
COPYright
i
DeJn P ",me. >\1 D. F\CS, p..\
Pr~SCI1l Past Hypertension : ____________________ Cancer: _________________________________________ C'heI1lOlhcmpy: _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ __
RadiatIOn therapy · A1tcrn~lti\'c treatmcnts: ___________ Swollen glands: _ __ Muscle spasms: ___________________ Polio or post-polio syndrome: ______________ Quadriplegia paraplegia: _ _ _ _ _ _ _ _ _ _ _ _ _ _ __ Myelomeilingocele: Dl!creascd sensation Artlmtls: _ _ _ _ _ _ _ _ _ _ __ Decreased acti\ lIy: __________________ IIIV "rAIDS: _ _ _ _ _ _ _ _ _ _ _ _ _ _ __ Ikplltilis B: _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ __ Decrcast!d appetite: ________ Problems with mobility _ _ _ _ _ _ _ _ _ _ _ _ _ _ __ Changes ill \\elght greater thrln 10 pounds; _________ Pacemaker: _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ __
The Diagnosti(' Pro('e.\',\
Appendix I- B: Focused Assessment for Wounds Medical Record # _ _ _ _ _ _ _ _ _ _ _ _ Namc _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ __ Attcndmg Physician ' _ _ _ __ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ __ Referral Source: _ _ _ MD Site: _ Olliee _Acute Ilospilal _ FacIlity Namc
Addrcss
ursc Other Subacute Center _ Nursmg Ilome _
Assi sted Livmg _
Home
Other
Ilts, bed #: _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ __
Physical 1~ \all1 : - year old M F' acqUIred non-healing wound(s) on Prior wound management lIlc1udcs: Ilast Medical I "story is positive for the following: Alcoholism
Allergics:
CVA
NIDDM _ _ _ _ _ __
Gangrene
Complications of DM Weakness _--:-:-,-_ _ _ _ __ Paraplegia/quadriplegia Illlll10bi III yicontracturcs Parklllson:Ii
PVD Arh::ri ~11
InsulTiclcncy
CAD IDDM Vitals: TP R Braden Scale: Sensory MS Moi:-.ture ACIJ\II Y Mobilit y Nutnlloll Fnctlon Shl!ar
BP: LIR totally limited constantly moist bedfast I. 1000', llllllloblle I. \cry poor freqllent slidmg
(sil'stand ly ing)
2. very lillliled 3. slightly limited 2. very mOist 3. occasionally 1110lst 2. chairfast 3. \\.alks WI,ISSlst 2. vcry IUnited 3. slightly hnlltcd ) '2 daily porllon 2. 3. most of portion 3. independent correction 2. feeble corrections Braden Sca le Tota l:
4 4. 4 4
no lI11palrmcnt
dry
\\alks frequcntl y full lllobllll Y 4 cats c\ crythlll£
\.1ental Status: Alert & Orjcllled X 3 - Other Skill: (mol,t . dry. !laky, scaly. condition of nails) : _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ __ Rubor cyano:;:.I;' atrophy dermatitis hair loss. rash. erythema, [-FNT (Eyes s unken, swollt:n lymph nodes) _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ Mucous Membmnes MOISt : Nellro ('ral1lal nerves. sensallon): _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ __ Endocnne (Blood sligar other): Re:-.rmatory: I lings Clear Other' CardiaC: Regular Rate & Rhythm ' Qth~ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ __ Ahdomen: (i-Tube · Soft. Supnle/Withoul Mas:;:.es QrTendcrness· Other Penneal : Skin Intac! Other: _ _ _ __ Lo\\cr EXlrelllllles: Ankle Brachi.lI Index: _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ __ Iluiscs Palpable: Don;ail s PediS _ _ _ _ _ _ _ _ _ Posterior Tibial _ _ _ _ _ __ Popliteal Pulse Quality: lloundlllg Strong _ _ _ _ _ Weak B:lrciy Ilalpabk
Doppler: L +
R + _ _ _ __
Fdem3 Circumference: (L) _ _ _ _ :(R) I""unctional Assessment : ADLs: Independent _ _ _ _ MlllImal Assisl Mod ASSi st Total ASS ist Lahs:Nulnllon llet : ° 0: TP : Alb : Prcalhumin _ _ _ _ _ _ : Other
WBC
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. LYles _ _ _ _ _ _ _ _ _ _ _ _ _ __
27
28
W OUND C."RI
Appendix l-C: Form HCFA-700 Departmcnt Of Il ea lth And Ilu man Serviccs Il calrh Can: Flnancmg Adnllnlstratlon
FORM APPROVFD
MedIcare Part 0 A
0
13
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Appendix I-D: HCFA-700 Form with FOR Template To Guide Documentation in Italics Department
or Health And Human Services
Ilealth
Hnancing Adl11l11l~trJllon
Lin!
MEDICARE PART 181 A
DB
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20
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Appendix I - E: Sample Case Report Using HCFA-700 Dt!partl11cnt
or Ilcalth And Iluman Sen ices
Ilcalth Care i-Illanc ing Administration
I'LAI\
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181 A
0
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B
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,
COLOR PLATES PROGRESSION THROLJGH THREE PHASES OFWOLJND HEALING Plates 1-6
The paticm is a 97-year-old nursing home resident with Stage IV pressure ulcers in the bilateral rib cage and sacral area.
t.
3.
Chronic wound converted to acute inflammation phase.
(I) (2) (3) (4)
Yellow, strin gy slough; Edema; Skin color changes (rcd), erythema; Rib bone noted in superior ulcer. Wound healing phase diagnosis: acute inflammation phl.lsc. Wound severity diagnosis : Impaired integumentary in tegri ty secondary to skin involvement extending inlo fascia, muscle, bone. Source: Reprinted with permission, copyright © C. Sussman.
2.
Same wound as in Plate I. ( I) Rolled epidermal ridge around granulation base; (2) Brown hemosiderin staining . Wound healing phase: prolireration phase. Source: Reprinted with permission. copyright ~ C. Sussman.
Same paticni as in Plate I. Chronic wound: converted to acute proliferation phase. This is a sacra l wound with stringy. yellow slough evident. Predomi nant wound hea ling phase diagnosis: Proli reration phase. Wound severity diagnosis : same as in Plate I. Source: Reprinted with permission, copyrig ht rCl C. Sussman.
4.
Same wound as Plate 3 progressing through the prolireration phase or healing. Wound contracting and prolirerating. Note change in size, shape, and depth compa red to Pl ate 3. Source: Reprinted with permission, copyri ght C. Sussman.
Color Plates Page 2
3/31
AL
I!J
S.
Note sustained wound contraction evident between Plates 4 and 5. Wound is in both epithelialization and proliferation phases. Source.' Reprinted with permission, copyright,~ C. Sussman.
6.
The wound is completely resurfaced. II is
In
the remodeling
phase. Source: Reprinted with permiss ion. copyright ·(, C Sussman.
Color Plates Page 3
PROGRESSION THROUGH PROLIFERATION PHASE Plates 7-9 Plates 7 to 9 show a sacral pressure ulcer progressing from chronic inflammation phase through the proliferation phase of wound healing. In Plales 8 and 9 the wound edges demonstrate epithelia l migration with new epidermis clearly visible as bright pink 10 this darkskinned patient In Plales 7 to 9.
7.
Chronic inflammation phase. Note the following wound char-
actenstlcs: ( I ) Sangumeous drainage; (2) (3)
Muscle exposure; Hemosiderin staining surrounding the wound. Sourc:e: Reprinted with permission, copyrightt.. B.M. BatesJensen.
9.
8.
Acute proliferation phase. Note the attached wound edges from the 12-o'c1ock to 6-o'c1ock positions and how granu lation tissue fil ls up onc side of the ulcer. Source: Reprinted with permiSSion, copyright ·c, B.M . BatcsJensen.
All of the wound edges arc now attached to wound base Note the presence of fibrin (yellow) wlthm thc granulation tissue . Ready for eplthcllalization phase. Source: Reprinted with permiSSion. copyright (" B.M Bates-Jensen
Color Pl(l{es Page 4
ABNORMAL PROLIFERATION PHASE Plates 10 and II
10. Acu te proliferation phase . ( 1) Hemosiderin staining; (2) Sanguineous drainage. Source: Reprinled with permission , copyright to S.M . BatesJensen.
WOUND IN REMODELING PHASE Plate 12
10/27/87 Left hip healed
t 2. An example of a wound in the remodeling phase of wound hea ling. ( I) New epitheli um (scar); (2) Hype rpigmcntalion (Hemosiderin-staining). Source: Reprinted with pemli ss ion , copyright © I3.M . BatesJen sen.
1 J. Chro nic proliferation phase with attributes of infection . ( 1) Hemorrhagic area of tTauma; (2) Hypopigmcnlation ; (3) Dull pink gran ulati on tissue. SOl/ree: Reprinted with permission , copyright ~ B.M. BatesJensen.
Color Plales Page 5
ANATOMY OF SOFT T ISSUE Plate 13
13. FullMthickness skin resected from calf. (I) Vascularized dermis; (2) Yellow healthy rat tissue ; (3) White fibrous fasc ia; (4) Dark red muscle tissue; (5) Tendon covered with peritenon: (6) Blood vessel. Source: Reprinted with permission. copyright to 1. Weihe .
WOUNDING OFTHE SK I N Plates 14-18
15.
Intact skin with subcutaneous microvascular bleeding
suggesting deeper trauma located over a bony surface.
14. Superficial wound ing of skin . ( 1) This wound wou ld be classified as a stage I pressure ulcer; (2) This wound is perineal dermatit is. Note location over rectum . Source: Reprinted with permi ss ion, copyri ght © RM. BatesJensen.
and would be classified as a stage J pressure ulcer; (2) Maceration of periwou nd sk in. Source: Reprinted with permissio n, copyright
Color Plates Page 6
16. Penneal dermalltls with classic differentiating characteristics of dilTuse erythema across buttocks and permeal area and partial-thickness skill lo~s, ThiS wound IS In the acute inflammation phase and was not staged. (I) Multiple. partial-thickness lesions with Irregular borders; (2) Lesions occur across area smgly and In groups and may or may not be over a bony prommcncc. Sourc/!. Repnnted with permission. copyright(." B.M. Bates-
t 7. Acute mflammation phase. partial thickness stage II pressure ulcer located over bony prommence.
( I)
Erythema and edema;
(2)
Reticular layer of dermis
S{}urce: Repnnted with permiSSion. copyright ( 8.M, Bales-
Jensen.
Jensen.
IS. Full-thickness skin loss illlhc prollrer:.lIioll phase. The \\/Olllld was not duc to pressure and was not staged Sown' · Repnlllcd with permissIOn. copynght c C Sussman.
Color Plales Page 7
ASSESSMENT OF DA RKLY PIGMENTED SKIN Plates 19-22
12/12
19. Pressure ulceration with multiple, small, stage 11 open areas. Wound is in acute inflammation phase. Note onset date 12/ 12. ( I) There is a clear line of dermarcation between hea lthy tissues and inflammation; (2) Evidence of discoloration. edema. and induration suggest underlying tissue death . Assess tissue temperature and pain. Source: Reprinted with permission. copyright 0 C. Sussman.
2 1. Assessment of inflammation attributes in darkly pigmented skin. (I) Erythema gives skin a reddish brown glow; (2) Hemorrhage of mic rovasculatu re gives skin purplish gray hue; (3) Eschar- nolc tissue texture change to hard black; (4) Usc skin color of adjacent skin for reference of normal skin IOnes. Source: Reprinted with permission, copyright 0 B.M. BatesJensen .
20. Same pressure ulceration as in Plate 19. Three weeks later the skin now shows evidence of the severe tissue destruction that occurred at the time of trauma . Note delayed manifestation of injury at the skin level. The date was 1/3. (I) Continued demarcation of inflammation; (2) Irregular diffuse wound edges; (3) Eschar, black and adherent ; (4) Partial-thickness skin loss. There is enlargement of stage II ulcers compared with those in Plate 19. The correct staging for this sacrococcygeal pressure ulcer is at minimum a stage Ill. Once eschar is removed, true depth of tissue loss can be determined. Documentation should reflect a combined area of wounding, including all three visible ulcers and the area of inflammation. This is the overall size estimate for the pressure ulcer. Inflammation now chronic. Source: Reprinted with permission, copyright C. Sussman.
22. Assessment of epithelialization and remodeling attributes in darkly pigmented skin. (I) New epithelial tissue that is light red ; (2) New scar tissue that lacks melanin and is bright pink ; (3) Old scar tissue that lacks melanin and is si lvery white; (4) Residual hemosiderin staining. Source: Reprinted with permission, copyright C. Sussman.
Color Pililes Page 8
ABNORMAL WOUNDATTRIB UTES
Plates 23 and 24
23. Wound is in chronic proliferation phase. Hypergranulation tissue; absence of epithelia lization phase. Source: Reprinted with permission, copyright S.M . Bates-
24. There is an absence of epithelialization phase. Hyperkeratosis on heel ulcer of a IOO-year-old woman. Source: Reprinted wi th permission. copyright C. Sussman.
Jensen. NEC ROTI C T I SSUE TYPES
Plates 25-30
25. I-lard. leathery eschar in the chronic innammation phase. Notice how the eschar looks similar to a scab. Source: Reprinted with permission. copyright B.M. Bates-
Jensen.
26. Soft, soggy, black eschar in the absence of innammalion phase. Source: Reprinted with perm ission, copyright '0 B.M. BatesJensen.
Color Plates Page 9
27. Chroni c wound converted to ac ute inflammation phase with ye ll ow, mucinous slough. Source: Reprinted with permiss ion, copyri ght rO C.Suss man .
28. Necroti c fatty ti ssue . Source: Reprinted with permi ssion , copyri ght
29. Esc har before debridement . Absence of inflammation phase. Source: Reprint ed with permiss ion, copyri ght © C.Suss man.
30. Eschar a fter debridement. Necrotic fat and fasc ia often ca ll ed slough. Restart of inflammation phase. Source: Reprinted with permi ssion, copyright () C.Sussman .
C.Sussman.
Color Plates Page 10
WOUND EDGES Plates 31-34
• •
31. Absence of prolife rati on phase. Wound with no epithelial izatio n present. The wound is clean . bUi nonpro fil crating. Source: Reprinted with permi ss ion, copyri ght B.M. BatesJensen.
32. Same wound as in Plale 3 1. Wound is in acute pro liferati on phase with evidence o rnew epithelia l mi grat ion. Source: Reprinted with permi ssio n, copyri ght 10 B.M . BalcsJense n.
I ~ T
33. There is an absence of epithelia li zation phase. ( 1) Wound lacking epitheli ali zation due to chronic fibros is and scarring at wound edge. Chroni c pro liferation phase. Source: Reprint,cd with permission, copyri ght B.M . BatesJensen.
34. An exampl e of know ledge gai ned fro m care ful exa mination o rthe wound edge. Wound is in chronic proliferation phase. ( I) New pressure-induced damage (hemorrhage) ; (2) Maceration from wound fluid : (3) Fricti on injury with signs of inflammati on. Source: Reprinted with permi ssion. copyri ght 0 8 .M. BatesJense n.
Color Pla tes Page II
SU RGI CAL DI SSECTION FOR TUNNELING
Plates 35 and 36
35. Unobservable tunneling. Source: Repri nted with permi ss ion, copyright © 1. Wethe.
36. Same wound as Plate 35 with surg ical d issec ti on demonstrat ing the exte nt o f the tunne ling
process. Source: Reprinted wi th permi ssion. copyri ght
1. Weihe.
Color Plates Page 12
UNDERMINING AND TUNNELING Plales 37-39
37. Wound with tunneling before insertion ofa callan-tipped applicator. (I) Ulcer reoccurrence at site of old scar tissue; (2) Skin bridge between two open ulcers: (3) Surrounding skin has unblanchable erythema. Wound edges rolled under demonstrate chronic inflammation phase Source: Reprinted with permission. copyright ,0 B.M . Bates-Jensen.
38. Same wound as in Plale 37. The wound overall size is much larger than the surface open area. Tunneling is present. (I) Note bulge from end of cotton-tipped appl icator. Source: Reprillied with permission, copyright <,~, B.M. BatesJensen .
39. Undermilled wound. (I) Note shelf. Source: Reprinted with pCnlllSSlon. copyright
I..
C Sussman
Color Plate.. Page I]
REA DI NG T H E DR ESSI NG: WOUN D EXU DATE ASSESSMENT
Plales 40-45
40. Clean wound in chronic proliferation phase. The quantity o f exudale is detemlined by the amount of dressing saturated by the drainage. (1) M oderate to large amount of sanguineous ex udate; (2) Moderate to large amount of purulent exudate ; (3) Eva luate for infection. Source: Reprinted wi th permission, copyright 10 C. Sussman.
42. Wound wi th compos ite dressi ng. Dress ing s hows moderate amount of se rosanguineous exudate. The wound bed s hows gelatinous mass thai may be ge latinous edema . Evalu· ale for trauma. Bright pink ski n is scar tissue. Source: Reprinted with permi ssion, copyri ght C. Sussman.
4 1. Wound with packi ng still present. (I) Mode rate amount of scrous exudate on dressing; (2) Green co lor of ex udate s uggests possible infection. Source: Reprinted with permission, copyright C . ussman .
43. Wo und with co mpos ite dress in g s hows scant a moun t of serous exudate. Wound is in chroni c inflammatio n phase. There is an absence o f pro liferali o n pha se. Source: Reprinted with permi ss ion , copy ri ght C. Sussman .
Color Plates Page 14
44. ( I) Large amount o f serous dra inage; (2)
NOie how drainage fl ows into secondary dress ing;
(3)
Nole green tinge to edges of dressi ng, suggesting anaerobic infection (eg. pseudomonas). Mo nito r for a degenerative change in ex udate Iype from present scrous to puntlent (eg, greener. th icker, and more opaque). Source: Reprint ed with permission, copyright @ C. Suss man.
45. La rge amount of purul ent ex udate. ( I ) Thick, opaque cloudy appeanlnce: {2} Note green co lor. Assess fo r odor. Source: Reprinted w ith permi ssion, copyri ght
C. Sussman.
Color Piates Page 15
A RTERI A L ISC H EM IC WOUN DS Plates 46--48
46. Severe arterial ischemic disease with Illultiple ischemic ul cers below the ankle bilatera lly. Wounds are in
absence ofinf1ammalion phase with hard, dry, black eschar covering. ( I) Note trophic changes on foot, ev idence of sca ling. SOll rce: Reprin ted with permission. copyright
47. C lassic ischemi c ul ce r. Note: (1) Chroni c infl am mation with ce lluliti s: (2) Punched-out ulcer edges: (3) Coverin g of dry, black eschar: (4) Location over latera l malleolus. SOllrce: Reprinted w ith permission , copyri ght
C. Sussman .
E. Fow ler.
48 . Isc he mic u lcer in chronic pro li ferati o n and absence of epi thel iali zati on phase. Note : (1) Pun ched-out ulcer appearance wi th rolled wound edges; (2) Dependent rubor. Source: Rcprintcd w ith perm iss ion, copyri ght C. S ussman.
Color Plales Page 16
VE 'OUS DI SEASE Plates 49- 54
49. Isc hemic ulcer in a 55-year-old male smoker with a 4-1110nth history of having "blistered" hi s ankle wi lh the subsequent formation of a painful ulcer. He was diagnosed as having a venous stasis ul cer and was trea ted wit h wet- Io-dry dressing changes three times per day. Despite good comp liance hi s ulcer failed to improve. The physica l exam revealed absent femoral, popliteal. and pedal pulses with an AS! of 0.35 . The ulcer edge was irregular, bUI the base was clean and had adequate granulation tissue . Even though the ulcer was located proximal to the medial malleolus. the typical locatio n of chronic venous stasis ulcers, thi s patient did not ex hibit any of the physical signs of chronic venous insufficiency such as brawny edema, hypcrpigmclltation, or stasis dennatitis . Sec Chapte r 14. Diagnosis and Management of Vascular Ulcers. for photos of angiogram on same patient (Figure 14-4). Source: Reprinted with permission, copyright C. Donayre.
SO. Structure of the venous wall. Cross-section of a venous branch of lower ext remity reveals a relative standard wall structure. The intima is covered by uninterrupted endothelium which is connected to a thin connective ti ssue layer. The media is structured much morc loosely than corresponding arteries, and is composed of distinct layers of collagenous and clastic fibers between which narrow strips of smooth muscle are found . Source: Reprinted with permission, copyright C. Donayre.
ColoI' Plales Page 17
SI. Venous stasis ulceration. This 49-year-old male with a 3-year history of recurrent venous ulceration was being treated with Unna boot changes once a week. Physical exam revealed patent femoral, popliteal, and pedal pulses. An en larged. dilated, and tortuous greater saphenous vein was easi ly visua li zed with the patient in a standing position (white arrow). A duplex scan confirmed isolated greater saphenous vein incompetence, with a normal deep and perforator vein system. Source: Reprinted with permission, copyright C. Donayrc.
52. Shallow and irregularly shaped lesion wit h a good granulating base and the associated physical signs of chronic vcnous insufficicncy such as hyperpigmentation. ch ronic scarring, and skin contraction in the ankle reg ion are readily identified. Note the classic characteristics of venous disease: ( I) Irregular edges; (2) Shallow ulcer; (3) Evidence of hyperpigmentation (hemosiderin staining) surrounding ulcer; (4) Location above the medial malleolus. Source: Reprinted with permission , copyright 4:J C. Donayre.
Color Plates Page 18
53. Stasis dermatitis. There is an absence of Cpilhilia lization phase. Evidence of: ( I) Brawny edema; (2) Trophic skin changes; (3) Hemoside rin staining (hyperpigmen tation); (4) Multiple shallow ulcers . Source: Reprinted with permission, copyright B.M. Bates-lensen.
54. Close-up view of same leg as in Plate 53 and shows evidence of: (I) Edema leakage through wounds; (2) Scaling and crusting (trophic changes) due to lipodcrmatoscl cros is. Source: Reprinted wi th permission, copyrigh t B.M. Bates-lensen.
Color Plates Page 19
WOUND HEALI NG WITH ELECTRICAL STIMULATION-CHAPTER 16
Plates 55 and 56 Palient wi th vascu lar ulcer treated wi th ED and HV PC (sec Chapter 16 for details).
)
,
e.9 ,
•
55. NOie beefy red granulati on ti ssue and island of epidermal ti ssue in full thi ckness wound . The wound is in acute proliferation phase on 12128. Source: Reprinted with permission, copyright 10 C. Sussman.
56. Same wound as in Plate 55 . Note epidermal migration from wound edges, island and wound shape changes. ( I) It had progressed to the acute epithe li alization phase by 2117; (2)
Note hyperkeratotic ski n changes due to old burn wounds and poor circu lation. C. Sussman.
Source: Reprinted with permission, copyright
Color Plales Page 20
WOUND HEALING WITH PULSATILE LAVAGE WITH SUCTION- C HAPTER 17 Plates 57-59
57. ( I) Ex posed artery in infected bypass gra ft donor si te in lower leg. SOllrc:e: Reprinted with permi ssion, copyright H. Loehne.
58. I)yodcrma ga ngrenosum ul cer on med ia llowcr leg of 8 years' durat io n. Source: Reprinted with permi ssion, copyri ght H. Loehnc.
59. Pyoderm a gangrcl10s um ulcer (sa me ulcer as Pl ate 58) on medial lower leg after 2 wee ks of treatment with Pulsavac ll System. Source: Reprinted with permission. copyright l-I . Lochnc.
Color Plates Page 21
WOUND HEALING WITH PULSED SHORT WAVE DIATHERMY CASE STUDY I--CHAPTER 18 Plates 60-62 Palic ni with pressure ulcers treated wit h PSWD (see Chapler 18 for dC lails).
60. Pali en! wit h pressure ulcers. PSWO was sta rted on 8/ 16. ( t ) Black eschar on heel wound surrounded by partial-thickness skin loss. There is an absence o f infl ammation phase; (2) Black eschar over the 5th metatarsal head. There is an absence of inflammation phase. Source: Reprinted with permission , copyr ight ~ C.
6 1. Same ul cer as seen on heel in Pl ate 6210 days aOer start of PSWD.
( I ) Eschar removed to soft necrosis; (2) Reepi lhei ial iz3tio n of partial -thickness sk in loss; (3) Eschar removed 5th malata rsal. Wound healed. Source: Reprinted with pennission. copyright C. Sussman.
Sussman.
62. Same hee l ulcer as in Plates 62 and 63 ( 10/7). The ulcer hea led and is shown in the remodeling phase. Source: Repri nted with permission, copyriglll C. Sussma n.
Color Plates Page 22
WOUND HEALING WITH PULSED RADIO FREQUENCY STIMULATION CASE STUDY 2-CHAPTER 18
Plates 63 and 64 Patient with incisional wound treated with PRFS (see Chapter 18 fo r detai ls).
63. Patient with an incision from an above-lite-knee amputation left open for delayed primary intcllIion hea ling . Wound is in aClite inflammation phase. Start of treatment with PRFS 8/3.
( I) (2) (3)
Sutures placed; Edema; Erythema and ti ssue tension;
(4 )
Yellow muci nous sloug h in incision line. Source: Reprinted with penni ss ion . copyright
64.
C. Sussman.
Same incision wound as in Plale 63 on 8/ 17 (14 days later). Note outcomes: edema frec. nec rosis free, wound co ntract ion and granulation. The wound is in acute proliferatio n phase and ep ithelia lization phase. Source: Reprinted with permission , copyright © c. Sussman.
Color Plates Page 23
WOUND HEALING WITH ULTRASOUND CASE STUDY I - CHAPTER 19
Plates 65-67 Patient with a ve no us ulcer 24 hou rs after onsel. (See Chapter 19 for detail s.)
65. Wound is in acute inflammation phase and shows subc utaneous hemorrhage (ecc hymosis)
associated wi th ve nous disease. Source: Repri nted with permission, copyright
•
C. Sussman .
9/16 - EF 8/22 - EF
66. Same wound as Pl ale 65 , 4 days a fter 2 treatments with ultrasound . Shows absorpt ion of ecchymos is seen earlier. There is part ial-thi ck ness skin loss. The wound is in acute inOammalion phase. Source: Reprinted wi th permi ss ion, copy ri ght \C C. Sussman.
o
67. Same ul cer as in Plates 65 and 66. 4 wee ks after sta rt o f ult rasound. Note wound contraction co mpared w ith th at in Plale 66. There are so ft irregular wound edges an d new epithelizatio n. The wound is in epi the li aliza tion phase. Source: Repri nted with permi ssio n, copyright C. Sussman .
ColoI' Plate,· Page Z4
WOUND HEALING WITH ULTRASOUND CASE STUDY 2-CHAPTER 19 Plates 68-71 Patient with blood blister on heel secondary to pressure. treated wi th ultrasound (US).
68. Acute Inflammation phase. Blister with bloody nuid at day of identifi cation. Source: Reprinted with permission, copyrightc' C. Sussman.
69. Same wound as Plate 68 withou t blister roof. The pcriwound skin was treated with daily US for 4 days prior. ( 1) Note area of apparent necrosis, hematoma. There IS an absence of inflammation phase. Source: Reprinted with permission, copyright l C. Sussman.
10/8- MM
9/2- MM
70. Same wound as Plates 68 and 69 afler2 additional peri wound US treatments. Note absorpt ion of he mal om a by reduced size of necrotic area and mild erythema surrounding the area of necrosis. The wound is in acute inflammation phase. Source: Repnnted with permission. copyright c C. Sussman.
71. Same wound as Plales 68, 69, and 70. (1)
Note focal area of necrosis. Time of change in treatment ES and sharp debridement. The wound shows the start of proliferation phase. Source: Reprinted with permission, copyright C C. Sussman. 10
CH A PTE R
2
Wound Healing Biology and Chronic Wound Healing Carrie Sussman
This chapler reviews ri ve basic wound healing models, the biology of acute wo und healing, fetal wound healing,
letes are seen and treated immediately for superfi cial so ft ti ssue inj uries with reduced loss o f playing tim e and pain . In pati ents with functi onal impairments, pain and ti ssue tension from congestion in the ti ssues often li mit functional . activiti es and result in diminished mobility, placing th e individual at risk for furthe r wo unding. Part IV, Management o f Wounds with Phys ica l Therapy Technologies, points out benefits from intervention for superfi cial wounds (eg, reabsorpti on of hemat oma for faster healing, incl ud ing stage I pressure ulce rs and grade I ne uropathi c ul ce rs). Color Pltlles 65 10 71 illustrat e how early intervention reduces hematoma. Case studies are described in Chapter 19, Ultraso und.
and factors that affect chronic wound healing. The clinician must fi rst understand the norm al ac ute healing biology so as to recognize the current status of the wound and to diagnose ab normal wou nd healing leading to chronici ty.
WOUND HEALING MO DELS There are f ive basic wound healing models for acute wou nd s, and similarit ies exist in a ll : ( I) supe rfi cia l wound heali ng, (2) primary intenti on wo und hea ling, (3) delayed primary intenti on wound healing, (4) parti al-thi ckn ess wo und healing, and (5) secondary intention hea ling.
Primary and Delayed Primary Hea lin g
Superficia l Wound Healing
Primary healing is drawing the wound edges together to achi eve closure (eg, surgical wounds). There are three co nsiderations in closing wounds by primary intention: there is no major loss of subcutaneous ti ssue, the edges are smooth and cl ean cut, and the wo und is not contaminated with microorganisms or foreign bodies. Primary intention healing norma lly occ urs qui ckly but less visibly than parti al-thickness or secondary intention healing. Th e result is minimal residual sca rring with closure in 3 to 7 days. Delayed pri mary intention healing is chosen for wounds that are contaminated with microorgani sms or debri s, wh ere there is a large ti ssue loss, and cl osure by primary intention would result in intolerable ti ssue tension or put the patient at ri sk of infection.2 In delayed primary intention, the wo und is left open, although stitches are placed in th e subcutaneous and fasc ial layers. The wound is usua1Jy closed in 5 to 7 days, afte r the ri sk of infecti on is significantly dec reased or part o f the ti ss ue loss has been replaced.
An alteration in th e superfi cial skin such as by pressure, including shearing and friction (s tage I pressure ulcers), fi rstdegree burns, and contusion, produces an inflammatory repair process. There is reason lO believe that thi s begins, within hours, the response to tra uma seen in wound healing of open wou nds that a re described be low.' Superfi cial skin invo lvement may be an indicator of deeper so ft ti ssue traum a and needs to be investigated for changes in skin color, temperatu re (warmt h, followed by coo ln ess, indi ca tin g ti ssue devitalizati on), tension, and sensation indi ca ting tissue congesti on. If dee p tissue death occurs a few days after first observati on, th e tissues may rupture and become a deep cavity. This is a we ll-known phenomenon of pressure ulcerati on. The soft ti ssues usually heal by th emselves ove r time, but intervention at this stage may hasten return to functiona l ac ti vi ti es such as work and homemaking. For instance, alh-
31
32
W OUND CARr
Partial-Thickness Wound
~Iealing
Wounds that have partial-thickness loss or th e dermis heal by repair. which is the res urfa cing of the wound by new epidermal celis. Immediately afler injury. the body starlS th e process o f closing th e wound to protect the body from invasion by infecti on or debri s. beginning w ith the inflammation
phase. Epidermal ce lis at th e edges as weli as rrorn th e dermal appendages- sebaceous glands, sweat glands. and hair rollicles provide a supply o r intac t epith elial celi s to ass ist in res urfacing of the wound by migration. 1•4 I r th e derma l 3ppcndages arc presclll, islands of epider mis may appear on the wo und surface and speed the res urfac ing process. The resulting res urfacing is onen indi stingu ishab le from th e surrounding skin. Examples of partial-thickness wounds arc abrasions. sk in tears. stage II pressure ulcers. and seconddegree burns. Secondary Intention Healing
Secondary intention hea ling is the chosen method of healing when th e wound ex tends throu gh the full thi ckness of th e skin and may ex tend into underlyi ng tissues. For instance. when a large amount of tissue is removed and a gap occurs. the wound has irreg ul ar edges that cann ot be approximated, or th ere arc nonviabl e wo und margins. it is le n to c lose by secondary intention. Wounds wi th a hi gh microorga ni sm count. debris, or skin necrosis arc also left to close by secondary intention. I-iealing by secondary intention. or by COIltraction. as it is frequently ca lled occurs when th e cont ractile rorces produced by th e myoribroblasts draw th e wound toge th er. Wounds hea led by sccondary intention go th ro ugh a regenerati on process th at is nominall y divided into four overlappin g phases of repair: inflam mati on, pro li feration, epithcl ial izati on, and remodeling. Wou nds that regenerate by secondary intention and contraction have littl e ep ithelializati on. Regcncrati on of tiss ue by secondary intention invo lves scar ti ssue formation. In th is process, the anatomic stru cturc or th e sca r tiss ue docs not replicate th e tissue replaced (eg, muscles, tendons. and ncrves). In addition. the surface tissue will not be eq ual in elasti city or tensile strength to th e ori gi nal. Arter wound clos ure. th e remodeling phase cominues for 6 months to 2 years. l Sometimes there is a defect that is too small to close by primary intention and hea ling by seconda ry intention is prererred. Some wounds arc incompletely covered by split-thickness skin grafts and are best healed by secondary intention. I f a wound is in an area where contractio n wi ll produce disfi guring or nonfun cti onal deformities, th e process of hea ling by secondary intent ion may be allowed to develop a good, hea lthy wound bed. Then it may be interrupted and a sp litthi ck ness skin gran placed on the gra nulat ing wou nd bed.
Secondary intention is th e mechanism for healing associated with chronic wo und s. ~
ACUTE WOUND HEALING BIOLOGY
The process or hea ling by difTe rent phases has been de· scribed by Hunt et a l. ~ as a cascade of overlapp ing events thm occur in a reaso nably predictablc fashio n. Evc n though th e evenls overlap. th e se ri es or evenls can be divided imo phases. The literature describes the phases orrepair as either three or four phases depending on whether epithelial ization is included as part of proliferat ion or as a se parat e phase. In th e pro lirerati on phase. the ribrobl asts are the celis or rege neration th at build the co llage n matri x referred to as gran ul at ion tissue and con tract th e wound open ing. In the epithelial izat ion phase, th e function of the epidermal ce lls is to close th e wou nd by res urfacing. ~ A diagram by Hunt and Van Winkle" (Figure 2- 1) shows in fl ammat ion. the cent ra l ac ti vit y of wound healing, located in the center of the d iag ram. On either sides are the concurrent eve nts th at occur as a consequ ence of inj ury. proliferatio n and epith elialization. The lower porti on of the diagram represents th e comi ng togeth er of th e phases leadin g to the remodeling phase of wou nd heal ing. The interpret ati on of th e diagram is that four phases- inflammation, pro lifcralioll. epithel iali za ti on. and rcmodeling occur in an orderly overlapping fashion. The wound hea ling model used in this tex t is based on rour phases. The biologic repai r process is th e same ror ali wounds, open an d closed, regardless or etiology. However. the sequence of repair is completed more quickly in primary healing. and when there is superfi cial and parti al-thickness sk in invo lve ment. Slower hea ling occurs when th ere is full-th ic kn ess skin loss eXIC nding into and through subc ut aneous tiss ue.
Phase I: Inflammation
The classic observable signs and symptoms of inflammation. where recogn ized arc change in color frol11 surrounding sk in (red, blue, purple), temperature (heat), turgor (sweliing), and sensat ion (pa in). plus a loss of funct ion (Color Plates I. 19, and 2 1). The inflammation response is sometimes referred to as a " fl are" because of the suddenness of th e respo nse. th e co lor. and the assoc iated temperature chan ges that are remini scent of th e fl aring up of a fire . inflammat ion is th e body's immune system reacti on and is essential for hea ling. The biology of inflammation is well regulated in the norm al acute hea ling wound. The process lasts 3 to 7 days. Acute inflammation begins at th e moment of inju ry. sett ing into motion a biologic cascade that fun cti ons, according to Knighton. 1 like a three-compartment system (see
33
WOllnd I-l eafing Biology lind CJuVI1;C Wound Ilea/illg
INJUR Y
(
'I' COAGULATION ETS PLATI
\
\
INFLAMMATION 'I'
LYMPHOCYTES MACROPHAGES GRANULOCYTES
DEBRIDEMENT RESISTANCE TO INFECTION
.. FIB ROBLASTS
I
J 'I'
EPITHELI UM
•
('1' /
'I' 'I'
•
'I'
-
PROTEOGLYCANS SYNTHESIS 'I'
COLLAGEN SYNTHESIS
COLLAGEN LYSIS
)
/
REMODELING
l
'I' CONTRACTION
NEOVASCULAR GROWTH
'I'
..
HEALED WOUND
..
Fig ure 2- 1 Wound repair diagram, Reprint ed with permission frol11 TK Hunt and W Van Winkle. FlIl/damel/raJ:,- ofJl o/Uu/ Management in SlIrge,:v, H1:nmd Jleedi"g: Normal Repail; p. Ie, 1976, South Plainfield, NJ: Ch irurgecolll. Inc.
Bm/le Zone
the site of injury. Hemostasis is a major function of the platelets. Platelets, which are norma ll y present in the intravascular space, arc activated by collagen or microfibrils from the subendothelial layers exposed when injury occurs. In addition, activated platelets release biologically active substances, or signal sources known as platelet-derived growth factor and epidermal growth factor, bOlh of which facilitate cell migration of granulocytes and macrophages to [he area of injury. They have a life span of approximately 8 to 12 days.
The battle zone is defined as the area of tissue trauma where the vasc ular response to wounding begins. It is the location of the central activity, which includes perfusion, pain, temperature, infection, and nutrition. First there is clotting and vasoco nstriction, or hemostasis, to reduce blood loss at
Per/usi oll and N lI1r ilioll. Vasodilatation is accompanied by perfusion and increased capillary pressure and permeability, which permits the plasma protein molecules to migrale into the surrounding tissues. Fibrin plugs seal ofT the lymphatic flow to prevent spreading of infection. Increased
Table 2- 1). Kilighlon 's three-compartment system is used
and adapted in this chapter to explain the actions of the key components and the sequence of events occurring during three phases orhea ling: inflammation, proliferation, and epithelialization. In all phases, the battle zone is the center of the action. 7
10
Signal sources attract responder cells and regu-
late th e repair process.
34
W OUND CARl
Table 2- 1 Three-Compartment System-Inflammation Phase Battle Zone Trauma Perfu si on Pain Temperature
Infection Nutrition
Signal Source
Responder Cells
Wound space Hypoxia Hyperlactic environment Current of Injury Neutrophils Mast cells Macrophages
Fibroblasts Endothelial cell s Epithelial cells
Source: Adapted with permission from tables of the Three Compartment Concept lOT Inflammation Phase of Wound Healing, presented at San Diego. California, May 2. 1995, as part of a lecture, The Ro/eofOxygen in Wound Healing. C David Knighton. M.D.
perfu sion or blood fl ow brings needed flutri ents to meet the increased metabolic demands orthe tisslies. H igh metabolic acti viti es and th e increased bl ood fl ow rai ses tissue temperatures. Thi s casca de o f events is th e bi ologic basis for the
fami liar signs and symptoms of inflammation: a reddening of the surrounding ti sslies or, in individuals with dark ly pi gmented skin , a purpl e or violaceous discoloration, pain , heat, and edema . T he rise in ti ssue temperature provi des an enviro nment favorable for cell mitosi s and enhanced ce ll ul ar acti vities."·'J
PI/in. Bleeding into the ti ssucs releases histami ne and prosta glandins. which stimul ate dilat ion of injured vessels in adj acent ti ssues and pain aITerents of the sympatheti c nervo us systelll . Thi s ph enomenon is called refl ex hypcremia.
Research Wisdom : Supplemental Oxygen Oxygen can be supplemented through a nasal can nula at 40%, or 5 U min. If chronic obstructive pulmonary disease (COPO) is present it can be safely supplemented at 2 U min. This is a simple and useful method of enhancing the available oxygen. IO. 11
the wo und space, hypox ia and hyperlactic ell vironment. current of injury, neutrophils. mast cell s, and Illacrophages.
Signal So urce
H'OIl1ld Space Hyp oxiil alll/ Hyp er/actic E",·jrollm elll. Th e process o f hemostasis is to curtai l blood fl ow directly to the site of injury which reduces oxygen deli ve ry to the wound space, producing an enviro nmental change to a stat e of hypoxia. Hypox ia in the wo und space is a key signal th at co ntrols wo und hea ling. Too much oxygen in th c wo und space will impede wound hea ling. Hypox ia is a signal that recruits endothelial responder cell s and serves as a stimulant for angiogen esis or the process of new bl ood vesse l growth by the endothelial ce lls that occurs during the prol i feration ph ase. Local hypox ia also ca uses a shift to ana erobic glycolysis with increased lactate producti on that al so is invo lved in acti vati on o f both angiogenesis and co llagen synthesis. The wo und space thus becomes hypcrlactic and a c idoti c. ~·1J
Th e second compartment in the system are th e signa l source(s ). Signal sources include indicat ors from environmental conditions or from some cells to oth er cells of repair signalling them to migrate to the wound to begin repai r or regeneration. During inflammati on. th e signal sources are
Current of '''jury . An other component of hea ling is endogenous biologic electrical currents. Becker," in the I 960s, demonstrat ed th e ex istence ofa direct-current electri cal system that contro ls ti ssue healing. He ca lled thi s the "current of injury." The human body has an average charge on th e
Infection. An oxygen tension gradient develops across th e wo und that is uscd for rcgulatory purposes. Oxygen is cssential to prevent infecti on and to meelmctabolic dcmands of th e tissues, as we ll as hydroxy lat ion of proline necessary for use ful co ll agen producti on in th c remodelcd wound. Oxygen supplementat ion by nasal cannu la is one way to enhance oxygen avai lable for these ti ssue functi ons; oxygen has been demonstrated to function as an "antibioti c" and prevellt wound in fecti ons. 1O 12
WOllnd Ileating Biology and ChlYJl1;c IIbIUlt! Ilealing
skin surface of -23 mV, I' Multiple experiments demonstrate that a ncgati\e charge exists on the surface of the skin with respect to the deeper skin layers. This results in weak electrical potentials across the skin, creating a "skin battery" effecI. The bauery is driven by a sodium ion pump inilialed by Ihe sodium ions passing Ihrough Ihe cells oflhe epilhelium via specific channels in the outer membrane. Once in the cell Ihey diffuse 10 olher cells of Ihe epilhelium and Ihen they can be actively tran sported from these cell s via electrogenic "pumps," located in all of the plasma membranes of the epithelium except the outer membrane. The result is a IranSpOrl of A from Ihe water balhing Ihe epilhelium 10 the internal body nuids and generation of a potential in the order of 50 mV across Ihe epilhelium. " Iflhere is a break in Ihe integrily of Ihe skin. Ihere will be a nel flow of ionic current through the low-resistance pathway of the injured cells and fluid ex udale Ihat line Ihe wound; if Ihe wound space becomes dry.lhe voltage gradienl will be eliminated. " Use of moist wound healing methods is clinical applica ti on of this theory.n The ionic current nowing between the normal and injured tissue is a stimulus for the repair process. During the repair process there is a distinct pattern of current now and polarity switchi ng, and when healing is complete the curren t ceases. The bioelectric repair process is polarily regulaled. and cells of repair are amacled by Ihe positive or negntive pole. This is called galvanotaxis. The macrophages and neutrophils arc attracted to the positive pole ."u~ Mast cells seem to be inhibited by the positive pole.20 Weiss ct al. ~n found reduced mast cell representation in wounds aocr positi\e polarity stimulation and suggested that as a mechanism for reduced fibrotic scarring. When the wound is innmlled or infected, neutrophils are attracted to the negati\e pole. 'I The negati\e pole attracts fibroblasts. 22 which stimulatcs protein and D A synthesis and increascs CA'· uplake. fibroblasl proliferalion. and collagen synlllesis. ~\ 2~ Negative polarity facilitates migration of epidermal cells .~tI Negative polarity is also associated with suppression ofbactcrial growth. 27 10 In chronic wound healing, it is proposed thai the current of injury fails to occur. One rationa le for the use of electrical stimulation for wound healing ini~ tially is based on the theory that electrical stimul ation mimics the current of injury and will restart or accelerate the repair proces:,. Clearly. th ere arc significant research data to support the concept that electrical current plays an imporla,U role in Ihe cell physiology of wound healing. The use of electrical stimulation for wound healing is explained III Chapler 16. Eleclrical Slimulalion.
Nelllrophi/s. cutrophils (polymorphonuclear neutrophilic leukocytes) migrate into the wound space usually within the first 24 hours after wounding and remain from 6 hours 10 several days. Neulrophils are granu locylic leuko-
35
Research Wisdom : Attraction of Neutrophlfs and Macrophages Electrical stimulation has the ability to attract neutrophils and macrophages to the wound site and stimulate fibroblasts. See Chapter 16. Electrical Stimulation, for more information.
cytes Ihal funclion as phagocylic cells Ihal proliferale in Ihe hypoxic acidotic environrnent and produce superoxide to fight bacteria and enhance effectiveness of antibiotics. Length of slay oflhe neulrophils is minimal iflhe baclerial cou nl is low or declines. High baclerial counls prolong neulrophil activation and inflammation. 31 The neutrophil is considered to be a primary cell responsible for cleansing the wound of microorganisms. and lack of adequate numbers of neutrophils will relard healing in infecled wounds. When baclerial counts in the wound exceeds 10\ infection becomes apparent in the wound site. The wound begins to pour forth pus, which is the accumulation of dead ncutrophils that have phagocylized debris in Ihe wound. The neulrophi l has a shorl li fe span because il is unable 10 regenerale spenl lysoso mal and oth er cnzymes used in the destruction of foreign substances. In addition to pus formation , the neutrophil produces numerous toxic byproducts that, if there is excessive neutrophil aClivily due 10 high baclerial counlS. will negalively affect the wound tissue and even healthy tissllc. I
Mast Cells. Masl cells arc specialized secrelory cells Ihat. in the resting state. contain granules that arc largely a heparin-protein complex in which the protein carboxyl groups serve as histal11ine~binding sites. There arc a number ofbiologically active substances in mast cell granules, including neutrophil chemotactic factor.J2 Histamine is ini tially released from the mast cells after injury and plays an important role in vascular dilation and permeability, inducing tcmporary mild edema. In low doses histamine may stimulatc collagen formalion and healing. ".n Once Ihe body has produced enough platelet and prothrombin reaction, the mast cc ll wi ll produce heparin. Heparin stimu lates th e migration of endoIhelial cells. Olhe r subslances in Ihe masl ce lls. eosinophi l and neutrophil chemolaclic faclors. a"raCllhe leukocytic cells that in turn act as chemical signals for the recruitmcnt of macrophages. leading to a modulation of the innammatory phase. Macrophages promote later phases in the repair process through recruitment of fibroblasts .l~.l" Thc effect of the heparin is 10 acee lerale the aClivily of Ihe leukocyles (neulrophils and eosinophils) in Ihe phagocytosis oflhe hemaloma Ihal occurs in Ihe wound following damage 10 Ihe blood vessels at the time ofwounding. H
36
WOUND CARt
Research Wisdom :
Physical Agents Affect Mast Cell Function
Both ultrasound and pulsed radiofrequency stimulation have been demonstrated to affect mast cell function and to promote absorption of hematoma (see Chapters 18 and 19).
~·I(l cr(Jpllllge ..,.. Both neutTophils and macro phages funclion in a low-oxygen. high-acidotic environment. Macro-
phages perform several important functions during the innammatory phase. Macrophages phagocytose debris and control infection by ingestion of microorganisms and excretion of ascorbic acid hydrogen peroxide. and lactic acid. The body interprets the buildup of these excreted byproducts as
Respolt fler Cells
Fibroblasts. Responder ce lls include the fibroblasts that respond to the chemotactic signa ls from the macrophages. The fibroblasts are the cell s that build the collagen matrix produced during the proliferative phase. Fibroblast cells begin to difTerentiate. and some transform into myofibroblasts during the la tcr part of the infl amma tory phase . Myoribroblasts are able to contract and extend. They draw the edges of the \\-ound logether like the drawstring on a purse, and influence the rate and amount of wound contraction. Drawing together too tightly causes deformity of the repaired scar and an impairment of function. E"c/otheli,,1 Cell.... Endothelial cells respond to the AGF secretions of the macro phages and from the signal of the hypoxic environment that induces angiogenesis. Angiogenesis is development of the new blood vesse ls or vasculari,t:a-
tion of the tissue that wi ll grow on the collagen matrix and gives the bright red appearance of granulation tissue seen in the proliferative phase.
Epithelial Cells. Epithelial cells respond to the signal of trauma from a break in the skin from the wound edges and, if a partial-thickness skin trauma, from the dermal appendages. Epithelial cells begin the resurfacing process immediately after injury. The process is described later in th e section on the epithelia lization phase . A spec ialized function of th e epithelia l cells is debridement of necrotic tissue by release orlyt ic enzymes, whic h lyse the attac hm ent of the necrotic tissue that may be present in the wound bed. The migration of the epithelial cells is also oxygen dependent. When there are low levels of oxygen, epithelial migration cannot debride the wound. Wound resurfacing is hampered if there is a full-thickness wound that has lost the dermal appendages and as a consequence epithelial cells can on ly migrate from the wound edges. For example, full-thickness pressure wounds develop a buildup of the epithelia l cells at the wound edges, fonning an epidermal ridge that curls under the edges and slows closure. It is as if the epithelial cell s get tired of waiting for granulation ti ssue to fill in the wound defect. so they prematurely proliferate and migrate over th e edge. Phase 11 : Proliferation Phase The proliferation phase consists of two overlapping phenomena . Fibroplasia. or the laying down of the collagen matrix known as granulation tissue. is one phenomenon and wound contracti on is the other. The granulation is first seen as pale pink buds, which. as it fills with new blood vessels. becomes bright, beefy, red tissue. The thick capillary bed. which fills the matri x. supplies the nutrients and oxygen necessary for the wound to heal. This tisslle is structurally and functionally different from the tissues it replaces and will not difTerentiate into the nerves, muscles, tendons, and ot her ti ssue that it replaces. J Wound contracti on is seen as th e change in wound shape and reduction in the open area of the wound. The three-compartment system (Table 2- 2) is used to describe the next sequence of events th at occur during the proliferation phase in the battle zone, by the signal sources and from th e responder cells. Battle Z()ll e The battle zone rem ains the center of activity for wound healing during the proliferation phase. The vascularresponse start ed in the inflammation phase now is responsible for sustaining the perfusion 10 the new tissue fom13tion, bringing necessary nutrition and oxygen. Oxygen and nutrition demand remains very high to support the cell s of repair, ribro-
WOllnd Healing Biology alld Chronic WOllnd Healing
37
Table 2-2 Three-Compartment System-Prolife rat io n Battle Zone
Perfusion Infection Oxygen Nutrit ion Trauma
Signal Sources
Responder Cells
Curre nt of injury Neut rophils Macropha ges Moist environment
Fibro blasts Myofibroblas ts Endothelial c ells Epide rma l c ells
Tem perature Source: Adapted with permission from tables of the Three Compartment Concept for Inflammation Phase of Wound Healing, presented at San Diego, California, May 2,1995, as part of a lecture, The Role of Oxygen In Wound Heeling, C David Knighton, M.D.
blasts, myofibroblasts, endothe li al cells, and epiderm a l cell s, which are reprod ucing at a rapid rate to create the collagen matrix. Nutrients, includi ng zinc, iron, copper and vitamin C, and oxygen, are essentia l for fibroblast synth esis of the collagen ma tri x. T he macrophages and neutrophils work to control infection as long as th e wound remains open. The
comb inati on of activities raises ti ssue temperatures. The wound needs warmth at this time to promote cellular di vision and management of infection.
Sigllul Source The current of injury remains a signal source to anract cells of repair as long as the wo und surface remains open. Macrophages continue to produce growth factors that are chemotactic signal sources to fibroblasts. A mo ist wound environme nt contains ions th at att ract th e cell s required for current fl ow and migration.
It is fo und in skin , lungs, blood vesse ls, and the bladder and functions to maintain ti ssue shape. A thi rd fibrou s connective ti ssue component is the structural glycoproteins. Laminin and rib ronect in are two of these fiber-forming molecules. Toge th er these connecti ve ti ssues provi de stru ctu ra l and metabolic support to other ti ssues. Collage n matri x, whic h is e lastin togeth er with the new vascul ar netwo rk produced by the endothe lia l ce ll s, looks li ke red granul es piled on top of each other (see Color Plates 2.4. alld 8 for examples) and give the tissue the name "granulation ti ss ue." Pink "granul ati on buds" may be the first sign of repair seen ,n th e wo und bed, as see n in Color Plate 7. Not ice how th e granulation starts at one side of th e wound and th en " marches" across th e wound bed as shown in Color Plates 8 alld 9. A t thi s time, th e granulat ion ti ssue is ve ry fragi le and un able to withstand any tra uma. Tra um a may reiniti ate the inflammatory process and cause th e laying down of excessive collagen, resulting in poor elasti city and a less desirable scar.
Respollder Cell., Fibrobillst,'i. T he ac ti vi ti es of the responder cells, fibroblasts, myofibro blasts, endoth elial cells, and epidermal cells du ring this phase are ve ry high. Fib roblasts ex trude collagen matrix as polypepti de chai ns th at agg regate into a tripl e helix, ca ll ed proco ll age n . The proco ll age n und e rgoes a process of c leavage and become tropocollage n molec ul es. The tropoco llagen molecules spontaneously associate wi th othertropocoll agen mo lecul es to for m a coll agen fibril , producing an array of disorganized filaments. Th e organization and bonding of th e fil aments is ca lled intermolecular crosslinkage. Cross- li nkage is the we lding toge ther o f the collagen matrix fo r wound durability and te nsi le strength. The better the deg ree of organi zation and cross- li nkage of the collagen ma tri x, th e better the tensile strength or strength o f the remodeled scar tiss ue. T he process is called fibroplasia. Elastin is anoth er connec tive tissue that is synthes ized by th e fi brobl as t. It deri ves its name from its elasti c properti es.
Clinical Wisdom: Granulation Tissue Complications
1. Cha nge from beefy, red granulation tissue to a du s ky pink is an evaluation point. Wound fluid may also change at the same time in ei ther color or
quantity, o r both. This is often a sign of infection. 2. Trauma to the new granulation tissue will cau se
bleeding , whic h will lead to sc a rring . Protec tion of the new granulation ti ssue is very important.
MyoJibroblasts and Wound Contractioll. During the inflamm ati on phase, it was desc ribed how the fibroblasts differenti ate into a specia li zed cell called the myo fibroblast. T hese cells contain th e contractil e propert ies of smoo th mu scle ce lls. The myo fibroblast co nnec ts itse lf to th e wound skin ma rg ins and pull s th e epiderm a l laye r inward. The myo fibrobl ast rin g forms what has been described as a " pi c-
38
W OUND CARE
lure frame" beneath the skin of the contracting wound. The contracting force s start out equal in all wounds, but the shape of the "picture frame" predicts the re sultant speed of contraction. Linear wounds contract rapidly. square or rectangular wounds contract at a moderate pace, and circu lar
wounds contract slowly. One characteristic of pressure ulcers is tha t they take on a circular shape. and this is an indicator that they will CQl1lract slowly. 1ft Wound contraction is a process that pulls the wound edges together for the purpose of closing the wound. In efTect. this wi ll reduce the open area and. if successful. will result in a smaller wound with less need for repair by scar formation. Wound contraction can be very beneficia l in the closure of wounds in areas such as the buttocks or trochanter but can
be very harmfu l in areas slich as the hand or around the neck and face. where it can cause di sfiguremcnt and excessive scarring . Rapid, uncolllrolled wound contraction in the se arcas must be avoided. Surgical wounds that are closed by primary intention have minimal contraction response. Skin grafting is used to reduce avoided contraction in undesirable locations. The thickness of the skin graft influences [he degrec of contraction suppress ion. Pressure garments are another method of controlling wound contraction.
Research Wi sdom: Best Time To Apply Skin Grafts Split-thickness skin grafts suppress contraction by 31 % and full-thickness skin grafts diminish contraction by 55%. The best time for application of skin grafts is during the inflammatory phase before contraction begins.36
I'hase 111: Epith elializa ti on The epithelialization pha se commences immediate ly after trauma as a priority for the body to protect itself from invasion by outs ide organ isms and occurs concurrently with
the other pha ses. Once again the three-compartment system mode l (Table 2- 3) is used to describe the activities that occur in the three aspects of the recpithelializa tion process.
Battle Zone Trauma. as described, triggers perfusion to the " battle zonc" area. During this phase. as during all of thc wound healing processes, perfu sion is a key component for delivery of the oxygen, nutrients, and warmth necessary for ce ll mitosis.
Sigllal Source The signals for epithelialization begin during the inflammation phase from the macrophages. neutrophils, and current of injury to stimulate the response of the epithelial cells to migrate from the wound edges and dermal appendages.
Responder Cells Epithelial cells make up the layers of the dennis and epidermi s as well as lining various body organs and derma l appendages (eg, sebaceous glands, sweal glands, and hair follicles). Epithelial cells respond to signals from the macrophages. neutrophils, and current of injury. Responding epithelial cells advance in a sheet to resurface the open space. The leading edges of the advancing epidermal cells become phagocytic and clean the debris, including clotted material, from their path. A moist wound environmcnt will speed the migration toward one another from the edges of the wound and from the dermal appendages. Full-thickness skin loss injuries sutTer loss of the dermal appendages as an important source of new epithelial cells. The advancing front of epidermal cell s cannot cover a cavity. so they dive down and curl under at the edges. In surgical wounds that are sutured epidermal migration begins within the first 24 hours and is lIsua lly complete. in healthy adults, within 48 to 72 hours postoperatively. In other wounds, trauma to skin results in ti ssue degeneration with broad indistin ct arcas, where any edge is difficult to sec.
Table 2-3 Three-Compartment System-Epithelialization Battle Zone Perfusion Temperature Nutrition Trauma
Signal Source
Current of injury Moist wound environment Macrophages Neutrophils
Responder Cells
Epidermal Stem cells
Source: Adapted With permission from tables of the Three Compartment Concept for InflammatIOn Phase of Wound Healing. presented at San DiegO, California. May 2.1995. as part of a lecture, The Role of Oxygen in Wound Healing. C Oavid Knighton. M .D.
Wound Healing Biology alld Chronic WOllnd Healing
This forms a shallow lesion with more distinct, thin , separate edges. As tissue trauma progresses, the reaction intensifies with a thi ckening and ro lling inward o f th e epidermis. The edge is well defined and sharp ly outlines the ulcer with little or no evidence of new ti ssue growth. Repeated trauma and attempts at repair to the wound edges resu lt in fibrosis and scarring. The edges of the wound beco me indurated and firm,n which results in possible impairment of the migratory ab il ity of th e epithe lial cells." If the epithelialization process becomes arrested, the result is a chronic wound. Elast ic ity of the replaced epiderm.llayers wi ll affec t the function of the skin as it overrides bony prominences and moving muscles or tendons. Once the wound has been resurfaced by epithelial cell s, the cells beg in the process of different iat ing and maturing into type I collagen. The tensi le strength of the remodel ed skin will not exceed 70% to 80% of the orig inal. The qua lity of the sca r ti ss ue is an indica tion of the final outcomc. Because closure had been achieved by epithel ialization, it does not mean that the wound is fu lly healed. The new ski n at thi s time has a tensile strength of onl y roughly 15% of normal. The new skin must be treated carefully to avoid trauma, which can cause edema and in fection and lead to reinflammation. Chronic inflammation wi ll cause a thi ckening of the skin and less-clastic remodeled tissue. J6
Phase IV: Remodeling Phase Collagell Lysis Collagenase is an enzyme produced during the inflammati on phase and throu ghout the proliferation phase as a regulator of fibroplasia. Collagenase has th e capability of cleaving or breaking th e cross-linkage of th e tropocollagen molecul es. This is called collagen lys is. In the healthy wound, collagenase is a regu lator o f the balance between synth esis and lys is of collagen. It is this ab il ity to break down collagen that makes collage nase useful as a debridin g agent. Breaking of the cross-linkage has the effect of making the tropocollagen molecule soluble so that it can be excreted from the body. The balance between collagen sy nth esis and collagen lysis is fine tuned with a goal that one process should not exceed th e oth er. However, as th e wound matures during remodel ing, collagen lysis increases. The organization of the collagen fibers as th ey a re la id down by the fibroblasts is part of this regulatory process. Better organization produces a bett er functional outcome of more elastic, smoother, and stronger fibers for the repaired scar ti ssues. Collage n sy nthesis is oxygen dependent, but collagen lysis is not. Too mu ch oxyge n is believed to ca use hypertrophy of th e granu la tion ti ss ues , ca ll ed hypergranu lation. Hypergra nul ation c reates a humpin g of the ti ssue that inhib-
39
its the epiderm al cell movements against gravity to cover and re surface th e wound (see Color Plare 23). This is usually the res ult o f an imbalance of co llage n synthesis to collagen lysis. Some individuals have a geneti c inhibit ion of lys is, meaning that the balance between collagen synth esis and co llagen lysis is not balanced and hype rtrophi c scars and keloid scars form. One way to control hypert ro phic granulation and hypertrophi c scarring is by app lica tion of pressure garment s to the scar ti ssue area to reduce profusion and oxygen inflow. In th e ischem ic area, synthesis is suppressed and lysi s continues. Thi s is an accepted meth od for flattening scar bulk. Continuati on of this process is requ ired unti l the remodeling is complete.
Clinical Wisdom: Controlling Hypergranufation Tissue If proliferation of granulation tissue overlaps the wound edges due to hypertrophic granulation, cauterizing the undesired tissue with a silver nitrate stick should be tried to suppress the overgrowth. Repeated applications may be necessary. This will knock down the granulation tissue and allow the epithelial cells to migrate over the granulation tissue base.
Sellr f'Ormation Scar formati on progresses during th e remodeling phase. when th e fibronectin laid down in the granu lation phase is eliminated and large bundles of type I collagen accumulat e. Mature scar is formed from type I collagen. The ex ternal scar undergoes contracti on, and the small vessels that gave the new scar its red appearance gradually retract. As long as the scar exhibits a rosier appearance than norma l, remodeling is under way. 16 The purpose of this process is an att empt by th e sca r to blend in both cosmeti cally and functionally. An example is th e surgical scar on th e incision line that initially is bright red and then over time blanches and conforms to the body contours. The entire process of remodeling of wounds is described as taking from 3 weeks poslinjury to 2 years.J6 At thi s time, the clinician has lim ited ability to con tro l the amount and location of scarring, but thi s may change in the near future . Much research is being done on pharmacolog ic interventions that may be used to manipulate the scar formation. Two theories are being tested on the forces that direct the alignment of the collagen fibers . These two theori es are induction theory and tension th eory. Briefly stated, according to induction theory scar ti ssue att empts to mimic th e characteri stics of th e ti ssue it is healing. Tension th eory refers to internal and externa l stresses that affec t th e wound
40
WOUND
CARl
during the remodeling phase. Severa l studies of the tension theory suggest that adding tension during the healing process increases the tensile strength of all soft tissue structures, as well as bone, and that immobilization and stress deprivation have been shown to produce loss of tensile strength and collagen fiber organization. Dynamic splinting, seria l casting, repetitive motion devices, and exercise are ways of applying long-duration stress on healing scar tissues to remodel to new positions. Physical therapists are often involved in selecting and providing these interventions. They are, however, beyond the sco pe of this book and are not included in the interventions for wound healing. F'ETALWOU DHEALING
Resea rchers arc looking to sec what can be learned from feta l wound healing. It has been known for some lime that there is a lack of scar forma tion in fetuses thai have fetal urgery in utero. \1/ oil One feature of feta l wounds is that they are continually bathed in amniotic fluid, which has a rich con tent of hyaluronic acid (HA) and fibronectin as well as growth factors crucial to feta l development HA is a key st ru ctural and functional component of the extracellu lar matrix and fosters an environment that promotes cell proliferation and tissue regeneration and repair.oIl HA is laid down in the matrix of both fetal and adult wounds, but the sustained deposition of HA is uniquc to fetal wounds. An example of the cffects of HA and amniotic nuid on healing of surgical wounds was reported by Byl et al. in two studies. oIJ .4-I Amniotic nuid, HA, and normal saline were applied to controllcd incisional wounds. The surgeons were blinded to the nuids applied. Both the amniotic fluid- and HA-treated incisions healed faster than the saline-treated wounds. In fact, the wounds treated with the amniotic nuid and HA appeared to close wi th in minutes of the app lication. The healing was qu icker and the quality of the scar was beller in the l-IA and amniotic nuid gro ups than in the saline-treated incisions. The tensile strengths of the amniotic nuid- and HA-treatcd wounds were slight ly weaker than those of the sa line-treated group at thc end of I weck, but aftcr 2 wecks all groups had equa l tensile strength . There remain many questions to be answered about fetal wou nd healing. There are many differences between fetal dcvelopment and adult repair and regeneration. For example, the transplacental circu lation provides a partia l pressure of oxygen of20 mm rig, which is markedly lower than that in adults. signifying that the fetus lives in a hypoxic environment.oI ~ This is in marked contrast to the adult environment, where oxygen is a critical factor in prevention of infection and in the repair process. Other factors arc the differences in the fetal and adult immune systems, the histology of fctal skin during development. the function of adult versus fetal
fibroblasts in collagen syn thesis, and the absence of myofibroblasts ....·" CHRONIC WOUND HEALING
A chronic wound is defined as one that deviates from the expected sequence of repair in terms of time, appearance, and response to aggressive and appropria te treatment.>l8When the response to wounding does not conform to the described cycle of wound recovery aner a period of 2 to 4 weeks, the wound may become stuck and unable to progress through the phases of hcaling without intervention . The chronic wound often does not have the cardinal signs of heal. swelling, redness. and pain observed in aClIte wounds. Chronic wounds may be surrounded with a halo of redness or a purple/ violaceous color around the wound ca used by overactive macrophages and mast cells, which release histamine. A brown staining of the skin by hemosiderin from the lysing of red blood cells often surrounds chronic wounds or scars (eg, pressure ulcers or vc nous ulcers). The typical way to diagnose chronic wounds is to use the pathophysiology leading to the ulcer and apply that as the medical diagnosis. For example, thcre are ischcmic arte rial ulcers, diabetic ulcers (both vascular and neuropathic), pressure ulcers, vasculitis ulcers, venous ulcers, and rheumatoid ulcers (Exhibit 2- 1). The disease processes are contributing facto rs to the ulceration. For example, diabetes and peripheral vascu lar disease are comorbid itics. The impairment of functions such as impairment of seilsali on due to long-te rm diabetes or the impaired circulation due to the vascular disease process are the coimpairments. Intrinsic factors are usually comorbidities. Extrinsic factors and iatrogenic factors arc impairments to healing. This book uses both management s trategie s for the \vound pa th ophys iology and comorbidities and for the wound coimpHirments to guide the nurse and physical therapist to interventions. There are a number of factors. including intrinsic, extrinsic, and iatrogenic factors (Table 2-4), that influence whether the wound wi ll go on to heal or will become chronic. intrinsic factors arc those that are related to mcdical status or physiologic properties within the patient that may effect the healing. Examples or intrinsic factors include age, chronic disease, circulatory disease, malnutrition. neuropathy, and immunosuppression . Extrinsic factors are those th at come from sources in the environment that affect the body or the wound such as medication , irradiation. psychophysiologic stress, wound bioburden from necrotic ti ssue or infection, or other therapies that are impai rments of hea ling. Iatrogenic factors are those factors related 10 the specific way that the wound is managed. These include local ischemia. inappropriate wound care, trauma, pressure, inattention to contributing pathology, and patient noncompliancc.oI9 These arc also il11-
WOl/lld Healillg Biology alld Chrollic lVol/lld J-/ealillg
Ex hibit 2-1 Examples of Chronic Wounds
• • • •
tive function of epiderma l cells diminishes wi th age and replacement is slowed. Elastin fibcrs are lost. and the skin becomes less elastic. The dermis atrophies, which slows wound contraction and increases risk of wound dehiscence. There is diminished vascularity of the dermis.4? Aging a nd chronic
Ischemic arterial ulcers Diabetic vascular and neuropathic ulcers Venous insufficiency Vasc uliti s ulcers
disease states often go together, and both delay repa ir processes due to delayed cellula r response to th e st imulus of
• Rheumatoid arthritis • Pressure u Jeers
pairments of hea ling. These items are not an a ll-i nclusive listing of factors th at impair wo und healing and comribute to chronic wound s. but are presented to raise awa reness of the nurse and the physical therapist to some common fac tors that have been implicated in th e problem. The nurse and the physica l therapist have responsibility in management of the patient with a chro nic woun d to evaluate the comorbiditics and impairment factors that may contribute to chronic wound healing. Much of this information is available in the medical history. from the systems review, or the physical examination as described in Chapter 1. The following information describes facto rs listed in the three groups. Early identification of wou nd hea ling factors that contribute to chronicity wil l help the clinician to triage cases, reduce variabi lit y in cost and care, and improve the prognosis and outcomes for planned interventions. Intrinsic Factors in C hronic \ Vo und Healing Agillg
Skin changes occur with ag ing. The epidermis becomes thinner with increased risk of injury from shearing and friction, resulting in ulceration and skin tears. The skin also loses its impenetrabil ity to substances in th e environme nt. Irritants and certain drugs arc more rcadily abso rbed. The reproduc-
injury, delayed co ll agen deposition, and decreased tensile strength in the remode lcd tissuc. The regeneration process may be diminished as a result of impaired circu latory function. Ag ing alone is not a major fac tor in chron ic wound hea ling. Research now demonstrates that in elderly persons without chronic disease states, healing is only slightly retarded compared with that of a young population. ~o Ch,.ollic Di.,·ellse
Chronic diseases of all kinds, renal , pulmonary, and other system ic diseases. affect the cardiopu lmonary system and the oxygen tran sport pathway that de livers oxygen from the lungs to the tissues and removes carbon dioxide. The ca rd iopu lmonary systcm is affected by conditions that are hemato logic, neuromuscular. mu sculoske letal, endocrine. and immullologic .5 1 For example, depending on the location or level ofa neuromuscular lesion, breathing func tions will be affected. This may contribute to reduced respiratory muscle fu nctio n, which will afTect lung vo lumes, now rates, inspiratory and expiratory lung functions , and the de li very ofoxygen to and removal of carbon dioxide from the tissucs that are requi red for healing. Impaired cardiopulmonary function will affect mobility and l11ust be cons ide red as a ri sk for skin ulceration. In thi s case, the nurse and physica l therapist must be aware of how to op timi ze the positioning and mobility of the patien t to compensa te for the effects of chron ic d isease on the body, Morc discussion about chronic diseases and the ir effects on wound hea li ng follow under specific ca tegories.
Table 2-4 Factors in Chronic Wound Healing
Extrinsic-Related
Intrinsic-Related to Medical Status
to Environment
Iatrogenic-Local Wound Management
Age
Medication
Circulatory disease
Irradiation
Local ischemia Inappropriate wound care
Neuropathy
Psychophysiologic stress Wound bioburden: necrosis or infection
Trauma Pressure
Malnutrition Immunosuppression
41
Inattention to contributing pathology Patient noncompliance
42
W OUND CARE
Circulatory Disease C ircul alO ry disease is a comorbidi ty of chro ni c wo unds that res ult s in vasc ul ar c ha nges that are coimpai rments o f wo und hcaling beca use of decreased de li very of blood supply bringi ng oxygen and nutrie nt s. A ll phases of wound healing req ui re adequ ate oxygc n. Oxygen is carri ed in th e blood a nd di ssolved in th e plas ma by the red blood cell s bound to the hemoglobin . In ane mia, the re is red uced hemoglo bin and redu ced oxyge n-ca rrying ca pac ity of th e blood. However. resea rc h data sugges t tha t anemia does not impair wo und hea ling when th ere is adeq uate pel/usioll and blood ,'o/lIme. 52 Hypovo le mi a, the lack of adeq uate intravascul ar vo lume, has bee n shown to impair hea ling beca use of insuff ic ient vo lume to transport th e oxygen and nutrients to th e ti ssues and re move waste products. ~2 Pro lo nged hypovo lemi a impairs coll agen produ cti o n and dimini shes leukocyte ac ti vit ies. so Ex terna l sig ns of mild hypovolemi a are not ev ident. Diagnos is of hypovolemi a is made by measurement of tra ns-cutaneo lls parti a l pressure o f oxygen in th e blood. Hypovolemi a sho uld be considered in s ituations th at a re com mo n to the chro nic wound pop ul ation. such as use of diureti cs. rena l di a lys is. o r blood loss. Flu id ad ministra ti o n ca n be used to co rrec t fo r hypovolemi a, but care mu st be taken to max imi ze intravascu lar vo lume wi th o ut ca using fluid overl oad ..so T heo ri es and resea rch abound in looking at reasons why th erc is a fa ilu re to respo nd to th e sig na ls of injury. In Chapter 14 , Diagnos is and Management o f Vasc ul ar Ulcers, th e theory abo ut white blood cell inhibitio n is ex plai ned. A no ther th eo ry o f the etio logy of ve nous ulcer chro ni c ity attrib ut es the problem to a dysfun ctio na l f ib rino lyti c system" Accordin g to thi s th eo ry. li poderm atoscleros is is part o f the pathoge nes is of veno us ul ce rs that impairs th e prog ress io n of th e infl amm ati o n phase. prog ress ing to th e prol iferati o n phase.
supplementati o n have been encouraged for wo und healing. Hydrati o n should also be considered as part of the nutri ti o na l assess ment. Malnutritio n, whi c h has lo ng been recogni zed as a pro blem for pressure ulce r patients, is now being co nsidered as a problem for the pati ent w ith ve nous ulcer di sease.'" Figure 2- 2 is an a lgorithm from the AH CPR g uideline fo r treatment o f pressure ulcers H to guide management o f nutriti o na l needs. Ex hib it 2- 2 is a n assess ment form from the sa me source.
No
....
......."
-""'-
No
,--_ _L.._-{oo
A'i ll/llutritioll
Ma lnutr iti o n of pro tei n a nd ins ufTicie nt ca lories is a comorbidi ty related to c hro nic wo und hea lin g. Mult ip le studies ci te ma lnutritio n as a ri sk fac to r fo r wound healing.54 511 A nutri ti ona l assessme nt should be considered fo r a ll pati ent s wit h chro nic \vo und s and is requ ired fo r th ose ind ividu a ls who are unabl e to take food by mo uth o r who ex peri ence wc ig ht loss. Th cAge ncy for Health Ca re Poli cy and Resea rch (A II C PR) publ ished a n algo rithm fo r nutrit io na l assess ment and suppo rt as a g uide fo r c linicia ns to manage nutrit io na l needs of pe rso ns w ith pressure ul cers. n Serum alb umin leve ls be low 3.5 mg/dL is a cli nical ind icato r of a di ag nosis of s ig ni fica nt ma lnutri tio n ifacco mpani ed by tota l lymphocyte co un t less than 1,800 mm 1 or bod y we ig ht has decreased mo re th an 15%.H ln adequate absorpt io n may be a part of th e prob lem . Dietary restri cti o n s uch as re na l die ts will effec t the prote in ava ilab le fo r wou nd repair. Vi tamin C and zinc
'-____-'--+1 - -
"
NOle: TLC = total Iym phocytc count: TPN = total pa renteral nutriti on.
Figure 2- 2 Nutri tional asscssmcnt and support. Source: Rcprintcd from N. Bergstrom. M.A. Bennett. C.E. Carlson. et al.. Treatmelll o!Pressllre Ulcers. Cli ni cal Prac tice Gu ideli ne No. 15. Deccmbcr, 1994, U.S. Depa rtment of Il calth and Il uman Services, Pu bli c H C~llth Scrvice. Agency for Healt h Ca n! Policy and Research. AII CPR Publi c. tion No. 95-0652 .
Wound Healing Biology and Chronic WOl/nd Healing
Ex hibit 2-2 Sample Nutritional Assessment Guide for Patients with Pressure Ulcers
Patient Na me: _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ Date: _ _ _ _ _ Time: _ _ _ _ __ To be filled out for all patients al risk on initial evaluation and every 12 weeks thereafter, as indicated. Trends wi ll document the
efficacy of nutritional support therapy. Protein ComparlmenlS
Somatic' Current Weight (kg) Previous Weight (kg)
Percent
( _ _ date)
hangc in Weight
Height (cm) • leight/Weight Current Body Mass Index (BM I)
[wtl(ht)'l
Previous BM I
(
date)
Percent Change in BMI
Viscera! '
Serum Albumin (Normal !! 3.5 mg/dL) Total Lymphocyte CO li'" (TLC) (op tion al) (White Blood Ce ll count x percent LymphocyteS/IOO) Guide to TLC: • Immune competence
• Immun ity partly impaired • Anergy
::=: 1.800 mm}
< 1.800 but !! 900 mm' > 900 mm J
Stat e of Hydration 24-l-Iour Intake
Note:
rnL
24-Hour Output ___ mL
Thirst. tongue dryness in non- mouth breathers. and tenting orce rvical skin may indicate dehydration. Jugu lar vein disten-
tion may indicate overhydration. [slimaled Nulritional Requiremenl
Estimated Nonpro tein Ca lori es (NPC)
_ _!kg
Estima ted Protein
_ _ (glkg)
Actual NPe
_ _ !kg
Ac tual Protei n
_ _ (glkg)
Recommendalions/Plan I.
2. 3. 4. Source: Reprinted from N. Bergstrom, M.A. Bennett. C.E. Carlson. et al.. Treatment of Pressure Ulcers. Clinical Practice Guideline No. 15. December. 1994. U.S. Department of Health and Human Services. Public Health Service. Agency for Health Care Policy and Research. AHCPR Publication No. 95-0652 .
43
44
WOl
Nil
C,.,
Neuropathy curopathy is a C0l111110n complication of chronic diabetes and alcoholism. Three types of neuropathy are found in individuals with neuropathy: sensory, motor. and autonomic. Neuropathy affects autonomic nervous system function of the sweat and sebaceous glands. resulting in impairments of these sweat and sebaceous glands. When sweat and sebaceo us g land function in the feet is impaired. the skin becomes dry and crackclL providi ng a portal of entry for infection. The skin acidity is also changed resulting in impairment orthe skin's ability to control surface bacteria normally controlled by the skin acidity. Patients with diabetcs also hmc an impairment orthe body's immune system. which is simply unable to generate an inflammatory phase of repair and subscqucntly unable 10 overcome infcction. Combining al l of these functional impairments results in a chronic infected wound in a paticnt with a comorbidity of diabetes. Chaptcr 15 describes the examinations to test for and thc consequences of the trineuropathy, including photos of the consequences.
EX lrinsic Factors in C hronic \Vound I-Iealing ftle(/i(:lIfioll lIlId Imlllull e Suppression
Research Wisdom : Topical Vitamin A to Restart Inflammation
Application of topical Vitamin A will effectively counteract the effects of steroid and restart the inflammation process in chronic wounds and set them back on track. for breakdown and poor hcaling. The cxtel11. dosage. frequcncy. and location of irradiation in rc lation to the wound site will determine the cITect on wound hcaling. The effects of irradiation on tissue arc not easi ly revcrscd:'11 P.\)'(·/r op" ysi%gic Siress
Understanding the role of psychophysiologic stress is allother area of chronic wound research. Psychophysiologic stress has been shown to lengthen Ihe time for wounds to heal. Paraplegics who were college students were found to ha\'c morc skin breakdown during final examination periods than at other times of the school ycar.fII ) Caregivers of chronically ill patients who cxperienced wo unds were found to takc longer to heal than persons not li ving in slich stressfu l situations. The chronica ll y ill patient wi th multiple cOl11orbidit ies has psychophysiologic strcss frol11 multiple discasc processes.
In body systems sufTering immune suppress ion. such as is common in those who have diabetes. human immunodeficiency \irus infection. and acquired immune deficiency syndrome. the body lacks the ability to produce an inflammation phase. \\ hich is the body's immune response to injury. As described above. the inflammatory response sets ofT the cascade of rcpair. Absence or impaimlent of inflammation at the onset of trauma will impair the healing cascade. Medications are ollen prescribed to control inflammatory responses in the body including anticoagulants. immunosuppressive agen ts. antiprostaglandins. and antineoplastics. Steroids are immunosuppression medications that may be applied topica lly or systemica ll y. Steroids arc prescribed for diverse disorders ranging from asthma to polymyalgia rheumf.ltica. Stcroids in hibit macrophage levels and delay wound repair. ~It Application of topical vi tamin A and systcm ic vita m in A suppl ementation have proven efficient in cou nteracting the efTects of steroid medication. Vilamin A shou ld be part of the medical management of the \'.;ound paticnt on steroids. (II
Excessi\'c bioburden from necrotic tissue and infection h3\'c been associated with development of a chronic wound. For example. epidermal cells normally march forward as a sheet and lyse the necrotic debris from the wound edges. but they are impaired in this process of phagocytosis ifobstructed by a large quantity of de\'itali7cd material. De\itali..:cd tissue and foreign matter debris contribute to the proliferation of bacteria in the wound wh ich in turn wi ll overwhelm the body with infection. possibly leading to sepsis. In sllch situations. the body will not be able to clcanse the wo und without intcrvention. It is imperati ve to clean the wound down to hcalthy bleedi ng (issue to restHrt the inflammatory phase and the biologic cascade of hc~lli ng. Blecding creates a new acute batt le zone and signa l source for the respondcr cell s. Il owevcr. thc response may fail to occur or be inadequate to initiate a new inflammation response if there is inadequate circulation .
Irradialio"
Iatrogenic Factors in C hronic \\'ollnd I-Iealing
The purpose of radiation therapy is to kill cells. The damage may not be visible on thc surface. Injuries to the ce ll s of repair. fibroblasts and endothelial cells. and to the vasculature of the area make tisslies that have been irradiated at risk
BiobllrtJell and III/el'lioJl
Isd,emill
Ischcmia is the result of constricting blood suppl y to tissues. Ischemia occurs in differcnt ways. such as from pres-
Wound Healing Biology lI li d Chronic Wound Healing
sure over a bony prominence or an inadequat e vascular functi on, and may result in mi xed ve nous and arte ri a l di sease. If the patie nt is th en inappropriately placed on co mp ression treatm ent, ischemi c tra uma may ensue. 50
Inappropriate ' YOWIt/ Care AI(11lt1gemellt Inappropriate wo und Inanagement, inc luding a misuse of topica l agent s (eg, ant ise pti cs) or poo r technique in appli cati on of dressings and tapes that results in tears and bli sters on surroundin g skin or wound bed, have all bee n implicat ed as factors in development of a chroni c wo und.49.so Wound desiccati on, from lac k o f a dressing or inappropri ate dressing choice, is not uncomn'tO n. Drying Ollt o f the wound inte rferes with th e "current of injury" functi on as we ll as the mitoti c and mig ra tory fun ction o f cell s.!O
T rauma Trauma to wo und ti ss ue occurs frequent ly and impedes wo und repa ir. Tra uma ca n be attributed to many different ca uses. inc luding th e foll owi ng: • High-press ure irrigati on such as in th e whirlpool or with WaterPikn.! or removal of wet to dry dressings used for c leaning granul ating wound s ca n cause trauma. • Imp ropcr pressure to new g ranul ati on ti ss ue traumati zes th e frag ile ti ssue and initiates a new innammatory response, which retards hea lin g and ca uses abnormal sca rfin g. • Improper handlin g during removal of dressings, compression wraps, or stockings, frequentl y results in trauma to vc nous ul ce rs whose surrounding skin is oft en extreme ly frag ile.
Clinical Wisdom: Avoiding Adverse Treatment Effects
I
45
wound healing: innamm ation, proliferation, epit he lial izati on, a nd remode lin g. The chapter has focused on the fo ur phases subdi vided into three co mpa rtm ent s to di fferen ti ate the acti vities occur ri ng in th e wound space, called the bail ie ZOIlC: these are th e signal so urces-chemica l and bioelec tri c produced by th e body a nd by th e res ponder ce ll s. T he inte nt has bee n to descri be key as pects of eac h phase and then conn ect th e re lati onships to th e cl inica l ma nagcment. Much morc has bee n wri tt en abollt th e bio logic process of wo und hea ling than is presented here, and funhcr reading is suggestcd. T he goa l of wo und manageme nt is to provide inte rventi ons that prog ress wo un ds th rough the biologic sequence of re pa ir or regene ra ti on in an orde rl y and time ly manne r. In ord er fo r th e nu rse and phys ica l therapist to have successfu l wound healin g out co mes, it is c riti ca l to und ersta nd and be able to recognize thi s key sequ ence of event s. T he ab ility to recogni ze the benchmarks of wo und phase c ha nge are c ritical 10 monitoring the e ffects o f trea tm ent interven tions and recogni zing whcn the inte rve nti on is successful or not SllCcess ful. Early identifica tio n th at the wou nd has become " stuck" and unable to progress shoul d tri gge r an app rop ri ate response to avo id chro nicit y. Chro nic ity ca n happen du ri ng any phase o f recovery. A wo und ca n a lso have an abse nce of a phase of repair. T his occ urs whe n th e body simpl y fai ls to init iate the phase (eg, when there is inadaq uate ci rcula tion). T hese co nce pts are ex panded in Chapter 3. Assessment of Surroundin g Skin and Wound Tiss ue. In the sectio n on chroni c wounds, three majo r facto rs (i ntrinsic, ex trin sic, a nd ia trogenic) we re descri bed. Care ful assess ment o f th e patient wi th respec t to these three fac tors in conn ec ti on with the wo und are requ ired to ident ify potenti a l interfe rence with th e process of hea ling. T he fo ll owing chapte rs are arranged so as to gui de th e nurse and physica l th erapi st th ro ugh assess ment and diagnos is, ma nage ment strategies to manage the fac LOrs that a re coi mpa innc nts to heali ng, a nd selecti on of inte rve nti ons that will provide optim a l wound healing outco mes. REFEREN CES
Careful evaluat io n of each treatm e nt and technique based on wound assessment can avoid adverse treatmen t effects and change th e co urse of the wound .
I.
Hunt TK. Hussain M. Can wound healing be a paradigm fo r lis,",ue repair? Med Sci Sports E:rerc. J994;26:755 758.
2.
Cohen K. Principles of II olllld lIe(lliflg (video) . Richmond. VA. Wound Healing Center. Medical College of Virginia. Virginia Commonwealth University: t990 .
3.
Coope r D. The physiology of wound heali ng: an overview. tn: Krassner D. cd. Chronic m)tlll(/ C(lre. Ki ng of Prussia. PA : Ilcalth Manage ment J'ubl ication ; 1990: J II .
4.
Winter GO. Epidermal regeneration stud ied in the domestic pIg. In: Hunt T K, Dunphy JE. cds. FIII/dtll/wnwl.'} oj WOllnd Mallagemelll. Ncw York : ApplclOn-Ccntury-Crorts; 1979:71 II I.
5.
Hunt TK , Hcppcnstal t RB. I'ines E. Ro\'cc 0 , cds. Soft "nd Hard Tissue Rep(lir: Biological alld C/illictt/ Aspecls. New York : Pmegar Publishing; t984.
CONCLUSION T he begi nning of thi s chapt er ex plains fi ve methods by whi ch wo unds heal : superfi c ial, partia l thi ckness, primary intenti on. de layed primary intenti on, and secondary intenti on. Biologically they all heal similarly. The bio logic sequence o f healing was described for fo ur phases of ac ute
46
6.
WOUND C'\ltl
lIunt Tf\.. Van Wmlde \\
FIIII"'1I11('I/f(l/'
of
/J()IIlId MmwXi'III/.'II/
III
28
l3arnmco S. Spmlaro J. el ai, In \llro cOCct of weak direct current on staphylococcus aurcu<.;. CIII1 Orf/wp, 1914.100:250 255.
29
Kinciud C La\oic K, InhibItion of bactcnal gro\\th 111 \lIro fol100\lI1g slImul:ltlon ,\ith high \olt'lge. rnonophasu.:. pul~cJ current Pin ...' Tiler Il)XI};()I);2 1) 33
30
lurninksky S. et ai, ureet of narrow. pulsed high \Oltagcs on baclerial \.lability. Pin'S TIt"r 11)94;74:660 667.
11
Kmghlon DR. lIunt TK The defense ... of thc "ound. In: lIoward RJ, SImmons RI. cds. SW):im/llljeUlml\ /);\('11\('.\ 2nd cd Nom·all.:. CT: Appleton & I.ange; 19t-J!U 88 193
32
Dyson "'I. Luke D. InductIOn of mast ccll degnll1ul;1110n tn sktn by ultr.JsoLLnd. I£E£ Tram l..:tlmwtlio. fi.:rmeh·(·/nmin. FI'I.:qllelltT COlllml 1')1'16;]:\ :194 2UI
31
lJabrowski R. Masinski C Ole/akA The role ofhi<.;t.unine in wound heJling: Ihe effect of high dose .. of histallllllC on collagen amI glycosamlOoglyc:1Il 111 wound~. '1-:1'11/\ .kfwl/~. 11)1)7;7:2 19 224
Slirgar. IImlllti II( '/I/ill~, .\'''1"111,11 Repair. South Pl:lInficld. ~J
Chlrurgccom Inc .; 1976: le 7
Knlghlon D The rnlc ofoxygcn Ln wound hcaling. Ilrcscnlcd allhe SymposLum lor Ad\;1I1ced Wound C:lrc. S:m DIego. CA. 1995.
X
LOl:k PM I he elleet or temper-uurc on nlLtOlic aell\ ity at the edge 01 ellpcmncnlai \\oum]!>.. In Sandell B. ed .~WIIH)\illm Oil lIi)/wll lhollllllg. 1'111"1(', SlIrXU'tJ/ (1/111 Dt'rt1ll1fo/agi{' 111'1.'1,:/\ S\\cdcn MulndilL 1979: 10.1 107.
\)
Myers JA \\ound heilling and the usc of modern surgical dressing. P/um"./ 19X2;229: 10J 104 m~plred
10.
Kl1Ightun DR. el ai, O.\ygen a ... an antiblollc: the errcct of oxygen on IIlICCtl()Il lI"d, S"rg 1984.119: 199 204.
11
lIohn DC. el al. Ln'cct of 0 , tcn ... ion on Ilucroblcldal function of leukocytes III \HllInds ilnd 111 \ itm. Slit): Furulll 1976;'17: 18 20.
12.
(ioO(holl \\ II. et al Wound oxygclltension of large III 1ll'1Il. SlIrX [(mlllr 1979;30:92 95.
wound ...
34
Dexter TM. Stoddart RW. Quana/ STA Whllt
11
Knlghtun DR. SII\ er IA. Ilulll TK. Regulation of \\ound-angiogenesis cfli!ct of uxygen gr,LdLenh itnd in"plred oxygen concentratIon ..\'III"g('1'l' 19K I ;90:262.
35
14
Uecker RO The "Igmficance of blOeleclnc potenll
Ro .. s J Ul1h/allUll of pulsed high peak plmcr electromagnellc energy (diupulse Iherapy) to accelerate hC;llIng proces ..cs Prc:-.entcd .11 the DI£e ... 1 InternatIOnal SymposllllTl. Anlennas and PropagatIon Society. Stanford, CI\; Stanford UIH\erS1ty. June 2() 22. 1977; 146 149
15 .
Fnuld .. IS. Barker AT. Iluman skin battery potcntiab and their po .. ... ble rolc 111 \\ound healing 81'./ f)/.'rlllllfol. 19S3;109:5 15 522
36
lIanly M lhc biology of ...car formation Pin ... Tlla 191'19;69:21,' 1()14 102112.
16.
Vanablc J Jr Natur.J1 and applied \oltagc ... in vertebrate rcgencratmn and hcallng. In IlIfl'.f{III1/{,,,1tJ1'l' l'ole"fitt!., ttm/ "imm/Hettlillg Nc\\; York : Alan R. Liss; 191'19 chllp 5.
37.
\'S ... mall
Shell JI), Prcssure .. orc~ clas!>.ifieilllOll nnd 1ll;ltIagelllcnl ellll O,.,IIop. 1975;112 :1<9 Wf)
3X
17
Jaffe [I'. \ '.. nable JW t-Iectric field and wound healIng. Oi" f)cUlldWI. 1984;1:233 234
Seller WD. St.lhelm liB ImplLcalltllh for rescan:h 1994;6:101 IOl)
39
11'1
Onnda N. Iddman JI) DLrecllonal prolfLhlve p~eudopodial acll\Ity .lIld motLllty III macrophagc .. IIlduced by eXir.lcel1ul;lr electric field.. ('dl \to/il II)X2;2 :243 255.
Ad7lek NS.llarri"'on \IR. Glick PI. ct al Cump.lrisunoffctOiI. ncwborn ,lI\d adult wound healing hy hi ... tuloglc. en/Yllle-hl ... tochemlcal and hydroxyproline dctcnTllnallon. j I't'dftl fr Slirg 19X5;20:315.
40
19
luku ... hlma 1\. . et al Studlc" of gahilnotaxLs of leukocytes. Aft'll J ()m/.;II {I//\'. 1953A: 195 20X
Ilarri~on ~IR. lilnger Jc. Ad/1ck. NS. ct al. Correcllon of'congctlllill d1:lphra£lllatic hcrni;1 in utl.!ro. V: milia1 clinical e"(pericnce .//hlitlfr Surg 1<)I)O;25A7
\\'Cl ..... DS . ct al. I'ulscd electrical ... tll1lUllition dccrca ... cs scar thickat .. plit-Ihlcknc .. s graft donor .. ile~ j Im'l'\I /Jall/ttWI 19X9;92 :5JI)
4I
lIarri~on MR. AJ/ick NS. Longaker MT. ct ai, Successful rep:ur in utero of a fetal dluphragnmlle hernlil aOer remO\.11 of he filiated ",i ..cem from the leO thont'.; ..'V t;"gl,/ '\ fed 1990;322: 1582.
21
KIOIh L( I:leclrical stimulation III tissue repair. In: McColloch JM. Kloth LC I'ceder JA. cds,. "(mmJ Ih·(I/illg .-lir/!rnulil '{','i i"o\IalllIxmu'/If 2nd ed Philadelpilla: I·.A. Da\is; 1995:292.
42
Ilarri .. Me. MCllnulI M"C Khne JA. ct al. Am1l1otlc flUid fibrolicclIlI conccntmllon<.; \\Ith ad\ancmg gestallunal age. Oh~/(,t Gym'co/ 19X8;72 :593
22.
I,richnn CA. NuccllellL R l-mbryonic fibroblast motility and orientatIon can lk! IIlfluenced by physiological eleclric field~. C/!II /Jill!. 19XI;\)X :296 107.
43
Byl N. McKell/Le A. Stern R. et al . AmniotLc flUHJ modulate .. \\ound healtng. EI/r./ R"/wh \1('(/ 1993;2 : I~4 19(J
44
21.
Buurgulgnon (d. Bourguignon LY\\ lIeclnc sllmulatlon of prote1ll ilnd DNA ... ymhcsl'" til humun fibroblast ... F·ISEB J Il)S7; I :J9X
13)'1 N. McKen/le A. ct al I)ulscd mIcro ampcmge ,lImulallon: a controlled stud} ofhcaling of surgicilily IIlduccd wounds in Yucatan pigs Phy\ TII"t: 1994;74 :201 211'1.
24
BourgUignon (JJ. Jy W. Bourguignon LVW Liectric slllnulation of human flbn.lbla~ls cau ...es an lI1erea<.;e in Ca' influ'.; and Ihe exJlu .. urc of '1(ldLtlOl1al in .. ulll1 receptor<.; J C('// I'It.niIJ/, 19X!); 140.119 1Xl.
45
Ilock RJ The physiology of high allL1udeln.Jm{'r 1987;22' 52
46
Chang ll. Longolker MT. Tuchlcr RE. et al 1)0 human fctal \\ound~ conlr:lct" Prescnted al the 35th Annual MCCtlllg of Ihe PlastIC Surger} Rescarch CounCIl. Wa<.;hlllgton. DC. Apnl 199()
25.
Uuurguignon LY\\. Jy \V. MaJereik Mil. et al Lymphocyte actl\alion and cilpplng of hormone receptor... J Cdl Bioduml. 19K~U7 ' 1.11 l.'il)
47 .
2()
Cnopcr MS . Schlma "'I ,",CClrical and iomc contro,,", oflis~ue cell IOCollmtloll III DC electric fields . ./ Ve/lro.\d Res. 19K5;1J :223 244
Longaker MT. Ad/ick. NS. et al Studies III fetal wound healing. VII fetal \\ouml heallllg Illay be modulated by ele\ated hyalurol1le aCid sllIllulalLng :tCII\ Ity III amniotic Illlld .! p"ditHr SlIr}! 1990;2H10
48.
RQ\\iley llA. McKenna J. Cha ...e G The mfluence of electrical currcnt on an infecting nllcroorgillll ... m III wounos /"tI.\') ,Icad Sd 1974;2JX'.'i43 551
Mulder GD. Jeler KJ-. I'alrcilltd PA. cd ... Clil/iriall:l Podet Gllide to Cimmic JliJlmll Repair. Sp'lrlanbur~. SC' Wound I !cOlling Publications: 1991
49
"luldcr G. 13r:llinsky SA. Seeley J. Factors complicating wound repmr In: t\-kCulloch JM. Kloth LC. reedcr JA. cd<.; lIill/,,1I 111'11/-
20
nc~!>.
27
lIinul//'.
Wound Ileafilig
mg A/lerll(llil'£'\ ill \/wwg£'melll 2nd cd. Philadclphia : F.A . Davis:
55.
1995:47 59
SO.
Stott:,. NA. Wipkc-Tc\ is D, Co-faclOrs in Impaired wound healing. O~tomy.IIlJ/lfl(' Mal/llge. Murch 1996:42:44 56.
5 I.
Dean E. Oxygen transport deficit:,. in systcmic discase and implications for physical thcrapy. Phys Ther 1997:77: 187 202.
52.
lIum TK. Rabkin J. \011 Smitten K. Effect.) of edema and anemia on wound healing :lI1d lIl/cction. Cllr,.. S'lld Hemato/ Blood TrailS! 1986:53: 101 111.
53.
McCulloch J\\. Treatmcnt of wounds ca used by vascular insufTicieney. In : McCulloch JM. Kloth LC. Feedcr JA. cds. IIhlllll/ lleaimg A/I£'rll(lI;l'£'\ ill ,\/tlIwgemC'lIt. 2nd cd. Philadelphia : EA. Davis; 1995 : 2 16 217 .
54.
Allmun R~·1. Laprade CA. Noe l LB. ct al. Pressurc sore!> among hO'lpltalizcd patients . .'11/1/ illfern Med. 1987:105:337 342 .
56.
57 .
58. 59. 60.
8iolog~ '
alld Chronic WOllnd Ileafing
47
Berg:,.l rom N. Braden B. A pro'>pectivc sllIdy of pressure sore risk aillong in s titutionalized elderly. .I Am Cerial/" Soc 1992 :4 0 : 747 758 . Breslow RA. Ilallfrisch J. Goldberg A P. r. 1:,lnutrition in wbefed nursing home patient:,. with pressure sores. J P(I/"ellfel" Emera! Nlltr. 1991:15:663 668 . Bergstrom N. Bennet! MA. Carl son C. ct al. Trcatmcnt ofprcsslirc ulcers . Clinica/ Practice Gltideline, no. 15. Rockvi ll e. MD: US Dept of Ilcalth and Il uman $cnices. AIICPR Publication No. 95-0652, December 1994 . Leiebowitch SJ. Ross R. The role of the macrophage in \voll nd rcpair. Am J Parhol. 1975:78:7 1 91. Hunt TK. Vitamin A and wound healing . .I Am Aead DermalOl 1986:15 :8 17. Crenshaw R. Vi:,.tncs L. A decade of press ure sorc research . .I Rehah Re.~ f)l"l'. 1989:26:63 ·74 .
CHAPTER
3
Assessment of the Skin and Wound Carrie Sussman
This chapler continues the methodology of the diagnostic process described in Chapter 1 with step II. the assessment and functional diagnosis of the wo und. Assessment is a process of assigning numbers or grades (0 events systematica lly. Tests arc the instruments or means by which events arc assessed or measured. Examination is the process of detennining the values of the lests. To evaluate something properly or acc urately, ski lis of evaluation are necessary. That is, a backgro und is required in selecting appropriate tests. understanding the significance of the lests and measurements, and kn ow-
two diagnoses- wound severity and biologic phase of wound hea ling. Additional examinations that are related to the wound etiology or coimpairmcnts are described in chapters re latcd to specific problems such as the chapters on noninvasive . vascular testing, management of exudate and infection, management of edema. and therapeutic posi tioning. During the initial assessmcnt, the clinician may find that data co llected triggc r concerns that require another opinion or a difTerent leve l of care. For example. the initial assessment may indicate that the patient is not a candidate for sharp debridement because of concerns about circulatory or med ical status. The nurse or physica l therapist communicates these findings to the referring physician. The term for this is prospecfil>e manogement, and physical therapists and nurses are clinicians who have the ability to do prospective management of wound cases. Utili za tio n manage ment beg ins at baseline and is really prospective management because it is manage ment of services to be de livered to the patient ahead of the actual delivery. Utili zation management continues with every follow-up reassessment. At the end of thi s chapter. referral criteria are discussed. Why li st referral criteria in a chapter on assessment? Utili zation management mandates that at the earliest possible time the patient be diagnosed, appropriate medically necessary services identified and proper referral made. Prospecti ve. appropriate utili zation management of health care services is critical under prospect ive payment and ca pitated delivery systems.
ing how to interpret th em. Both th e examination and th e
eva luation require specific skill s and understanding of the condition. how the information wi ll be used to recognize its importance and va lue. and how to coll ect it appro priately and in an organ ized manner. I Examination and performance of tests are wit hin the scope of practice of both physical therapist assistants and licensed practicaUvocational nurses; however, evaluation of the data is a skill that is the purview of licensed physical thera pists and registered nurses who have some knowledge of wound manage ment. Simple monitoring of tissue attributes can be performed by unskilled persons after instruction and then reported back to the professional. The purpose of this chapter is to instruct the clinician in the why, who. when, where. what, and how to assess wound attributes leading to a functional diagnosis. Accepted tenninology and the significance of each tissue attribute to be assessed are described and illustrated with color plates located in this book. Chapter 4 describes techniques for measurement of size and extent of woundin g. Chapter 5, Tools To Measure Wound Healing. teaches how to use two methods to assign numbers or grades to the attributes described in this chapter. Assessment of the wound and surrounding tissues through examination of various attributes provides data leading to
T HE ASSESSME 'T PROCESS Purpose a nd Freq uency
Wound assessment data are collected for three purposes: (I) to examine the severity of the lesion, (2) to determine the 49
50
WOlNIl CARl
phase of wound healing, and (3) to establi sh a baseline for
the wound and to report observed changes in the wound over
Clinical Wisdom: Monitoring Wound Progress
lime. Assessment data enable clinicians to communicate
clearly about a patient's wound provide for continuity in the pl an of care, and allow evaluat ion of treatment modalities.
Baseline assessment, monitoring. and reassessment arc the keys to establishing the plan of care and evaluating achievement of target outcomes and progress toward goals. Valid
significant tests and measurements should be selected for the assessment process. Usc the tests se lected initially and for each retest throughout the course of care to eva luate progress toward target ou tcomes and to revise the treatm ent plan as required.
Attributes are assessed at the initial or baseline examination and at regular intervals. usually week ly or at most biweekly. to measure progress or deterioration of the ulcer. Rcassessment is done to measure change in either the status of the ulcer or change in risk factors ' One study of stage III
and stage IV pressure ulcers found that the percentage reduction in the ulcer area afler 2 weeks of treatment was predictive of time to h eal. ~ Expect improved status in 2 to 4 weeks.' If the reassessment indicates that the wound has deteriorated or has failed to improve with appropriate treatment afler 2 to 4 weeks. the physician should be notified.
Monitoring is a means of check ing the wound frequently for signs and symptoms that may trigger a full reassessment ~ u c h as increased wound exudate or bruising of the adjacen t or peri wound skin. Monitoring includes gross eva luation for signs and symptoms of wound complications such as erythema (change in color) of peri wound skin and pus sec-
ondary to infection and progress toward wound healing, stich as granu lati on tissue growt h (red co lor) and reepithelialization (new skin). Less skill is required for monitoring than for assessment and may be performed by unskilled caregivers such as the palient's family or a nurse attendant. Monitoring ta kes place at dressing changes or other treatment application times. Different care settings will have different requirements and wi ll designate specific individuals to perform the assessment funct ion. For example. in the home setting the nurse or physical therapist may function as professional wound "case manager" who assesses the findings but they may instruct a nonprofessional caregiver in wound attributes to be monitored. The caregiver would gather the data at dressing changes and predetermined intervals and report changes to the professional wound case manager who would eva luate the results of the treatment plan. The professional wound case manager may see the patient's wound only intermittently for a complete reassessment. In a skilled nursing facility (SNF),
there are lIsually requirements by federal licensing agencies that prescribe interva ls for reassessment. If the patient is in an acute or subacute setting where there are very short lengths of stay, there may be on ly a single assessment.
Teach family and other caregivers to monitor the wound at each dressing change, looking for the following: signs of wound infection such as large amounts of purulent exudate (pus), peri wound erythema (reddish, purplish), warmth, increased tenderness or pain at the site or elevated temperature, and signs of healing characteristics (bright red color and new skin).
Attributes to Assess
Evaluation of the severity of the wound by obscnation of the depth of tissue destruction. tisslle response to injury. and signs of wound healing phase arc presented. These compo~ nellis are used to provide a wound severity diagnosis and wound healing phase diagnosis. Assessment of the wound is separate from the assessment of the etiology of the wound although the examinations chosen for the assessment may relate to or provide clues to the etiology. Wound etiologies are presented in Part III . For example. wounds with an etiology of venous insufficiency wi ll have characteristics of the adjacent and periwound skin that are differelll from those of a pressure ulcer. A patient with a diagnosis of diabetic ulcer and insensitivity will have distinctive adjacent skin and tissue characteristics. Therefore. soft tissues adjacent to the area of wounding should be assessed for attributes of sensation,
circulation, texture, and color. Findings of the adjacent soft tissues will be useful in determining medical necessity. establi shing a treatment plan. and predicting outcomes of care for the wound.Adjacellf refers to tissues extending away from the peri wound. Therefore. it is a good clinical practice 10 include examination of the adjacent skin characteristics as well as peri wound skin characteristics. Assessment encompasses a composite of characteristics. A single characteristic cannot provide the data necessary to determine the treatment plan nor will it allow for monitoring progress or degradation of the wound. The indexes for wound assessment include all of the following: location. size of the wound stage or depth of tissue involvement, presence of undermining or tunneling. presence or absence of tissue attributes not good ror healing (such as necrotic tissue in the wound and erythema of the peri wound tissue), and attributes good for wound healing such as cond ition of the wound edges, granu lation tissue. and epithelialization. For many clinicians, the wound exudate characteristics are also cssential indexes. There are IWO schools of thought regarding tissue assessment. One looks only at the wound tissue. The second examines both the wound tisslie and periwound skin and soft tissue structures. Because the peri wound skin is intimately in-
Assessmellf off/Ie Skill and I1huml
volved in the c ircu lato ry response to wo undin g as well as the risk for infeclio n, il is prudent 10 eva luate both areas. The exa minati on of til c wound and pcriwound skin providcs the data related to th e wound heal ing phase diagnosis desc ribed latcr in th is chapt cr. Wou nd severi ty attributes to assess include determination of tile tissue layers involved in the wound. Wounds that penet rate through more ti ssue layers are more seve re than those th at are less deep. This is th e wo und severity diagnosis. Depth of ti ssue invo lvemen t indicates the wound seve rity a nd has an impact on further wo und assess men t strategies and determinati on o f an approprialc treatment plan. For exam ple. a partia l-thickness wound would not be assessed for tunneling or undermin ing. II a lso has impact on prediction of ri sk for nonh ea ling and on re imbursemcnt . For exam ple. third-party paye rs kn ow lilat a stage IV pressure ul ccr requircs mo re care and a longe r leng th of stay th an a stage II pressure ul cer and th at thc ri sk of com pli ca tion s is g rea ter. The most co mmonly used method of diagnosing wou nd severity is with classification sys tems.
51
ably one of th e most wide ly known wo und classificat ion systems. T he stagi ng system is most onen applied to press ure ulcers, but it is used (sometimes inappropriately) to classify ot her types of wo unds as we ll. It is best lIsed for wo und s with a press ure or ti ss ue perfusion eti ologic fa ctor such as a rte ria l/ischemi c wo unds or diabet ic ne uropath ic ulce rs. The N PUA P and theAgency for Health Care Policy and Research (A HCPR) used the initial pressure ulcer stagi ng system proposed by Shea6 as a basis for recommending a un iversa l fOllrstage systcm for describing press ure ul cers by anatomi c depth a nd soft ti ssuc layers invo lved. The pressure ulcer sta ging system does not descri be the who le wo und and is limited to a desc ripti on of th e anatomi c ti ssue loss and is a diagnosis of seve rity of ti ssuc insult before hea lin g sta rts. The A I-I C PR adopted the NPUA P staging system for use in two sets o f c li nical practice guidelines. '·' ll is wi del y accepted und commonly uscd to com muni cate wound severity, to orga ni zc treatmcnt protocols. and as crite ri a for selectio n and re imburseIll CIll of treatment products for pressure ul cc rs. Table 3- 1 presents the stag ing c riteria for pressure ulcers.
\Vound Classification Systems Table 3-1 Pressure Ulcer Staging Criteria
Allhc prescnt tim e. a va ri ety of wound classification systems is used to describe wou nd seve rit y for different wo und etiol ogy. Allhough the classification systcms were dcsigned and researc hed wit h onc specific wou nd type. they are often (sometimes inappropriately) used for any wo und type. A lthough there are many wou nd c lassification syste ms. such as meth ods of classifyi ng surgica l wo unds and scvcri ty scoring of lower leg ulcers, four wo und c lassifica tion systems are presented in thi s chapter. The Nat ional Press ure Ulcer Advisory Panel (NPUAP) pressure ulcer stagi ng cri teria deve loped for lise wi th pressure ul cers, the Wagner staging system for grading seve rity of dysvasc ular ul ce rs, partialthickness/full -thi ckn ess sk in loss criteria. and Marion Laboratories red/yellowlblack color sys tem arc desc ribed and di scussed."5 The NPUA P pressure ul cer stagi ng systc m and the Wagner stagi ng syste m are c lass ifications based on ti sslie layers and depth of ti ssue destru cti on. The partial-thickness and full-thickness sk in loss classi fi cat ions are tissue layer desc riptions o f skin loss that a re also com monly used. The final method discussed groups wounds based on co lor of the ti ss ue. Marion Laboratori es, in Europe, deve lopcd a system that classifies the wound based on th e color of the wo und surface red. ye ll ow. or black. No wound c lassi fi ca ti on system when lIsed in isolati on is a n appropri ate meth od ofmcasuring wo und hea ling (sec Table 3- 5). NPUA P Pressure Ulcer Sfllgillg System
Classificatio n by stages is used to descr ibe the anatomic depth ofsofl ti ssue damage observed after the path ology has declared itsel f.' The pressure ulcer staging system is prob-
Stage
Definition
I·
Nonblanchable erythema of intact skin , the heralding lesion of skin ulceration. In individuals with darker skin , discoloration of the skin, warmth, edema, induration, or hardness may also be indicators.'
11
Partial-thickness skin loss involving epidermis and/or dermis. The ulcer is superficial and presents clinically as an abrasion, a blister, or a shallow crater.
III
Full-thickness skin loss involving damage or necrosis of subcutaneous tissue that may extend down to, but not through, undertying fascia. The ulcer presents clinically as a deep crater with or without undermining of adjacent tissue.
IV
Full-thickness skin loss with extensive destruction, tissue necrosis or damage to muscle, bone, or supporting structures (eg, tendon , joint capsule).
"In 1997 the NPUAP proposed a new definition of stage I pressure ulcers to reflect better the ethnic diversity of persons With pressure ulcers. The new definition under review is as follows : ~an observable pressure related alter· ation of intact skin whose indicators as compared to an adjacent or OPPOSite area on the body may include changes in skin color (red. blue. purple tones). skin temperature (warmth or coolness), skIn stiffness (hardness. edema) andl or sensation (pain). "!ltPlIlSource: Reprinted with permiSSion from Pressure Ulcer Staging Criteria from Pressure Ulcers: Prevalence, Cost. and Risk Assessment, Consensus Developmenl Conference Statement. 0 1989. National Pres· sure Ulcer Advisory Panel.
52
WOUND CARE
Clinical Wi sdom: Reverse Staging or Back Staging of Pressure Ulcers Once the ulcer is staged, that remains the stage and wound severity diagnosis. Correct terminology is healing stage II, III, or IV.
The pressure ulcer staging system is not an ideal system.
It has many problems. Staging systems measure only one characteristic of the wound and should not be viewed as a comp lete assessment independent of other indicators. Staging classification systems do not assess for criteria in the healing process and hinder tracking of progress because of the inability of the staging system to demonstrate change over tim e. The definition of a stage I pressure ulcer does not account for the severity of soft tissue trauma beneath the unbroken skin such as is seen with purple stage I ulcers.
Stage I lesions vary in presentation and pose validity concerns. Some stage I lesions may be the indicator of deep
tissue damage just beginning to manifest on the skin, and others may indicate only superficial insult where damage is somewhat reversible and not indicative of underlying tissue
death. There are problems with the reliability of assessment of stage I ulcers in dark-skinned patients. In fact, in 1997 the NPUAP proposed a new definition of Stage I pressure ulcers to renecl better the ethnic diversity of persons with pres-
sure ulcers (see footnote to Table 3- 1). Identification and meaningful interpretation of skin color changes in darkly pigmented skin requires special assessment strategies. These strategies arc described in the sect ion on assessment of the peri wound and wound tissues. Stage II pressure ulcers are lesions that are not necessarily caused by pressure and are more likely due to shearing. friction , or incontinence. The latter should be distinguished
and treated in a different manner than pressure ulcers. Theoretically, pressure ulcer trauma starts at the bony tissue interface and works outward, eventually manifesting damage at
the skin. However, stage II lesions are usually caused by fricti on or shearing of the tissues, causing superficial and par-
tial-thickness damage to the epidermis and dermis. Stage II lesions start at the epidermis or skin and may progress to
deeper layers. Staging of pressure ulcers covered by eschar and necrotic tissue cannot be accomplished until removal of necrotic tis-
sue allows determination of the extent of depth of tissue involvement. Pressure ulcers with necrotic tissue filling the
meaningful communication is difficult, as clinicians may not have the experience necessary to recognize the various tissue layers that identify the stage or grade. In addition, clinicians may be defining stages difTerently. Slaging requires practice and a certain amount of skill that develops with time spent examining wounds Unfortunately, the staging system has been misinterpreted and applied in clinical practice as a way to monitor healing.
It was not designed to do this. Biologically wounds do not heal in the manner suggested by reversing the staging system. For example, a stage IV pressure ulcer cannot "heal" and become a stage " pressure ulcer. taging pressure ulcers is lIsed to document the maximum analOmic depth of tissue involved after all necrotic tissue is removed. Staging of pressure ulcers is a diagnostic tool useful to determine the extent of tissue damage only. Staging is a diagnostic tool to aid examination of the wounding severity and not wound healillg. Elimination of reverse staging has left a void in the
system to report and document wound healing quickly and efficiently. The situation has been complicated because ofa
reporting system developed by the Health Care Financing Administration (HCFA) that requires that providers must continue to reverse stage in order to stay in compliance with
HCFA regulations. Specifically. the Minimum Data Set (MDS) developed by HCFA relies on the reverse staging of wounds, both pressure ulcers and ve nous ulcers, to demonstrate progress ofa wound toward healing. This has created a dilemma for the conscientious practitioner. One pragmatic suggestion is to stage for the wound severity at baseline and then on subsequent reassessment report with decreasing
stages as the wound shows attributes of healing (eg, initial stage IV wound has bad-for-healing attributes of eschar, slough, and exposure of tendon. muscle. or bone indicators
progressing to a stage III wound with presence of some goodfor-healing attributes: absence of necrosis and presence of granulation tissue to a stage II recpithelialization beginning
and stage I healed).' While this is a misuse of the staging system, it does have some merit, and until there is broad
acceptance ofa research-based tool to monitor healing and a change in the government reporting system, this may be the
only route open to the thoughtfu l clinician. The MDS documenting system can be supported by using the Pressure Sore Status Tool, or the Sussman Wound Healing Tool, which are research-based tools for monitoring wound healing attributes.
The tools are presented in Chapter 5. Wagller Ufeer Grade Clas.' ijieulioll
wound bed are full-thickness wounds or stage III or stage IV
Thc Wagner Ulcer Grade Classification system is used to
wounds. The clinician cannot determine the level of tissue insult until th e necrotic debris is removed. Another di fTiculty with staging occurs with patients with supportive devices
establish the presence of depth and infection in a wound.
because of the difficulty in accurately assessing the wound without removal of the supportive device. Finally. accurate,
The Wagner grading system was developed for the diagnosis and treatment of the dysvascular foot .' It is common ly used as an assessment instrument in the evaluation of diabetic foot ulcers. It is useful for both neuropathic and artc-
Assessmel1l of the Ski" (Jl1l/ lffJII"d
rial/ischemic ulcer classification. There are six grades progressing from 0 to 5 in order or seve rit y. Table 3- 2 presents the Wagner grading criteria and Figure 3 I shows how the natural history ofbreakdowll in the diabetic, neuropathi c foot corresponds to the Wagner 0 to 5 classification. The 0 classificatioll evaluates for predisposing ractors leading to breakdown and, a long with grades I 10 3, is used for risk managemelll as described in Chapter 15 .
Table 3-2 Wagner Ulcer Grade Classification Grade
Characteristics
o
Preulcerative lesions; healed ulcers; presence of bony deformity Superficial ulcer without subcutaneous tissue involvement
2
Penetration through the subcutaneous tissue; may expose bone, tendon, ligament, or joint capsule
3
Osteitis, abscess or osteomyelitis
4
Gangrene of digit
5
Gangrene of the foot requiring disarticulation
Source: Reprinted With permiSSion from F.E.W. Wagner. The dysvascular foot a system for diagnosis and treatmenl.Foot and Ankle. 2:64-122. 0 1981 . WilUams & Wilkins.
53
CllISSijiClllioll by ThiL'klless of S kill Loss Classification by thickness of skin 1055, parlial- or I'ullthi ckness skin loss. is another classification sys telll and is cOlllmonly used for wounds whose etio logy is ot her than pressure wounds such as skin lears, donor si te s. vascu la r ulcers (venous ulcers in particular), surgical wounds, and burns. Wound thickness refers to partial-thickness or full-thickness loss of the skin with or without penetration into subcu taneous tissue and deeper structures. Partial-thickness wounds extend through the first layer of the skin or epidermi s, and il1lo. but not through. the seco nd layer of th e skin or dermi s. Full-thickness wou nds extend through the epidermis. the dermi s, and beyond. Full-thickness wounds may be further ca tegorized accordi ng 10 dcpth of involvemcn t by using the term slIbclIIlIlleolis tisslle wOUl1ds. Subcut aneolls ti ss ue wounds extend into or through subcutaneous ti ssues and may extend into muscles. tendons, and possibly down to th e bone. Depth of injury classi fication identifies the speci fie anatomic level of tissues involved but does not report their condition or color. Anatomic deplh is predictive of healing.uo Partia l-thick. ness wounds heal by epithe lializ.1Iion and heal faster th an full-thickness and subcutaneous wounds. Full-th ick ness and subcll taneous wounds heal by secondary intention, whic h is a comb ination of f ibroplasia or granulation tissue formation and con traction. Table 3- 3 provides the definitions of partia l- and full-thickness skin loss.
Figure 3- 1 Diabetic neuropathic progression of foot breakdown. Courtesy of William Wagner. MD.
54
WOUND
CARe
Table 3-3 Partial-Thickness and Full-Thickness Skin Loss
Definition
Thickness of Skin Loss
Clinical Examples
Partial-thickness skin loss
Extends through the epidermis, into but not through the dermis
Skin tears, abrasions, tape damage, blisters, perineal dermatitis from incontinence; heal by epidermal resurfacing or epithelialization
Full-thickness skin loss
Extends through the epidermis and the dermis, extending into subcutaneous fat and deeper structures
Donor sites, venous ulcers, surgical wounds; heal by granulation tissue formation and contraction
Subcutaneous tissue wounds
Additional classification level for fullthickness wounds, extending into or beyond the subcutaneous tissue
Surgical wounds, arterial/ischemic wounds; heal by granulation tissue lormation and contraction
Mario" Laboratories Red, J'ellow, BIOl:k ,roulld Classificatioll Classification by color is a popular system because of the simplicity of the concept and th e ease of use of the system. A three-color concept, red, ye llow, or black, is used for assessing the wound surface color. II The three-color system was originally conceived as a tool to direct treatment , with each color corresponding to specific therapy needs. The red
wound is clean, healing, and granulating. Yellow signals possible infection, need for cleaning or debridement, or the presence of necrotic tissue. Finally, the black wound is necrotic and needs cleaning and debridement. Red is considered most desired, yellow less desirable, and black least desirable. I f all three types are present, select the least desirable as the ba sis for treatment. Table 3-4 shows the red, yellow, and black
classification system with clinical manifestations. The four wound classification systems discussed in this section and the type of wound most appropriate for use with each sys tem are presented in Table 3- 5. Wound Severity Diagnosis
Nurses use nursing diagnoses to classify skin and tissue impairments and assist with developing care plans for wound care patients. Nursing diagnoses are expressed as specific diagnostic statements, which include the diagnostic category and the related to stem statement. Impaired (issue iJlfegrity is the broad diagnosis and would be correctly applied to stage III and stage I V pre ssure ulcers, for example. Impaired skill iJlfegri(y is a subcategory and correctly applies to partialthi ckness or full- thi ckness loss of sk in . Impaired skill illtegrity should not be used for surgical incisions or deep ti ssue wounds. The diagnosis risk for infection related to surgical incision is more appropriate because of the di sruption of the
ski n during surgery, making it more vulnerable to infection.
Table 3-4 Red, Yellow, and Black Wound Classification System Color Red Yellow Black
Indication Clean; healing; granulation Possible infection; needs cleaning; necrotic Needs cleaning; necrotic
Source: Data from J.Z . Cunell, The New RYB Color Code, American Journal of Nursing, Vol. 88, pp. 1342-1346, C 1988, American Nurses Association and NA Stotts, Seeing Red & Yellow & Black, The Three Color Concept of Wound Care, Nursing, Vol. 2, pp. 59-61. 0 1990. SpnnghOuse Corporation .
The related to stem statements aid in communicating with other hea lth care professionals and in planning care by targeting the defining characteristics for the diagnostic statement. For example, the diagnosis statement impaired skill illtegrity would be followed by a re lated to stem statement such as impaired skill i11legrity related to frictioll (llld moislUre fivm urillGlY illcolJlinence. For nurses, the related to stem
statement usuall y reflects etiologic factors in wound development and directs the plan of care and specific interven-
tions.12 Physical therapist s will also use a wound severity diagnosis that relates to depth of penetration of wounding. The wound diagnosis statement wi ll have a stem statement impaired ilJlegumentGlY ;11Iegri!y secolldwy 10 - . The ending part of the statement will include the depth of ski n involvement. End statements read superficial ski" ;nvolveme11l or partial-thickness skill illvolvemelltalld scarformation, full-thickness ski" involvemellt and scar formatioll, or involvement extending ;1110 fascia, muscle. or bOlle. A total statement would read impaired illlegumelltmy i11legr"ty secondmy to partial-thickness skill involvemelll and scar formation. Il The statement refers to the functional impairment
Assessmellf o/the Skin alld Wound
55
Table 3-5 Wound Classification Systems and Wound Types Wound Classification Systems
NPUAP pressure ulcer stages
Pressure Ulcers
Venous Ulcers
X
Arterial, Ischemic Ulcers X (Those with pressure component)
Wagner grades
Diabetic Ulcers (Neuropathic) X (Those with pressure component)
X
X
X
Other Wounds
Stage II classification will be appropriate for skin tears and tape damage.
Depth of skin loss (partialthickness to full-thickness skin loss)
X If the wound is full thickness, it requires examination of level of deep tissue involvement.
X If the wound is full thickness, it requires examination of level of deep tissue involvement.
X If the wound is fu ll thickness, it requires examination of level of deep tissue involvement.
X If the wound is full thickness, it requires examination of level of deep tissue involvement.
Useful for skin tears, burns, and other skin wounds. If the wound is full thickness, it requires examination of level of deep tissue involvement.
Marion Laboratories red, yellow, and black system
X
X
X
X
Surgical wound is healing by secondary intention.
of the integument and different ti ssues. which has implications for fu nctional impairmelll and disability. Physical therapists use the severity diagnosis to se lect examinations. plan treatment. and predict functional outcomes. Diagnosis statements for bOlh nurses and physical therapists arc similar. Both usc impairmcnt diagnoses that affect function of the involvcd tissues.
tu s. Two tools, th e Pressure Sore Status Too l (PSST) and the Sussman Wound Hea lingTool (SWHT), can bc used to record the findings and to measure each attribu te objectively. Both are described, with forms and instruction provided in Chapter 5. Useful forms for assessment oftissllc wi ll usually include the following items:
• Peri wound skin attributes ASSESSMENT OF WOUND STATUS
• Wound tissue attributes • Wound exudate characteristics
Data Coll ec tion and Documentation Forms Information collection is easier. beller organized. and more consis tent when a form is used as a collection instrument. Forms may be paper-and-pencil instruments or templates on the computer screen. There are many forms bcing used, with the most common being thc skin care now shect used by Illirses. Mcthods of recordi ng assessment data should allow for tracking of each assessment item over tim e in objective and measurable terms that show changes in the wound sta-
Regardless of which instrument is used 10 collect findings. all attributes on the form should be considercd. I f the attribute is not applicable the notation N/A shou ld fill the blank. Ifan attribute is absent, record a O. If present, a grade or check is required. Leaving a blank space on the form impIies the attribute was not considered or assessed. If th e patient 's medical diagnosis suggests possible related impairments associated with th e wound and peri wound sk in (eg. neuropathy or vascular disease), multiple form s may be
56
WOUND
CA.'
req uired to report all the necessary elements that relate to
th e patient's condi ti on. Chapter 6, Noninvasive VascularTcsti ng. and Chapter 15. Management of Ihe Neuropathic Fool. have sample fOfms specific to recording data related to those problems. Documentation requ irements for wound assessment should be part of the facility policies and procedures. Documentation should be accurate and shou ld clearly reOect the patient's condit ion. the examinations performed, the find ings, the care rendered, and proper notification of the physician of sign ificant findings. Documentation of similar findings by practi-
tioners in the same department or facility should be consistent and reflect the facility policics. I " Remember that some
day. maybe 5 years from the time of initial assessment, the medical records may be subpoenaed into court. "Documentation can be either your shield against a potentia l malpractice lawsui t or the sword that strikes you down."I-lIfl401
Case Study: Dangers of Differing Clinical Procedure and Facility Policy A physical therapist (PT) debrided a toenail on a patient with a medical history of neuropathy associated with diabetes. The toe went on to become infected. leading to below-the-knee amputation of the leg. The PTs action was called into question in a malpractice lawsuit. The debridement procedure followed by the PT was acceptable and documented. but it was the facility policy to have a patient with diabetic neuropathy evaluated in the vascular laboratory for transcutaneous oxygen levels before debridement. The PT did not document anything about evaluating the patient for circulatory status prior to performing the procedure. The case is pending.
Observation and Palpation Techniq ues
Observation and palpHtion are classic components ofphysical diagnosis used to determine alteration in soft tisslie characteristics. including the skin. subcutaneous fascia, and muscles leading to a son tissue or structural diagno s is. '~ Proper lightin g and positioning of the patient and tissue to be assessed wilJ improve observation. Begin the examination of tisslies by eva luating for symmelry with th e opposi te side of th e body and adjacent Slruetures by both observation and palpation. Look for consistency of symmetry of tissues in color. texture. contour, hardness/softness. temperature that represent changes in the attributes of the skin, subcutaneous tissue, fascia. and muscle compared with an area of normal sk in and soft tissue.
Palpation requires the use of the hands as important sensitive diagnostic inslruments. The hands shou ld be clean and the fingernails of appropriate length. It is important for the clinician to development a palpatory sense in the hands. For example. difTerent pans of the hands are valuable for difTeren t tests. The back of the hand is more sensitive to temperature. the palms of the hands are best used to detect changes in tissue contours (induration. edema). and the fingerpads are more sensi tive to texture (fibrotic tissues) and fine discrimination. The thumbs are useFul to apply pressure to check for hardness or so ftness at different tissue depths. Techniques of palpation include the usc of slow. light movements. Avoid pressing too hard and trying to cover the area of examination too quickly. This will provide confusing messages to the sensory receptors of the examiner's hands. Palpation skills require practice to refine the practitioner'S palpatory sensc. The first requiremcnt is for the examiner to reduce other sensory inputs in the environment (noise. traffic, conversation) so as to concentrate and focus on the palpation examination. The ncxt requirement is a coml11OI1 language to communicate the findings, in easi ly understood terms. Paired descriptors such as superficial-deep. moist-dry. warm-cold, painful-non painful, rough-smooth. hard-soft. thick-thin are useful. The state of ti ssue changes can be reported as acute. subacute. chronic, or absent. They can also be graded on a scale of 0 to 3+ as a way of diagnosi ng the severity of the problem. A familiar example of thi s type of grading system is pitting edema; another is pulse strength. The use of this type of grading system is also helpful in reporting response to treatment intervention.
Clinical Wisdom: Four Requirements for Palpatory Examination 1. 2. 3. 4.
Concentration Language to communicate findings Light pressure Slow movement
Assess ment of Adjacent Tissues The ti ssues adjacent to and surrounding a closed or open wound provide many clues that identify the health of the skin. the phase of wound healing, and the patient's overall health stat us. For clarity. the term atijacelll is lIsed to separate tile tissues that may not show signs of wounding but that arc predictive ofhca ling from the tissucs immcdiately surrounding the wounded tissue. referred to as periwound skin. Skin or trophic changes arc important predictors of the body's ability to respond to wounding. The attributes of the adja-
Assessmelll oJlh e Skill alld Wound
cent ti ssues th at should be assessed are described in the following sections including: • • • •
Anatomy of the skin Skin texture (eg, dryness, thickness, turgor) Scar ti ssue Callus
• Maceration • Edema • Color • Sensation (pain, th ermal, touch, protective)
about 0.5 mOl thick (Figu re 3- 2). Each of the primary layers is stratified into severa l layers. The dermis is the true skin. It is tough, flexible, and elastic. The thickness of the skin varies from extremely thin over the eyelids to one third of an inch thick over the palms of the hands and sales of the feet.
The epidermis is avascular, whereas the dermis is we ll vascu larized and contains the lymphatics, epithelial cells, connective tissue. musc le, fat , and nerve ti ssue. The vascular supply of the dermis is responsible for nourishing the epidermis and regulating body temperature. The we ll- vascu larized dermis will withstand press ure for longer periods
of time than wi ll subcutaneous tissue or muscle. The col-
• Temperature • Hair distribution
• Toenails • Blisters Allutomy o[tll . Skill
The skin is composed of two primary layers: the epidermis, which is about 0.04 111111 thick, and th e dermis, which is
OpenIngs ot sweat ducls
lagen in the dermis gives the skin its toughness. Hair fo llicles and sebaceous and sweat glands, located in the dermis, contribute epithelial cells for rapid rcepithelialization of partial-thickness wounds. The sebaceous gla nds are responsible for secretions that lubricate the skin and keep it soft and flexible. They are most numerous in the face, and sparse in the palms of the hands and sales of the feet. The sweat gland secretions control skin pH to prevent derma l
Hair shaft Dermal papilla
Sensory nerve ending lor touch
Stratum corneum
Pigmenllayer
l
EPIDERMIS
S',,"um
Stratum germlnatJVum
57
splnosum Stratum basale
Sebaceous (011) gland
II
Hair follicle Aneclor muscle
Paclnlan corpuscle
DERMIS
I
J
Papilla 01flair
Sweat gland SUBCUTANEOUS FATTY TISSUE
Blood vessels ------l~.,
Figure 3- 2 Anatomy o f Lhc skin . Courtesy of Kn oll Pharmaceutical s. Mount Olive. New Jersey.
58
WOUND CARE
infections. They are numerous in the soles of the feet and palms of the hands. The three togeth er are referred to as dermal appendages. The sweat glands, dermal blood vesse ls, and small mu scles in the skin (responsible for goose pimples) control tempera ture on the surface of the body. The nerve endings in th e skin inc lude receptors for pain, touch, heat, and col d. Loss of the nerve endings in the skin increases risk for sk in breakdown by decreasing the tolerance of the tissues to external forces. Nails are a lso considered as appendages of the skin. The deep or reticular layer of the dermis consists of fibroelastic conn ecti ve tissue that is ye ll ow and composed mainly of coll agen. Fibroblasts are present in thi s ti ssue layer. The deep layer of the dermis merges with the subcuta neous fat and fascia and may be confused with yellow slough, but it shou ld be eva luated for texture and vita lity. A healthy reticular layer will be adhered and firm, not soft, mushy, or stringy like slough. Often g ranulati on buds are seen protruding through the mesh of the reticular layer. Color Plate 17 shows the reticular layer of the dermis with the red granu lation buds poking through the mesh layer in a partial-thi ckness wound. Skin color varies greatly in humans. but the structure and th e ski n arc ve ry similar. Melanin produced from melanocytes account for th e varia ti on in pigmentation from very
light to extreme ly dark. Numbers ofmelanocytes in dark and light skin arc similar, bur the size and activi ty of the melanocytes are greater in black skin th an in li ght skin. The melanin pigmentation is concentrated in the stratum corneum layer in a dark horny layer that can be wiped off when washin g clean, black sk in. Of course, this docs not mean that all the color is removed, just th e superficial layer. The thickness of th e stratum corneum in both dark and light skin is the same, but the cell s in dark ski n are morc compact with morc cell layers. For thi s reason, dark skin is more resistant to external irrita nts. Healthy dark skin is usually smooth and dry. Dry dark sk in may have an ashen appearance. 16
Clini cal Wisdom: Care of Darkly Pigmented Skin Care of darkly pigmented skin requires keeping the skin lubricated. Petrolatum, lanolin-based lotions, and sparing use of soaps are recommended. 16
loss of turgor. The areas most affected by loss of subcutaneous fat are the upper and lower extremities. This thinning of subcutaneous fat resu lts in more prominent bony protuberances on the hips, knees, ankles, and bony areas of the feet with a higher risk of pressure ulcer formation . Elderly skin also experiences a loss of elasticity due to shrinkage of both collagen and elastin. There is a weakening of the juncture between the epidermis and dermi s. making the skin layers "slide" across each other and placing the person at ri sk for skin tears. Sebaceous glands and their secretions are diminished, resulting in skin that is dry. often itchy, and easily tom." Impaired circu lation also contributes to changes in the skin; it is usually associated with aging but may be due to a disease process such as neuropathy associated with diabetes. Neuropathy impairs the secretion of swea t and sebaceous glands. Death of sweat and sebaceo us glands co ntributes to slow resurfacing of partial-thickness dermal ulcers. Loss of sweat changes the pH of the skin. making it marc sllsceptibl e to infection and bacterial penetration . To assess skin texture the clinician uses observation and palpation . Observe the skin , looking for evidence of dryness such as flaking or sca ling. To check skin turgor, gently pick up the tissues with thumb and forefinger and observe how th e ti ssllcs respond. For example. in oldcr patients loss of elasticity may be exhibited by the ti ssues' slow rerurn to normal after pinching. In older patients it is best to check for general skin turgor on the forehead or sternal area. Palpate by gently rubbing your fingers across the patienrs skin and feel for sliding of the epidermis away from the dermis.
Clinical Wisdom: Skin Texture Assessment
Observe skin for moisture content; look for evidence of dryness such as flaking , scaling, and excoriations (linear scratches). Palpate the skin to assess turgor; gently grasp the tissues between thumb and forefinger and observe for any delay in the tissues' return to normal position . Finally. rub your fingers across the patient's skin and feel the sliding of the epidermis from the dermis due to weakened epidermal-dermal juncture.
Scar Tissue Skill Textu re Smooth, flexible skin has a feeling of fullness and resistance to ti ssue deformation that is called turgor. Turgor is a sign of ski n heallh. Aging sk in often shows signs of dryness due to atrop hy and thinning of both the epithelia l and fatty layers of tissue in the dermis. The feel of the skin renects a
Inspection of the adjacen t skin should include checking for scar tissue. Check scar for smoothness, ncxibility, thickness, and toughness. Scar tissue that is mature has greater density and toughness and is less resilient than surrounding sk in. New scar tisslie is thinner and more nexible than mature scar and is less resilient to stress. Wounding in an area of scarring will have less ten si le strength when healed than a
Assessment oJthe Skill alld "'ouml
new wound and will be more likely to break down (see Color
Plate 37).
New scar tissue will be bright pink. As the scar tissue matures it will become nearly the same color as the periwollnd skin except in persons with darkly pigmented skin . Hypopigment3tion frequently follows injuries to dark skin. Loss of skin color may create more anxiety for the individual than the wound itself. If the wounding disruption is less than full-thickness loss of the epidermis. rcpigmcnt3tion wi Ilusually occur over lime. However, new skin covering deeper lesions and new lesions will appear pink. IS The area of scar
59
imbalance and subsequent uneven weight distribution along the metatarsal heads resulting in callus formation in those areas. The location of the callus is a clue to the underlying bony pathologic condition.'" Untreated. the ca l lus buildup will continue creating additional shear forces between the bony prominence and so ft ti ssues, resulting in breakdown of the interposing soft tissues. Hemorrhaging seen on a callus indicates probable ulceration beneath. Callus is an indicator of need for further assessment of the foot. Chapter 15 contains more information about callus management, and pictures of ca ll us.
may even turn white. Hypopigmented areas are morc susceptible to sunburn than arc normally pigmented areas. For some individuals. burns and physical trauma may be followed by locali zed areas of hyperpigmentation . Like hypopigmention. hyperpigmcnt3tion leads to anxiety for many individuals. Observe for abnormal sca rring characteristics. Hypertrophic scarring results from excessive collagen deposition , causing a very thick scar mass that remains within the area of the original wound. These scars are ugly and disfiguring and may be bothered by itching or pain that may interfere with functional mobility. The scars are differentiated from keloid scars, which are also thickened scars , but ke loid scars extend beyond the boundaries of the original woulld. 19 Although keloids arc known in persons of all races, scarring is of special concern to persons of the Negro race and some Asians as opposed to other dark-skinned individuals because of frcquency of keloid formation in this popUlation. thus suggesting a genetic factor. Frequency of occurrence is equal among men and women. Keloids are like benign rumor growths. Ke loids continue to grow long afier the wound is closed and may reach large size. Any attempt to cut or use dermabrasion to buffaway the keloid will only result in even more scarring. IS The mechanism of collagen deposition is totally out of control. Areas with keloids may be itchy and may be tender or painful. 16 New therapies are being used to contro l this phenomenon, but if a patient reports having had this problem or reports a familial tendency to form keloids, special attention should be made to address this problem at the time of initial assessment. Hyperkerototic scarring is hypertrophy of the horny layer of the epidermis. It is commonly seen in diabetic patients and may be located in adjacent and periwound tissue (see ColoI' Plate 24).
ClllIllS The most commonly encountered calluses occur on the plantar surface of the foot. They are usually found along the media l side of the great toe, over the metatarsal heads, and around the heel margin. Callus fonnation is a protective function of the skin to shearing forces ofa prominent bone against an unyielding shoe surface. Neuropathy often leads to muscle
Clinic al Wisdom: Observation and Palpation of Cal/us The callus will appear as a thickened area on the sole of the foot and it will usually be lighter in color (often yellow) when compared with the adjacent areas. When palpated, the callus area will feel firm or hard to the touch. There may also be some scaling or flaking, roughness, or cracking of the callus. Cracked callus is a portal for infection . Further examination is recommended.
~lacerll lio ll
Maceration is defined as "the softening ora tissue by soaking unt il the connective tissue fibers are so dissolved that the tissue components can be teased apart."17I PI·Ut l Macerated skin is drained of its pigment and has a white appearance and a very soft, sometimes soggy, texture (see Color Plate 15). The kin is often described as being wrink led l ike a prune. A familiar example is di shpan hands. Softened tissue is easily traumatized by pressure and is a contribu ting factor in the development of pressure ulcers. 17 The source of moisture that soaks and macerates the skin may be perspiration, soaking in a tub. wound exudate. or incontinence, as well as from wound dressing products. Macerated skin wi ll be thinner than adjacent skin. Palpate very gently so as to avoid trauma. Protect from pressure and shear. Edemll Presence of edema may be associated with the inflammatory phase. the re sult of dependency of a Ii Illb or an indication of circulatory impairment or congestive heart failure . Edema is defined as nuid excess in the ti ssues due to overload of interstitial or intracellular Ouici, causing congestion. A consequence of trauma is increased extrace ll ular fluids in the tissues that both blocks the lymphatic sys tem and causes increased capillary permeability. The function of edema fo llowing injury is to block the spread of infection. The resu lt
60
W OUND CARE
is a swe ll ing that is hard, and the app lication of pressure to
lhe swollen area docs not distort the tissues. The term "brawny edema" refers to this type of swelling and is assoc iated with
the inflammatory phase. Traumatic edema is usually accompanied by pain. Swe lling rcsulting from lymphedema or from systemic causes is usually painlcss, 21
There are two types of edcm3- nonpitting and pitting. Nonp itting ede ma is identi fied by skin that is stretc hed and shiny, with hardness of underlying ti ssues. Pitting edema is identified by firml y pressing a fin ge r dow n into the ti ssues and waiting 5 seconds. When pressure is released, if ti ssues fail to resume th e previo us position and an indent ati on re-
mains, there is pitting edema. Pitting edema is observed when there is ti ssue congesti on associated with congesti ve heart
by usi ng wate r di splacement. This is a qui ck and accurate meas urement using a vo lumometer fill ed with wat er. Vo lumometers are made o f a heavy Lucite and come in diffe rent sizes for immersion of a foot and ankle, leg above the knee. and the hand (see Figure 3- 3). They are strong and durable. Both methods work best when edema in a limb is being measured. A simple form , such as Ex hibit 3- 1, either handwritten or preprinted, listing the measurements of both limbs side by side is a useful guide for consistency and completeness of the measurements and to make compari son between baseline and retest measurements qui ck and easy. Change in edema measurements is one way to assess the treatm ent outcomes. The procedure for girth measurements is as follows:
failure, venous insuffic iency. and lymphedema, or dependency ofa limb. It is meas ured on a severity scal e of 0 to 3+, whe re 0 = no t present , 1+= minimal, 2+ = mode rate, and 3+ = severe. Eva lua te for body symm etry wh en examining for edema and also refer to the patient's medical history. Bilateral edema of the lower extre mities can be a sign of a systemic problem such as congesti ve heart failure, cirrhos is, ma lnutrition, or obcsit y or may be caused by depe ndcncy or usc of ce rtain drugs. Drug-induced edema is often pitting edema and may be caused by hormonal drugs, incl uding corti costeroids. estrogcns, progestcrones. and testosterone. Other drugs to consider include nonsteroidal ant inflammatory and antihypertensive drugs. Symptoms usually resolve i f the drug is withdrawn .:!1 Systemic edema may extend from th e lower ex tremiti es up into the abdomen. Unilateral edema of the lower extremity of suddcn onselmay be due to acute deep vein thromboph lebitis and requires immedia te refe rral to th e phys ician. Other cau ses of unilatera l edema are chronic venous insufficien cy, lymph edema, ce lluliti s, abscess , osteo mye liti s, C ha rco t's j o int , po plitea l a ne ur ys m, de pe nd e ncy, and revasc ul ari za ion. Deep vei n thrombophlebiti s, chro ni c venous insufficiency, and lymphedema are th e three most common callses.21 I fin doubt about th e eti ology of th e edema, co nsult with the physic ian before planning furth er testing or an interventi on. If edcma is left in th c ti ssue th e large-protein molecul es will cl og th e lymphatic channels and cause fibrosis. Chapter 9. Ma nagc ment of Edema, descri bes the management of eden1a with compression. IWellSllrelltelll of El/eIlt U. Ti ssue volume increases when edema is present. Edema ca n be evaluated by palpation for change in COlllour of th e ti ssues and by pholOgraphs. Two meth ods used for measurement of th e ex tent of edema formation are girth and volume. Girth measure ment or the limb is th e mosl common meth od used in clinica l practice becau se it is simple to perform . Although limbs are mos t casily measured, th e torso can also be assessed for edema by taking gi rth measurements. Volumetri c measurement is made
I. Mark and record the bony landmark s on the limb to guide th e measurements, includin g the metatarsa l heads, both ma lleoli, 3 cm above the lateral malleolus, 12 Col above th e lateral ma lleolus, 18 cm above the lateral ma lleolus. and th e lowe r edge of the patella. 2. Use a fl ex ible tape measure to measure th e circumference around th ese landmark s. 3. Measure both limbs. 4. Record measurements (for both limbs) side by side. Repeat at nex t assessment. Compare.
Figure 3- 3 Vo lum etric Edema Measuremenl. Source: Reprinted wi th permission frolll G.M. Pennington, D.L. Danl ey, and M.H. Sumko . Pul sed. Non-Thermal, High-Frequency Elec tromagnetic Energy (DI APULSE) in the Trea tment of Grade I and Grade II Ankle Sprains, Military Medicine: The O.Dicial JOll rnal ofAMSOS. Vo l. 158. No. 2, p. 102. 1993, Associa tio n of Milia ry Surgeons of the United States.
.h.H.',\'.\'11/(11II (~rtlte St.ill
E,hibit 3-1 Lo\\cr h.lrcmlly Girth
Mca~lIrements
umllHnmd
61
Form
Dale
-
-
Righi
Len
Righi
Len
Righi
I ell
MclnlJrs
r l
12cm
1 lalcralmallcolu~
1~
1 lalcralmal1colu:-,
cm
-
-
Lower edge of p.IIc1Ii1
The proccdure for volume di~placement measurements is as follows: I. Fill \ollimomcter \\ ith tepid wmer (abollt 95' F). 2. Immerse the atTected extremity II1to water. 3. Catch O\erno\\ in a graduatcd cylindcr to measurc volumc displaced. 4. Repeat \\ IIh both I"nbs. 5. Record volume displaccments to both limb~ ~ide by side on a form.
Target Outcome.\ for Edemll Illten'elltioll\ The edcma \\ ill be absent. rcducc(l or controllcd. Bascline girth or volumc mcasurements were larger for the atTected IlInb or area at baseline and arc now equal to or closer 10 the measurements of the unaffected limbs. Ifboth limbs arc afTcete
edema could be an Indication of change from absence of the innammation phase Lo thc acute inflammation phase. The increased edema \\-'Quld be accounted for by increased perfusion to the tisslie. This cdematous rcaction may bc more appropnate ly palpated than measured by lIl"rll",ents. The cdcma should be transitory and reduce as the IIlflammalion phase passes. Color Assessmcnt of adjacent skill color i!'l a clue to skill circulation and dlsfllptions in circulation associated with trauma or Infcction. Skin color tones reflect the condition of underlying blood vessels. In lightly pigmented skin. pressllre closes capillaries and induces a blanching of the sk in color that returns to normal color tones when pressure is released. Irthe color does not return to the color or the adjacent skin Wllhlll 20 minutcs aftcr removal of pressure. this IS called lInblanchable erythema. Unb lanchable erythema III lightly pigmented skin is redness that docs not disappear when pressure is rcmoved. Ilistology of un blanch able erythema shows crythrostasis in the capillaries and \'cllulcs. followed by hcmorrhage ' (see Color PI"les I. 17. "lid 25 for lInblanchablc erythema). The same indexes cannot be used in darkly pigmented skill.
Color A,\.\e.'i.\llIellt for Darkly Pil:lllellt(!ll Skill. Idcntification of stage I pressure ulcers has historically relied heavily on color changes in the skin. Erythema may bc scen in some situations in lighter-toned persons of colo r, but III darkly pigmented skin the redness may not bc seenY; Darkly pigmented skin is defincd as skin toncs that "rcmalll un-
62
WOUND ('".,
changed (docs not blanch) when pressure is applied over a bony prominence. irrespective of the patient's race or cthnicity."H( rJ~ 1 Darkly pigmented skin is usually found in African Americans, Africans, Caribbeans. Hispanics. Asians, Pacific Islanders. Middle Easterners. NativcAmc ricans. and Eskimos. When aSSeSSI11CIlI is made of darkly pigmented
skin in patients with high risk for pressure ulcers, careful attention should be paid to color changes at sites located over bony prominences. Look for color changes that differ frol11 the patient's usual skin color (as described by the patient or those who arc familiar with the patient's usual skin co lor or 3n area of healthy tissue).:!-' Consider conditions that can cause changes in ski n color. such as vasocon-
as observed in
striction (pallor) causcd by lying on a cold surface or hyperemia (redness or deepening of skin tones) from lying on a bony prominence. Allow the area to be assessed to be exposed to ambient room tcmpcrature for 5 to 10 minutes before examining. When darkly pigmcnted skin is intlamcd the site of inflammation becomes darker and appears bluish or purplish (eggplant-like color: sec Color P/(lIe,. 19 alld 21). This is comparable to the erythema or redness seen in persons with lighter skin tones ..B Changc in color. as mentioned, is an indicator of hcmorrhage of the microvasculature in the skin and may also be an indicator of deep tissue trauma that will later rupture and form a crater. When there is an extremcly high mclanin content. the color of the skin may be so dark that it is hard to assess changes in color at all. l7
Another complicating factor in identifying erythema in darkly pigmcnted skin is difTerentiating intlammation from the darkening of the skin caused by hemosiderin staining. Hemosiderin staining usually occurs close to the wound edges, whereas injury-related color changes usually extend out a considerable distance and are accompanied by the other signs of intlammatioll. Color Plate 10 shows hemosiderin stain ing at the margins of a wound in a dark-skinned person. Ilemosiderin staining is a symplOm of wound chronicity or repeated injury. The mechanism of hemosiderin staining is dcscribed later. Color changes are apparent around acute (in named) and chronic opell wounds (pigmentation). If color is not a reliable indicator, use other clinical indicators such as sensation (pain). temperature (heat. coolness). tisslle tension (edema or induration and hardness) to confirm the diagnosis of innammation in darkly pigmcnted skin. Assessment of tissue circulatory status by use of color is also difficult in darkly pigmented skin. Consider the efTec ts of gravity on vasomotor changes in the tissues of the extremities in elevated and dependent positions. Color changes will appear more subtle than those in light skin. Assess from a neutral position, then with the area eleva ted about 15° and dependent for about 5 minutes and comparcY Asscssment
of capillary refill time for persons with darkly pigmented skin shou ld be tried at the tips of the second or Ihird fingers." Also consider the examining the nail beds. If they arc not pigmented apply pressure to the second or third finger; if the skin under the nail blanches. it will give a color comparision for assessing pallor or cyanosis. Thc speed of color return following the slow release of pressure is an indicator of the quality of vasomotor function. The slO\\'cr the return of color the morc diminished the vasomotor function. Compare the speed of return wit h that in your own nail bed or that of another person with normal vascularity.!4 Assessment should be made with good lighting. Avoid nuorescent light. which casts a blue color to the skin. Use natural or halogen lighting to assess skin tones. Flash photo· graphs arc recommended becausc the flash makes 'he demarcation between normal skin tones and those that arc traumatiled easier to see and the picture provides a visual record of the patient's skin status.~\ Not ice the demarcation between the normal skin tones and the traumatized area in C%r Plare 19. The patient or family member who is familiar with the patient's natural skin tones shou ld be the primary person to provide information relative to skin color changes. E('c/tJ'IIIosis (lIelllorrlwge). Trauma to the skin and subcutaneous tissue causes rupture ofthc blood vessels and sub· cutancous bleeding or hemorrhage called ecchymosis. Ecchymosis is seen as a purple discoloration in white skin and a deepening to a purple color in darkly pigmented skin. The ski n over the hemorrhagic area may be taut. shiny. and edema· tOllS (see Color Plate 34). Hemorrhage and clotting occur as a consequence of an acute injury such as trauma from pressurc, a bump, or shearing and includes trauma to new granu· lation tissue as well as veno us leakage from venous insufTj· ciency (sec Color Plate 65). Clotting cuts ofT oxygen 10 the lissues with subsequent hypoxia and ischemia. If the blood is not reabsorbed into the tissues in a timely fashion. tisslle necrosis will occur. It is not known exactl y how long clolled blood can remain in the tissues before necrosis occurs. but electrica l stimulation. pulsed radio frequency stimulation. and ultrasound facilitate reabsorption of hemorrhagic materials if started soon aftcr injury (eg, 48 to 72 hours). EfTicacy studies reported in the literature and photographs that show the effects of these interventions are described in Chapters 16, 18, and 19. Rupturc of the vesse ls around a wou nd and also scep~lgc from venous hypertension cause deposition of blood in the subcutaneous tissues. The blood stains the tisslies by deposition of hemosiderin from lysed rcd blood cells and turns the skin a rust brown color. Hemosiderin staining is seen as a ring around pressure ulcers (sec Color Plate 2) or as the brown discoloration or the skin of the lower Icg ill patients with venous discase (see Color Plates 491111l/50). The discolora· tion may be permanent or it may gradually disappear.
As~essmel1l
(dille Skill lind " 'bulIll
For those who cannot communicate verbally. but who can understand and respond cue with questions such as. Show me where it hurts? Docs it fcc I like it is burning? In noncommunicating patients. observe during guided movement and palpation for facial grimacing, tenseness, and! or withdrawal response to noxious stimu li . Testi,,!: with a VbmalAllalog Se(de: A visual ~lI1a l og sca le (Exhibil3 2) is a line marked wilh 10 perpendiclilar li nes and numbered 0 to 10. where 0 = no pain and 10 the worst pain imaginable. Ask the patient to give a number on the line or point to a number to indicate pain severity. Record. This is a common procedure for assessing pain severi ty. It can be repeated to determine change in pain severity as a measure of Ireaim en I efTcct. Reliabilily may be qllestionable. Palients with either very high or very low pain thresholds may more accurately report pain level by another method. Keeping a PaiJl Diary: The patient or caregiver can record the information on a pain diary form such as Exhibit J 3. This will be a va luab le tool to measure change in pain over time and wi ll provide feedback to the patient that pain is altered. Iflest resliits indicate Ihal pain is presenl and a problem. management of the pain with an intervention wou ld be indi cated with a target outcome of pain free, pain reduced, or pain controlled. A change in pain status will be a functi onal outcome if there is a change in the patient's functional activities as a result of the chan ge in pain status. such as th e patient is ab le to tolerate active assistivc range of Illotion to the wounded area and is able to sit lip in a wheelchair. Outcome measures to report after an illlcrventioll for pain management include the following:
Semwtio" Sensory testing procedures and expected outeomcs are described in this section. They include pain. protective sensation, and thermal sensation.
Pai". Severe pain or tenderness either within or around the wound may indicate th e presence of infection, deep tissue destruction. or vascu lar insufficiency. Use of a pin to lesl for pain sensmion is considered oUldaied and is nOi recommendcd. Absence of pain or insensitivity to touch and temperature may indicate neuropathy. Sometimes pain-level reports arc more a report of anxiety than pain. Observation ofmO\'el11ents by the patient in the area of reported pain and reaction to gentle palpation are useful in distinguishing between the two. Ideally the beM and most reliable way to determine the intensity of pain is by report oflhe palient. Of co urse. Ihis is not always possible. Se\cral methods can be used to test and retest for pain. Retesting is very important if one of the expected outcomes from treatment is pain reduced eliminated, or controlled. Use the same testing measures before and after the use of an intervention. Commonly used tests for pain include pain questionnaires that arc either verbal or pictorial. visual analog scale. pain diary. or palpation and observation for those who cannot communicate except by response to noxious stimuli. Testi"g with (I P(li" Que.,·tio""aire: If the patient can communicate verbally, ask the patient to describe the pain. Guiding questions would include the following:
• Pain free-the patient is pain free by observation or report of the patient or caregiver. • Tension free- tissue tension reduction is tc:stcd by palpation or by checking for increased mobility of the area. • Pain medication free- the patient may no longer require pain medication. or the amount or frequency may be reduced. • Sleeping- the patient'S pain is controlled and he or she has morc hours of undisturbed sleep. • Unreactive (to noxiolls st imuli ) the patient no longer responds 10 movement or palpation that produced pain.
• Where is the pain? • When do you have Ihe pain? Ilow long does il last? • What type of pain do you have? Is it burning, throbbing. cramping. or prickling? • Docs the pain affect your sleep? • Does it afTect your mood? • Do you take medication for the pain? What do you take? • What are th e eITects of the medication? • What positions or activ ities affect the pain?
Ex hibit 3- 2 Visual Analog Scale for Pain Measurcmcnt
o
2
3
4
63
5
6
7
8
9
10
64
W OUND CARE
Ex h ibit 3- 3 Pa in Diary Form
Dale
Time
Location
Activ it y
Clinical Wisdom: Premedication for Pain
Res ponse to the pain testing will guide the clinician about the need to premedicate the patient before performing a procedure. Sometimes relaxation and antianxiety medication will be more appropriate than pain medication .
Protective Sell.lfDtioll. If neuropathy is suspected by medical history or observatio n, testing fo r se nsati on is indicated . A safe, accurate method for testin g se nsa ti on has bee n de-
veloped usin g Semmes- We instein mono fil aments. The l11onofilam cnts come in different force levels. Levels 4. 17, 5.07, and 6. 10 are used to check for protecti ve sensation. Force leve ls increase as the numbers increase. The object of
the test is to see if the patient can detect pressure when the monofil ament is placed against the skin and force applied that is sufficient to buckle the monofil ament. Testing is usuall y performed on the sale of the foot. The procedure for
meas urement of sensation with Scmmes-Wei nstein monofi lame nts is as fo llows:
Pa in intensity
Medicat ion
Other symptoms
sensitive to thermal sensation.26 If the pat ient is unable to sense warmth, there will be a high risk of burns if heat is applied to the skin. If th e pati ent is un ab le to sense cold, th ere is a ri sk o f injury from ex posure 10 co ld; Ihe fee t shoul d be protected from fros tb ite if th e pati ent is going to be exposed to ve ry co ld te mpe ratures.
Adjacent Skin Temperiltllre
Baseline sk in temperature is one objective measurement of circulation. The baseline can be used to monitor circulatory response to treatment or to eva luate innammation. Temperatu re can be tested by palpation or by a skin surface thermometer. If greater acc uracy is required, there arc several commercial instruments avai lable. A thermistor is the least costly of the three commercial dev ices described here fo r measurement of skin surface tcmperature.A probe is placed agai nst the skin and a reading taken. Another dev ice is a radiometer, which determines tcmperatu re by measurement of surface re n ection o f in fared rad iati on. Anot her way of
taking temperature is with liqu id crystal thermography, which produces multicolor pictu re maps of the wo und and adjacent tissues. These devices have good reli ab ility but arc usua ll y used for researc h. The thermistor and th e infra red
I. Start by applying to the so le of the foo t.
2. Place thc monofi lament against skin.
scanner. however, could be lIsed in the clinic easily with minimal training. Usc of the in fra red scanner is described in
3. Appl y press ure unlil the fil amenl buckles.
Chapter 15.
4. Ask the patient to identify where the monofilament was appl ied. The patient should be able to detec t th e mono fil ament at Ihe tim e il buc kl es. The inability to detect th e 5.07-levelmono fil amelll ind i-
cates a limited ability to use protecti ve sensations. If the patient can distinguish th is level of sensation at several points on the feet, the protecti ve sensation is considered to be adequate to avo id ri sk of trauma. 25 A photograph of SemmesWeinstei n filaments and the appropriate interventions for patients wi th loss of protecti ve sensation arc given in Chapter 15.
Thermal Sell.m tioll. The test for thermal sensation is performed by using test tubes or small narrow bottl es fi lied with
warm and cold water. Be sure to test in a normal area before app lying to possible insensate areas to avoid burns. Research reports that the lateral aspect of the foot is the area most
Use of an inex pensive (about $2) skin fever thermometer strip that changes color with temperat ure change is a si mple and useful way to assess the tcmperaturc ofpcri wo und skin. This is best done in areas that have adeq uate ci rculat ion, such as on the trun k. It is more sensiti ve to changes in temperalure than the back of the hand, although not se nsitive enough
to record temperatures below 95°F, which are found in the distal parts of ex tremities. Sk in feve r thermomcters usuall y have six thermochromic liqu id crystal ind icator lights in shades of brown. tan, green, and blue. which respond to temperature shi fts. To read the temperature usc the highest telllperature window indicated by a color. Ski n temperature is shown in 1°F intervals. The normal skin temperatu re in areas of good ci rculation is usuall y abollt 95°F. An increase in temperature of the sur rounding skin measured on the fever thermometer. compared with adjace nt area temperatu re. is an indication of an area of circulatory perfu sion. This is the heat descri bed as a classic sign of in nam111atio l1 . Absence of
Assessment of the Skill alit! WOllud
an increase in periwound skin temperature from adjacent ski n may be an indicator of an impaired or absent inflammatory respo nse. Ski n tempera ture below 95° F wi ll not record on this thermometer. Other more sensitive tests for temperature or blood now should be considered. Skin temperature is a useful measure for assessing many kimis of wounds. including stage I pressure ulcers. An increase in skin temperature may indi cate pressure ulcer formation o r the presencc of infection . It is a very useful 1001 for assessing inflammation in darkly pigmented individuals, in whom the margins of eryth ema are hard to see. Skin temperature can be taken at locations on the Inargins of discoloration and at the ce nt er. The c lock mcthod. taking Ihe lemperalUre at Ihe 12-. 3-, 6-, and 9-0'c lock posilions around the wounded tissue, is usefu l for recording this measurement. The procedure for measuring skin temperature is as follows : I. Make sure that the area of skin to be tested has been pressure free and exposed to ambient air tempenllure for al leasl 5 10 10 minules before lesling ils lemperatu re (a sheet can cover the paticnt for privacy). 2. Place a single layer of plastic against the sk in as a hygieni c barrier (this docs nol interfere wit h tempera ture accuracy). 3. Lay temperature strip flat on th e plastic barrier. 4. Hold Ihe slrip in place at bOlh ends lighlly so as nOI 10 compress capillaries, and wait for color of strip to change color. Allow at leas t I full minute for the color change to occur. In very inflamed tissues. it may occur immediately, but may change further as it is held for the fullminutc. 5. Read the temperature whi le the strip is still against the skin. 6. Measure at the wound edge at the 12- and the 6-o'clock positions and ncar th e expected outer margin of the periwound erythema/discoloration. Repeat at the 3- and Ihe 9-0'c lock posilions. 7. Record temperature at each point. Interventions afTect tissue perfusion and thus skin temperature. Skin temperature would be expected to increase if there is enhanced perfusion following superficia l heating with whirlpool. Temperature changes in deeper tissues may occur following pu lsed short wave diathermy. However. the fever strip may not be sufficient ly se nsiti ve to measure any of these changes. If that is the case, the thermistor or infrared sca nner thermometer is recolllmended. To measure the effects of an interventi on. take a baseline measurement before treatment and repeat the measurement after treatment. Skin temperature sho uld rise aller treatment. If th ere is an ab ence of inflammation and the target outcome is to initiate the acu te inflammation phase. repeated measurement of tissue temperatures would help verify the outcome.
65
Coolness a lso ca n be used as an assessment of ci rc ul ation. Sometimes th ere is an initial increase in skin temperature fo ll owed by cool ness after trauma. Like warmt h. coolness wi tho ut trauma may be an indicator of circ ul ato ry statu s. Some areas oflhe body nalUrally have less war mlh, including the feel, toes, and fingers . The areas of the trlln k or over we ll-perfused Illuscle tissues have greater warlllth. If there is coolness in the digits or the feet, it is importa nt to eval uat e o ther signs and symptoms such as hair grow th. sk in colo r, pulses, and skin tex ture for circulation. If those signs arc also suggestive of circulatory impairment. they shou ld trigger further c ircu latory examinat ion as described in Chap ter 6. Cool ness may also be an indicator of impaired ti ss ue viability o r ti ssue death following isc hemia. A quantitative measure of tissue temperature as part of the assessment of wounds is not yet a standard of c linical practice. However. articles are appearing regu lar ly in journal s describ ing temperature measurement as an assessment procedure fo r inflammatory processes and tissue viab ility. All or lh e procedures described arc simple. noninvasive, and quick but most importantly have clinical significance.
Hair Distribution Norma l body hair is dislribuled over all four eXlrem ilies, extending down to the digits. Over time body hair diminishes and is even tu ally lost. A dimini shed presence of hair is seen in aging skin or where there is impaired circulation. As circulati on in a leg decreases. hair is lost dis tally. lI air distribution may be used as an indicator of the level or vascu lar impairment and an indication for vascu lar testing. I-lai r folli cles are important to wound healing because they contribute epidermal cells for resurfacing partial-thickness wounds. Absence of hair should be conside red a fac to r in the prognosis ofwollnd healing ift herc is a partial- th ickness wound in an area where hair is usually found suc h as th e lower leg. Clinical Wisdom: Assessment of Hair Distribution as an Indicator of Peripheral Circulation 1. An easy checkpoint for adequate tissue perfusion to the lower extremities is examination of the great toe for hair growth. Hair growth on the great toes implies adequate circulation to support the hair follicles. When working with female patients, prior to examination remember to ask whether they shave the hair on the great toe. 2. Move up the leg proximally from the ankle and assess the most distal point where hair distribution stops. Th en palpate for skin temperature and pulses, and observe skin color in the area denuded of hair for circulatory changes.
66
W OUND CARE
Toell uiis Part of a comprehensive examination of the feet includes not only the skin but also the toenail s. Look at the color, thi ckness, shape, and any irregularities. Toenail pathology commonly seen includes hypertrophic, thick nails. Some toenail s may look like a ram's horn . Ingrown toenail s and fungal and pseudomonas infection, which give the toenail a green color. may be observed. Findings of toenail abnormalities, as described, arc referral criteria unless th e cli nician has
knowledge and training in
fOOl
and nail care.2'
Blisters Trauma to the epidermis gives rise to a blister. The blister
may be filled with clear fluid or, if the trauma is deeper than the epidermis and ruptures blood vessels. the bli ster nuid may be bloody or brown (see Color Plate 68). The bli ster roaris nature s best dressing, but it can hide deep tissue damage. Removal of the bli ster roof is controversial. If the blister fluid is clear, ti ssue damage may not extend into the dermi s or deeper, and the wound will heal under the bli ster roof; th e epidermis will eventually just fall off. I( should not be di sturbed and in fact may requ ire protection. However, if the fluid is bloody, brown. or cloudy, as shown in Color Plare 68, deep ti ssue damage may be present, and unroofi ng the blister may be the only way to determine the extent of trauma, as shown in Color Plate 69. Assessment orthe ti ssue under the blister without breaking the blister is helpful in evaluating when the blister needs to be unroofed. Gently press down with a fingertip on the ti ssue beneath the blister roorand compress it; release, and reel ror the resilien cy of the subcutaneous tissues. If there is
good resi lience, that is, it bounces back when the pressure is removed, the deep ti ssues may be mildly congested, but if (he tissue feels SO f1 , spongy, or boggy there is high probability of ti ssue congestion and probable necrosis. Practice and carerul concentration are needed to perrorm thi s palpation examination. One tip is to try pressing down on the skin on the opposite side of the bod y in the same location (eg, on (he heel) and compare the resiliency when compressed.
ASSESSMENT OF T H E PERI WOUN D AND WOUND TISSUES Assessment of the peri wound and wound tissues is described in the following section s according to clinical signs and symptoms that wou ld be expected in each wound healing phase. There is a close relationship between assessment of the wound and periwound ti ssues and diagnosis of wound healing phas e. Care ful assessment of the wound and peri wound tissue establishes the present, predominant wound healing phase. The predomil/a/lt wound hea ling phase is the primary functional diagnosis for (he wound at that time. There will also be a secondary functional diagnosis signifying (ransition to (he next phase(s) or absence of subsequent phases(s). In thi s section , ti ssue assessment is presented by describing three aspects of healing, acute, chronic, or absent, for each phase of wound heal ing (inOammation, proliferation, and epithelialization). Each aspect of each phase is a potential wound healing phase diagnosis. Table 3-6 li sts the wound healing phase and the re lated wound healing phase diagnosis. Also an expected prognosi s applies to each diagnosis and is also li s(ed.
Tabl e :HI Wound Healing Phase Diagnosis and Prognosis
Wound Healing Phase
Acute Wound Healing Phase Diagnosis
Chronic Wound Healing Phase Diagnosis
Absence of Wound Healing Phase DiagnOSis
Inflammation
Acute inflammation
Chronic inflammation
Absence of inflammation
Proliferation
Acute proliferation
Chronic proliferation
Absence of proliferation
Epithelialization
Acute epithelialization
Chronic epithelialization
Absence of epithelialization
Prognosis
Progression through phases of healing
Reinitiate acute phase, then progress through phases of healing . Reinitiate acute phase of healing and progress to a clean,
Initiate healing phase, if able, and progress through phases. If able to initiate healing phase, progress to a clean, stable wound. If unable to initiate healing phase, refer.
stable wound.
Assessment aI the Ski" (lnd Ift)t{m/
Acute Phase A s normal acute wounds heal. there is an orderl y progres-
sion through the wound healing phases (inflammation. proliferati on. cpithciiaiizHlion. and remodeling). Chapter 2 describes th e normal biologic phases of wound repair. Chronic Phase
Failure of the orderl y progression of hea ling results in a chroni c wound. The chronic wound may fail to initiate or stall in any phase of wo und hea ling. When a wound siall s, platea us, or simply gels stllck in one wound healin g phase, th e wound becomes chronic with respect to that phase. For example. a press ure ulcer often will become stuck in the innal11l11alory pha se of wo und healin g. thu s th e term cJuv llic illjllll1lmarioll. Another example is the wound that fill s with
granulat ion ti ss ue but does not stop proliferating and goes on (Q form hypcrgranulati on ti ss ue (Colo I' PllIle 23). Th is is termed chronic proliferation . A ri na l exa mple is th e wou nd with impai red scarri ng. such as with hypertrophic scars or keloid fo rm ati on. A wound in thi s condit io n does not stop laying down collagen. Thi s is termed c:lllvnic epit/w/ia/i=arion.
67
and create a care plan based on a diagnosis of wound healing phase. The wo und hea ling phase di ag nosis is used for the prog nosis and to targe t treallnent out comes. Prog nosis fo r a wound with a diagnosis of th e ac ut e healin g phase (innammatioll. proliferati on. or epithelializmion) is prog ression through the phases of hea ling. A chro ni c wo und heal ing phase di agnosis indicates a prognosis th at the wound will progrcss th ro ugh the phases of hea ling following rein iti atio n of the ac ute phase of hea ling th at is impaired. Alternati ve ly, th e prognosis may be a clean, stable wo und th at may not heal or may need anoth er interve nt io n to achieve clos ure. If there is inabil ity to initiate the abse nt phase and prog ress thr o ug h th e ph ases. th e prog nos is fo r th e wo und is nonhea ling. Such a findin g may suggest re ferral to anoth er practitioner. Mo re th ;:111 one predo minant wound healin g phase can be apparent at the same time. For example. a wound with the chroni c innammat ion phase is also in abse nce of the pro liferati on phase and in absence of th e epitheliali zati on phase. Chron ic innammati o n wo uld be th e primary wo und healing phase diagnosis and abse nce of th e proliferati on phase and th e epitheliali zation phase wo uld be th e sec~ ondary functi onal di agnosis, signifying th at th e wound is not prog ress ing through th e phases ofhealing. The wo und heal ing phase di agnosis is use ful to demonstrate medi cal necessity for intervention by the nu rse or physical therapi st.
Absent Phase
Innammation Phase
The wound that fai ls to pass th rough a wound healing phase is lac king attributes of that phase and is refe rred to as absence of inn aml11ation, abse nce of proli ferati on. or absence of epithel ializa ti on. Wounds that fail to prog ress th rough a wo und healing phase dirTcr from those that gel stuck or exhibit characteristi cs of chroni city in one phase. Those wounds that are nbse nt an innammatory response. for example. will not demonstrate signs of innam1l1ati on, whereas wounds with chroni c innammati on wi ll show signs of a continued innammatory response. Abse nce of the wo und hea ling phase is a way of indicating th at the wound has not initiated the phase fo r whatever reasons. Absc nce of th e wo und healing phase signifi es either th e inability to hea l or the need of help fro m an intervc ntion to initi ate th e acut e phase leading to progression th ro ugh phases. for example. reperfusion th rough surgica l intervention or enhan ced bl ood fl ow from a phys ica l agent.
Assessment of the peri wound and wo und ti ssues during th e infl ammatio n phase includes att ribut es assoc iated with the vasc ul ar response to wo unding desc ribed in Chapter 2. The appea rance of periwo und and wound tiss ue will chan ge as the wound prog resses through th e phases of healing. Colo,. Pla te.\· I and 2 show a wo und that went fro m th e chronic inflammati on phase to th e ac ute infl ammation phase and subsequ ent progression to the pro liferat io n phase. Four catego ries of wound characteristics are considcred: peri wound and adj acc nt tissue appearance (color. edema/indurati on. temperature). wo und tiss ue ap pea rance (colo r and tex turc). wound edges. and ex udatc charac tcristi cs (odor. type. and quantit y). The majo r att ributes of adjacent and pcri wound tiss ue that are observed and palpated in th e inflammatory phase include co lor. temperature. firmness/tex ture. se nsati on. and ecchymosis (hemorrhage) bruising. In this secrion, the att ri butcs of the wo und and the peri wound ri ssues are desc ribed durin g ac ut e inflammati on. chro ni c inflammati on. and abse nce of inflammation.
WOUND HEALING PHASE ilIAGNOSIS AND PROGNOSIS
ACllte Inflammlltioll
When the pcri wound and wo und tissue assessment is completed the clinician wi ll be able to rev iew altribules prese nt or abse nt. intcrprctlhc wound healing phase status obse rved,
Signs of acute inflammati on often ex tend we ll beyo nd the immedia te wound and pcri wo und ti ss ues and ex tend into adjacent ti ss ues as we ll ; they indicate a hea lthy res ponse and
68
WOUND
CAR'
arc a prerequisite to norm al healing. Compare the characteristics seen during acute inflammation as a reference point for the eva luat ion of impaired responses. A djucelll Tissues. Skill Coillr. Erythema is defined as redness of the skin
and is one of the classic characteristics of the inflammatory phase. Sk in color attributes found in light and darkly pigmented skin are described in the section on assessment of adjacent tissue. discussed earlier. Reddened sk in wit h streaks lead ing away from the area may indicate the presence of cellulitis. Ifassessed. check the patient's history for fever, chill s. history of recu rrent ce llul itis, or medical ions being used to treat the condi tion. Ifno treatmen t has been initiated. these findings shou ld be reported immediately to the physician. £delllll alld I"duratioll, The edema of acute innamma-
tion phase is a loca li zed brawny edema that feels firm and di storts the swollen ti ~sues causing the skin to become taut, shiny. and raised from the contours of the surrounding tissues. This edema results from trauma (eg. pressure ulcers. burns.
Differential Diagllosis ofllljTllltlllllltioll alll/Illfection
A differential diagnosis between innammat ion and infection shou ld be performed by the nurse or physical thcrapist during the tissue assessme nt. Innammation with periwollnd characterist ic symptoms of color change (red or purple). edema, pain, heat, and loss of function may progress to infection and necrosis. If the innammatory process alone is present, there will be exquisite tenderness over the involved area. If, however. there is cellulitis or other infection, there wi ll be streaks of redness extending away from the wound and pain may becomc intense (sec Color Pl(l(e 47). Wound exudate may be thick, yellow. tan. brown. or green color with malodor. Amount may be moderate to large. Monitor for signs of systemic infection that can Icad to sepsis including fever of 10 I OF (39.4°C) or higher. chills. manifestation of shock including restlessncss. lethargy, confusion. and decreased systo lic blood pressure." Management and diagnosis of infection is discussed in Chapter 8. " VlIllll Tissue Assessment. A partial-thickness skin loss creates a shallow crater that looks rcd or pink or shows the ye llow reticular layer, a thin. ye IlO\\, 111eshlike covcring. that is the deep layer of the dermis (sec Color Plllle 171. If it is bright and shiny, it is healthy and viable and should be len intact. Culor Plate I J shows the anatomy of the tissues beneath the skin. Ir the wound penetrates through the dermis into the subcutaneous tissue. the wound will look as ifit contains yellow fat. such as chickcn fat. or \\ hile cOl1l1eclh e tissue called rascia. The fascia is a connnective tissue that covers and wraps around all muscles. tendons. blood vessels. and nerves. Wounds that extend th rough the subcutaneous tissue into the muscle may have a pink or dark red appearance with a shiny layer of fascia on top. UlltiermillillgiTlIlln elillg. Excavation of the subcutaneous tissues during debridemcnt creates a "cave" or un dermining of the wound edges. Undermining can lead to separation offascia l planes (sec Color Plale 371. Muscles lie together in bundles held together by fascia. Separation of the muscle bundles occur~ when the rascia is cut. Separat ion of the fascia l layers opcns tunnels along the rascia l planes between the muscles under the skin (see Color Plate 37). Tunnels may join together and form sinus tracts (see Color Plate 36). The tunnels are areas where infection can travel. leading to abscess. A wound in the acute illnamm3tion phase wit h undermining, tunneling wiJlnot havc signs of in fccti 011 or necrosis in those species. Differential diagnoses ofi nn ul11!nation and infection has been discussed previously. Muscle ti ssue is striated and jumps or twitches when palpated. Muscles are connected to bones by tendons. Tendons arc covered wi th white rascia and look like ropes. The shcath of
Asse.~·:mlelll
fascia covering th e tcndon is called peritenon. New granulation tissue will grow over intact peritenon. Penetration of a wound into the joint may expose several anatomic st ructures, including ligaments that are white and striated, joint capsu le that is white and shiny, and cartilage that is whi te. h~lrd and smooth and is on the end of bones. Bone is white. hard and covered with a c lear or white membrane called periostellm. The level of tissue exposed is used to stage or grade th e wound severity as described previously. Loss of pc rite non or periosteum wi II compromise a skin graft.
WOUlld EdKes. During acu te inflammation the wound edges are orten indistinct or diffuse and change shape as wound contra ction and epitheliali za tion begins. Wound edgcs may be attached to th e wound base or may be separated from it, forming walls with the base of the wound at a depth from the skin surfacc. Wound edges should be palpated for firmness and texture. Observe th e margins for curlin g. See Color Pillfes 31 ami 31to observe wound edges. WOllnd Drllillilge. Wound drainage during the acute inflammation phase is an indication of the status of the clotting mechanisms and of infection. Wound drainage that contains dead cells and debri s is called exudate. Clear nuid dminage is called transuda te. See Chapter 8 for more descriptions of exudate charac teristics. During assessment record the presence or absence. color, odor. and quantity and quality of the wound drainage. Sllllgui"eolls. Initiall y there will be bleeding into the wound space that is controlled by clotting. Wounds that have bloody exudate a re called sa nguineous and may have impaired clotting. This may be due to anticoagulant pharmaco· logic products that contain substances such as heparin or to di sease processes such as hcmophilia . The amount of exudate will vary. Medical hi story. inc luding a pharmacy history. and systems review should c larify th e causes of the sanguineous drainage. Copious or persistent sanguineous drainage should be reponed to the physician.
Research Wisdom: Management of Heavy Sanguineous Drainage
If there is heavy sanguineous drainage, a dressing that promotes hemostasis and is very absorptive, such as an alginate, should be considered.
Serous. Scrous tran sudat e is clear fluid that exudes from the wound. It is usually ye ll ow and odo rl ess and is see n in
o.llhe Skin alit! H1J11l1d
69
va rying amounts during the inflammation phase (sec Color Plares 41 alld 43).
Chrollic Inflammatioll Inflammation that persists for weeks and months is referred to as chronic inflammation. Chronic innammation occurs when the mac rophages and ncutrophils fail to phagocytose necrotic matter, ingest foreign debri s. and fight infection .2M Thcrefore. necrotic matter or foreign debris is the type of material that would be expected to be found in the wound bed. Chronic inflammation is also related to th e release of histamine from the mast cells and renex hyperemia associated with vasodilatation of the surrounding vascu lature. Repeated trauma to the wound wi ll also develop into chronic inflammation . PeriwolIllll Skill. Chronic inflammation is seen as a halo oferythcma in lightly pigmented skin or a dark halo in darkly pigmented sk in located in the peri wound area. The latter may be easily mi staken because of its similar appearance with hemosiderin staining. There is minimal temperature change or cooling compared with adjacent uninjured tissues. There may be some minimal firmness from edema in the peri wound tisslles. There is usually minimal pain response or there may be intense pain associated with arterial vascu lar disease or infection . Arterial ulcers over the malleolus and press ure ulcers arc frequentl y see n wi th a halo of erythema but lack th e blood now to progress the wou nd (sec Color Plate 47). J"OIiIlC/Tisslle. Wounds in the chronic inflammation phase uSLIally have necrotic ti ss ue covering all or part of the wound surface. Necrotic tissue varies in co lor and may be black. yellow, tan. brown. or gray. Soft necrotic ti sslle. such as fibrin or slough , may be prese nt in the wound bed. Fibrin forms on the wound surface and is associated with venous di sease. Slough is necrotic fat and fascia adhering to the layer beneath it. Sec Color Plates 25 10 30 for different appearances of necrotic ti ssues. Pale pink wounds may have chro ni c infection (see Color Plate 24). Chapter 7 describes the significance of the different qualities of necrotic ti ss ue. Wounds that arc chronically inflamed ollen have a portion of the wound surface that is in th e proliferation phase with gra nu lation tisslle prese nt. but the proliferation fail s to progress. Not a ll pink ti ssue is granulation. however, as muscle ti sslle that is beneath newly removed necrotic ti ss ue is pink or dark red (sec Color Plate 13). During assessment record the presence of necrotic ti ss ue and the color. Wounds in the chronic inflammation phase of healing often have a comb inati on of seve ral a ttribut es present. For example. a wound can have black and yellow necrotic ti ss ue as well as pink granula ti on tissue or healthy mu scle ti ss ue (Sec Color Plate 7).
70
WOUND CARE
Clinical Wisdom: Distinguishing Granulation Tissue from Muscle To distinguish granulation tissue from healthy muscle, palpate the tissue with a gloved finger. Granulation tissue is soft and spongy and will not jump if pinched, but it may bleed. Muscle tissue is firm and resilient to pressure and will jump or twitch if pinched or probed.
plasma proteins from damaged or irritated capillaries. allowing moisture to accumulate and form an opaque ge latinOliS mass in the base of the wound. The edematous mass contains many substances, all of which are contributory to sustaining a chronic inflammatory respo nse. This mass is visib le on examination. 29 Record ifprcse nt (sec Color Plate 42).
A bsell ce of 11lj1(mimalioll Abscnce of the inflammation phase or inability of the body
IVoUlld Drainage. C% r(lIId Odor. Wound drainage that is foul smel l ing and!
or viscous yellow/gray or green exudate is oncn referred to as pus. The pus is a result of the demise of ncutrophils after
they have phagocytosed debris and excessive bacterial loads. W hen there is a high bacterial count (greater than 10' ), signs
of active infect ion will be seen. Prolonged, chronic in nammatio n is the resu lt when there is a bacteria-filled wound. 211 Not all ma lodorous or yellow/gray exudate signifies infection. The odor and fluid may come from solubi li zation of
necrotic tissue by enzymatic debriding agents or auto lysis. Enzymatic and auto lytic debridement are described in Chapter 7. C lea nse exudate from lhe wound to determ ine whet her odo r is transient or in terna l. If enzymatic or autolytic methods of debridement are used, the odor and debris should be
removed by the cleansing. Ifodor remains or ifexudate can be expressed from the wound or adjacent ti ssues that has color or odor. consider infection. Check for other symptoms of infect ion such as heat , fever, and lethargy. Exudate color can suggest the type of infec ti on. No rma lly, wou nd exudate is serous- a clear or light-yellow fluid . Green is usually assoc iated with an anaerobic infection (see Color Plates 40 10 45 and Chapter 8). Record co lor, texture. and odor on the
assessmcnt form. Vollllll e. Exudatc volume is considered an indicator of wo und outcome. l The amou nt of wound exudate volume should be estimated as scant/minimal, sma ll. moderate, or large/copious. It is hard to record exudate quantity froln a dressing or by expressing it from a wound so these estimates arc considered appropriate ways to record estimated quantity. Absence of exudate or dryness of the wound bed may indicate desiccation and the need for adding moisture. During assessme nt record th e presence or absence, color. odor,
to present an immune respon se to wounding may be due to many causes, inc luding an immune-su ppression state (eg. human immunodeficiency virus infection/acquired immune deficiency syndromc. cancer. diabetes. drug or radiation therapy, overuse ofantisepties. or seve re isc hemia).Absence of an inflammatory response prevents the wound from progressing through the biologic phases of repair. It is different
from chronic inflammation, with distinct signs and symptom s. In order for the wound to heal. interventions need to be considered to restart the innammatory response. However. because of the coimpairments related to the problem thi s may not be realistic. For example, a patient with an ischemic foot and an eschar over a wound on th e heel has an absence of inflammation. This is nature's best protection from entry of infcction . Protection of the eschar and the limb from trauma to prevent opening of the body to infcction and new wounding \lIould be the preferred treatment strategy' (see Color Pl{I{e 46).
Periwolllid S kill. Absence of an innamma tion phase is recognized by absence of a vascular response to wounding. including absence of color changes in the peri wound skin and absence of tension or hardness: however, there may be a boggy feeling, and minimal temperature difference or coolness compared with adjacent ti sslle. Minimal pulscs arc palpable. Such findings would trigger further investigation of vascu lar status of the patient (see Color Plale 46). IYOIlIll/ Bed Tissue. Wound bed ti ss ue may be cm ered with harcl dry eschar to sea l 00" debris and infection from
the wound (see Color Plale 46).
'''oulld Draillllge. Wound drainngc may be sca nt or the ti ss ues may be dry. Dryness may be due to sca ling off of tissues or due to improper treatment.
and quant ity of exudate. T he PSST has a Likert sca le to rate each one of these aspects (Chap ter 5).
S ummary of Three IIIj1ammll(;oll Phase Dillgll osis alld Progll osis
Ge/lIlillOIiS Edelll ll. Following a secondary trauma to the wound bed such as sharp debridement or enzymatic debridement, wound edema forms as a result of the leakage of
A diagnosis is the summary of data collected during the assessment process. Wound healin g phase diagnosis is a diagnosis of the functional status ofhcnling.,u Tablc 3 7 Sllm-
Assessmel1l (~rthe Skill al1ll ll hllllll
marizes the findings for cach aspect of the innammation phase.The presence of edema. induration, erythema. elevated temperature. pain. or diffuse or indi stinct wound edges is an indicator that the wound hea ling phase diagnosis is acute inflammation. The chronic ;,~flammalio" wound hea lin g phase diagnosis wi ll be recognized by an inadequate circulatory response to the area of trauma. There wi ll be a mild or Iimitcd erythcma, minimal or absent edcma and indurati on. and no elevat ion in tisslle tcmpcrature. OOen the assessmen t findings include a wound with a large bioburden of necrotic tissue. There may be a copiolls and malodorous exudate signifying an infection that the body cannot adequately suppress. Absence oIinjlammatiol1 wou nd healing phase diagnosis is recognized by an absence of circulatory response to trauma. Sealing ofT the wound from the rest of the body by a
hard, dry eschar gangrene is oOen nature's way of protecting the body from imasiol1. Absence of the innammation phase may also be due to scabbing over the wound surface or letting the deep wound tissues dry out. Because the phases of healing overlap. the wound healing phase diagnosis if the \\o und is transit ioni ng from one phase to the next is defined by the prill/my phase appeara nce. 11/flammation is the wo und hea ling phase diagnosis if the attributes of in flamm at ion are at least 50% to 75% of what would be ex pected in an acute innammatory res ponse (see Color Plate I). If the wound attributes are chron ic inflammation for at least 50 0 0 to 75 0 0 of the symptoms assoc iated
71
with chronic innammation. the diagnosis is cluYJl1ic i,!f1amlIlatiOI1 (see Color Plate 7). When the wound attributes of ac ute innammation are less than 50°0 of what are expected and there is significant proliferation of granu lation tissue in the wound bed, the primary wo und phase diagnosis changes to proliferation phase (see Color Plate 8) .
Proliferat ion Phase Like the innammation phase. the proliferation phase is broken into three aspects: acute proliferation (the active biologic process of proliferation. includi ng gra nulat ion ti ssue formation and contraction). chronic proliferation (the wound is stuck in the proliferation phase and not progressing to the next phase of epi thelializat ion and remodeling). and absence
of proliferation (the wound bed is clean but the wound is not proliferating or is not contracting). Each of the three aspect characteri stics of proliferation arc described . A('lIIe Proliferation Phase I'eriwolllll/ Ski". Periwou nd ski n during proliferation regai ns co lor and contour sym metry with that of adjacent skin (edema resolved); if it is a recovering chro nic wound howeve r, expec t to see hemosiderin stai ning (pi gmentation) around the wo und margins (sec Color PllIfe 2). Ecchymosis should be resolved. Skin turgor is normal and is not stretc hed
Table 3-7 Wound Healing Phase Diagnosis: Tissue Characteristics for Inflammation Phase Periwound Skin and Wound Tissue Characteristics
Acute Inflammation
Chronic Inflammation
Absence of Inflammation • Pale or ashen skin color • Absence of erythema or darkening • Hemosiderin (ru st brown) staining • Ecchymosis (purplish bruising)
Periwound skin color
• Unblanchable erythema in light-skinned patients • Discoloration or deepening of normal ethnic color in darkskinned patients • Ecchymosis (purplish bruising) • Hemosiderin (rust brown) staining
• Halo of erythema or darkening • Hemosiderin (ru st brown) staining • Ecchymosis (purplish bruising)
Edema and induration
• • • •
• Gelatinous edema may be seen on wound tissue • Minimal firmness • Absent • May feel boggy
Firmness Taut, shiny skin Localized swelling Consolidation (hardness) between adjacent tissues
continues
72
W OUND C A RE
Table 3-7 continued Periwound Skin and Wound Tissue Characteristics
Chronic Inflammation
Acute Inflammation
Absence of Inflammation
Tissue temperature
• Elevated initially, decreases as inflammation progresses
• Minimal change or coolness
• Minimal change or coolness
Pain
• Present; wound is tender
• Minimal pain unless
• Minimal or no pain unless arterial etiology, then may have intense pain
Wound tissue
and painful unless
arterial etiology or
neuropathy is present
infection, then may have intense pain
• Blister with clear or bloody
fluid • Shallow or deep crater with
red to pink color • Red muscle • White shiny fascia • Yellow reticular layer of dermis with granulation buds
• Necrotic, varies in color from yellow to brown to black • Necrotic tissue covering full or partial surface area • Soft or hard necrotic tissue • Yellow fibrin or slough • Portion of wound may have granulation tissue • May also appear as clean, pale pink
• Covered with hard, dry eschar • Necrotic, varies in color from yellow to brown to black • Scab
Undermining/tunneling
• May be present in deep wounds • Has potential for infection and abscess
• May be present in deep wounds • May extend poten tial for infection and abscess
• May be present in deep wounds • Has potential for infection and abscess
Wound edges
• Diffuse, indistinct, may still be demarcating from healthy tissues
• Distinct, edges may be rolled or thickened • Is not continuous with wound bed if deep wound cavity
• Has distinct well defined wound edges • May be attached to necrotic tissue
Wound drainage
• Serous or serosanguineous
• • • •
Infection Viscous Malodor Pus (yellow, tan, gray, or green) • Moderate to large amount
• Scant or dry
Color Plates
1, 14,15, 17, 19,36,37, 39, 68
20,25,27, 42,47
26,29, 46
, 1\.\'('.\.\/1/t'1I1 of"rlu: SAin lIlUl U(mllli
73
or taut because the edema and IIlduratlOn me resolved (absent). Firml1l.!s~ IS absent or minimal.
to measure undermining, tunneling and then calculatc the extent of the o\'crall wound.
Periu'ollltli Ski" Temperatllre. pf.!riwound skill tcmpcrature "hcn palpated or measured on a skin thermometer is the same [IS skin in adjacent arcns or mny bc slightly ele\'ated due to enhanccd perfusion of the tissues and higher metabolic acti\ ities associated \'vith healing.
IIlJlllld Ti~.\lle. Wounds that ha\ e a bO\\ 1-llkc shaped C;1\'ity will fill \\ ith granulation tissue during the acute prollferativc phase to create a surfac.:e across which epldennal cells may migrate. Tissue that develops during this phase has been given the term granulatiol1 lissue because thc tisslIe has the appearancc of granules piled upon olle another. BIOlogically. this tbsllc is the collagen matri,. GfHnulation buds arc clearly seen in Color PlaIt's .J £I1U18. Note hO\\ the cavity is filling in those photos to create a Icvel surface wllh the adjacent skin. Acute proliferation starts when the wound bcd tissue begins to shO\\ red or pink granulation buds and o\'erlaps the late inflammatory phase. The collagen matrix is laid dowll and is infiltrated by and supports thc grO\\ ing capillary bed gi\ing it the red color. Reduced depth in a full-thickncss wound is a measure of proliferation activity. The collagen l11<'lIrix docs nOI replace the slructures or functions of the tissucs that occupied the cmity prior to IIljury. fhis is scar tIssue. The prevailing OPIllIOI1 IS that thiS deep red color indicates a hcalthy hcaling wound. A contrary opinion is explained later under Chronic Proliferation Phase. Another featurc that has bet.!n rcportt.!d to appear during the acute proliferation phase ofhcalillg in a Ilumber ofpatients is the dc\'clopmcilt of a ycllow. fibrinous membmnc on the surface of the gr~Jnulation tlsSllt.!. Removal of this membranc has been allemptc(l but it will recur in a fcw days. Wounds that dc\'elop this ycllO\\ 1llt.!ll1bnll1t.! appear to bc less susceptible to IIlfection. Thesc wounds c.:ontlllut.! to hcal in a normal fashIOn. Rccoglll/ing this mcmbrane during examination will pre\ent unnecessary disruption of the wound bcd "
Pai". MIIlIl11al or no pain is e\perienced dUring this phase.
It
IS
an lIlappropriate Indicator if there is neuropathy.
UlIllermillillglTllllllelillJ:. The acute proliferation phase progresses aner the wound has been debrided of necrotic tissue. Dcbriuclllclll of necrotic tissue creates a disruption of the tissue integrity of the skin and the underlying structures. The proliferation phase is concluding when the wound tisslie intcgrity is reestablishcd. Undcrmining is defined as a closed passagcway under thc surface of the skin that is open only at thc skill surfacc. As prc\ iously described wound UIldermining occurs foJlo\'vlllg debridemcnt of the skin and subcutaneous tissue and is erosion of the tissue, forming a ca\'c undcr the \\oUlld cdge (sec Color Plate 39). Both undermining and tunllellllg an: loss of tissue IIltegrity. The loss oftissuc integrity allows separation orthe fascial plan!.!s between thc bundles of muscles. TUI111elll1g is like a subway progressing from the initial undermined excavation and occurs ,,,hen there IS debridement Into the fascial and muscle layef\. Tunncling may be unobsenablc from the surface and yet ha\c a great e\tent. as shown in Color Plllfl!S 35 lIml 36 of the same \\Olllld. Undermining and tunncling close as the tissues reestablish contllluity during thc laying down of the l'ollagen matrix and gmllulation tissue during the proliferation phase. Thc e\tent of undermining is a measure of the lOla I son tissuc in\ol,'ed In the wound. Reduction of the extent of undermining, tunneling is a measurc of the progression of proliferation and reduced O\erall wound size. Note findmgs of undermining and tunneling as part of the tissue assessment. Ir the tunneling extends beyond about 15 cm, this is causc to notify the physician. Chapter -l dcscribes hO\\
Clinical Wisdom: Assessment of Abscess by PalpatIOn
Palpation to assess for an abscess is done by pressing down over the undermined area. If there is a lump accompanied by pain or fluid expressed by the compreSSion, an abscess should be suspected and referral made to the physician.
HOUlld Edge.\. Thc \\ound edgt.!s arc soft to firm and nre nCXlble 10 louch. Edges wlil rolllflho \\ound IS fulllhlekness. but when thc wound tissue fills the cavity even with the cdge of the wound the edges will flattcn and epithelialization and contraction will continuc together (sec Color Plat£'\ 3105 amI 8 10 9). At this POlllt. the wound acqlllrcs a distincthe wound shape or "picture frame." The cc lls thai control the 11l0\cment of the picture frame. the myofibroblaslS, arc locmed bCl1calh Ihe wound edge. The cells arc contractile and \\ill mO\e forward drawing the wound together. During thIS proccss the wound cdgcs arc dra\\ ntogcther like the drawing together of purse strings. shnnk lng the si/c ofthc open area measllmbly. The shape that the \\ound 110\\ assumes predicts the resultIng speed of contraction. I Incar wounds contract rapidly. Square or rectangular wounds contract at a moderate pacc. Circular wounds contract slO\\ Iy.
74
W OUND CARl
Wound contraction is a major activity of the acute proliferation phase of hea li ng. Contract ion reduces the areas needing
to close by epithe lia lization . Contraction in areas slich as the g lutcal s and abdomen wi ll be finc , but examples of locati ons where con tract ure is troublesome include the head neck.
phase when thc g ranulation ti ss ue may s how these characteri stic s of infection, about 10 days postopera tively and at the cnd stage of healing. when thc wound has progresscd sa ti sfacto rily and then bcco mcs indolent. 31 Color Plales 10 alld II show the same wound . In Color Plate 10 the wound
ti ght ly in those areas w ill
was progress ing through the proliferation phase. Seven days
cause a defect or contracture that will impair function and
later the wound has attributes of in fecti 0 11 . th e proliferation ha s ceased, a nd the wound is now in the c hronic proliferation phase. Trauma can al so retard proliferation, Pale pink.
and ha nd. Drawing together
(00
cosmesis. Wounds that wou ld have a poor outcome ifal lowcd to close by contraction would have a prognosis of need for surgica l intervention at the start of the proliferation phasc. n IYolIlIII Draillllge. During the acute pro li feration phase the wou nd drainage is serosanguineous and of moderate to minimal quantity and odor.
Chrollic Prolife ratioll PlllI.\·e Periwolllul Ski" Color lind Edema. Color of the s kin at the wound edge may blanch or begi n to draw together very tightly (see Color Plate 34). Gelatinous edema may be present. sig nify ing an episode of trauma. PeriwOIllld Skill Temperuture allil Pai". Co mpared to the te mperature of the adjacen t skin. periwollnd skin durin g the chronic proliferation phase may be cool or mildly e levated, and there may be so me sig ns of intense pain. This could indi ca te th at the wound ha s bee n traumati zed and is having another episode of acut e inflammation, or there may be presence of infection . Ullilermi"i"g {/lui TUllllelillg. C hronic proliferation deve lops when the ti ss ue integrity is not reestabli s hed , The tunneling can extend a long di stance and present s an opportu-
nity for infection to travel up the fascia l plane. Tissues in the tunn e l may be necrotic. Tunne ling can become a sinus tract, which is defined as a cavi ty or cha nn e l unde rl yi ng a wo und that involves an area larger than the visible surface of the wound. An abscess may form in the tunnel or sinus tract. 2 When undermining/ tunneling pers is ts in a proliferating wound a nd the assess ment findings include a black hole that ha s no reac hab le bottom, th e wound need s urgent medi ca l manageme nt.
' Youlld Tis.'tue. A wound in chronic pro liferation may exhibit attributes of infectio n, poor vascular supply, des iccation , or hypergranulation . Poor vascu lar slipply wi ll appcar as a pale pink , minimall y g ranulating wound , A contra ry op inion of so me c linicians is that certain wounds that deve lop a li vid red surface color may be infected and slow 10 hea l (sec Color Plote 40). Infection in granulaling wounds is di sruptive to healing. The features of infection that may be observed in g ra nula ti ng wounds a re s uperficial bridgi ng, friab le tissue. bleeding on contac t, pain in the wound. and a delay in hea ling, Th ere arc two stages in the proliferation
blanched 10 dull dusky red granu lation tissue indicates poor vascular s upply. Desiccated g ranulat io n ti ss ue is dark , dull ga rn et red. Hcmorrhaging or bleeding of til e granu lat ion tissue vesse ls causes an acute innammation to the a rea and promotcs sca rring. Hemo rrh agi ng on the gra nulmi o n ti ssue looks like a purple brui se on the surface. In Color Plate II note the small hemorrhagi c area at thc center of lhe wound, indica ting rupture of blood vessels. In C hapter 2 the processes tha t result in di s rupt io n of granu lat ion ti ss ue regulation that allow ilyperg ranulation to occur are exp lained. Normally, the process of granu lation decreases as the wound space decrea ses and the wound integrity is recovered. The g ranul ation ti ss ue fi lls th e wou nd space to th e s urface; the epit helialization process then cove rs the wound , Bul whcn the " nowering" of th e granulation ti ss ue ovcrflows the wound bed, the epitheli a l cells cannot climb the hill of granu lation ti ss ll e against gravity and the result is th.1 the epi thelialization process is halted. See Color Plote 2J for hypergranulation . Ifhypergr.nulation persists, the wou nd moves into a chro ni c proliferation phase, The C linica l Wi sdom below de sc ribes some methods that are common ly lIsed to co nt ro l hyperg ranula lion. Th ere have becn so me s uggcsti ons about th e usc of dre ss ings to control hy pergranulation, but these method s are unproven and rcmain anecdota l.
W(Jlllld Eliges. The chronic proliferation phase deve lops when the wound edges roll in and become hard and fibrotic. whi ch inhibits further wound contraction, See Color Plate
33 for an example of rolled fibrotic edges. Wounds of different pathogeneses develop thi s problc m, inc ludin g press ure ulcers and venous ulcers. This finding may trigger a referra l to a surgeon to excise the ro ll ed edge to restart th e hea ling process.
IYolll1t1 Draillilge. C hronic proliferation exuda te may be a ye llow. gelatinous, viscous matcria l on the wound granulati o n base that indicates th e wound has been traumatized. This should not be co nfu sed with wo und dressings s uch as amorphous hydrogcls or treatmcnts s uch as antimi crobia l oin tment s, An infec ted wound in chronic proliferation may have a malodorou s. visco lls, reddis h brown . green, or g ray exudate. Color PllIfe 40 shows an apparc ntly clean WOUll(~ but the wound dressing shows signs of modc rate to largc amo unt s
AsseSSlll elll o(rlte Skill alld IliJlllld
Clinical Wi sdom: Management of Hypergranulation
Since hypergranulation will inhibit the reepithelialization of the wound surface, it must be prevented or controlled. Two methods used to achieve this purpose are as follows: 1. Cauterization by applying silver nitrate sticks to the surface will necrose the superficial granulation tissue, which can then be wiped off. 2. Trim the excess hypergranulation tissue by rubbing with a gauze sponge or snip with scissors.
of sa ngui nco us and purul c nt reddi sh brown exuda te. This wound is in th c chroni c prolife rati o n phase and needs trea tment to recover.
A bl'elJ('e of IJrolijeratioll Phase PeriwolIlJll Skill; Color, EI/eml', I'llill , ali i/ Temperature. Th e presence o f hem os id erin sta ining or a hal o of eryth ema wi ll surround thc wound signifyi ng a wo und that is a lso in the chro ni c inn aIlll11ati on phase. The skin may show sig ns of ecchymosis. Ede ma and pain wi II be minima l o r abse nt . Temperature c hange is minima l inc reasc o r coo ln ess. Wo""d Ti,'i,m e. A wo und in an abse nce of pro liferation phasc is e ither not producing gra nulati o n tiss ue or no t co ntracting (sec Color Plate 3 I). The wo und tiss ue may look dry. dull red. a nd de siccated o r may cO l1lain palc pink gra nulation ti ss ue, There is la ck of change in wound de pth . No t much is writt en describing an abse nce of pro liferat ion. The wound th ..lt is in th e chroni c inn aml1lati o n phase or absence of inn al11l11at ion phase a lso has absence of a proliferati o n phase. The wou nd is no t prog ress ing throug h the pro liferati ve phase, Wounds in thi s si tu ation often ha ve a s urfa ce appearance of necroti c tissue and/or hemorrha ge/ecchymosis. Any s igns of ecc hy mosis would sig nify a res tart of an innammato ry process w ithin th e wound. The c hro ni c innammati on phase and absence of th e pro liferation phase ca n both be used as fun ct io nal diagnoses for th e same wound. The prognosis would bc for the wo und to progress to the acute pro liferatio n phase. T he med ical hi s to ry and systems rev iew sho uld g ui de the c lini c ian to investigate th e impa irme nt s to the proliferation process. WOllnd Edges. Wound edges may be ro ll ed or jagged and th e s hape is irregular. The wound does no t change s hape. sign ify in g lack of wound co nt rac ti o n. Dee p wounds may have absence of continuit y of wo und bed and ed ges. The wo und is not reduc in g in s ize.
75
'''011111/ Draillage. Wo und s have absence of ex udate o r sca nt se ro us ex udate. The wou nd in Color PlllIe 43 is in thc chroni c inn amm3tion phase and ha s a bse nce of a proliferatio n phase. Note the scant amount of sero us ex udate on the wound dressi ng. Treatment interventions s hould be rev iewed to see why the wound lacks moisture. Summary o!Three Prolifera tion Phase Diag u Q.';is alld IJrogllo."'i,f; Tabl e 3- 8 summarizes the findin gs for eac h a~pcct of the prolife ration phase. Thc presence of the fo ll ow ing attributes s ignifies that the wound hea lin g phase diagnos is is acute pml{/elrHioll phase: beefy red g ranulat ion tissue in the wound bed (red uced depth) ; wound con tractio n (reduced surface opcn area. regu lar wound ed ges and shape); se ro us or scrosa ng uin eous ex udate o f mode rat e to minimal amount : and normali zed pe riphe ral sk in te mperature. turgo r, and color. T he prognosis is that reassessment will show reduction in depth and clos ing of thc undcrminccUtunne led s pace wi th meas urable reduc tio n in overall size estimate as th e integrity or th e ti ssue is reestabli shed. Failure to prog ress as ex pected through the pro li fera tio n phase signifies a wound hea lin g phase diagnos is of c:Il1Ymic prolijeration or ahsence ofprolijeration. The eva lu atio n of a halt to proli feration s ho uld be give n carcful co nsiderat io n, For examp le, infection during proliferation retards hea ling and causes a chro nic pro li fe rat io n phase, (fs uperfi c ia l bridging. friabl e ti ss ue. bleeding o n co nt act. pa in in th e wo und, and a de lay in hea lin g are obse rved, the eva luati o n wo uld be posi tive fo r infection. Wound s wi th ea rly s igns of in fec tion arc treated wi th a reg ime n of o ral antibiotics for 2 to 4 weeks and th ose th at ha ve late healing s ig ns of in fecti 0 11 arc treated with topica l ant ibio ti cs. 11 T he prognosis is that the wo und will res ume progression th rough the phases of hea ling fo llowin g in tervent io n with antibiotics. Fa ilure to init ia te a n innamJ11a1ory phase will ca lise absence of a pro l i ferati o n phase. Iatroge nic wou nd ca re may also cnuse th e wo und to have abse nce of a prol iferation phase. The prognosis is th at th e innammation phase will be initiatcd (if body systems ca n support it) and w ill progress to th e pro li fe rati o n phase. Another possibility or prognos is is th at th e proiireration phase will be ini tiated fo ll owing change in treatment. O nce again. the phases o f heal in g overlap; the wo und hea lin g phase diagnos is if the wo und is transit iollin g from onc phase to the nex t is de fined by the primm:\' phase a ppearance. A wound healing phase diagnosis of aClIte prolij~ emtioll phase mcan s that 1110st (50% o r grea ter) o f th e wou nd surface appearance attributes, g ranulati on ti ss uc and contraction, arc observed , If less than 50% of the pro li fera ti o n attributes are ident ified, the wound is primarily in a n infl a mmatory phase and has no t yet reac hed the pro li fe rative ph ase
Table 3-8 Wound Healing Phase Diagnosis: Tissue Characteristics for Proliferation Phase Periwound Skin and Wound Tissue Characteristics Periwound skin color
Acute Proliferation
wound
• Ecchymosis (purple bruising)
• Hemosiderin staining if chronic wound • Halo of erythema if in chronic inflammatory phase • Ecchymosis (purple bruising)
• Absent
• Gelatinous edema may be
• Minimal edema present
• Continuity with adjacent skin • Hemosiderin staining if
recovering chronic
Edema and induration
Absence of Proliferation
Chronic Proliferation • Continuity with adjacent
skin • Paler than adjacent skin • Hemosiderin staining
present signifying trauma
Tissue temperature
• Temperature may be
• Minimal change or coolness
• Minimal change or coolness
• Painful, may be indicator of local inflammation; if
• Intense if infection present
minimally elevated if wound is well perfused Pain
• Pain free or minimal • Inappropriate indicator in presence of
• Minimal or absent
intense, consider infection
neuropathy Wound tissue
• Shiny bright red to pink granulation • Sustained reduction in
wound depth • Sustained wound contraction • Reduced size
• Livid red
• Hypergranulation • Desiccation (dark red color) • Poor vascularization (pale
pink) • Ecchymosis (purple bruising) on granulation
• Covering of yellow fibrinous membrane on granulation tissue
• Necrotic tissue-stuck in chronic inflarpmation phase
• Ecchymosis (purple bruising) on granulation inflammati on restarting • Dull red-desiccated granulation • Pale pink granulation • Lacking change in wound
depth • Unsustained contractionno reduction in size of surface area
Undermining/tunneling
Wound edges
• May be present in deep wounds • Closes as proliferation progresses
• Soft to firm • Flexible to touch
• Rolled if full thickness • Change in wound shape from irregular to regular • Reduction in size of surface area • Drawing together • Adherence of wound
• May be present in deep
• May be present in deep
wounds • Fails to close or may extend • Has potential for infection and abscess
wounds • Fails to close or may extend • Has potential for infection and abscess
• Tight drawing together to
• Unchanged size
reduce size----contracture • Absence of continuity of
• Rolled or jagged irregular edges
wound bed and edges • Rolled
• Fibrotic • No change of shape-not
• Fibrotic
• Ecchymosis (purple bruising) on wound edge
drawing together • Absence of continuity of
wound bed and edges
edges by end of phase continues
Assessmellf o/lhe Skill alld lVolilld
77
Table 3-8 continued Periwound Skin and Wound Tissue Characteristics
Wound drainage
Acute Proliferation • Serosanguineous or
serous in moderate to minimal amount for wound size
Chronic Proliferation
• Yellow gelatinous following trauma • Infection: viscous malodorous, red/ brown, green, purulent
Absence of Proliferation
• Serous drainage scant to minimal amounts • Desiccated and dry
• Large amount
Color Plates
3 to 5, 8 to 10, 18
11 ,34 to 36, 39, 40
for diagnostic purposes. The diagnosis would be wri tt en 111//ammarioll phll,\"elprolijertlfiul/ phase. A wound with infection of the granulatioil lissuc has impaired healing and wou ld carry a wound healing phase diagnosi s of chrollic plVlijertllioll. A clean wound that is not producing granu lation ti sslie or cOlllraclillg is in a wound healing phase of absence of pro life ratio II .
30,31 , 43
epidermis may occur from leakage of wound exudate or use of products thalll10i sten the s kin and sat urate the ce ll s. Maceration is especially damaging to new epithelium. Macerated skin look s pale and wrinkled and fee ls soft and th in to t.Quch, making it ve ry s usceptible to traum a such as from press ure .
Clinical Wisdom: Describing a Wound in the Proliferation Phase
Clinical Wisdom: Protection of Skin from Maceration
Example of a narrative note describing a wound in the acute proliferation phase:
Skin barriers are products that can be used over the periwound skin and new scar tissue to protect them from maceration.
Evaluation: A wound on the right hip has beefy red granulation tissue. The wound edges are firm and soft. Wound is contracting in to a rectangular shape. Wound healing phase diagnosis: The wound healing phase diagnosis is proliferation phase.
Epilhelializiltion Phase Acme i:.jJilhe/ill/i:lIIioll Phase
Perin'olllul Skill. Since acute epitheliali .!3tion begins at the time of wounding concurrently with the inflammation phase and overlaps the other phases. expect the signs of acute inflammation to also be observed in th e peri wound skin. As the acute innnmmation process subsi des. the peri wound skin shou ld return to the usual color for cthn icity, tempera ture of adjacent tissues, and should be firm but not hard, edematous. or fibrotic . Mac era tion of the periwound skin and new
Wotlllli EI/ges (IIul 'Yollml Bell Tissue. Epithelia l ce ll s start migrating toward th e center from th e wound edges to cover the defect with new skin within hours of wou nd ing . Ep ith e li alization occurs from several directions. The edges arc a source of keratinocyte s that cover the wound surface wi th epithelium. The wound edges mus t be adhered to the wound base for epithelia l ce llm igratioll to cover the wound. The leading edge of the migrating celis is one cell thick. Gradually the epithelium sp reads across the wound bed, as shown in Color Plates 5 and 6 of the same wound. The migrating tiss ue is connected to the adjacent s kin and will pull it along to cover the opening. '-' The new ski n will be brigh t pink regardless of normal pigmentation and may never regain the melanin factors that color sk in (see Color Plates Ii and 22). New s kin is formed as a very thin s heet. and it la kes several weeks for the new skin to thicken . If the wound is less than fu ll thickness. is lands of pink epi th elium may appear in the wound bed from migrating ce ll s donated by the
78
WOLNIJ CARl
dermal appendages. the hair follicles. and the sweat glands. Cells from these islands and edges spread out and cover the open arca. C%r PllIIe 55 shows a wound with an island of epithelium. C%r Platl! 56 of the same wound shows the migration orthe epithe lium across the wound frol11lhc edges
and from the island. Notice in Color Plate 56 how the edges ort lle new epitheliul11 arc jagged. Fu ll-thickness wounds lose these island contributors and they never regenerate.'2 Fu llth ickness wounds begin to cpilheliaiiLc when the edges arc attached and even wilh the wound so that there arc no sides
or wa ll s. <.Ind the epithe lial cells can migrate from the edge across the wound surface. Edges arc soft 10 firm and arc ncxiblc to touch, as shown in Color Plate 18. Th is wound well t on to hea l by epithelialization from the wound edges. The wound environment is critical to a successful epithe lialiLation phase. The wound must be kept warm, moist, and free of trauma at all limes. Wounds may bypass thi s pha se of repair ifit is preferable
to place a skin graft or muscle nap to close the wound. Large wounds and wounds in areas where contraction will be harmful or where it wi ll simp ly take too long to cover the wound may benefit from surgical repair. The wound shown in Color
lides. sweat , and/or sebaceo us glands. The wound shown in Color Plate 57is in the chronic epithelialization and chronic innammation phase. The appea rance of adjacent and periwound skin changed as chronicity was altered and acu te cpithe lia liLation and proliferation phases werc initialcd (Colo/" PllIle 59).
' VoUlld £l/ges. Epithelia lization of deep wounds occurs on ly at the edges and may involve thickcning and rolling under of the edges. If the cells cannot continue to migrate across the wound they will build lip an epithclia l ridge along the edge of the wound as seen in Color Plate 40. Pressure ulcers typica lly deve lop a round shape when this occurs. Wounds in chronic epithelialization have ce lls piled on each until the rolled thickened edges become fibrot ic. The wound edges need to be mod i fied and the wound bed filled before
wound epithelialization wil l be reinitiated. Hyperkeratosis is another abnormality of the cpithelinli za tion phase. Hyperkeratosis is overgrowth of the horny layer of thc skin. Color Plate 24 shows a wound with hyperkeratosis and an irregu lar shape of a heel ulcer of a I aO-year-old woman.
Plare 56 was closed at that time by a split-thickness skin
graft to speed the repair process.
Clinical Wisdom: Maintaining a Moist Wound Bed for Epithelialization Amorphous hydrogel dressings are useful wound moisturizers and, along with moisture-permeable fi lms and sheet hydrogels, provide the warm, moist homeostatic environment critical for epithelialization.
IYOIIIll/ Draillllge. A scant or small amount of serous or serosanguineous wound exudate is expected. The wound must be kept moi st during this phase of healing because desicca-
SClIr Tissu e. The majority of wound closure in humans is by gra nulation tissue formation followed by epithelia lization. l~ New epi thelium of scar tisslle is bright pink. rega rdless of the pigmentation of nOT ma l skin . In dark ly pigmcnted skin. the scar tisslle may neve r be repigmcnted. The bright pink color may fade mer time to a lighter shade of pink as the vascular system is fully reestablished. H1wm/ Tis!w e. The wound bed tissue that is hypcrgranulating may develop a chronic epithelialization phase because the epithelial cells cannot migrate over the hump of granulation tissue agai nst gravity (see Colo,. Plate 13). The granulation ti ssue must be trimmed back to be level with the periwound skin for epithelia lization to resume.
tion wi ll destroy th e epithelial ce lls.
Chronic Epilhelillli: lllion PlllIse PeriH'olilld Skill. The characteristics of the skin may be the same as chronic or absence of inflammation phase. The peri wound ski n may show signs of ischemia such as a pale or ashen color in the elevated position, which deepens to dark purple with dependency (rubor). Pain may be a constant, throbbin g pain or intermittent c laudication during walking. if it is associated with arterial occlusive di sease. The "ppearance of the adjacent sk in is usuall y dry, shiny. taut. and/or hairless. These arc indicators of loss of hair 1'01-
IVolllld Drllitlllge. Wound drainage may be noncxiMcllt and the wound dry. I fno or scanty exudate is assessed, add itiona I moisture may be needed to facilitate the migration of the epithelial cells. Epidermal cells migratc best in a warm moist environment. Wound dryness can be due 10 improper dressi ng sclection, loss of dressing. dehydration of the wound or patient. or other iatrogenic conditions. On the other hand, there may be heavy exudate from a partia l-thickness ulcer that should be epithelializing, but the exudate washes out of
the epidermal cells fa ste r than they can migrate and attach to the wound surface. Excessive moisture associated with wound products may also cause this to occur. Management of the wound moisture would be required.
Assessmellf a/fhe Skill (llId "bund
Absell ce of Epitheliali:ll1ioll Pha ....e Absence of the epithelialization phase may bc due to intrinsic. extrinsic. or ia trogcnic causes that may be iden tified during the assessmcnt. Color. The color of the adjacent and periwollnd skin of-
fers clues to the etiology of absence of the epithe lia lization phase. Absence of the epithelializalion phase may be related to an intrinsic condition such as arterial obstructive disease (AOD). AOD limits blood supply and oxygen to the tissues and impairs the func tion of the skin to repair itse lf. Examination of adjacent skin will reveal absence of ha ir, dependent rubor. and pallor on elcvcHion. The wound will have a punched-out appearance and a very limited ring of epidermal tissue around the wound that will not migrate across the wound as shown in Color Plate 48. Ifno prior vascular testing is reported, thcse findings would indicate the need for further assessmcnt of the vascular system. Chapter 6 should be consulted for testing suggestions.
Textu re. Peri wound skin that is dry and naky. has an irregular texture. or is macerated provides limited epidermal cel ls to resurface the wound. The wound will lack epithe lialization activity. Skill Temperll1l1 re. kin temperature is a renection of blood sllpply. Skin temperature cooler than 92° F to 96° F on the torso and lower in the extrcmities (75°F to 80° F) is an indicator that blood sliPply to the sk in may be limited: warmer ski n may be due to infection. Edema. Chronic edema caused by tissue congestion such as lymphedema. congestive heart failure. or venous insufficiency stretches the skin and fills interstitial spaces v·lith excess fluid. including large protein molecules. When the capacity of the tissue to hold nuid is exceeded. the nuid leaks through the skin. Because of the di sease process. changes occur in the vascularity of the tissues. leading to loss ofdermal appendages and dry stasis eczema. The changes are known as lipoderm3tosclerosis. \.I Skin changes associated with thi s disc::lse proccss are shown in Color Plates 53 (Ind 54. Patients with lipodenmlloscierosis may show absence of epithelialitation phase. More information on lipodcrmatosclcrosis is presented in Chapter 14 . Edge.5. Anothe r example of an intrinsic factor that causes absence of epithelialization is decreased epidermal proliferation due to de laycd cellular migration attributed to aging. There is slow or absence of new skin growth from edges or islands. Absence of epithelialization attributes W Ollllli
include dry, naky. hyperkeratotic skin at the wound edges. The dryncss may be associated with a dry wound environment.
79
' Vound Ti.\·.'Hle. Hypogranulation results from an absence of the proliferation phase and failure to fill the wound bed and provide a surface for the epidermal cells to migrate across to cover the wound. S Ullllllu ry ofTirree £ pitireliali:lIfioll Pir ase /)iagll osis 1111(1 Progn osis The epilheliali=alioll phase of healin g begins with epithelial migration during the inflammation phase of healing. Partial-thickness wound epithelialization may progress from is lands in the center of the wound as well alol frolll the wound edges. Full-thickness and deeper wOllnd healing by epithelialization will be arrested if a large amount of wound debris interferes or if the wound edges fall ofT into a decp wound bed with stee p wa ll s or are nonadhered to the wound bed. Throughout the wound healing process the phases overlap. and it is not at all unusual for the epithelialiLation, innammation, and proliferation phases to overlap and attributes of each to be identified. Table 3 9 summarizes the findings during the epithelialization phase. A wound phase diagnosis of epitheliali=ariol1 phase is . based on findings that the wound is resurfacing. Pa rtial-th ickness wounds that arc resurfacing from the middle or edges are in the epitheliali=arioll phase. Wounds that are greater than 50% attached HI the edges and do not have steep walls tha t are epithelializing are also diagnosed as being in the epitheliali=arioll phase. Wounds in the acute epithelialiL3tion phase have an excellent prognosis for hea ling. Wounds in the chronic epithelialization pha~e need an interven tion that wil l restart the healing process. The prognosis then wou ld be wound will heal with intervention . For example. the surgeon may need to excise the fibrotic wound edges. An nbsent or chronic proliferation phase may need initiation before cells can migrate over the surface. Wounds that have absence of the epithelialization phase of healing have high ri sk for nonhealing unless intrinsic or iatrogenic conditions can be altered for example, by rcperfu siol1 or app lication of moisture-retentive dressings.
Clinical Wisdom: Describing a Wound in the Epithelialization Phase Example of narrative note describing a wound in the epithelialization phase: Evaluation: A wound on the left medial ankle is adhered at 75% of the edges and epithelialization is progressing over 50% of the open area. Wound healing phase diagnosis: The wound is in the the epithelialization phase.
80
WO UN D CARL
Table 3-9 Wound Healing Phase Diagnosis: Tissue Characteristics for Epithelialization Phase Periwound Skin and
Wound Tissue Characteristics Peri wound skin
• Early phase has same
characteristics as acute inflammation phase • Returns to normal color
for ethnicity as inflammatian subsides • Hemosiderin stain if chronic wound
Wound tissue
Chronic Epithelialization
Acute Epithelialization
• Even with wound edges • Pink/red granulation
• Reduction in wound surface area
• May be same as chronic or absence of inflammation
phase • May be ischemic (pale) or ashen • May be purplish with dependency • Dry, flaky (hyperkeratoticmay be due to desiccation or aging skin) • Maceration: pale, wrinkled, soft, thin • Hemosiderin stain
Absence of Epithelialization • Scar tissue • Same as chronic or absence of inflammation phase • Dry with hyperkeratosis or lipodermatosclerosis
• Not connected with wound edge • Hypergranulation
• Absence of resurfacing from edges or dermal appendages • Hypogranulation • Presence of scab or necrotic tissue
Undermining/ tunneling
• Steep walls limit migration
• Steep walls limit migration
• Steep walls limit migration
Wound edges
• New skin moves out from wound edge and dermal appendages in irregular pattern • Bright pink color regardless of usual skin pigmentation • Texture is soft to firm and flexible to touch, thin
• • • •
• Fibrotic wound edge • Rounding off of wound shape and edges • Macerated • Dry flaky skin
Wound drainage
• Minimal to scant serous or serosanguineous
• Absent, dry; if hypergranulation, minimall moderate
• Absent, dry
Scar tissue
• Thin layers of scar tissue • Thickens over time • Deep pink color initially; changes to bright pink color regardless of usual skin pigmentation
• Hypertrophic scarring • Keloid scarring • Hyperkeratotic scarring
• Weak, friable epithelial tissue • Breaks or washes out
Color Plates
5,22, 55, 56,59
24, 48
33, 37, 48, 54 58
Epithelial ridge RoHed under or thickened Dry flaky skin Rounding off of wound shape
XI
·h,\es.\11/ellt atlhe SkilllllU/ UfJllJU/
REFERRAL CRITER IA
Utili/alion management requITes that the patient's problems be identified and triagcd carly (0 the medical care provider most appropriate to the patlent's wound severity or wound healing phase diagnosis. Referral should be made \\ hen there .:lre rindings that require the attention of another di scipline morc skilled or morc knowledgeable in management orthe identified problem. Referral will depend on where the patient is to be seen, the available resources, and other very significant factors. For instance. skin lesions that ha\c not been described in this c1wptcr include scales associated \\ Ilh psoriasis. papules such as warts and tumors. vesicles such as chickenpox. and shingles. which nfe examples of sk in comillions that may be seen on the adjacent skin and should be referred to a dermatologist. Wounds that have a history of nonhcaling for long pcriods of time may be cancerous. and they should be referred to a dermatologist for biopsy evaluation. Deep wounds that can be probed to the bone should be considered positi\'e for osteomyelitis and need c\aluation by the orthopaedic surgeon. Wounds that are in the chronic inflammation phase need enhanced perfusion to achic\ c comcrsion to an acute inflammation phase. Vascular assessment would be a primary consideration. and the vascular techniCian may be the most qualified to pro\'ide the sen ice. Reperfusion reqUIres the expet1ise of the \ascular surgeon. A wound \\ ith dcep tunneling should be referred to the plastic surgeon. The physical therapist has skills in exercise. usc of physical agents. and elcctrotherapeutic modalities. all of which enhance perfusion to tissues. Exhibit 3---4 is a list of possible referral so urces.
E\hibit 3-4 Rererral Sources Ph~
"'ursin~
\lIied lIealth
Dermatologi<;t
Dermatology Nurse
PhYSical "iherapisl
Orlhoraedic Surgeon
1·, lllerostomal Nurse
Podlairisl
Plastic Surgeon
(ienalric Nurse Practllloner
\ ·ascu lar li:chnu: ian
V'lscular Surgeon
Vascular Nul'c
the collector. For cxample. cxalllinat Ion and rccording of the different wound characteristics Illay be collected by a properly trained physical therapi st assistant or a licensed practical nurse. and the evaluation orthe findings, the wound healing diagnosis. and the prognosis may be completed by the physical therapist. the registered nurse, or the enterostomal nurse. Collection tools to grade, record, and monitor findings are described in Chapter 5. Documentation requircments for wound asseSSlllent should be part of the facility poliCies and procedures. Documentation ~hould be accurate. c1emly reneci the patient 's condition. and bl! consistent with documentation by others in the same department or facility. I r it is not documented It did not happen .
\an RiJ s\\ iJk L, Frc"!ucnc)' of rca ... :-.c ..... mcnl of rrc:-.:-.url! ulr.:er:-.. NPUAP Proeccdlng:-. leb' U'I/oul Ctln· Juiy /f\ugu'l 199~; Kf4 Surp):19 24
CO\CLUSIO",
Wound c1assd'ication systems are used to identify the \\Qund seventy by the depth of tissue impairment leading to a functional diagnosis of impaired ski" integrity (i f the dermis is not penetrated) or impaired tisslle integrity (if the wound extends through the dermis and deeper). Wound healing assessment by biologic wound healing phase includes three aspects for each biologic phase : acute. chronic. or absent. Fach pllllSC describes the Httributes of the acute, chronic. or absent qate of the phase by sy mptoms found in the pcrivv'ound skin and Ihe \I,'o und tissues. Thc nurse or physical therapist needs to know where in the trajectory of healing the wound IS at baseline assessment 10 plan treatment. make a diagnOSIs and prognosIs of heal mg. select interventions. predict outcomes .•l11d triage patients. The assessment is lIsunlly completed by the same person, but this is not always the casco Thc evaluator may be a person more highly skilled and trained in interpreti\'e skills than
sicians
2
\an RiJs\\ Ijk l.. Po lan,k ), M PredIctor, uilllnc 10 healing deep prc",urc utcc~ {)'((111/1' H(wlIll \I(II/rl.l.:t' 1'J94;4()(X):4t1 42
J
Bc rg:-.lrom N. ct .. 1. 1il'(I(ml'II( of Pn.·H'l/rt· lInn ("lllllt.:all'mcllce (jUldellne '0. 15. AII(PR Publicallun 1\0. 1}5-0M2. Rock\llh:. MD: Agency ror lIealth ("arc Ilillie), and Re~e.w.:h. 1 S IkrartIllenl of Ilcallh and Ilulllan Scn lecs~ ()ecel1l~r 1994
4
t-.allonal Prc ...... urc lltcer Ad ... l ...ory Panel (' PliAP) I'n: ...... un: uker ... prevalence. co ... l .lnd n ... k asscssl1lcnl con,cn ... us de\cluplllCnl cunfercnce statcmcnt. /)n'lIhiflll 19!N;2(:!):24 21( .
5
\\lcm fl.lrdlilgno'>ls and trcat· mcm: FoOl .-Inklt,. 1IJI(I;J:64 122.
6.
Shea JD. Prc-;'>Ure ..orc: c!a ..... lflcallon .1I1d I1mnagcl1ll."nt 1975 ; 112 :1019 IOU
7,
l3crg:-.trom N. Cl al l'n'Hl/n· l kt'T\ til ·'111111\ J>I"I"IIi('/WIl flild !In·· Rock\illc. MD .i\g..:nc) rur Ikallh ("MC I'oli!.:)' and Rc· <'carch. U.S, D.:partOlclllllf 11.:.lllh and Iluman Scnlcc,; \101)' 1992.
(·"11
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I(
Il cndcr... oll cr. el al Draft dt.·fllliIIOIl of .. tilge 1 prc",ure ulcer.. II1duslOn of pcr-;on .. \\ I1h dilrkly plgmcllh!d ,kill ItII' U(lUml (·all· 1997; 10(5):16 )I)
82 9.
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II 12 11. 14 15.
16
17,
18
19.
20
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WOlll\1) CARt
Kr.hlll.:r D. \\!!Ir D. Reconullcndallon<; ror u"lIlg rc\crsc "ta£lIlg to complete the M D.S.·2 0.\101111' IIi",,,,! .\I(IIIt1IW 1997;43(3): 14 17 I'errell BA. O,>tcrwcil D. Chri<;t~l1<;on P A r.:mdoml/cd chnicaltrial 01 low·.ur·lo\,> b!!ds for treatment or pressure ulcers. J.., \1.1 199):269:494497 . ('uncll J./. The IlC\\ RYB color code !.IV 19M!UUI( 10): 1342 1146 ('arpelUlo LJ. \funillg DillXllo.\I\.I"plil"tlliotl to Clil/inti Pri/C"Iin' 6th cd. Pllliadclphia: JB LlpplIlcon Co: 1995:7()1 713 Integumentary Pallcl. GUIde to phY"lCal thcrurl<,t pmctlce. II, 1'11\',\ TlI('1" 1997;77' 11f13 1(ISO, Abeln S Repurtlng risk chcck·ur. PT\laX"=uw OCHlhcr tt)97: ~( IO)lM (ireenmill1 PI Pnm:lplc" of structured dmgno<;I'>, In Prlll{"lpl('\ 01 \It''I/I (I/ \1e(JiC/l/t· 2nd ed Baltimore : Williams & WilkinS; 1996:11 20 Milckclbust J. Slcgrecn M Glossary. prcs\urc ulccN. In : (illitit·· '/Iln lor Pn'I'{"I/Iiol/ (//U/ \III'.\/IIx\lwWXf!mf!1I1, 2nd cd Springholl'lc. PA . Spnnghotl'>c; 1996:X IJ M'lcl..elbtl~t J. Slegrccn M Glo,,-sary. pre"<,.tlre ulcer .... In : (illitlt,· 11111,'.\ lor 1'1'l'I'l'",IOI/ (mJ IVllnlflJ.: UtllltlXl'mt·"" Wc"-t Dundee. IL S.N I'ubhcalions; 19QI 14 15. Throne N The problem of the bl:lck skill \"unifiX 7/11/('\ Augu ... t IIJ(J9;9W 100 I Wci ...... LL. ('onnCcll\c II'>"IIC In wOllnd hcallllg, In: McCulloch J. Klolh L, I'e~dar J. cd... , Ifrllllld /It'a/i llX ,II/{,,.,ltlllH'.\ 1I/\I(lII(lge· mel/I. 2nd cd Philadelphia: 1./\ D,n i~; 11}95:26 2X II;\rkle,,~ l B. Dellni~ K Role of the podil, In: LC\ln MI: . O'Neal tW. I)(mker JII. cds 11/1' Diaht'lic Foot ;th cd. St. Louis. MO Mo"hy Year Book; 1993:516517 Ruschh
23.
Bennell MA Report of the la .. k furce on the IInplicallons for darkly pigmented inlact ... 1..111 In Ihe predlcimn and pre\ ~ntl(," of pre\'1l1rc ulcers "III' Ifillmd Cal'l' 1995;M(f1):H 1~.
24
Roach L.B. A... sessment color changcs III dar1.. ... 1..111 January 1977:4X 51
25.
Cahillagh PR o Ulbricht JS Biomcehalllc~ uf the fOOl III dla!:>cte\ Illellllu .... In : Le\'lll Mr.. O'Neal LW. Bo\\k..:r JII . cd\ Til(' Dlt/hel/{ fiml ;th cd, SI I.\lUl ". \10: I\1m,by 'IC;lr BI)(II.. . 1993 :225
26.
MI Jlillhogclle~l\ amlmanagemenl of d ... hctle fool lesion" In L~\lI1MI.O·Neall\\.BO\\l..erJII.ed ... ]1,,'Oillhl'fi('/-imt 5th ed, SI L.Otl\\. "10: Mosby Ye;lr Buol..; 1991:<11
27
1'I ... hmanT fiml flllt! \'ail CIII''' Pr~sentcd I!\ llIlu.11 Wound Management Work<.hop. l)~erfle1d i1e;u:h. Boca Ralon. I L 01.:10· ber 19')5.
21(
('ooper IJ Ihc phpiology of \\oUIHI he.ll,ng' an O\~nle\\, In ('lmll/it'IUmml (·an'. Wayne. PA II..:a1th i\.lanagernclll PubllC;ltHlIlS. 1(1)(l1 II
29
Fcedar J ('llllle,,1 management of dlrOillC \\(lund". In: 1\1c("ulloch J. I\.100h L. I cedar J. ed~. II(}(Iml Jk(lhl/~ IItt'rmll/l'c, /1/ \ftllltl.~t'· IIIt'/II, 2nd cd l'hl1 .. delpllla. I.A Da\Ls; 199; :1 40
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Sussman (" ('11\(, / '1"(,1('11/(111011 p"fI,'1I1 1\1111 tI Pn'II/ln' {ka. APTA SClcntlflc Meet1llg; MlIlneapnlj<,.. MN. JUIlC I'N6
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Ilartling KG Wound care: pUllmg Ih~ory Into climcal pral"IlCe, In Krasner D. cd, ('hnmi(' IIillm" (""",' I ("1111/1'1// .')11111'1"1' 8001.. lor /lm/lh ('an' I'mk\\iO/w/, I ~t cd Wayne. P'\ IIcilllh i\.I,magelllenl Publicallon,>. 1990:24
32
KtlIghlon D. /'Icgd VD. DOlieCII!! :\IM Wound r!!palr' Ihe grm\lh faclor r~\'oIUII(lI1. In "r.I~ller D. cd Chromc Uil/lllt! ('lin': I Cli"l· ntf SO/ll'("(' Bllol../ol" /le,t/,II CarL' Pm/n\lIl11l1/\ \\;Iync. (1.-\ lIe .. llh ~hnJgcl11cnl Puhhc ••IIlIll'>. 19l)():.:141 44~
3J.
liard) i\.1.\ The blllingy of ... car formation 19N9;69' 1014 ION
34
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nil
G, Ulcers nfthc
UOllllt/\/tIllIlf,:"lI/t'lII
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1')\\er~\:trell1ltlc .... In. G,)gla JlP. cd ('"",. I hllruf.lrc. NJ Slilel... 11}t)5 : I UO 10 I
CH A PTE R
4
Wound Measurements Carrie Sussman
ments can be used as the best legal defense. They also provide strokes for the clinician, who can review the measurements and feel a sense of accompli shment. They may also be the alarm that all is not well. Because the information gathered is important to the interdisciplinary team, the language used requires llni form and consistent terminology to encourage good communication between all.
BASELINE ASSESSMENT
This chapler describes quantitative measurements to mea-
sure size and change in size of wounds and extent. Assessment means to test and measure, to perform an examination. It is imporlam to distinguish between examination and eva lu-
ation. The examination provides the data that are evaluated. The data may be collected by the physical therapist assistant or the licensed practica l nurse. The evaluation of the significance of change in size measurements requires skilled judgment orthe registcred nurse or licensed physical therapist. This chapter provides information and step-by-step procedures for performing many measurements of wounds and the surrounding tisslies. It also provides a guide to the most commonly lIsed measurements. benefits, and disadvantages. User-friendly helpful hints and clinical wisdoms are sprinkled throughout. Measurement done at the start of care establ ishes a baseline wound size. Measurements are performed at regular intervals. The rationale for measurement is to quantify and measure the progression of wound healing.1 In the home care or long-term care settings measurement is usually recommended at least week ly. The professional case manager, nurse. or physical therapist may choose to select measurements that can be made easily. afler training, by an unskilled individual in the home and reported to the skilled professional at a specified interval such as weekly. Linear measurement of the size of an open surface area is an examp le of a type of measure that might be delegated. Significance \\lould bc interpreted by the professional case manager. Tests and measurements of wound size and extent arc important to providers, payers. and regu lators, as well as the patient and the family. Well-documented wound measure-
ACCEPTED MEASU REMENTS
Table 4- 1 is an overview of the three different common ly used methods to monitor healing. ~ The table highlights purpose, requirements, and information derived from each method. Many measurcment methods and suggestions are included in this chapter. Not all will be useful in all settings. Different ski ll and interest will determine the methods and measurements used. A table of common usage patterns for wound lest and measurements (Table 4 2) is a guide to current practice patterns. Measuring with planimetry and sophisticated computer-assistcd or technologic equipment ha been omitted because these devices arc usually research tools rather than c linical practice approaches. MEASUREME T ASSESSMENT FORMS
Examination must be consistent. complete, and accurate. One way to manage uniformity, consistency, and completeness is with the use of forms. Forms guide the examination in a logical sequence and organize the information gat hering. Forms may be papcr-and-pencil instrumcnts or templates on the computer screen. They arc real tin'Jcs(1vcrs because one simply fi ll s in the appropriate information on the preprinted form. Forms become a part of the documentation 83
Table 4-1 Monitoring Recovery of Chronic Wounds: Photo, Tracing, Measurements Purpose
Photo
Tracing
Measurements
Objective
Records change in recovery phase or wound stage
Records change within a recovery phase
Linear: estimates size Perimeter: estimates boundary Oigitization: approximates surface area
Treatment planning
Validates overall treatment plan
Demonstrates short-term response to treatment plan
Demonstrates rate of recovery
Frequency
Monthly or change in phase/ condition
Weekly
Weekly
Time reference
Retrospective
Interim
Ongoing/ interim
Requirements
Photo
Tracing
Condi tions
Correct light, body position, and device to indicate relative size
Use of standard anatomic landmarks and method to transfer tracing to medical record
Use of standard anatomic landmarks
Equipment
Camera and film
Tracing kit
Measurement tool and recording notebook
Information
Photo
Tracing
Measurements
Measurements
Type
Displays full color picture
Gives black and white three-dimensional picture on two-dimensional form
Provides numeric information
Comparison
Provides color comparison
Represents topographic effects
Summarizes quantitative changes for use in a graph
Use
Clinical medical review, program management, referral source, reports, survey team , legal
Clinical medical review, program management, referral source, reports , survey team, legal
Clinical medical review, program management, referral source, reports , survey team, legal
record . There are numerous forms in usc for documenting wound measurements. Exhibit 4-1 is a sample form for performing the wound measurement examination . The form fits into a 4 x 6-in pocket notebook. A new form is used each week. and the form s arc kept together in the notebook during the course of care for easy reference to prior week measurements. A sample completed form is gi ven in Exhibit 4 2. I-laving the measurements togeth er in one place facilitates monitoring of the si7c changes on a weekly or biweekly basi s. ""hen the case is completed the measuremcnt sheets
are tiled onto pages of note papcr with tape and put into the permanen t record . This notebook functions like the nurses' treatment or drug record books. When not in lise it can be kept in a specific location at the nurscs ' station or in the physical therapy dcpartmcnt for rcfcrence. Thc form uscs the clock method described later for monitoring wound depth and undcrmining. Other mcasuremcnts can also be taken, using that method or another. Methods of mcasurcnlcnt are described later in thi s chaper. Thc sample wound form includes thc following items:
HV lIlid A1easliremellls
85
Table 4-2 Common Usage Patterns for Recording Wound Measurements Always
Often
Sometimes
Rarely
LxWarea
Clock L x W area
Depth-greatest
Polaroid grid photo
Tracing shape
Undermining-longest and "mapping"
Tracing on grid
Stereophotography
Instant photo with flash Point and shoot with flash
Planimetry Digital photography with computer technology
New
Depth four points of clock
Undermining four points of clock Undermined estimate
Area of erythema or discoloration in darkly pigmented skin Tracing "wound map"
Tracing "wound map" with graph report
• Wound anatomic location is noted which on th e form is called the wound ID. • Size is given. including length by width open area. length by width area or erythema (color change). depth. undermining/tunneling. and overall wound size estimate
(explained below). • Period of the wou nd assessment is given: initial. interim observation week number (OB), and discharge
(DC). • The form al so captures information abollt the wound
healing phase. Initials arc inserted next to U'o1l11d phase
to identify the current wound phase. The initials stand for the phase as follows: I for inflammation phase. P ror proliferation, and E for epithelialization as described in Chapter 3. • Di scharge outcome status also should be checked as healed or not healed . The sample form works well when used in conjunction with the Sussman wound healing tool (SWHT)' deseribed in hapter 5. Data can be entered into a computer database and program outcomes monitored.
86
WO UND CARt
E xhibit 4- 1 Wound Measurement Form
Wound Measurements Imtial Di scharge OUWK#: DC Status:
Patient Name: _______________________________
Date: _ _ _ _ __
Wound 10:_ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ Mod Rec #' _ _ _ _ _ _ _ _ _ _ _ __ Wound Phase: _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ __ (all measurements in em) Linear Size (CI1l~): Erythema Size (Clll~): Undermined:
12:00 6:00 12:00 6:00 J 2:00 (A I)_ _
(A) _ _ (A) _ _
6:00 (A2)_ _ 3:00
Depth: 12:00 Overall Undermined Estimate: A+AI +A2
(a) _ __
B + BI + B2
(b) _ _--:
(a)x(b) ~
x x
3:00 9:00 3:00 9:00 3:00 (81) _ _ 6:00
(B) _ _
(8) _ _
9:00(82)_ _ 9:00
_ _ _ _ cm'
EX3miner_ _ _ _ _ _ _ _ _ _ _ _ _ __
(OB
the observation week II since start of care)
Ex hibit -1- 2 ComplclCd Wound Measurement Form
Wound Measurement s Initial _X_ Discharge OBWK#: _0_ OC Status:
Patient Name: \,Gz..,-'LJ,u"'c"kv:L-_ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ __
Date: 01/03199
Med Rcc#.0"'3"'9,,7'-_ _ _ _ _ _ _ _ __
Wound ID:_R Trochanter Wound Phasc:.Chroojc inflammation ("II measurement s in elll)
12:00 6:00 12:00 6:00 12:00 (A I).Q.. 12:00Q,L
Lmear Si7C:
Erythema Size:
Undermined: Depth:
(A) 4.4 em
6:00 (A2)..Q2 3:00 !U
Overall Undermined Estimate:
A+AI +A2= (a) 4.9 B + B 1 + 132 = (b) 4.8 (a) x (b) 23.52 cm'
Examiner: B Sweet PI COB
Ihe
observ~lIion
week # since
Sian
x
(A)~x
of cme)
3:00 9:00 3:00 9:00 3:00 (B1).J2...
9:00 (82) -'2...
6:00~
9:00~
(B)~~cm (B)~
~cm'
Hhufld ,\leo.mrellleIllS
WOUND SIZE MEASUREMENT ACCURACY AN)) RELIAB I LITY
LOCATION
Document the wound's anatomic location. Location can be an indication of the wound etiology (Table 4-3). For example, wounds located over bony prominences are usually press ure wounds, wounds on the soles of the feet may be due to pressure and insensitivity (diabetic wounds), and wounds
over the medial side of the ankle often are venOliS ulcers. Location provides important inrOfmation abo lit the expected wound healing. Wounds in areas of diminished blood Oow, slich as over the tibi a. heal slowly. The anatomic name thai clearly describes the wound location should be written. For examp le, trocltalller is a clearer descriptor than hip and signifies that the wound lies over the bony prominence (Figure 4-1). A circle over the anatomic site on the body diag ram g ives quick. easy identification of wound location on thc doc umentation fOfm (see sample of recording form, Exhibit 4- 3). If several wounds are c lustered close together in a locati on, they should be noted by either different lellers or by references such as o uter. inner. upper. or lower. It is important to keep the same reference loca tion I D for all the wounds by name throughout the course of carc. If one of the wounds in the cluster heal s, thi s should be noted in the documentati on. and the sa me reference names for the remaining wo und s should be retained for further documentati o n. I f severa l wounds join together and become one. thi s should be recorded and a new ID name given to the revised wound site. Exhibit 4-3 shows documentation o f wound location for multiple wou nd s.
Accurate, complcte, uniform , and co nsistent wound measurements are required to establish a wound diagnosis, plan treatm ent , and docume nt rcs ult s. Ways to maximi ze accuracy include th e following : • Take the measurement the sa me way each timc. from a noted reference point on th e body. • Use the samc terminology and units of mcasure for eac h measurement . • When poss ible. have the sa me pe rson do re peat measurements. Carefu l measurement records eve n small changes and shows the improved wound status or deterioration. Recording the wound mcasuremcnt is a lso ~1O impo rtant part of acc urate. consistent measurements. I f it isn °t recorded, it didn ' t happen . • An assistan t is helpful as a record er of the measurements as they arc taken. Usc a pre pared form and then fill in a mcasurement number at each space indicated on the form . This form can be preprinted or handwri tten so nothing is forgottcn . Reco rd as soon as each parameter is measured . Memory is nOl accurate. • Record a 0 if a characte ri stic is asscssed and found absent. The 0 says that yo u observed the charac teri sti c and assessed it. For exampl e. partial-thickn ess wounds are superficial. By th e depth meas ures spaces, a 0 should be written. A blank space does not show that thi s characteri stic was assessed .
Table 4-3 Common Locations for Chronic Wounds by Etiology Arterial Ulcers Lower leg dorsum Foot Malleolus Toe joints Lateral border of foot
87
Pressure Ulcers Bony prominences:
Ears Shoulder Scapulae Sacrum Coccyx Trochanter Ischial tuberosity Knees-condyles, patella Tibia/fibula Malleolus Heel Metatarsal heads Toes
Neuropathic Ulcers
Venous Ulcers
Plantar surface of foot Metatarsal heads Heel Lateral border of foot
Above the ankle Medial lower leg
88
W OUND CARL
IV~'---- OcCiput
__ .,--· Ac,onllonP~. Thoracic Vertebrae -~::4
lumbar Vertebrae
~~-Scapu la Olecranon
--.,:.II-
Coccyx Trochanter - - - - - . /
k l--lateral Knee Medial Malleolus (Inner Ankle) lateral Malleolus (Outer Ankle)
Metatarsals (Toes)
~.~~_--=Cako~' (Heel)
Figure 4- 1 Common IOc'lt ions for chronic wounds. Courtesy o f Kno ll Pharmaccuticn l Company, Moum Olive, NJ.
Ex hibit 4-3 Document ing Wound Location
Documenting Wound Location with Narrative Note:
Example:
is measured across the diameter of th e grea test length and the greatest width. Then the length is muhip lied by the widlh. which gives the estimated sq uare area of the wound or OA. This meas urement inflates th e size area of the wound. The product results in a si ngle number that can be easily moni !Ored for c hange in size. These two dimensions are always meas ured a nd may be the onl y measureme nt recorded. Less frequently measured arc und ermining/tunnels and depth. Anoth er way to measure is called Ihe clock melhod. The face of th e clock is used to guide th e meas urement (sec Figure 4-2). Seleci a 12:00 refe rence posilion on the wound. Twe lve o'c lock is usually loward the head of the body but in s ituati ons such as seve re contrac tures of th e trunk and lowe r extre miti es it may be more co nvenient and easier to rep roduce the meas urements if anot her conve ni ent anat omic landmark is selected . For exa mpl e, meas urcments in the foot may usc the heel or th e lacs as Ihe 12:00 refcre nce poinl. In a fe ta ll y contracted person. a troc hanteric pressure ulcer may be more easi ly tracked if the 12:00 refercnce point is IOward the knee. Usc a clock face and take th e mcasuremen t from 12:00 to 6:00 and from 3:00 to 9:00. Both wo und meas urement methods are acccptable. Choose a method that is co mfortab le and record whi ch method is used, th cn lise it co " si.well/~\ ·. Ex hibit 4-4 lists some advantages a nd disadvantages o f cacho
I. Si ng le wou nd location : coccyx 2 . Multiple wo unds at a location: Initi a l note : 71/re(! lI'Ollllds are loeared IIppe,; middle. and OIlier side 01/ 'he rig'" flvclwmer.
The upper and middl e wou nd s merge. Since they arc upper to the o uter wound the same term upper is retained and the merger noted as in this example: fo ll ow- UI) note: The upper and middle wounds have merged and wi ll in the ruturc be referred to as the upper wound on th e right trochanter.
LINEAR WOUN D SI ZE MEASUI{EMENTS Three types of wound meas ure ments that track th e c hange in the wound size over tim e arc described in thi s section : open a rea (OA) measure ments (length by width), unde rmin ing or tunn e ls, a nd de pth . Th e mos t co ml11 o n wo und Illeasureme nts are the ope n area length and open a rea width. The ope n a rea length and width of the wound are meas ured from wound edge to wound edge. The greatest lel/gth lIlld greatest width method of measurement mea ns that th e wound
Figure 4-2 Orientation of 12:00 to 6:00 position on the body rchued to a clock face . Courtesy or Knoll Pharmacellti cal Company. MI. Olive. NJ.
Wound A1easuremellls
Ex hi bit 4-4 Comparison orTwo Wound M easurement M ethods
G REATEST LENGTH BY G REATEST WIDT H MET HO I) Ad ,'anl ages • Simple and casy to learn and usc • Most cOlllmon method • Reliable Disadva ntages Diamcter~ change as size and shape change. so different diameters are Il1 c,lsurcd each lime • Wound open area will be larger than in clock method
•
CLOC K
• Gauze paper. fo rlll . or pocket-size notebook to record data (see Ex hibits 4-1 an d 4- 2)
How To Measure Before measuring. the wound should be c1eancd and examined closely. Look ca refull y at the wound edges and see if they are di stinct so you are measuring from wound edge to wound edge. Use Ihe foll owi ng sleps: I . Posi ti on patient. 2. Don gloves and remove wo und dressing and packing. 3. Place in disposable infectious waste bag. 4. Clean wound with normal sa line and syringe with
~ I ET H O I)
Advan tages
5.
• Simple '.II1d easy to learn and use • Tracks sa me place on the wound ovcr lime • More co nservative measure of area
6.
Oisad\'unl ages • Requires morc sleps to perform • More preci sion required to line up wound points along the clock "fucc" • Less commonly uscd
89
7.
8.
9. 10. II .
IS-gauge needl e or angiocatheter (sec Chapler S for wound cleansing procedure). Take measurements with disposable wound measurement ruler. M easure the open area greatest length and greatest width from wound edge to wound edge. Record each measurement liS il is takel/ . Dispose of wound dressing, measurcment instrument, dressing. and gloves in infecti ous waste container after th e procedure is complet ed . Dispose of the syringe with IS-gauge needle in sharps container. Ca lc ulate wound open area. Repeat week ly or more frequently if indi ca ted.
T he Cloc k Melhod To Meas u re O pe n Are a Sup plies Needed ror Linear Meas ure me nl Replace step 6 with the foll owing. Everything elsc remains the same. Supplies assembled in advance help improve eITiciency and red uce examiner and patiel1l fatigue (sec He lpful Hinls for Measuring).
• Pen or pencil • Disposable plasti c straight edge ruler wi th linear measure rul ed in centimeters • Disposable g loves • Normal sali ne • Di sposa ble syrin ge with I S-gauge needl e or angiocatheter (for cleaning)
6a.
6b. 6c. 6d.
ESlablish Ihe 12:00 posilion by c hoosing an anatomic landmark Ihat will be easy to identify, a nd make a record for all following mcasurements. Example "" 12:00 toward head. Mark 12:00 with arrow on the skin . Re peat with marks at 6:00. 3:00, a nd 9:00. Measure from wound edge at 12:00 to wound edge at 6:00 position. M easure from wound edge al 3:00 to wound edge at 9:00 position.
90
WOUND CARE
Clinical Wisdom: Using a Template To Improve Measurement Accuracy
...
To improve accuracy and keep the measurements better aligned, cut a circle from paper folded in half twice and mark the four clock paints at the four paper folds. Place over wound to use as a guide. Tape paper guide to the periwound skin to keep from shifting.' Take all measurements with the template in place for uniformity of tracking the same wound locations for open area, undermining, and depth (see Figure 4-3).
...
, ,
Figure 4-4 Mapping undermining around the entire wound perimeter. SOllrce: Copyright c Evonne Fowler, MN, RN. CETN.
Method 2 fig ure 4- 3 Using a template to improve measurement accuracy.
Measurement of Undcr miningITu nn cl in g Measurement of undermining/tunneling shows the extent of wound damage into surrounding deep tissue. Three methods to measure undermining/tunneling arc described. Choose one and usc it consistently (see Color Plates 37 alld 38).
Methotl I I . Map undermining around the entire wound perimeter by inserting a moist, co tlon-tipped applicator into the length of the undermined/tunneled space and continuing around the perimeter. Dip the cotton tip into normal sa line before insertion to make it slide in easier and be less likely to cause tissue trauma (see Figure 4-4). 2. At the end point do 1101 force further entry but gently push upward until there is a bulge in the skin. Mark th e points on the skin with a pen and connect them . Measure two diameters as in the length by width. Calcu late by multiplying length by width for ol'erall 1/1/del'milled eslimale (explained later).
I . The Sussman method for wound measurement applies the four points of the clock method 10 measurement of undcrminingltunneling,2 The four card inal points of the clock, 12,3,6, and 9. are used. Twelve o'clock will be toward the head unless otherwise noted (see section on clock method of measurement). 2. Wet the callan-tipped applicator with normal saline and insert gently into tunnel. The place on the sk in where the cation tip causes a bulge can be marked and th e callan-tipped applicator can be wit hdrawn . 3. The callan-tipped applicator is gripped at the point where the skin and the wound edge meet and withdrawn. This is the length of the tunnel. 4. Next place the length of the cation-tipped app licator up to the withdrawal point against a centimeter ruler or measure from wound edge to mark on skin. Record length.
Methocl 3 I . Test the perimeter for undermining with a colton-tipped appl icator and then select the longest llInnel to record. 2. Use the clock to identify the locat ion(s) on th e wound perimeter where there is tunneling and then track the tunnel over time.
Jl hUllll J\/e(l\llremellls
Research Wisdom: Accuracy and Reliabifity of Wound Undermining Measurements Taylor' studied the variability of the measurements of wound undermining among physical therapists trained to use the Sussman wound undermining measurement method. Her findings show that the biggest variation occurred when 12:00 was chosen to coincide with the greatest length of the wound open surface area. This produced an inflation of the area measurements. Her results of reviewing measurements by 39 physical therapists over the 4-week study period demonstrated some interesting findings. For instance, there were three common errors: misreading the measuring device, errors in transferring the numbers, and calculation errors. As would be expected, there was more error in measurement when the wounds were smaller compared with larger wounds. Overall the coefficient of variation for open wound area measurements was 5% or less for intra tester replication for 69% of the physical therapists and between 5% and 10% for the balance. The wound overall estimate had intertester variance of 10.5% or less for 100% of the study participants. Validation of the measuring technique was proven as highly reliable and suggests that this measurement can be used to document progress in the healing of undermined wounds. "
Q'
91
Helpful Hint: Wound Stick Tunneler and Wound Stick Wand
Two devices are available to aid in wound measurement: the Wound Stick Tunneler and the Wand. Both devices are long, thin rulers. The Tunneler is made of very thin, flat metal (see Figure 4-5). The Wand prototype resembles a fever thermometer and is made of smooth, unbreakable plastic. Both devices have centimeter ruling along the length of the device and can be gently inserted into the undermined space to the pOint of tissue resistance. Never force th e instru ment into th e spa ce. To use either device, insert the "1 cm" end into the length of the undermined space. The distance from the inside point of resistance to the edge of the wound is read on the ruler. Read the length from under the wound edge, not the visible number. Otherwise extent of undermining will be overstated. These devices can also be used to measure across the open area and from the wound bed to the skin surface for measurement of the depth as described. The depth is read directly from the ruler device. Both devices come in sterile packages and are for single-use application.' If the wound undermining/tunneling exceeds the length of the instrument it would signify that a . physician should be notified of possible sinus tract formation. Figure 4-6 shows how undermining is measured on a mock latex wound model. Extent can be read to nearest millimeter. See section on accuracy of measurements for more information.
Wound Stick$ Tunne ler
Figure -'- 5 Wound Slick Tunneler. Courtesy of USMS. Mi:1mi. Florida.
Figure 4-6 USlllg the Wand to measu re wound undermining on a latex wound model. Courtesy of Des myrna R. Taylor. Loma LlIlda. Ca lifornia.
92
WOUND CARL
Overall Undermined ESl imalcd Size
lier, betwecnAugust and Septcmber. Whereas notice the linear reduction in wound extent from September to December. As the wound healed undermined/tunneled spaces closed and ti ssue integrity was restored the overall size reduced. Another finding observed from graphing is how the change in undermined estimate also parallels the change in wound phase. Note the abrubt jump in wound overall undcrmined estimate from 42.25 cm to 122.43 cm. This is frequently coincident with the early proliferative phase. The expansion of the wound extent reneets the efTects of wo und debridement on loss of subcutaneous tissue integrity (the separalion of fascial planes), producing tunne li ng. Loss of subcutaneous tissue integrity produces increascd risk ofinfcction. Subcutaneous ti ssue integrity is restored as the wound progresses through the proliferative phase to the remodeling phase. Graphs, like the one illustrated (Figure 4- 7), are a very useful visualmcthod to monitor healing over time. The graph can be generated as part of a database program or can be manuall y drawn on a piece of graph paper.
Undermining/tunneling adds to the extent of tissue involved in the wound. The linear measurement of the extent
of the wound undermining/tunneling al the same four points on th e clock is added to the open area length and width. This
is the overa ll length and overall wid th . Next the overa ll length is multiplied by the overall width to derive an estimate of the o\'erallulldermilled estimated si::e of the wound area 2 (calcu lation is shown below). The product is a si ngle number that can be monitored and graphed over time in the manner shown in Figure 4- 7. Figure 4-7 shows graph ically how the overa ll undermincd estimated s ize compares with the surface area estimate.2 If on ly the open surface area is moni-
tored as change in size. the wound appears significantly smaller than it actually is, and incremental changes in size information arc lost. Other information can be read from the graph. For example. large variations in the extent of lhe wound noted car-
". ,,.
". '00
•• •~
• ~
•u • ••
§
' ''''' UNoeRMINEo eSTIMATE
••
..
_
SURFACE ARU ESTIMATI:
11.80
,.
. 50
42 . 25
••
3 • • 72
.....••.••
,.
............
.. "" .... ~~~.~r---+---~--..... ..... =.. t-;;,,".....--+---
» +---~---+--~----+-~~~
•••• 22 .M
u....
oJ.
14.00
::-
'.
,Dt---M~kfu~H······~·~ ,~ ~ ~ = ' . ..-. ---~ ... .. L-__~--_+----+_--~--~__ -=+===~==~~ ~~D
""'UL
I I NFLAMMArORT
MAT
JUNI:
JULY
AUO
I
""
.""
PROL'''I!RAnVI! _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _•
66-YEAR -OLD FEMALE WOUND TYPE: PRESSURE WOUND LOCATION: LEFT HtP
Fig ul·c 4-7 Wound healing prori!c; recove ry O rH pressure wound.
DOC
I
REMooeUNO
Wound Mellsllremellls
93
Ca lculatin g th e Ove rall Es timat e Exa mpl e: Ovenl ll Size Es tim ate
I. Add the length of the open area from 12:00 to 6:00 to the undermined lengths at both 12:00 and 6:00. Thi s is the overall length of the wound . 2. Add the width of the open area from 3:00 to 9:00 to the undermined lengths at both 3:00 and 9:00. This is the overall width of the wound. 3. Multiply the overall length by the overall width. 4. This equal s the overall size estimate of the wound .
d"
12: 00 6:00 Icngth + 12 :00 undermining t 6:00 undcrmining - overall length 3: 00 9:00 width + 3:00 underminin g + 9:00 undermining overall width
Ovcralllcngih x overall width
=
o\erall estimated area
Helpful Hints for Measuring
1. Wound M easurement Kit
If wound measurements are taken frequently, the job may be easier if you assemble a kit made up of the supplies in the supplies needed list for wound measurement that you keep with you in a small plastic carrier. 2. Use An Assistant
An assistant is helpful to: • • • • •
Position patient Comfort patient Act as recorder Control wound "sagging" (see below) Seek additional supplies or assistance
3. Patient Positioning
It is easier for everyone if both the patient and measurer are comfortable during the procedure. Some patients and some wounds are difficult to position for accurate measuring . Once a convenient and comfortable position to measure is found, record the position that works best. This will save time and effort and improve the uniformity of measures from time to time. Example: coccyx wound-position: right sidelying; heel wound-position: left sidelying. 4. Order of Measuring If measurements are always taken in the same order, the tracking of the wound will be more consistent. Suggestion is to take the length first , the width second. If the clock method is used, take 12:00, 6:00, 3:00, and 9:00 in that order for improved consistency.
5. Controlling Sagging Wounds
Full-thickness wounds with undermining may sag because of lack of subcutaneous support and the pull of gravity. Tension on the tissue is hard to maintain. Try to keep sagging to a minimum and maintain uniform tension for accurate length and width measurements. 6. Wound Measurement Pocket Notebook (see Exhibits 4-1 and 4-2) A 4 x 6-in pocket notebook is useful for recording wound measurements. This can be a spiral notebook or a ring binder. If the information to be gathered is listed in the spiral notebook before doing the measurement, sort of like a handwritten form, it will help consistency, uniformity, and completeness. Another way is to use a preprinted form (see sample) with holes punched to fit a loose leaf notebook. An alphabetiC index is also helpful in keeping the records separated by patient name. The small sheets can be taped to a large sheet and placed in the medical record in a cascading fashion. Then numbers do not have to be rewritten. They can also be entered into a computer.
94
\VOUND
CARl·
Calculating Pcrcclllagc Rate of Changc in \\-'ound SiLc An interesting way to see how a wound is progressing is to look at the percentage rate of change. ThiS is a way to measure and predict successful outcomes. It is a simple statistical calculation that uses the follo\vlIlg formula: I . Baseline (week 0) wound size (OA or overa ll OA size) measurement is used as the original si/e. 2. Subtract the next \!':ound size OA or overall OA size measurement (IIltef1lll) taken from the baselint.!. 3. Divide by baseline wound measuremelll and muhiply by 100"0.
Formula for (·omputillg rate of dUlIlge ill woulld opell area: (Baseline open area (OA)
Example:
Interim open area (OA). BaselIne open area)
Wound open area (OA) baseline week 0 Wound open area (OA) week I (inlerim) OA baseline OA week I (inlerim) Divide Ihe remainder by lhe baseline OA To ca lculale pcrcelllage muhiply 0.066' 100°'0
IO()Oo
30 em' 28 em' 30 28 2 2/30 0.066 6.6%, Percentage rate of change
Note: A weekly percentage of change would use the prior \veek size measurement illS Lead of baselllle. Wounds oOen change drastically in size from one week to another in the early phases of healing and then the ralC slows. Referring 10 the percentage of change measure on a weekly or biweekly basis is a good guide to how the wound IS healing.
Measuremenl of Wound Oeplh Wound deplh is defined as diSiance from Ihe visible skin surface to the wound bed. ~ A melhod to track wound deplh is desirable and needed because this measurement is an in"lportant indication of the proliferation phase of wound healing. Wound bed surfaces arc irregular, and repair is not uniform. It is common practice to try to find the deepest site in the wound bed. This method is diITicult to reproduce from measurement Lo measurement because the wound bed fills in irregularly and what is the deepest spot one time may not be the same spot at the next measurement. Depth measurement accuracy is limited regardless of how this measurement is made; ho\vevcr. the clock mcthod se ts repeated measurement sites th at can be 1110re closely reproduced at each measurement test than the use of a single "deepest" spot measurement. There is controversy. especially among researchers. abo lit usefulness of the depth measures because of the inaccur~lcies recorded." The Clock Melhod for Measuring Wound Oeplh I. Take deplh measuremenlS allhe 12:00,3:00,6:00, and 9:00 posilions.' 2. Insen a calion-lipped applicalor perpendicular 10 Ihe wound edge. 3. Grab stick of applicator with fingers at wound skin surface edge.
4. Ho ldin g this position on the applicator ~tick. place applicator stick along a centimeter-ruled edge. Record for each position. S. These depth measurements mayor may 110/ be at the deepest area. 6. A separate measurement may be taken and noted at Ihe deepeS! area. Partial-thickness \'v'Olll"lds hmc a depth less than 0.2 CI11. Wounds with . . 0.2 em depth arc difficult to measure. and should be recorded as >0.2 em. Mea,ure Ihe deplh of fullthickness \\.:ounds of greater than 0.2 em depth. When a wound is undergoing debridement of nonvlUble tissue. the wound depth usually increase~; but then a~ the wound bed fills with granulation tissllc. the depth decreases. Reduction in wound depth IS a measurement of progression through the proliferation phase of healing. Measurement of wound volume is difficult and is usually reservcd for rescarch . T".."o mcthods ha\e been reportcd. One method involves filling the wound with a measured amount of normal saline from a syringe. This wo rk s best for wounds that can be positioned hori/onH.llly so liquid doesn"t spill OUI. Anolhcr mel hod is Ihe use of JeIl"'le, an alginale hydrocolloid used by denliSis. II has been rcponed Ihal by pouring the rapidly selling plastic into the wound a mold of the wound can be made. Jell",le is reponed 10 be well loleraled by Ihe wound tisslle." Regardless of \\hlch method of measuring wound volullle is used there will be significant inac.:cura-
Wound A1easilreme11fs
cics. Is it necessary to measure wound volume? At this time, thcrc is qucstionablc value to thc taking ofvolumc measurements. Use of this paramc ter ofmcasurcmcllt appea rs 10 be of most concern in the research arena and should not be of concern to the cli nician.1> Measurement of S urrounding Ski n Eryt hema
Erythema of th e sk in surround ing a wound may be a measure of the inflammation phase of healing or a sign of in fection. Chronic wounds often show a halo of erythema but lack the other signs of inflammation. The peri wound erythema can be identified as unblanchablc redncss or a darkening of the skin in darkly pigmented sk in, See the C linical Wisdom box rcgarding measurcmcnt oferythcma in dark ly pigmented skin. Streaking or significant signs of eryth ema projecting out a distance from the wound may be an indicat ion of celluliti s, and medica l measurcs are needed. Meas uremen t can be taken using the greatest length and greatest width method, or the clock method can be used. The clock method is described.
The Clo('k l\leth od To Mell ,m re Surrounding Skin Erythema I. Measure across th e wound open area at th e 12:00 to the 6:00 position to the outer margin of the periwound erythema. 2. Measure across the wound open area at the 3:00 to the 9:00 position to the ou ter margin of the peri wound erythema , 3. Comp ute th e peri wound area of erythema.
95
Clinical Wisdom: Measurement of Erythema in Darkly Pigmented Skin Skin color changes reported by clinicians and in the literature' indicate that, when inflamed, the skin color of darkly pigmented people darkens to an eggplanV purplish color. It may be difficult to differentiate darkening of imflammation from hemosiderin staining. If this is true, proceed with temperature and edema examinations. For a fu ll description of assessment of darkly pigmented skin, see the section on assessment of darkly pigmented skin in Chapter 3. The following are guidelines for measuring the extent of inflammation/trauma in darkly pigmented skin: • Use natural light or halogen light, not fluorescent light. • Outline the margins of color change on the surrounding skin with a marking pen. • Select a reference point for future measures. • Measure the greatest length and the greatest width or use the clock method. • Calculate the area of color change (as described for all length-by-width measurements).
household plas ti c wrap with a plastic transparency mark ing pen (the ink does not bead up). Tracings taped to a sheet of
paper can be put in th e patient reco rd . However. because raped-o n tracings can come loose or ragged in a chart, the tracing and form can be photocopied and the copy placed in the chart. A tracing is a picture of the wound shape. Repeated tracings show change of size and shape over the course of recovery. Accuracy of measurement with tracing is dependent on how carefully the wound edges are followed as the
Est imated area of erythema: 12:00 to 6:00 length x 3:00 to 9:00 width ~ _ _cm '
Example: 9:0 cm x 6.0 em
= 54 cm 2
"Vound Tracin gs
tracing is drawn. Kloth and Fecdar lO documented measurements for patients in a research study. Sussman II sugge sted use of tracings app lied to a g raph form wi th a key for ti ss ue assessment called wou nd assessmen t form" for c l inical practice report in g wo und healing progression. Foll owing are suggested ways thai tracings can be used : • Tracings show change in the wound perimeter shape over time. Wound shape is a helpful indicator of the rate of
Making a wound tracing is reported to be the most popular and practicalmcthod for measuring wound area. It is easy to learn. inexpensive. and readily ava ilable.s Measuring the wound area from transparency tracings and plac ing it on graph paper to determine size by counting the centimeters have shown high intra- and inte rtester reliability (0.99). Com-
pared with linear measuremcnts with a ruler th ere is less overestimation of the real wou nd arca. a lthough some error can be expected. Using the I-cm graph papcr to coun t sq uares has been reported to be qu ick a nd efficient.\! Tracing can be made on acetate measuring sheets such as those th at are given out free by many companies for measuring wounds or on
healing. As de scribed in Chaptcr 2. linear wounds contract rap id ly. square or rectangular wounds contract at a moderat c pace, and c ircu la r wou nds contract slowly,9 • Tracings can be placed on a metric graph form. This shows th e wo un d size as we ll as shape and provides a three-dimcnsional pictograph of the wound on a IwOdimensional form " (see Exhibit 4- 5). • A tracing can become a "wound map" showing fca tures of the wound bed such as necro ti c tissue and adjacent tissue c haracteristics such as erythema (sec Exhibit 4-6). Household plasti c wrap is better for th is because it is clear.
96
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II 'cJlllld A1ell.wrel1lell/s
Exhibit 4-6 Wound Assessment Form \\ IIh TraclIlg
NAM I-: _ _...lG.z..lJL!,/lJC.tK.rY_ _ __ _ _ _ _ _ _ DATE: 4120/01 WO UN D I.D. (I)
_....:C:::O:::C:::.CYX~_ _ _ _
BLISTER
CD
II SB
®
Io RYTIIE ~ IA
II EMORRH AG IC SCAD NEC ROS IS
DRAI AGE : V ISCOUS PURUU.NT
B S wee t
(2) _ _ _ _ _ _ _ _ _ _ (3) _ _ _ _ _ _ _ _ _ __
INFLAM MAI"ION X B
PT
PROLIFERAT ION F C
FT PT U
FIBRO I'LAS IA CONTRACTION FULL THICKNESS PARTIAL TH ICK l:SS U Dl:RMINING
EP ITH ELIALIZATION EP M R -
EPITH ELlALI ZATIO M ACE RATION REMODIoLED INTACT
DRA INAGE:
DRAINAGE:
S SS -
S DY
SEROUS SEROSANGU INOUS
~ ~
SEROUS DRY
SOl/rce - Adapted rrom Su"man . CA ' Physical Thcrnpy Choices for Wound RccO\cry. OW)IIU lI o",/(1 \{C/lwg('flU' ,,'. 1990: 29:20 2M. (
l1 ealth M .umgcmcnt Publi cations. Inc.
1990.
• The wound map, if placed on the metric graph paper, can have features such as aellla! amount of undermining/tunneling around th e wound perimeter drawn in using the actual measurements and a ruler. • The wound map tracing becomes the ti ssue attributes assessmcnt documentation by the addition of information about thc tissue. A key of ti ssue attributes with assigned letters for each attribute at the bottom of the graph form makes thi s an easy way to mark the ti ssue in the drawing. This is then a paper-and-pencil instrument to track wound healing over time. NOIe: The ti sslie attributes arc the samc as those representcd in the Sussman wound healing tool described in Chapter 5. • The wound tracin g can be scanned in to a computer and a digiti zed measurement of the wound can be made, the area calculated and stored in the computer.
2. Draw an arrow on the pla stic wrap in the location and direction of the 12:00 position. 3. Trace the wound edges.
Clinical Wisdom: Tracings on Plastic Sandwich Bags A plastic sandwich bag can be placed over the wound and tracing made on top layer. The bottom layer of the bag makes a wound barrier. Slit the bag in half and discard the contaminated layer with infectious waste. The top layer can be put on the graph form or placed in a zippered sandwich bag and kept for comparison measurements. This is very useful for home care.
S upplies Needed Assemble all equipment needed: • Two acetate measuring guides or one each plastic wrap over wound lopped by measuring guide • Two pieces of plastic wrap cut to approximately 6 x 8-in pieces or larger ifwollnd plus periwound erythema is larger • Fine-point tran sparent film- type marking pen so ink won't bead up on the plastic (Dark Pentel or Vis a Vi s) • Paper towel. folded in half lengthwise • Paper or graph form • Transparent tape
Ma ke a IVotwd Tracing
I . Place two acetate measuring guides or two pieces of plastic wrap over wound so that the bottom piece is going across wound from 3:00 to 9:00 and the second piece is going from 12:00 to 6:00. Thi s helps when separating the top layer from the bottom layer. Smooth each one to avoid wrinkles. Two layers are used to prevent contamination of the layer with the drawing. The layer thflt was in contact with the wound will be discarded with infectious waste after tracing is completed.
Optiollal Additiolls 10 Tracillgs I . Draw any notable features within or around the wound open area slich as outline of the necrotic ti ssue, exposed bone, etc. Label with a letter from wound assessment form 11 key. 2. Mark areas of erythema/darkened darkly pigmented skin with broken lines around the wound open area. 3. M ark area of necrotic tissue or eschar with diagonal lines. 4. Mark other features with a circle and dots and label. 5. Place the film with drawing so the 12 :00 arrow is in the conventional 12:00 po sition on the graph form . Tape wound tracing onto graph form . Make sure that plastic is taut and free of wrinkles. ee instructions for completing th e wound assessment form which follows. 6. Copy wound tracing with copier for permanent record. Di scard graph with plastic tr3cing. 7. Mark wound features with lines drawn at right angles to the feature and label.
\Vound Assessme nt Form
W
Helpful Hints for Tracings
1. A grid printed on an acetate film that peels off a plastic backing sheet can be used to make wound tracings. The sheet acts as a barrier to infection and is discarded . The tracing is then ready to place in the medical record. 2. The Polaroid Wound Photograph system has a grid available to be used when taking a wound photograph.
The wound assessment form l1 is a papcr-and-pcnci l instrument that consists of a centimeter graph sheet, a linear measurer lined lip with the graph coordinates to show size. and an anatomic figure front and back to mark loca tion . The tissue characteri stics arc listed by phase: innammation , proliferation. and epithelialization. The key assists the clinician in the evaluation and the development of the wound phase healing diagnosis. The form is shown in Exhibil 4- 5 and the completed tra cing is shown in Exhibit 4 6.
"bUIld AleaSII,.emellls
Supplies Nee(/e(/ • • • • •
Wound assessment form \Vound tracing Transparent tape Fine-tip marking pen Copier (optional)
Use the 'Youlld Assessment Graph Form I , Prepare wound tracing (sec above). 2. Place tracing on assessment form graph with arrow lined lip with lines at 12:00 position. 3. Tape tracing in place unless adhesive backed. 4. Draw lines exactly th e same length as length measurement taken from the undermining at clock points arollnd wound perimeter starting a1 wou nd edges outward. 5. Draw lines from tissue characteristic out to side of graph and label with letter from key. 6. Print wound location at bottom of picture. Mark location on anatomical figures. 7, Thi s "\\ound map" is also a tissue assessment report.
mised by the problem caused by measuring wound area on curved surfaces. 1I Periodic photography is a method often used to validate th e overall treatment outcome. Serial photos are great teaching tools for in-services, for referral sources, and for patient encouragement. Photography can be done as simply as shooting an instant camera or by using more complex camera equipment. For example, an instant camera with a grid printed on the film is one method. See Figure 4-8, A to C, for an example of grid photography. Digital camera equipment is now avai lable that interfaces with compu ter so ftware and performs wound measurements as well as records the color. The cost of such equipment is still high and not readily available to the clinician. Ano ther new option is co lor print film, which can be shot with a standard 3S-mm camera and is processed and returned in three forms : photos. slides and compu ter disc. One company that offers this service also sells inexpensive (abou t $20 to $25) so ftware that can read the disc and upload the photos on screen . The computer could store the photographic records. Additional information can be added to each photo for record keeping. Scanning is yet another method for computer inpUlling of photographs. Complex camcra set ups arc usua lly ' used by researchers. Regardless of wh ich method is used, for good pictures follow these tested suggestions:
Note: Tissue characteri stics arc described in Chapter 3.
• Usc a good light source. • Position patient and wound carefully. en suring that the patient's private areas are screened from the camera. • Position a linear measure (ruler) in the photo to show re lative size. • Use a string of known length to measure distance from the camera to the wound for more uniform recording. • Use an identification sign with patielll lD, wound location, and date in the photograph (unless dated by th e camera). • Select a camera with a close-up feature if possible to take the best close-up view of th e wound . • Use an assistant to help maintain the posi tion and perhaps to position the marker. • Record wound and patient position for repeated photographing sessions, ie, right sidelying.
Clinical Wisdom: Using the Wound Tracing for Compliance The wound tracing is used as an incentive for compliance in diabetic patients. Two wound tracings are
made on acetate film or plastic wrap. A date is placed on the tracing next to the wound edge. One copy is placed in the patient records and the other is given to the patient. The next assessment day the patient brings in his or her copy and the copy from the chart is also presented. The wound is redrawn on both pieces of film and dated. The size change is then visually compared. Patients receive positive reinforce-
ment for their compliance by seeing their wounds getting smalier (N. Elftman, personal communication, 1996).
Q>
WO UN D PHOTOGRAPHY "A picture is wo rth a thousand words" best describes the value ofwollnd photography. Serial color photographs record wound ti ssue characteristics.The lighting will affect the color. Flash photography tends to give a blue tone to the photograph. Incandescent light gives a ye llow tone. Photographs are used also to measure the wound si ze. The accuracy of wound measurcmcnt taken from a photograph is compro-
99
Helpful Hint: Making an Identification Marker for Photographs
1. Tape plastiC measuring sheet to a 3 x 5-in index card. 2. Put card into a plastic sandwich bag. 3. Put two strips of white tape on plastic sandwich bag. -
Write patient ID, wound location on first strip (example:
w.J. , coccyx). - Write date on second strip (example: 1/23/99). 4. Throwaway the plastiC bag. 5,
Reuse the card with measuring information .
100
W OL'If) CARt
A
B
c Fi gure 4-S Grid photography (A- C). Shows change in wound
SilC
and :ltlribUlcs mer time.
WOUlld A.feu.wremeflls
REFE RR AL C RI TE RI A Why include referral criteria with the chapler on measurement? As wo und measurements and rcmca$uremcnts are
performed, it
1l1 3Y
become immed iate ly appa rent that a
prompt refe rra l is necessa ry. Following is a li st of referral
criteria to guide clinica l decisions: • Exte nt of wound invo lves bone and/or dee p subcuta neous spaces- may indicate osteomyelitis or other infecti on. • Impendin g expos ure o f a named anatomi c structurc-
wo und extent should be eva luated medica lly.
101
of many caregivers. Tracing the wo und will also hel p the caregive r to sce that the wou nd is ge tting smaller as the report number decreases or to sec the changes in drawing shape and size. This reinforces both the caregiver's and the patient's compliance. If the wound is not getting smaller, it will be an anent ion getter and encourage change in treatment planning. A form such as the one illustratcd (sec Ex hibit 4 7) can be faxed to the wound case manager ifvisits cannot be made on a frequent basis. and the progress of the wound can be followed. If the person to moni tor the wound is a paraprofessional. physical therapist ass istant , or licensed prdctica l nursc. other wo und measurements can be taught and with a hi gh Icvel of expected reliability and confidence.
• Black holes or tunnels that ca nnot be mcasured- hi g h-
ris k situation. • Wound tunnel ing may perforate the peritonea l cavity either in the abdomen or rectum .
• Wound
SiLC
is enlargi ng morc than expected.
' YOllllll lltl easlI rem ellts
Supplies: plastic measuri ng sheet. pen, plastic wrap, plastic sandwich bag (o ne or two). hand-held pocket calculator. Wound measurements are take n once a week or biweek ly.
REFER RAL SOLJ RCES There are many hea lth care practitioners who have experience in complex wo und manage ment One or more of these professionals shou ld be contacted for follow-up management if any of the referral criteria listed above are met. Some choices include the following: Physicians ~ DcnmHology nurse Derma to logist Orthopaedic surgeon En terostomal registcred nurse Plast ic surgeon Geria tric nurse Vascul ar surgeon practitioner Vascull.lr nurse
Sa mple Instru ction Sheet
Allied Il ea lth Physica l therapist Vascu lar tec hni cian Podiatrist
I. Note the date. 2. Measure the longest diameter of the wo und in cnch directi on, head to toe (length ) and side to side (width). Record the length and width in the ap propriate boxes on the form as the measurements arc taken. 3. Then multip ly the two numbers togcther for a single total size measurement. IlIstr lll'tioll'" To A1l1ke II ' YOIIII(I Tradllg lit /Jolli e
I. Use either two pieces of plasti c wrap or a plastic sandwich bag. 2. Place onc layer of plastic against the clean wound . If the plastic becomes foggy, that is. li ke wa rm air condensing on eyeglasses, lin a corn er of thc plastic to
SELF-CA RE TEAC HI NG GLJ IDELINES In loday 's hea lth care environment. many leve ls of caregive rs may be callcd upon 10 measure and monitor the wound size parameters di scussed in thi s chapter and then report to the ex pert clinician their findings for interpretation. The most successful results occur when step-by-step instructions and return demonstration are given by the designated data collector. Prepa re an instruction sheet for measurin g and/o r for tracing. Include a chart like the one in Exhibit 4-7 for recording the data . First, make an assessment of the person 's abilities to follow the directions. If the patient or a lay caregiver is to do the measurin g, limit the measurements to length and width. Teach the simple length by width multipli cation so that only one number needs to be reported. Makin g a wo und tracing is also within the abil ity
Ex hi bi l 4- 7 Wound Measurement Record
Name: _ _ _ _ _ _ Medica l Record # _ _ _ __ Datc
Lcngth
Wid th
Total
4/30/04
5cm
3clll
15
5/1 5104
4.5 cm
2.5 cm
11.25
5/30/04
4.0cm
1.75cl11
8.8 cm!
6/1 5104
2.5
1.25 elll
3. 13 cm!
Clll
Cll1 l
crn ~
102
Wm,NI) C\RI
allow the heat and moisture to escape and the fog will go away. 3. When you can sec the edges of the \vound usc a fch-
REFERENCES \un RIJs\\ IJk L t·rcqucney of rea ....essmclll of" pn:s .. ure ulcers Na· tional Prc ..... ure UkerAd\ isory Panel Proceeding.... 11)95 . -Id\" lIiJllI/d CtlI""i.'. July /A ugu .. t 1995:19 24
tip marking pen and draw around the wound edges.
4. Mark the date or the drawing next to the edge or the wound. Anerthe ink is dry (about 10 seconds). lin the top layer or plastic 'Hap or cut orr the top layer or the plastic bag.
2.
Su<,sllMn C. S\\.;IIl'tOn (j A uniform mcthod to tnlee and mea~urc chromc "ound ... Po .. ter prc\entallon. Sympo... llull for ·\d\;lnecll Wound Carc. S:1n IrJllcl"'cO. CA. Apnl 11)1)1
5. Save the wound tracing in another clean plastic lunch
J
Su .... man C. Sw;m ...on GIL The ulllily of Su ...... man wound healing tool 111 prcdll:tll1g wound heOlhng outcome .. 111 phy .. iealtherap)' Pre· sented 3t the NOIllonnl I)re ...~ure l!\cer Athl ...ory P,lIlci hfth Bien· nial Confcrcm.:e. Wasillngton D(', February 1')97.
4
Taylor DR. Reliability ufthe Sus ... man method nfme....urmg \\ound .. that eontOlin underrmlling Po.. ter prc ...cnlallun at Amcricill1 Phy ... i· cal Therapy A"'SOClalion Scientific \
5.
lie!) .. ("T"·lIn(·:~ ("/illlwJ Springhull',c; 1995.
6.
(ienl.ll.o\\ (i \1ethod!' for mca .. uring SI.le III pre ...... ure ulcer"'>...... a· tional Pre ..... ure Llcer.·\d\ I..ory Panel Pnx:eedlng.... 11)\)5.ld,·II(lIImJ Cllre. Julyl·\ugust 1995:4] 45
7
Bennett MA Report of the liI .. 1. force on IInpIH;allon ... for lIarl.l)' pigmented IIltact skill in the prediction anll pre\enllon uf pre ..... ure u\ce ...... Itll" 1Ii-1II1Il1 elm..'. NO\cmha Dcccmlxr 11)1)5;34 35
M
Ilardlllg K. Method .. for ""se ...... mg change III ulcer .. taw .... It/l- Hi-mIltJ Curl..·. JulyiAugu ... t 1995:37 -12.
I}
MaJc .. ke C Rcliability of \\ouml surface area meOlsurelllent !'lin TI't'r 11}9:!;72:t:\X loll
10
Kloth L. I·ecdilr J. Accclcr;:ltlon of "ound healinJ:! wllh high \011agc. monopha"'lc. pulsed currclll. 1'1/1"1 TIlt·,. 19XK61'1:5UJ SOX
II
Su ..... man ( Phy .. icOIlthcrap)' ehUlce .. Ii.Jr \~\nlnll rec,l\cr}. IIrJ/md \JUMgl>. July Augu .. 1 199()::!() 11'1
bag. 6. Discard the dirty plastic sheet,
CONCLUS ION This chapter described a number of different measurement strategies for monitoring wound extent and wound healing
by tracking change in four dilTcrcllt parameters ofsi.lc: open surface arca, undermining-tunneling. depth. and overall wound estimate. Obviously, to perform all of the abo\c measurements would be overload for Illost people. All arc lIsed
cOlllmonly. One method will appeal to one facility's practitioners and another to {Ulother facility·s. This is an opportunity for collaboration. Ilave a team meeting and decide on the Illethod that meets the needs of the majority of praetilioTH.:r~ and conveys the desired infonmttion. There is enough similarity between melhods Ihal thc information communicated through Ihe continuum of care can and will be readily interprcted. The key to successful measurements are consistency and accuracy. Once a method is selected usc it with rigor by all clinicians. Report on a regular. consistent basis.
RESOURCES
~UGGESTEO
• The Wound Slick Tunneler. USMS. Inc .. 1172 S. Dixie IIlghway. Coral Gables. FL 33146
• TIle Wand
~lIld
latex \vound models: D. Taylor. Loma
linda University. School or Allied I Jcalth Professions. Loma Linda. CA
• Plastic/acetate Jl"lc<.lsuring sheets are a\"ailablc frolllmi.1ny wound care products companies listed in Appendix A.
(iI/ide.'
lIill/lltJ Om' SpnnghoU'.c. PA
0\1",11\·
READI\G
lI:mly MA Biology of scar fonn:llion 1'11\·,7111'1' 191'19;69·1014 1{)24
CHAPTE R
5
Tools To Measure Wound Healing Carrie Sussmal/ al/d Barbara M. Bares-Jel/sen
INTROD UCT ION
Prod uct manufacturers also appl y th e stag ing system as a crite ri a for produ ct selecti on and use as wcll as marketing. Stagi ng systems have been misa pplied as methods of evaluating hea ling by using a dow n or reve rse stag ing system to ·s ignify hea ling. The assump t ion has been made that stage II I and stage IV press ure ulcers hea l by replac ing lost tiss ue with tissue of th e same type and qu ality as th e ori g inal. This meth od of monitorin g hea ling is biologically inacc urate because granulation tissuc and scartisslIc arc not the same structu res and lac k the fun cti on of tissues such as musclc, tcndons, subcutaneous fat , and dermi s that they rcplace. 6 Thcre is a need, there forc. for a va lida ted tool that measures hea ling in a bio logica ll y acc urate mann er.
Va ri olls instruments have been proposed to add ress the question of mOil itorin g heali ng, includi ng th e Press ure Sore Stat us Too l (PSST).' th e Sess ing sca le.' th e National Pressu re Ulcer Adviso ry Panel (N I' UA P) Pressu re Ulcer Scale fo r Hea li ng (PUS H).' the Wound Hea ling Scale (WH S).' and th e Sussman Wound HcalingTool (S WH T).' No ne has de monstra ted predi ct ive va lidity fo r wound hea ling and none has been val ida ted for meas uri ng hea ling or wo rsenin g of ulce rs mer ti me. Ta ble 5, 1 shows th e fac tors of wo unds and surro undi ng sk in and oth er fac tors used in these too ls as we ll as th e scoring system used by each. Eac h o f the tools is in deve lopment a l th is time wi th the idea of deri ving a 1001 th at wi ll be va lid. reliable, responsive, and pract ical for the wound care commu nit y including prov ide rs and payers. Hi storica lly, meas uremelllS used to eva luate imp rovc men t ovcr time inc lude change in ulccr size. change in surface appearancc, tisslie type prcsent, and surroun ding skin charaC leristics (see Table 5- 2). No single meas urement or combination of meas urements has been satisfactori Iy combi ned into a 100 110 monitor hea ling. Stagi ng systems such as th e NPUA P stagi ng system€> and th e Wag ner sca le. 7 (see Chapter 4) are approp ria te for determini ng initi al severit y at tiss ue trauma based on depth of tiss ue destructi on. The inform ation that is reported by assigning a stage of severi ty is static as opposed to healing, whic h is dynamic. Stagi ng systems are uscd in many ways; some arc appropriate and oth ers are not. For example, wou nd stagc is used as a criterion for inc lusion or excl usion in research st ud ies. The rei mburscment system uses the staging system as a crit eri on fo r eli gibility for products and services.
Criteria for a Wound l'lea ling Tool Criteria to eva luate th e appropriateness and util it y of a 100 1 include reliability, va lidi ty. res ponsive ness, se nsiti vity to change. and clinica l prac ti ca lit y.8 Validity
Fo r an instrument to be va lid the instrumcnt should measure what it is supposed to measure. Fo r instance, a wound hea ling toolmllst measure change in att ribut es hi ghly correlated with wo und healing. To be use fu l, the meas urements must be Cl/rrellf . In ord er fo r a too l to have pred icti ve va lidit y, the tool I11ust pred ict out comes characteristi c of healin g. Predi ctivc va lidity is of great import ance. Screenin g too ls th at have predictive va lidi ty are based on th e ass umpt ion that after detecting specific varia bles, an in tc rve ntion CB n be applied th at wo uld affect th e prcdi cted outcome.
103
104
W(JlI~()
C!\RI
Table 5-1 Factors and Scoring Methods Used in Wound Healing Tools
Factors
Wound Factors Size DOOth/Staae Ednes Necrotic Tissue
TvDe Amount Siouah Exudate Tvne Amount Odor Infection Granulation Contraction Undermininn Epithelialization
Surrounding Skin Factors Color Edema Induration Maceration Hemorrhaae Other Factors Location Risk of Skin Breakdown Wound Healing Phase Sha,;; Debridement Healed Scoring:
PSST
x x x x x x x x x x x x x x x
x x x
Sessing Scale
PUSH
WHS
SWHT
x x x
x x x x
x x x x
x x
x x x x x x x
x x
x
x
x
x
x x x x x
x
x x x x
x
x x x
x x x x x
Likert scale: 1=best; 5=worst. Scores for 13 items are added. Score changes as wound improves or worsens.
Scale 0-6 Uses the numerical value most closely associated with description . Score by calculating change in numberic value over successive assessments. Positive score = improvement; negative score = worsening .
3 Weighted subscores for: surface area, exudate. and surface appearance are added to obtain total score. Score changes as wound heals or worsens.
Eight letter modifiers are used with the Pressure Ulcer Staging System (eg.4NStage IV necrotic). Method to measure change in status over time not clear.
Scores presence or absence of each of 19 wound attributes. "good for healing" or "not good for healing" and other factors. Measures change by noting change from "not good" to "good for healing" attributes.
Tools To Measure 110 ulltillealillg
Table!>-2 Historical Measures of Pressure Ulcer Improvement Measures Change in ulcer size
Definitions
• Area (length x width) • Depth (for volume) • Perimeter/circumference
Surface appearance
• Red
• Yellow • Black Tissue type
Surrounding skin characteristics
105
tial. Both tool s are in various stages of development and th e ir reliability, validi ty, responsiveness, se nsitivity to change. and clinical practicality for monitoring wound hea ling are still to be determined. There are simi larities in some aspects of the tools: both 100is eva luate tiss ue attributes of the wound and surrounding skin. Methods of evaluat ion and scoring are different. A t thi s time, ncither author knows for certai n that a ll items li sted in the tools are useful. The processes of devclopmcnt and application of the two tools will now bc presented .
• Necrotic • Granulation
• Epithelial • Singly or in combination • Erythema (color change) • Edema • Undermining or Tunneling
$ource.- Sussman C, Swanson GH . The utility of Sussman Wound Heating Tool In predicting wound healing outcomes in physical therapy. Advances in Wound Care , September 1997.
Re/i"hilily
Rcliabili' y Orn tool is its ability to be used with minimum error. There are seve ral kinds of reliabilit y tests for a tool. Intrarater reliability means th at the sa me raler gets the same sco re with repeated measurements . Interraler reliability means that two or more individuals get the same results after administering the sa me instrument. Re!11JOIIS;,'ellesslSeJlsili'lily 10 ChaJlge
Responsiveness or sensitivity to change is the next test criterion for a tool. An appropriate tool or method must be ab le to detect changes in the condi tion of the wou nd over time with repeated administrations. CIi"iclIl Pmclicllfily
Cl in ical pmcti ca lity mcans the tool mu st be simple, easy to learn and to use with clear instructions, and must be reliable with the sa me and multiple lIsers. It must be time efficient and cost effective.
Two Tools To Monitor Wound Healing This chapter desc ribes two tools to monitor wound healing. the Sussman Wound HealingTool (SW HT) and the Pressu re Sore tatus Tool (PSST). each developed by one of the authors of this chapter. Both c linicians recognized many years ago that the ability to monitor hea ling ou tcomes was essen-
SUSSMAN WOUND HEALING TOOL Introduction and Development of the S ussman Wound Hcaling Tool The SW HT was developed by Sussman and Swanson' as a physical th erapy (PT) diagnostic tool to monitor and track the effec ti veness of PT technologies used for press ure ulcer healing. The ability to predict pressure ulcer hea ling and treat ment outcomcs in PT has yet to be done reliably. The monitoring and tracking of healing and treatment outcomes is essentia l for clinical decision making and triage and provides payers and providers improved utilization management. The basis forthe SWHT is the acute wound healing model (see Chapter 2) that desc ribcs the changes in tissue status and size ove r time as the wound progresscs through the biologic phases of wound healing. Some atlributes of the wo und that are observed during each phase are considered related to failure to heal or " not good for healing" and others are co nsidered indicators ofimprovcment or "good for hea ling." For example, a tissue attribute such as necrosis is thought to be negative or not good for healing. whereas wound attributes such as granu lation tissue, which represent s fibroplasia. and ad herence of the wo und edges are cons idered good for hea ling. The concept of the SW HT is to benchmark the wound attributes as it recovers and progresses throughout the healing phases. For example, the "not good" attribute, necrosis, sho uld change over time from preselll to abselll. thus moving from "not good for healing" to "good for heali ng." The "good for healing" attribute, fibroplasia- significant reducti on in depth , sho uld be g ranul ation obse rvcd as th e wou nd heals and changes from absem to presef1l, in-dicating improved tissue status. The initial design of the SWI-IT is a qualitative instrument. meaning that a wound would be described a s having certain ti ssue atlributes. Subsequcntly, th e tool wi ll be refined an d each SW HT variab le will be measured. weighted. and ranked to produce a quantitative tool. In total , 19 attribut es are defined. It is composed of 10 wound attribut es combined wit h 9 descriptive attributes of size. extent of tissue damage plus loca ti on. and acute wou nd healing phase. wh ic h are not
106
WOUND CAR'·
measurable. The 10 wound tissue attributes described were each ass igned a score as prese/JI or abseil! and ranked as /lot good or good for healing. Five attri butes ranked as 1101 good
include hemorrhage. maceration, erythema, undermining. and necrosis. Five attributes ranked as good include adherence at the wound edge. fibroplasia, appearance of co ntrac-
tion , sustained contraction, and epithelial ization. The lists defining and describing each attribute are shown in Exhibit 5- 1. S uss man \Vo und Hea lin g Tool Attribute Definitions Purl I: ThislieAllribufes
The first five attributes described are classi fied as "not good for healing" and the second five listed are classified as "good for hcaling:'Thc "not good for healing" attributes arc
all related to the inflammatory phase of healing.The att ributes that are "good for healing" are re lated to the proliferation and epithelia liLation phases of healing. As the wound at-
tributes change from "not good" to "good" the wound is progressing th rough the phases corresponding to those of (lcute wound healing. I. U emorrllllge. Hemorrhage is defined as a purple ecchymosis of wound tissue or surrounding skin (see Color PI"tes 65 "fld 68). The color plates show the deepening of
tissue color or distingui shable purple ecchymosis whic h is an indicator of significant subcutaneous bleeding or hemorrhage. Wounds with hemorrhage have high probability of tissue death and thus enlargement of the wound. This attribute is classi fied as "not good for healing."
Clinical Wisdom: Assessment of Hemorrhage
3. Ultclermill;IIg/Tlllllle/illC. Underm ining is defined as erosion under the edge of the wound and tunneling is defined as separatio n of the fascial planes leading to sinus tracts, Locat ion of undermining for thi s attribute means undermining at any location arou nd the wound perimetcr. Color Plates 37 to 39 show wounds that arc underminincd or wit h tunneling . The ex tent of the undermining/tunneling is not recorded or included as part of the assessment. on ly the presence or absence of this attribute. If undermining is present, it is an attribute that is classified as "not good for healing:' 4.
£~"Ilrelllll,
Erythema is defined as reddening or dark-
ening of the skin compared wi th surround ing ski n. Erythema following trauma is due to rupture ofsl113 11 venu les and capillaries or may be caused by inflow of blood to start the innammatory process, or both events. Disti nguishing between the two is oftcn difficult. Erythema is usually accompanied by heat. but it may be accompan ied by cooling. indicating dcv italizat ion of tissuc. lU Di stinguishing and assessing erythema in darkly pigmented skin is described in detai l in Chapter 3 (see Color Plate /9). The abi lity to sec the mar-
gins of the change in sk in color is enhanced by lighting and may be seen morc easi ly in a photograph than in the living tisslles. especially in very dark skin tones. Color PI"te.l' 6. 14. "fld /5 show erythema in both lightly and dark ly pig-
mented skin. Erythema is an attribute that is classificd as "not good for hea li ng."
Clinical Wisdom: Differentiation between Erythema and Reactive Hyperemia
Erythema should be assessed after pressure has been relieved from the area for about 20 minutes so as to eliminate effects of reactive hyperemia.
Triggers Further Examination
The presence of hemorrhage would be a trigger for further examination, including temperature testing as described in Chapter 3 to determine tissue vitality. Hemorrhage may trigger vascular consultation. The chapters in Part IV on electrical stimulation, pulsed short wave diathermy/ pulsed radio frequency, and ultrasound describe how these interventions promote absorption of hemorrhagic materiaL
5. Nec:rosis. All types of necrotic tissue, including eschar and slough, arc included when assessing for presence or absence of th is attribu te. Necrosis is defined as dead devitalized tissue. Color may be black, brown, gray. or yellow. Tex-
ture may be dry and leathery, soft, moist, or stringy. Odor may be present or absent. To determine if the tissue being assessed is necrotic, see Chapter 7. Management of Necrotic Tisslle, and Color PI(ltes 3, ]5 to 30. 46, (If1d 47. One com-
2. A1(1('erlltiolt . Maceration is defined as a softening of
mon error in assessing necrotic tissue is to assess all yellow and wh ite tissue as necrot ic. Yellow ti sslle may be either
connecti ve ti ssue fibers by soak ing un til they are soft and friable ." Macerated tissue loses its pigmentation. and even
a tendon . White tiss ue may be connect ive ti ssue. fascia. or a
darkly pigmented skin looks blanched. Th is weakened tis-
ligament. Color PI(lte 13 shows healthy yellow and white
sue is highl y susceptible to trauma, leading to breakdown of the macerated ti ssue and enlargement of the wound. Maceration is an attribute classified as "not good for healing."
tissue. Healthy tissue usually has a gleam not seen in devitalizcd tisslle. Note, however, that the topica l treatmcnt or exudate is not the source of the "gleam." Ilcalthy tissue is
healthy ye llow fa t, the rcticular membrane of the dermis. or
107
Tools To A1easlire WOllnd /-Iealing
not friable and has resilience whe n compressed. Dead tissue tears and does not spring back when compressed. Waiting 24 hours helps to sec if the ti ss ue c hanges color to gray or
brown. indicating loss of vital it y. Reassess. Necrosis is an attribu te that is classified as "not good for healing."
6, Al/herell('e af WOIIIU/ El/ge. Adhere nce at the wound edge means that there is continuity of the wound edge and the base of the wound at any location along the wound perimeter (Cnlor Plales 8, 9, 56, alld 57), A partial-thic kness wound will be adhe red at the wound edge by definition, A
full-thickness or deeper wound will have closed by either granulation or contraction to the point whe re some area of the wound edge will be even with the skin surface. Some wound edges curl under because of epithelial migration over the edge of the wound. Thi s can halt wound contract ion and lead to fibrosi s of the scar tissue. Edges may not adhere when this occurs. and wound healing will not proceed. Adherence of the wound edges is an attribute that is classi fied as "good for healin g," 7. Grtlllll/afitm Tisslle (Fibroplasia-Sigltijic:allf Rel/Ilcfioll ill Depth). Granulation ti sslle formation or fibropla sia
is the action of the fibroblasts laying down collagen matrix during the proliferation phase of healing. The collagen matrix fills the wound.. causing a measurable or significant redu ction in wound depth . For determining the presence of fibroplasia signi fi cant reduction in depth. a linear measurement of thi s attribute is required (sec Chapter 4), A signifi-
cant reduction in depth is at least 0.2 em si nce the prior assessment. Color Plates 7 to 9 show a significant reduct ion in depth. Granulation is an attribute that is classified as "good for healing:' 8. AppellrtlllCe o/Confracfion, The appearance of contraction is defined as the first measurement of the wound drawing together, resulting in reduction of wound open surface area size. 'ompare Color Plate 3 with Color Plares 4 lind 5 to see the onset and progess ion of contraction . It is identified by a change in wound open area size and may be identified as a change in wound shape (eg, from irregular to symmetric, such as the circular or ova l formation and rounding ofT the edges of the wound seen in pressure ulcers; see Color Plate 2). This item is scored at subsequent assessments as the contraction continues or ifit has stopped. Irthe wound enlarges, however. this itcm wou ld change from present to absen t, and a new appearance of contraction would be required to have a score of "present" again. When present, adherence at thc wound edge is an attribute that is classified as "good for healing."
9. SlIsfaillell COllfrlU:lioll, Sustained contraction means there is a continued drawing together of the wound edges that is measured by a reduction in wound surface open area size. It is usuall y accompanied by a change in wound shape.
Color Plales 3 10 5 show the same wound as it goes through wound contraction . Sustained contraction is scored 0 at the appearance of the contraction benchmark and then scored I at subsequent reassessment following the appearance of contraction. Occasionally something interferes with the wound contraction and the wound does not reduce in size or increases. Thi s attribute would be marked O. absent, if the wound size docs not reduce or enlarges after the appearance of contraction. Sustained contraction is an alLribute that is classified as "good for healing,"
/0. Epifhelill/;Zafioll. Epithelia liza tion refers to the appearance of and continuation of resurfacing of the wound with new skin at the wound edges or surface. Color Plate 5 shows the sa me case as Color Plates 3 10 5, now in the epitheliali za tion phase. Epit helializat ion may first be noticed during the innammation or proliferation phase of healing as a lightl y pigmented pink ti ssue, even in individuals with darkly pigmented skin (Color Plates 7 10 9), In partial-thickness wounds, the epithclia l cells may migrate from islands on the wound surrace or from the wound edges. or both. Color Plales 55 alld 56 show an example, Full-thickness and deeper wounds have epithclial migration, usually from the edges only, Color PI",es 5 alld 6 show the sa me full-thickness wound as seen in Color Plates 3 and 4, that is, resurfacing rrom the wound edges. Many peo ple confuse new bright pink scar ti ssue or skin as erythema. Color Plate 22 shows new pink scar tissue in a person with darkly pigmented skin. Epi thelialization is an attribute that is classified as "good for healing." Parf II: Size Locafiollllllli H'oUlli1 Healillg Pllase Measures
Wound depth and underminin g indicate extent of wound. If a wound has a depth less than 0,2 cm it is scored as
°
at all
four points and at general depth . Depth and undermining are two indicators of "'not good for healing." 1/- 15, W"'/Ild Depl", Five items on part I! o f the SWI-IT arc related to presence of depth of 3t least 0,2 c m both in ge neral depth and at the four points of the c lock. 12-. 3-. 6-, and 9-0'clock posi tion s, Depth is meas ured as desc ribed in Chapter 4 , and if it is at least 0,2 c m it is recorded as
present. Extent of depth is not significant for this assessment as lon g as it is at least 0,2 cm, (Sec Color Plales 2, 7, 27, alld 30 for full-thi c kn ess depth ,) /6-19. TUllllelillglUllllermillillg. Undermining and tun-
neling are measured at a ll four points of the c lock. like depth ,
However, the objective measure used to report this attribute is also present or absent. With further testing and analysis this attribute may prove to be redundant with part I. For the present time. it remains a part of the 1001.
Additional Descriptille Attriblltes 'Yound Locution. Wound location is noted as the anatomic description most closely related to the wound site. Because lower torso and lower extremity wounds are most frequently seen, the locations have been broken down into th e common sites for chron ic wounds and they have been clustered together for the upper body. Letters are also used to represent Ihe wound local ion: UB ror upper body, C ror coccyx, T ror troc hanler, I ror isc hial. " ror heel , and F ror root. Wounds in other locat ions can be added to the list if they are commonly seen in the practice setting by using letters on the rorm and adding a local ion descriplor 10 Ihe key (eg, K = knee, A = abdomen, Til = Th igh). One needs 10 be sure 10 include Ihe side orlhe body where Ihe wound is localed, righl or left, by putting an R or an L next to the location leHer. Wound location has been shown to be an indicator of healing. However, the specific locations that indicate healing are slillio be delermined . I¥ol/nd He(lfillg Phase. The wound healing phase refers to the four biologic pha ses of wound heal ing: inflammatory. proliferative. epi th elializa tion. and remodeling. Letters are used to repre sent the current wound healing pha se: I for inflammation, P for proliferation. £ for epithelialization. and R ror remodeling. As described in Chaple r 2 Ihe wo und hea ling phase may be chronic, acute, or absent. A letter is placed berore Ihe phase suc h as Ihe leller C be rore Ihe phase ror chronic. no letter before acute, or the letter L for lacki ng or absent can be used as modifiers of th e current phase. A change in pha se over time is an expected outcome. Chronicity of a pha se should change to an active state of the pha se followcd by progre ssion to the next pha se in the traj ectory. Absence of a pha se indicates need for investi gation as to why thc pha se has not been achicved. This itcm is listed but unscored. Tesling Ihe SW HT One or Ihe rirsl questi o ns applied 10 Ihe SW HT was whether a tool design based on the four phase acu te wound healing model could be applied to chronic wounds such as pressure ulcers. The SWHT is in Ihe process orbeing lesled on a dala sel or I 12 pressure ulcer cases. All or Ihe palienls who were included in the dataset were long-term care residents with prcssurc ulcers. Many experts consider pre ssure ulcers to be chron ic wounds from the time of ol1set.The ana lyses are as yet incomplete.
SWNT for MOllitorillg (Illd Trackillg WOIIIll/ fleldillg The utility of the SWHT in the clinica l setting for monitoring and tracking healing is easy and practical. Each of the
allribules orl he SWHT is scored ir lissue allribules or Ihe wound or surrounding skin are present or absent. The total number orpresenl (I) "nol good" ror healing allribules shou ld diminish as the wound heals, and the total number of prese nt (I) "good" ror healing attribules should increase in number. Change of score measures the change in hea ling and reduced severity of the wound. The scores are al so useful for measuring the level orhea ling indiealing progress. lack orprogress, or regression or healing. The SWHT has proven ulilil y bOlh as a diagnoslic loollhal difTerenliales phases by assess men I of healing attributes and as a tool for measurement ofcJulIIge in ti ssue statu s (eg, ti ssue attribute) and size (eg, change in deplh and undermining) over lime. Thus, Ihe SWHT is designed to monitor and track healing based on the acute wound healing model , and can be applied to acute or chronic wounds such as pressure ulcers.
SWNT Reliability alld Practicality The SWI-IT has been clinica ll y lesled ror reliabilil Y and clinical praeliea lily by phys ieallherapisls and physicallherapi sts ' assistants working in a long-term carc faci lity during ils 5 yea rs or developmenl and round 10 be very reliable ror monitoring and trackin g healing and nonhca ling ofprcssure ulcers. It relies primarily on visual observation skill s. No linear measurements, arithmet ic calculations. or estimates of amount of ti ssue characteristic present arc required. To health care proressionals who treal wounds. Ihe SWHT information communicatcs clea rl y wound progress or risk. Documentation is very simple and outcomes arc visual. For example, it takes the clinician about 5 minutes to complete the assessment. In a trial educat ional session to train new learners 10 use Ihe WHT, a group or 10 physicallherapisls and physical th erapists' assistant s who recei ved I hour of training in the classroom using verbal description and photos 10 teach the method of assessment and definitions of the attributes, fo llowed by 1 hour of clinical pract ice on pressure ulcer patients. learned to use it well. An'essmenf o!Tre(/fmenf Ollfcome~'
Assessment of treatment outcome was the initial reason ror developmenl orlhe SW HT. Mosl palienls arc rererred 10 Ihe physical Iherapi sl by Ihe nurse ror treatmenl arter conventionaltreatI11ents failed to heal the wound. To qualify for an intervention by the phys ical therapi st, the patient and the wound often need to meet a criterion of 110 progress or regression or a halt of healing. Therefore, it is critica l for the physical th erapist and the nurse to be able to set target outcomes and then assess the response to the treatment intervention. A wound assessed with the SW HT as nOI progressing after a course of conven ti onal care by the nurse would meel Ihe crileri on ror referral. Once rererred, Ihe SWHT is use ful for rcporting wo und outcomcs associated with the
Tools To A1ellsllre Wound lIealiug
intcnelllion prescribed by the physical the rapist. s uch as physica l therapy technologies. Response to treatment with these interventions shou ld demonstrate co nsistent c hange in tissue status that co rresponds to th e biologic model for acu te wou nd healing. A change in ti ssue status benchmarks th e heal in g process and becomes a ta rget functional o ut come for reporting purposes. such as the wou nd w ill be hemorrhage free. undermining free. nec rosis free. and so forth. Reviewers ca n quickly determine a c hange in wound tiss ue status during the co urse of care because. as already descri bed, the wound attribul cs sho uld change fro m those "not good for healing" to those "good fo r hea ling."
6.
7. 8.
Usin g th e SW II T
Two Pllrl.' o/SWU T Exhibit 5 I ,how. th e two pans of the SW ill' The SWI IT is a paper-and-pcncil instrument comprising 19 attributes. Part I is th e coll ection form of 10 tissue att ributes. Part II is the list of II other attributes, inc ludin g ex tent. location. and \\Olilld hea lin g phase. All items on the SW HT arc scored c'(cept locatio n and the wo und hea lin g phase. Omission ofa score indicates th at the assessmen t was no t comp leted. Sco ring begins at baseline. week O. The meth od of scoring for the tool is a number I fo r present and a 0 for absent. This reporting format is readily compatible wi th comp utcr tec hnology and simplifies using the tool to build a database such as the one described later. Completi o n of the form rcq uires understanding of the dcfini tions for each of the scored itc rn s (see Exhibit 5 2 for definitions of att ributes). The aSsessmcnt process is visua l except for detcrmining the presence of undermining tunneling. which cannot be seen at the surface. and Il1ca~urement of the open surface area of thc wOllnd.
Proteilllre/or Usil/g I/l e SWII T (see Ex/libil 5- 1) Compl etion of th e Wi lT is by observa tio n an d physical assessment, as follows : I. Each wo und of each pa ti en t needs its own SW HT attrib utcs forl11 . 2. The patient's name a nd medical record number and da te ofasscssmcllt are wrilten at the top of the form . 3. The examiner has a place to sign the document. 4 . As the wound is assessed. th e rarer marks a I or a 0 to signify present or abscnt on thc form nex t to each of the 19 attributes. The squares in the co lumn must be marked \\ ilh one of the two scores. 5. The wo und l oe~lt i on a nd the current wo und hcaling phase arc marked wi th the appropriate letter. Choose the appropria te letter to represent thc ana to mi c loca-
9.
I O.
109
tion of the wound and place it in th e squa re at th e time of the ini tial assessmcnt and subscquclll reasscssments. The locat ion will not change. Letters are a lso used to reprcsent th e current wound healing phase: mark a nI fo r innammati o n, P for proliferatio n. £ for epilh e li aliLa ti on. and R for re modeling. In the a ppropriate box, th e phasc is no ted ini tially a nd at eac h rea ssessment. The wound hea ling phase sho uld chan ge as th e wo und hea ls. Undermining and depth require some physica l assessme nt to determine prese nce or absencc. Open area measurements a rc Illade and li sted o n a separate form (see Chapter 4) and thell co mpared wi th subsequent measurements of these cha racte ri sti cs to detennine contraction and sustained co ntraction. measured as reduction in linear si/e. Scoring part L Add th e number of·· not good for hea ling" at tributes and the number or"good for healing" attribut es li sted. The sco re of "not good for healing" shou ld diminish as the wo und hca ls. and th e sco re of " good for hea ling" attrib utes shoul d increase. A grap hi c representation o f the chan ge is show n in Ex hibit 5-4.
SW I·/T For ms
Two SW HT forms arc shown (Exhibits 5 2A and 5 28). Part I of th e long form (Exhibi t 5- 1) contains the 10 ti " ue attributes. listed in descending o rder ofse\e rity. next to definitions. followed by a co lumn li sting th e rat ing option for the attribute as present o r nOI present. The ncxt column ranks the relatio nship to hea lin g as " not good" o r ·'good ." The last column is where the rating is listed as a score of present or absent. Part II li sts measures and ex ten t. The same scori ng syste m of"p rese nt" or "absent" for 19 attributes o f ex tent is appli ed. The attributes a re th e ge ne ral depth of grea ter than 0.2 e m, th e dc pth at th e four c lock poi nt s. and unde rminin g at the four clock po ints. Date and week of care sho uld be noted o n th e form . The benefit o rlh e lon g fo rm is havi ng the definitions on th e form. This wou ld be he lpful to a nurse or physical thcrapist learning th e system o r for medical reviewers and surveyors looking for information abou t th e rating system used for documentation.
Short Form The short form (Ex hib its 5 2A and 5 28) of the S WIIT is thc same as the lo ng form except that th e sho rt form lacks the defi nit io ns printed o n the forl11. T he sho rt form lists o nl y the attributes and has co lumns to record data for Illultiplc
Elhibit 5-1 Long Form SWHT o Sussman \\ound lIealing Tool (S\\ Hn \\OL '0 ASSESS'IE'\T FOR;\I
=E
o
'A'IE, _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ ___
\IEDIC \L RECORD
O\TE' ____________________
~O.,
_ _ _ _ _ _ __
EXA \II\"ER: _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ __
L Z
",." ~
CIRCLE \\ UK OF CARE, S\\'IIT
Tiss ue Attribute
\ariablc
2
B
3
~
5
6
7
Altribute Definilion ecchYlllosi~
8
9
10
II
12 Relationship 10 Healing
Rating I)rcsent or absent
Not good
Softening of a tissue by soaking until the connectiw tissue fibers afe soft and friable
Present or absent
Not good
UndcrmlRlng
Includes bOlh underOlimng and tunnding
Present or absent
Not good
~
Erythcltlj
Reddening or darkening of the sJ..:in compared to surrounding skin: usually accompanied by heat
Present or absent
i'l'ot good
5
""ecrosis
All types of necrotic tis:-.uc. includIng eschar and slough
Present or absent
1\1ot good
6
Adherence at \\ound edge
Continuity of wound edge and Ihe base of the wound
Present or absent
Good
7
Granulallon (Fibroplasia significant reduction in depth)
Pink red granulation tissue filling wound depth
the wound bed reducing
Present or absent
Good
8
Appearance of contraction (reduced size)
First measurement of the wound drawing together. resulting in reduc tIOn in wound open surface area
Present or absent
Good
9
SusUlined eontmctiol1 (morc reduced sile)
Continued dmwing together of wound edges. measured by reduced wound open surface area
Prl!$ent or nbsent
Good
EpithelialiLation
Appearance and cOnllllualiOIl of resurfacing with nc\\ skin or the wound edges or surface
Present or ab:;cnt
Good
I
Hemorrhage
Purple
2
\-Iaceratlon
3
10
of wound tissue or surrounding skm
10
~car
at
Score
',EASURES A1\D EXTE;r.,'T (Depth and Undermining: 'ot Cood) Oepth/ Location
SCORE
L nderminingi Location
SCORE
12:00
Other
II
GenerJI depth -·0.2 em
16
Underm
'll
12
Geneml depth
17
lindcrm
(j
3:00
Wound healing phase
13
Geneml depth a 3:00 >0.2 em
18
L:ndcrm
/L
6:00
Total "'Jot Good"
14
General depth
1I
6:00 >0.2 cm
19
Lnderrn a 9:00
15
GencrJI depth
(t/
9:00 >0.2 em
ill
12:00 >0.2 cm
-
Leiter
Location
TOlal "Good" -
---
--
Key: Present - 1. \bscnl - O. Location choices: upper body fUB). coccy\: (C). trochanter (T), ischial (lJ. heel (II). loot If): add right or left (R or L). \Vound healing phase' Innammalion Ill. prollfcration (Pl. epitheli.llizalion fE). remodeling tRI. SO/lrcl'.
Copyright
i:'"
1997. Sussman Physical Therapy Inc.
Tools To Measure It blfllll /-Iealillg
II I
Ex hibit 5- 2A SWIIT Short Form Parl I: Wow,d Tissue Allributcs
Namc: _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ Mcd Rec # ________ Examiner: _ _ _ _ _ _ _ _ _ __ \Vct'k
0
I
2
3
4
3
4
I. Ilclllol'rlm gc
2. Ma ceration
3.
Undcrll1inin~
4. Erythcma 5. Necrosis
6. Adherence 7. Granula tion (decreased deth)
8. Appearance of cOlllraction (Reduced size) 9. Sustained contraction (More reduced size)
10. Epilhcliali7tHion Total NO{ Good Total Good Key : Prc . . cnt SOI/I"/.·(':
1 Not preSC11I
CopY right
I
O.
1997. Su . . . . man I'hysical Thcr:tpy Inc.
Exhibit 5-28 SW II T Short Form Part II : Sile. Location. Wound lI ea llll g Phase Measures. and Extent
Date
0
I
2
II. General Depth >0.2 ern I:!. Depth ((/ 12:00 > 0.2 em
13. Depth (a l 3:00 >0.2 em 14. Depth
(ll
6:00 >0.2
CIll
15. Oqllh «(/ 9:00 >0.2 em 16. Undcrrn (al 12:00 >02 ern 17. Undl.!rrn (a l 3:00 >0.2 ern 18. Undenn ({II 6:00 >0.2 em 19. Undcnn
(ll
9:00 >0.2 em
Location Wound healing piw"c K\.'y: Present I Not prc:.cnt O. Location choices: upper body (UB). coccyx (e). troch:Ullcr (T). ischial (I). heel (I I). lllld foot (F); add right or len (R or L) Wound healmg ph:tsl.! : :lbsent (A). chronic (el, inflammation ( I). proliferation (P). epithelialization (E), remodeling (RI. S{l///'('(':
Cupyright
c'
1997. $us-;man Physical Therapy Inc.
W
112
Exhibit 5-3 \ SW II
r Part L \\iound Ti,<;sw..' Allnbutcs
\\ ee k DatI!: 20 10
I-f-
2
17
)114
J
4
I 11
I':!X
14
I kmorrhagc
I
()
0
()
()
2.
Maecrcltlon
0
()
()
0
0
0
()
I
I
I ()
3. Undermining
I
I
I
(I
I
I
I
0
()
()
()
0
I
1
7. (iranulallon (decre:J'<;cd depth)
0
0
I
I
1
H.
\ppcarance 01' con tract ion (reduced .., 17e)
()
()
I
I
I
9
Su'>talnl!d contraction (mon: reduced sil"l!)
()
(I
()
I
1
I· pJthcllalll" ..lt iol1
()
()
0
I
I
Total "Not Good "
J
2
J
I
I
Total "Good"
()
(I
2
5
5
4 I ryt hema f--5. NeCrthlS f--6. Adherencc
f-
1
I
I---
-
0
r----u,
I\.ey:
Prl'\l'nl
I. \b\l! 1I1
0.
S"un'(' Cupyright, 1997. SII\\milll PhY'l!;ill Therap) Inc.
[,hibil 5-38 SWIIT Part II : Si/c, Location. Wound lI ealing Phase Ml!a'<;un.:'<;, and Lxtent
Wee k f) .. tte: I-- II General depth '0.2 cm
I---
I
I 7
2
I
I
1'14
I
1,'21
J
I
12X
I
2~
0
I
I
I
12:00 '0.2 elll
(I
I
I
I
I
I
I
I
I
I
--
Depth
(a
I J.
Depth
(a
J:OO >0.2
CI11
0
14
Depth
(a
6:00 -0.2 CIll
0
I
I
I
I
Depth 'a 9:(10 '0.2 ern
I
I
I
I
I
0
0
I
I
(I
CIll
0
I
I
(I
0
Unde rm (a 6:0(1 ·().2 ern
0
I
I
I
()
0
0
I
I
I
RT
RT
RT
RI
Rl
I
I
I
r
I'
12
I--15.
16. Undcrm
-
0
17.
fll
12:0(1 '0.2 em
Undcrm (a 3:00 '0.2 ---
I X.
r- 19
f==
--
lindcrm
III
t):()O ·O.:!
Loc ..tlion f--Wound healing phase
Clll
I\.ey: Prc\cnt I Nnt prc\ent II LOI.:;ltlon cholee\: upper body (UD). eocc)\ «("). trochanter ( rl. I,clual (I), heel (II) .•lIld font ( I ): add nght lert (I< or I) \\Ilund healing pha\e' IIIllaml1l;1tlon (II. prolllcfUllon cPl. cplthchalil"atlUll (II. remodeling (R)
(If
Tools To A1ea.w re WOllnd Ileating
weeks. Part I can be printed on one side and part II on the olher and the paper can be CUI to rit in a small pocket-size 4 x 6-inch looseleaf notebook . Printing the forms as a pad punched with a hole paltern to match th e notebook makes it easy and convenien t to keep forms on hand . A printed set of the definitions and scoring can be printed on the same size paper and then kept in the notebook for reference . The notebook functions most smoothly ifan alphabetic index the size of the notebook is used. The wound progress notebook can then be kept like a nursing treatment record book with records alphabetica lly riled . The current patient wound healing records would then be readil y available. The benefit of the notebook is Ihal it will usually fit in a lab coal pocket and can be carried to the bedside or home. In a facility, like the treatment record book. il can be kept at th e nurses' stalion. when not in usc. for easy reference. An additional benefit of the short form is that it is easy to sec a comp lete hi story of the change in tissue status over l11ultiple weeks of assessment. Reading the report over time provides a quick and clear eva luation to 1110niror wound healing progress. Exh ibits 5 3A and 5 3B show a completed case rccord . At the time of discharge or monthly the completed record of wound attributes is then taped in ti ling fashion like telephone order prescription sheets onto a sheet of paper and filed in the medical record .
I 13
elise Exumple Usillg til e SIVII T Exhibits 5- 3A and 5- 3B show an example ofa case where wound healing was monitored over a 5-week course of care as reported on the shon form of the SWHT pan s I and II. A summary, Exhibit 5-4, of the case example shows how the SWI-IT can be used to document a change in wound tisslle status from a predominance of "no 1 good for healing" to a predominance of "good attributes." Exhibit 5 rencct s the following : • The patient had the presence at baseline. week 0, hemorrhage. necrosis. and erythema. and absence of any attributes "good for healing." The presence of these attributes at ba seline is an indication that thi s wound wi ll need aggressive intervention to improve. • At week 2 there were multiple attributes that were imticators that thi s patient wi ll be in the "risk for nol healing" group, including undermining and depth at all four clock point s. funher indicating the medical necessity for aggressive intervention to put the wound on a course of healing. • Ass uming that aggressive intervention was undertaken al week 2, the improvcment in the wound tissue stalus from " not good" to "good" is significant by week 4.
S uss ma n \Vound H ealing Tool Database
Clinica l Wisdom: Use of Forms for Wound Measurement along with the SWHT Since wound measurement and tissue assessment or reassessment are usually done at the same time it makes sense to record the information in the same record book. A wound measurement recording short form that fits in the same notebook as the SWHT meets this need. This form is used to record the size, depth, and undermining linear measurements. Each week a new measurement form is added behind the SWHT form . By having the two forms together in the notebook the examiner can check at a glance to see whether there is reduction in depth and open area. Chapter 4, Exhibit 4-1 , shows a sample wound measurement form designed to fit this model.
Although the SWI-IT is a paper-and-pencil instrument , the SWI-IT wound database is maintained in a computer. The scoring system of using a lora 0 is computer compa tible for data managemcnt and data en try. T he SWI-IT form s are printed on the compu ter as screens, and data are entered either prospectively or retrospectively. Data report s can be printcd and the captured data can be analyzed on an individual patient basis or by group. Further testing of the SW I-IT is planned at different sites.
Summa ry Physical therapists and nurses can utilize the SW II T present/absent scoring system 10 triage Ihe case, guide treatment interventi on, and repon functional outcomes. The SWHT is a simp le, easy-to-follow, and comp lete documentation system that provides payers and providers improved utilization management .
11 4
WOlNDC\RI
E,hibit 5-4 SUlllmary of Wound Attribult! Change o\er a Five-Week Course orCarc
\\ EEK 2
\\ EEK 0
\\ EEK 4
"NOT (;000 "./or/u.'ttfiflK
"NOr GOOD "Jor healing
".vOT GOOf) ",or healing
llcl11orrhagt!
Nccro!'ils
UnderminIng
Undcrlllllllng
UnderminIng
Depth 12. 3. 6. <):00
l~ rythcl1ln
Undermining 9:00
Erythema
Necrosis
Deplh 12. 3. 6. 9:00
Deplh 9:00
Undermining 11. J. 6. 9:00
"GOOf)" j(u' /wulillg
"GOOf) " Ii),. healing
"GOOf)" Ii),. hetllillg
None
FibroplaSia
"'Ihropla..,m
ApPc<'lrancc of contraction
Appearance of contraction
Sustained
COlllraCllon
Adherence
Fpllhcliali/ation /l{J/lI/(IIIl'tllillg plw\(1
IfiUlfltl he·alill}.! "I/alif!
HtJ/{m/ IWlIli,,}.{ "lwH'
Inflammation phase
Innammatlon phase
Proll fcralloll phase
SOlin"
Cnpynght ( 1997. Su ... ~Ill"n Ilhysic,ll Therapy. Inc.
TilE PIlESSUIlE SOIlE STATUS TOOL Introduction and Development of the Pressure Sore Status Too l The Pressure Sore Status Tool (PSST) is a penctl-and-paper instrument comprising 15 itcms (see Exhibit 5 5). Two items that are not scored arc 10c.Hion and shape. The remaining 13 items arc scored and appear with descriptors of each item rated on a modified Likert scale (I being the healthiest attr ibute of that characteristic and 5 being the worst a\tribute of the characteristic). The tool has a one-page sheet of instructions for u~c in addition to the item descriptions (Appendix 5 A). The PSST "as de,eloped to measure wound healing in pressure ulcers based all a clinical and research need in thi s area. The items on the PSST were de,eloped through the usc of experts participating in a modified Delphi panel. The COIltent va lidity of the tool was established with the lise of a nine-member expert judge panel (mean overall contenl nllidllY index 0.91." 0.05). Reliability "as demonstrated
on adult patients in an acute care hospital with enteroslomal therapy (ET) nurses. The mean inlerrater reliabi li ty coefl'icient was 0.91.11 Intrarater reliability estimatcs yielded a mean of 0.975. Although high re li ability estimates had been established with ET nurses. a question remained as to the emeaey of the tool's usc with practitioners who did not have extraordinary education or experie nce in wound assessment and management. The issue of re li ability of the PSST when used by "regular" health care practitioners was addressed in a long-tcrm care facility. Fifteen practitioners participated in the study. Their educational background and experience with wounds varied. Two physical thcrapist:s. three licensed practical nurses. and 10 registered nurses participated in the study. Pairs independently assessed 16 wounds across a broad spectrum of seventy on two occasions (2 hours apart). An expert ET nurse also independently assessed the same wounds as the practitioner pairs. Interrater rcliability estimates were calcu lated between practitioners thcmscl\'cs and between practitioners and th e cxpert rater. Int rarater relmbility estimates \\crc calcu lated in a simi lar manner except that each raters recordings were compared with a second assessment
Tools TiJ A1easure H'tJIIl1ll llealilig
I 15
E:\hibir 5-5 Pressure Sore StailiS Tool Form
PRI:SSURI' SORI S r\Il,S lOOL Complclc Ih~ r:lling ... h~et 10 .,-':,ess rm:-,:sure sore Maills. ...core 111 the Hem ...curl' cui ullin fix the appropriate date Loc:uion: AnatomiC ... ite . C'irde.
id~lltlry
Laterul ankJc Medial ankle Ilcel
Shape: O",:rall wound pattern; as<.;e ..." by ubscn ing Circle Jnd dale appropriate dl.: ...cnpllow Irrl.:g.ular Roun.J 0\:11 Squilre rectangle
1
"1 4
5 J)..:pth
1 ~
)
4
;
).
I t.lge,
1 ~
1 4
; 4
LJIldcr1ll11llng
1
2 1 4
;
;
Necrotic !'is... uc fypc
I ~ )
4
5 (>
Necrotic TI,>sue -\mount
Otl1l'r ,ile
perimeter :tnd depth I mear or elongated 130\\ I boat
Olher shapc _ _
BUllcrny
Asse:.slltrnl
Ilrllt
,
by pic"ing Ih~ re:.ponsc Ihat best tl~scribes the wountl,lIld cnh.:nng the
right (R) or lel1 (L) allli u... c "X" to mark site on body tlmgrarns :
S;lerUI1l :md ('()C;eyx Trochanter !sehi .. 1 tuberosity
1 Si/c
haillal~ ~ach it~m
1
2 )
4
;
Date
Hatr
Date
Score
~corc
Score
Length widlh'4 t:m Length x width ... 16 em: Leng.th width 10.1 36 em Length x width 36, t ~() cm; Leng.th wiJlh >HO cm~ Nonblanchuble crythcma on inlact ,,"til Partial-thie"ne ... s skin It)s~ in\'oh mg epIdermis and or dermi ... htll-thie!-.ne,,:. :.!-.in lu~s ttl\olvUlg damage or nccro ... is of suhcutaneous tts':'lIe: llIay extend dO\'..'11 tu hut not through utulerlying fa"cl;]: andor mi"(cd partial and full thidncss alldor tissue layers ob ...cured by granulation tissue Ob:scurcd by Ilecro.:,j:., rull~thickne ... s ... kin loss \\1Ih cxten\l\e destruction. tbsue necrosis, or damage to muscle. bone, m ... upporting ... trueturcs Indistinct. dilrusc. none clearly \ i... ible DI.,ttllcl. outline ckurly \Isible, all ached e\:en WIth wound base \Vell-defined not attached 10 \\ounJ ba ...e Well-defined not attached to bllse, rolled under. thickencd Well-defined fibrollc, scarred or hypcr!-'cr Undermining 2,-4 em 1IIvol"ing >5()'~0 wound margms Undcrtllll11Tlg >4 em tn any area Tunneling undior ... inu ... tract formation None visible While gray nonviable Itssue antI or nonudhcrent ycllO\\ slough Loosely adhercnt yellO\\ slough AdhcrCnI. sofi. black cschar Firmly adherent. hard blac" cschar None \ isible 25"" of \\'Ound bed covered 25"" to 50"'0 of wound covcred >50"" and <.75~'0 of wound emered 75°0 to 100')\1 of wound covered COl/fil/lles
WOl~OCA. '
116
E\:hibil S-S conllnucd \sSC'is m e nl
It e lll
l)nle
!o,corc 7. I "<-ullalc Type
I
!\iune ur bloody
2 .1
'-'(udale
X
Amollnt
5 I
None
" Skill ("olor
Surrounding Wound
2
SCiUlI
;
Small Moderate L .. rgc
I
PlIlk or normal for ethniC group
2 .1
Bnght red and or bl:lIlchc<; 10 tOllch Whitl! or gr.ly pallor or hypopigmcTlIl!d Darl.. rcd or purple and or nonblanchablc Black or hypcrplg.mcntc(]
4
;
Score
Sco re
- -
3 4
I)ah'
Scro:-.angulllcou:, thin. watery. palc red pink
Scrolls· thm. '\'alery. dear Purulen t thin or thick, opaque, Ian ycllm\ Foul purulent thick. opaque. ydlo\\ green \\ Ilh odor
4
--
Illtl t·
!--If! Pcnphcr.11
I
Ti"'im: l'demO!
'-II
f\:nphcral I i...... uc Induralloll
2 ..1 4
Ililtmg edema C'lend .... '" em around wound
;
CrcpillJ:o. ami or pilling c
I
4
Mlniuwl firllluc~s around \\(lund Indur.llion <2 elll around wound Induralloll 2 4 elll c"lcndmg 50" II armllld wmllld Indur.JtlOn 2 4 em c"lending .5(0)0 .. round \\(lund
I
Indur.lll0n A elll in any area
I
SI-Ill inl
2 ..1
r-12 (iranulatHHl
2
., 1"lIC
.1 4
; IJ
I plthelialinlion
MlOlInal ,>,\clllng around \HlUnd \jonpilllng edema c\lend ... <4 em around wound 'onplllll1g edema c\lcntl<. ,4 em around V.OUlllJ
I
2 .1 4
;
10(J°u \\ound cmcreJ. :-ouriilcc intact 75 0 010 < \C)()00 \\(1l1nd cO\~rcd itnU or epithelial tlS~UC e"h:n~"• .(); cm 11110 wound l1ed 50"010 ... 75°1) \\OU IU.I c()\ered and or epilhdi
II(H\L ~IG1\
~ ( Ol{t:
\ll lH. I)I{ E ~SL
I
I II
I
I
1, ...... lIe Ikillih
RE SORE
~T\Tl~
('QVn'L L \1
1.1
I;
20
25
JO
35
411
I
I
I
I
I
I
I
Wound Regeneration
4;
I
50
55
611
I
I
I
6S
I
\\(lund
Dq;encralilll1
Plot Ihe tolal ,core 011 Ihe Prc"ure Sore Sialu' ("UI1IlIlUUIll 11: pUllmg .111 •• X". (In Ihc Imc ilnd Ihe date I'lcncath the Imc Piol multiple 'C(lre:.. \\ Ith their dilh::.. 10 ...cc al iI glill1l:e regencr
-
("\)pyrighl •
19<)0. Barbam M
Ilille~-Jcn ..cn
-
Tools 70 Measure Wound fle(t/ing
(taken with in 2 hours of th e first) for the same wo und . Interrater re liabil it y for th e prac titi oners yie lded a mea n o f 0.78. Reliabilit y estim ates for the prac tit io ners ve rsus the ET ex pert yie lded a mean of 0.82. Int rarate r rel iabilit y for the practit ioners averaged 0.89. 12 Si nce the PSST invo lves a Likert-type ordi na l sca le and the probabi lit y of chance ag reemc nt s between two raters is 0.20 for any item , th e data were a lso subj ected 10 a nal yses using a polyc hoto mous data stratagem . Re sultin g K statisti cs for each item on th e sca le yiclded coeffic ie nt s above 0.60. Collectively, the resu lts from th e long-term ca re setting suggested thaI usc or th e PSST by ge neral health care practitioners resu lted in lower reliability th an usc by ET nurses, but certai nl y within an acceptable range. The Pre.\·.'Wre Sore Stalll.\' Toolllem .~ The PSST is mcant to bc used once a pressure sore has developed: it is not a ri sk assessmen t tool. It is recommended tha t the press ure sore be sco red initia lly fo r a baseline assessme nt and at regu lar interva ls to eva luate th erapy. Once a lesion has been assessed for each itcm on th e PSST. the 13 item sCOres ca n be added to obta in a total score for th e wou nd. The total sco re can then be plotted on th e press ure so re conti nuum at the bottom of th e tool to see at a g lance rege neration or degeneration of the wou nd . Total sco res ra nge fro m 13 (skin intact but always at ri sk) to 65 (profou nd ti ssue degene ration). Each of the items is discussed below in term s of how the PSST item measures th e cha rac teristic . LO('mio",- Assess the locati on or the pressure sore by identifying where th e lesion occurs on th e patient's anatomy and using th e bod y diagram on the tool. Remember. th e sacrococcygeal area is th e mos t com mon a rea for press ure so res; more severe pressure ulce rs often occur over th e grea ter trochan ter and th ere are ve ry few pressure so res on the hips (usually so meo ne has mi slabe led the lesion- it most often is the grea ter troc han ter that ca used the pressure sore). Shape. As wou nd s hea l they often begin to assume a more regular. c ircular/oval shape, The shape a lso he lps dcte rmine the overall size of the wou nd . Butterny-s haped wo unds occur in the sacrococcygeal area and are wounds wi th mi rror images on each side of th e coccyx. Color Plales 3 alld 4 show bu tl crny-shaped ulcers on the coccyx. To determine the shape of the pressure sore. eval uate the perimeter of the wo und. Is the wound ci rcu lar or oval? She. Use a tran spa rent mcasuri ng gui dc to mcasure in centimeters the longest and wi dest aspec t of th e wound surface th at is visible: multiply the length by the width to determine the sur face area of th e wou nd . It can be difficult to determine where to measure size on so me wound s, because the edge of the wound may be hard to visualize or the edge may be irregular. This is a ski ll that simply tak es so me prac-
I 17
tiee. Always look for the longe:';1 as pec t and th e pe rpendi cular lI 'idesl portion of th e wound ; the measurements then wi ll be more re liable. Deplh. Measure th e depth of th e wo und lIsi ng a co tl ontipped applicator. Inse rt the applicator in th e deepest portion of the wou nd ; mark the app lica tor wi th a pen, a nd measure the di stance from the tip to the mark, using a metri c meas uring guide. Pick the depth of tissue layers involved wit h th e wo und or th e thickness of th e wound most approp riat e using the add it ional guidelines on the PSST rorm (Ex hi bit 5 5).
Edges. Th e edges of the wound reflect some of th e most important characte ri stics of the wound. The wo und edges ca n be a wi ndow to th e history a nd health of the wo und. When assessing edges look for how clear and di stinct th e wound outl ine appea rs. If the edges a re indi stin ct and diffuse, th ere are areas where the normal ti ss ues blend into th e wound bed and the edges arc not clearly vi sibl e. Edges that arc eve n with the skin surface a nd the wound base are edges that are attac hed to the base of the wo und. Thi s mea ns that the wound is fl at, with no appreciable depth. Well-de f ined edges are clea r and di stinct and ca n be out lined on a transpare nt piece o f plastic easil y. Edges that are not attached to the base of the wound impl y a wound wit h some dept h of ti sslle invo lvement (Color Plate 3/). The wo und that is a c rater or has a bowl/boat shape is a wo und with edges that are not attac hed to the wound base (Color Pltlle 39). T he wo und has walls or sides. T he re is depth to the wo und. As the wound ages, the edges beco me ro lled under and thi ckened to palpation . The edge ach ieves a unique colori ng. T he pigment turn s a grayis h hue in both dark- and li ght-sk inned pe rsons (Color Plate 33). Wounds of long dura ti on may co ntinue to thicken, with scar ti ssue and fib rosis developing in the wou nd edge, ca usi ng the edge to fee l hard, rigi(~ and indurated . Hype rkeratos is is th e ca llus- li ke ti ss ue th at may form around the wound edges (sce Color Plale 24). Eva luate the wo und edges by visual inspection and palpation. C% r P/llfes 31 {() 34 show wou nds with different edges.
Clinical Wisdom: Tips for Assessing Wound Edges Definitions for help in assessing wound edges: Indistinct, diffuse-unable to clearly distinguish wound outline Attached--even or flush with wound base, no sides or walis present, flat Not attached-sides or walls are present; floor or base of wound is deeper than edge Rolled under, thickened-soft to firm and flexible to touch Hyperkeratosis-callus-like tissue formation around wound and at edges
I 18
WoeN" CARl
UIIlJermillillg. Undermining and tunneling are the loss of tissue underneath an intact skin surface. Undermining usually invo lves a greater percentage orthe wound margins wit h morc shallow length than tunneling. Undermining usually involves subcutaneous ti sslies and follows the fascial planes next to the wound. An undermined area can be likened to a
cave. whereas a tunnel is morc like a subway. Tunneling usually involves a small percentage of the wound margins: it is
narrow and quite long and it seems to have a destination . Assess for undermining by inserting a cotton-lipped applicator under the wound edge and advancing it as far as it will go withollilisi ng undue force . Rai se the tip of the app licator so that it may be see n or felt on the surface of the skin and mark the surface with a pen . Measure the di stance from th e mark on the skin to the edge of the wound. Continue this process all around the wound. Then use a tran sparent metric measuring guide with conccllIric circles dividcd into four (25%) pie-shaped quadrants to help determine perccntage o f the wound invol ved (see Color Plmes 3710 39).
Necrotic Ti ....me 1jlpe. Assess necrotic ti ssue for the color, consis tency, and adherence to the wound bed . Choose the predominant characteristic present in the wound. Necrotic ti ss ue type changes as it ages in the wound, as debridcmcnt occurs. and as further ti ssue trauma causes increased cellular death . There are two main types of necrotic tissue: slough and esc har. Slough gencrally indicates less sevcrit y than eschar. Slough usually appears as a yellow to tan mucinous or stringy material that is nonadherent to loose ly ad herent to Ihe healthy ti ssues of the wound bcd (Color Plme.. 3. 27. alld 38). Nonadhercnt material is defined as appcaring scattered throughout the wound: it looks as Ih ough the ti ssue co uld be removed easi ly with a gauze sponge. Loosely adherent refers to tissue that is attac hed to the wound bed; it is thick a nd strin gy and may appear as clumps of debris attached to wound ti ss ue. Eschar signifies deeper ti ssue dam age. Eschar Illay be black . g ray. or brown in color. Eschar is usually adherent or firmly adherent to the wound ti ss ues and may be soggy and so ft or hard and leathery in texture. A so n , soggy eschar is usuall y strongly attached to the base of the wound but may be lining from and loose from the edges of the 1V0und (Color Plate 16). Hard, crusty eschars are strongly attached to the base and th e edges of the wound (Color Plates 25. 29. and 46). Clinical Wisdom: Eschar Appearance Hard eschars are often mistaken for scabs. A scab is a collection of dried blood cells and serum on top of the skin surface, whereas an eschar is a collection of dead tissue within the wound.
Sometimes nonviable ti ssue appears prior to a wound's appearance. Th is can be seen on the skin as a white or gray area on the surface of the skin. The area usually demarcates within a few days and the wound appears and interrupts the skin surface.
Necrotic Tisslle A mount. The amou nt o f necroti c ti ssue present in the wound is one of the easier characteristics to assess. Place a tran sparent measuring guide with concentric c ircles divided inlo four (25%) pie-shaped quadrants over the wound. Look at each quadrant and judge how much necrosis is present. Add up the tota l percentage from judgments of each quadrant : thi s determines the percentage of the wound involved. Also measure th e length and width of the necrosis and determine surface arca. Exudate Type. Evalua tin g ex udat e type can be tricky beCiluse of the moi st wound hea ling dressings used on most wounds. Some dressings intcract with wound drainage to produce a ge l or nuid, and othe rs may trap liqu id and dmin· age at the wound si te. Before assessi ng exudate type. gently cleanse the wound with normal sa line or water and evaluate fresh ex udat e. Pick the ex udate type lhat is predominlllll in the wound according to color and consistency. Remember that a wound with necrotic tissue present will almosl a lways have an odor and this may not be true ex udate odo r. ExudateA molillt. Exudate amount can be difficult to assess accura tel y for the sa me rea sons it is difficult to deter· mine the type o f exudate in the wound. Moist wound healin g dressings interact with wound drainage to trap drainage at the wound si te. Others may absorb varying amounts of exuda lc. To judge the amount of exudate in th e wound, observe two arcas: the wound itself and the dressi ng used on the wound . Observe the wound for the moisture prese nt. Are the ti ss ues dry and desiccated? Are Ihey swimming in exudate? Is the drainage spread throughout the wound? Use clinical judgment to determine how wet the wound is. Evaluate th e dress ing used on the wound for how much it interacts with exudate. Color Plliles 4() 10 45 show dinercnt exudate characteristic s. S kill Color SlIrrolllll/illl: HfJIIlld. The tissues surrounding the wound are oneil the first indicalion of impending further ti ssue damage. The color of the surrounding skin may indicate further injury from pressure. friction. or shearin g. Assess the ti ss ues within 4 cm of the wound edge. Darkskinned persons show the co lors "bright rcd" Hnd "dark red" as a deepening of normal eth nic skin color or a purple or blacker huc (Color Plales 1910 2/). As hcaling occurs in dark-skinned persons, the new skin is pink and may never darken . In both light- and dark -s kinned patients. new epithelium mu st be di fferelltiated from ti ssues that are cryth cmi c. To assess for blanchability. press firml y on Ihe skin with a finger; lift the finger and look for blanching (sudden whit-
Tools Tb A1ellslIre Wound tIel/ling
ening of the ti ss ues) followed by prompt return of co lor to
th e area. Nonblanchablc erythema signal s morc severe tissue damage. Peripheral Tisslle Et/em ll. Edema in th e surroundin g ti ssues wi ll delay wound healin g in the press ure ulcer (C%r Plates 17 10 /9). It is difTi cult for ncoangiogcnesis, or the growth of new bl ood vesse ls in to the woun(~ to occur in edematous tiss ues. Assess tisslies within 4 cm orthe wo und edge. NonpitLing edema appears as skin that is shiny and taut, almost glistening. Identi fy pitting edema by firmly pressing a finger down into the tiss ues and waiting for 5 seconds; on release o f pressure, ti ss ue s fail to resume normal position
and an indentation appears. Crepitus is accumulation of air or gas in ti ssues. Measure how far edema extends beyond the wound edges. PeriplrertllTb,·sue luduratioll. Indurat ion is a sign ofimpending damagc to the tissllcs.A long with skin color changes, induration is an omen of fur th er pressure-induced tiss ue trauma . Assess tiss ues within 4 Clll of the wound edge. Induration is an abnorma l rirmness ofti ssucs with margins. Palpate where the induration starts and where it ends. Assess by gent ly pinching the tisslics. Induration results in an inabi li ty to pinch the ti ss ues. Palpate from healthy tiss ue. moving toward the wound margins. It is usua l to fcel slight finnness at the wound edge itself. Normal tissues feel so ft and spongy:
induration fee ls hard and firm to the tOllch. Crauu/tltioll Tis~·lIe. Granulation tiss ue is a marker o f wound health . It signal s the proliferative phase of wound healing and usually heralds the eventual closure of the wou nd. Granulation tissue is the growth of small blood vessels and connective tiss ue into thc wo und cavity. It is more observ-
I 19
Try to judge what percentage of the wound has been rill cd with g ranulation tissue. This is much casicr if there is history with the wound. If the same perso n follows the wound over multipl e observat ions. it is simple to judge the amount of granulation tissue present in the wound. If the initial observation of the wound was done by a different observer or if th e data are not available. simpl y use best judgment to determin e the amount of ti ssuc prese nt. Epitlr elillli:lItioll. Epithelia lization is the process ofepidermal resurfacing and appears as pink or red skin. Vi sualizing the new epithelium takes pract ice. C% r Plates 5. 6, 55. and 56 show the process of epidermal resurfacing. In partial-thickness wounds it can occur throu ghollt the wound bed as we ll as from the wound edges. In full-thi ckness wounds epidermal resurfacing occurs from th e edges only. usuall y after the wound has almost completely fill ed wit h g ranulation tissue. Use a transparent measurin g guide to help determine percentage of th e wound involved and to measure th e di stan ce the epithelia l tissue extends int o the wound. The assessment and ultimately the quantification ofclinica(judgment form s the foundation for determining treatments and for evaluating effectiveness o f therapy.
Clinical Wisdom: Evaluation of Reepithelialization in Partial-Thickness Wounds In partial-thickness wounds, reepithelialization wi ll occur from the wound edges and from throughout the
wound bed where portions of hair follicles and accessory glands remain .
able in fu ll- thi ckness wo unds becau se of the ti ssue defect
that occurs with full -thi ckness wounds. In partial-thickness wounds granulation tisslie may occur so quickl y and in concert with epithelialization that it is unobservabl e in most cases. Gran ul ation ti ss uc is healthy whcn it is bright, beefy rcd shiny, and granu lar with a ve lvety appearance. The ti ssue looks bumpy and may bleed easily. Granu lation ti ss ue can be seen in Color Plates 8. 9. lIud 18.
Clinical Wisdom: Appearance of Unhealthy Granulation Tissue Unhealthy granulation tissue due to poor vascu lar supply appears as pale pink or blanched to dull. dusky red cotor. Usually th e first layer of granulation tissue to be laid down in the wound is pale pink; as the granulation tissue deepens and thickens; the color becomes the bright. beefy red color.
Assess ment of Treatment Res ponse The PSST too l allows for temporal tracking of individual
characterist ics as well as th e total scorc. Each characteristic is asscssed as described above and given a va lue from the Likert scale ; thus th e sco res can be monitored for improvement or deterioration in cach characteristic. Addit ional ly. the 13 item scores can be summcd and the tota l sco re tracked over time to determine the wound status. This quantification of obser va tions allows for monitoring not only individual items and total score but also groups of characteristics. For examp le, the characteri sti cs of nccrotic tiss ue typc and amount and exudate type and amount may be tracked to eva luate debridement or infecti on manage ment. Another benefit associalcd wi th the assignment of numeric values to items on the tool is the ability to set rea li stic goa ls. Clinical experience shows that not all pressure ul cers heal and certainly not always in th e sa mc settin g. The PSST allows for more realistic goal sctting as appropriilte to the health
120
WOUND CARl'
care selling and the individual patient and pressure ulcer. For examp le. the patient with a large necrotic full-thickness ulcer in ac ute care wil l probably not be in the facility long enough for Ihe wound 10 heal eomplelely. However. Ihe 1001
enables clinicians to sct smaller goa ls, such as "The wound will decrease in type and amount of necrotic tissue:'
Clinical Wisdom: Realistic Goal Setting
format screen. The clinical assessme nt data field s provide basic Ireallnenl gu idelines ba sed on Ihe Agency for Heailh
Care Po licy and Research pressure ul cer treatlllcnt guidelines. Out-of-range va lues and certa in illogica l entries are not permitted. The Wound and Skin Intelligence ystem - captures related risk factor data and eva luates the overa ll wo und status in relation to risk factor data as we ll as the assess ment data disc ussed. Development of a large database wi th the system is currently being explored.
In some instan ces a pressure ulcer may never heal because of host factors or other contextual circumstances, so an example of a goal might be to maintain the total wound score between 20 and 22.
Usc of the PSST or a silnilar instrument should enhance com munication between health care professionals involved
in pressure ulcer care. By providing a framework for assess-
ment and documentation with an attempt at quantification. the communicati on process becomes more meaningful. An obj ect ive met hod of assessi ng pressure ulcers and monitoring changes over time allows for eva luation of the therapeuti c plan of care and may be used to guide and direct therapy. This is particularly true now that health care is moving into a managed care enviro nment. For example. if a speci fic treatment modality is in use and tile patient 's wound status as determined wit h th e PSST has not changed in 2 weeks. reeva luation of the plan of care is wa rranted. Several studies have demonstrated that wounds with a 50% reduction in surface area wi th in 2 weeks healed more expediently than those without a 50% surface area reduction .l.\ These data become an expectation with chronic wound healing. Use of the PSST ITIClY uncover other outcome criteria th at wi ll help identify criti ca l attribu tes during the course of healing.
An automated system with the advantages discussed will have significant rcgulatory implicatio ns. Third-party payers and managed care grou ps are looking for the most cost-effective methods of treating chronic wounds. Use ofa quantified tool can ass ist the clin ician in proving the effectiveness of a chosen therapy plan, explai n the course of the wound more clearly to payers, and provide ralionale for Iherapy de-
cisions. thus expeditin g re imbursement in particular cases. Use of this tool or a similar research-based 1001 can improve health ca re practitioner communication and the genera li za bility of research studi es, al low discrimination in studies dealing wi th treatment modalities. and may help improve understanding of wou nd healing in pressu re ulcers. It can provide increased sensiti vity. allowing g reater precision and clarit y in sludies related to the Ireatment and development of pressure ulcers. An instrument that is sensitive to change in wou nd status will be helpful in the development of criti ca l pathways for pressure ulcers and is useful as an outcome measure. REFERENCES
I. 2.
The PSST has been fully aUlommed as the Wound and
Skin Intellige nce SystelTI ~ and now incorpo rates grap hic capabilitics and tracking abili ty for all 13 pressure ulcer assessment items for monitoring progress or deterioration of the pressure ulcers. The system uses relational databases and prov ides ongoing monitoring capab il ities for determining changes in pressure ulcer status over time, produces essenti al documentation. and automatica ll y reminds users when additional assessmen ts shou ld be completed. The purposes of th e Wound and Skin Intellige nce System" arc clinica l assessmen t; management and documentation, providing feedback based on aggregate data within the system ; and monitoring. Data me co llected rOlltine ly on patients in the system
).
4.
5.
6. 7.
(u sually weekly) on Slandardized forms and Ihen tran sferred
8.
to the computer fi le by the nurse or designated clerk. Pat ient fi les consist ofdcll1ograph ic and cl inica l data, types and costs of treatments and support surfaces. and agency/facility and staO' data .A II data arc cntered into the system through a fixed-
9.
BUles·Jensen 11M. Indi ce~ 10 incl ude III \\ouml hC;lllllg asscssmel1l At/,' Il(wml ('till! 1995:8:25 )3. Ferrell BA. Arul11an BM. SesslIlg D. The Ses~lI1g sC:lle for u~ses ..meIH of pressure ulcer healmg. JAm Gel"/al,· Soc. 1995 :43:37--1.0. Thomas D. Rodchea\cr G. ct al. PI"I!_~ HI/"(' VIe(',· SClI/e lor 1I(!(l/mg J)eril'(llio" lIlUlll,lit/lIliu" (~/lh(' Pmh Trw/ Waslunglon. DC: Fifth NatIOnal Pressure Ulcer Ad\ i'iory Pand Co n ~en .. us Conference: February 1997. Krasner D. WIIS. II tJ/lird Ih'aliItK Scale I(!n/of/ UJ.- A Pmpowl Washinglon. DC : Fifth NU llonal Pressure Ulcer Ad\l i ~ory Panel COl1scnsu!- Conference: Fcbruary 1997. Sussman C. S\\anson G. The utility of Slhsmlm Wound Healing Tool 111 predlctll1g wound healing outcome .. 111 phy~icul Ihempy. tit/v II'OIII/d ('are 1997;10(5):74 77. Maklebust J. Pressu re ulccr slaging systems: NPUAP proceedlllgs. IId\' UOl/lld ('0/"('. 1'.195:8(4); 1 14. Wagner FW. The dys\:IS!.:ular foot : a system for dlugnosis and IreUImenl . FoOl tinkle. 19l5 l :M :122. Cuddlg;m J. Pre"","£' Ulcer C/mfi(icalioll _II'hlll Du fie II(II'('? 11'1/(/1 Do He Net't/? Washmgton. DC : l-iOh N:niona1 l'ressure Ulccr Ad· nsory Puncl Conscn:. u ~ Conference: Feburary 1997. Makicbusl J. Sleggreen M. Pn.'H //I"(' Ulct'!" Glllt!eU"e 1m· Pr(!'·t''' · lio// lIml Nuning ft/lIIwgell/t'nI West Dundee. 1L: S~N I'ubhcallons; 1991 : 19R.
Tools 7b A4easure Wound Ileafing
10,
I I.
IJcnnell A Rcporl on thc t.I~~ force Oil thc unpllcatlonil for durk ly plgmentcll mtact ... klLl in thc prcdictlOn ,HId prC\Cnt lOIl of prcv·,:urc ulcel"'i lt/,' Hinmt/ ClI"" 1996;~(6) :J5
12.
Bate:-.-Jcn:-.cn B\1. Vrcl!c\oc DL, Brecht ML. Val id ity and rcli:.bdIt) of the Prc:-. ... ure Sore Stalll~ Tool [)('l"/Ihifl/I 1992;5 (6):10 28.
13.
B;ltcil-Jcn~en
12 1
0, McNee .. P To\\ard un inte ll ige nt \\O llll d
a .. se ..... mcnl :-,y .. tcm . 0110111,' lIf1/lIIt/ MOII(lge. 1995:4 1( ... uppl 7A):
80 88 van R IJ~\\ IJk L. Polan~k~ t...1. P rcdlclor~ of [lIlle to hl:al ing dcc p prc .... urc ulcer.. 01101111 ' "(wild \lmwg{'. 1994;40(R):41J 50.
Appendix 5-A Instructions for Pressure Sore Status Tool GENE RAL GUIDELINES Fill out the attached rating sheet to assess a pressure so re's status after reading the definition s and methods ofasscssll1cnt described below. Eva lua te once a week and whenever a change occurs in the wound. Rate according to each item by picking the response that best describes th e wound and entering that score in the item score column for th e appropriate date. When you have raled the pressure sore on all items. determine the lotal score by adding together the 13 item scores. The HIGH ER the total
score, the more severe the pressure sore status. Plot total score on the Pressure orc tatus Continuulll to determine progress. S I' EC II'I C INSTI{UCTIONS I. 2.
3.
4.
5.
6.
Size: Usc a ruler to measure the longest and widest aspect of the wound surface in ccntimeters: multiply lcngth by width. Depth: Pick the depth and thickness most appropriate to the wound using th ese add itional descriptions : I Ti ssues damaged but no break in skin surface 2 Superficia l, abrasion, blister, or shal low crater. Even with a nd/or e levated above sk in s urface (eg. hyperplasia) 3 Deep crater with or without undermining of adjacent tissue 4 Visualization oftissuc layers not possi ble due to necrosis 5 Supporting structure s include tendon. joint capsu le Edges: Usc this guide: Indi stinct, dirfu se unable to c lea rl y di stinguish wound out line Attached even or flu sh with wound base. 110 s ides or walls present; flat Not attached sides or walls are present; floor or base of wound is deeper than edge Rolled under. thickened so rt to firm and Oexible to touch Jl yperkeratosis callus- like tisslie formation around wound and at edges ha rd rigid to tOllch Fibrotic, scarred Und erm inin g: Assess by inserting a cotton-tipped app li ca to r under the wound edge. Advance it as far as it wi ll go withollt lIsing undue force . Raise the tip of the applicator so thm it may be seen or felt o n th e surface of the skin and mark the surface with a pcn . Measure the di stance from the mark on the skin to the edge of the wound. Continue the process around the wound. Then usc a transparent metric mcasuring guide with concentric c ircles divided into four (25%) pic-shaped quadrants to help determine percentage of wound involved. NccroticTissueTypc: Pick the type of necrotic ti ssue that ispredomillallf in the wound according to co lo r. consistency, and adherence usin g thi s gu ide: White/gray, nonviable ti ssue may appear prior to wound opening; skin surrace is whi te or gray Nonadhercnt. ye ll ow slough thin , mucinous s ubstance; scattered throughout wound bed; easily separated rrom wound ti ssllc Loosel y adhe ren t, yellow s lough thick. strin gy clumps of debris: attac hed to wound ti ssue Adherent, soft, black eschar soggy ti ssue; stro ngly attached to ti ssue in ce nt er or base of wound Firmly adherent. hard/black eschar firm , crusty tissue: strongly attached to wound base amI edges ( like a hard scab) Necrotic Tissue Amount: Usc a transparenlmctric measuring guide with concentric circles divided into four (25%) pic-shaped quadrant s to help detennine percentage of wou nd involved. COl/tIllIteS
SOl/rce: Copyright ~ 1990. Barbam M. Oatcs-Jenscn.
122
Tools To A1easflre Wound Healill}!,
7.
8.
9.
10.
II .
12 .
13 .
123
Ex ud a teTy pe: Somc dre ss ings interact with wound drainage to produce a gel or trap liquid. Before assessing exudate type. gentl y cleanse wound with normal saline or water. Pick the exudate type that isprec/ominanf in the wound according to color and co nsisten cy. usi ng thi s guide: Bloody thin, bright red Serosanguineous thin , watcry, pale red to pink Scrous thin. wale ry. c lcar Purul cnt thin or thick . opaque tan to ye llow Foul purulent thi ck, opaquc ye ll ow to green with ofTensive odor Ex ud ate A mo un t: Usc a tran sparent metric measuring guide with concentric circles di vided into four (25%) pieshaped quadraJ1ls to dete rmine percentage of dressing involved with exudate. Use thi s guide: None - wound ti ssues dry Scant - wound ti sslies moi st; no meas urable exudate Small wound ti ssues wet; moi sture evenly distributed in wound: drainage involves ~25% dressing Moderate - wound tissues saturated; drainage mayor may not be evenly di stribulCd in wound; drainage involves >25°'0 to ~75% dressi ng Large wound ti ss ues bathed in Ouid ; drainage free ly expressed: mayo r may not be evenly distributed in wound: drainage involves >75% of dressing Skin Color S urro undin g \ Vo und : Assess ti ss ues within 4 Clll of wound edge. Dark-skinned perso ns show the colors "bright red" and "dark red" as a deepening of normal ethnic skin color or a purple hue. As healing occurs in dmk· skin ned persons. the new skin is pink and may never darken . Peri phera l T iss ue Ede ma: Asses ti ssues within 4 Clll of wound edge. Nonpining edema appears as skin that is shiny and taut. Identify pitting edema by firmly pressing a finger down into the tissues and waiting for 5 seconds; on release of press ure. ti ssues fail to resume prev ious position and an indentation appears. Crepitus is acculllulation of air or gas in ti ssues. Use a trans parent metric mcasuring guide to determine how far edema extends beyond wound . Pe r ip hera l Tiss ue Ind uratio n : Assess tissues within 4 em of wound edge. Induration is abnormal firmne ss of ti ssues with marg ins. Assess by gently pinching the ti ssues. Induration result s in an inability to pinch the ti ss ues. Use a tran sparent metri c measurin g guide with concentric circles divided into four (25%) pie-shaped quadrant s to determine perce ntage of wound and area involved. Gra nulatio n Tiss ue: Granulation tisslie is the growth of small blood vesse ls and connective ti ssue to fill in fullthi ck ness wounds. Tissue is healthy when bright, beefy red shiny, and granu lar with a velvety appearance. Poor vascular supply appears as pale pink or blanched to dull , dusky red color. E pit heli a li za ti o n : Epithelialization is the process of epiderma l resurfacing and appears as pink or red skin . In partialthi c kness wounds it can occur throughout the wound bed as well as from the wound edges. In full -thickness wounds it occurs from the edges only. Use a transparent metric measuring guide with concentric circles di vided into four (25 %) pic-shaped quadrants to help determine percentage of wound involved and to measure the di stance the epithelial tissue ex tends into thc wound.
C H A P TER
6
Noninvasive Vascular Testing Anne Siegel
INTRODUCTION
What time of the day is the pain experie nced? Describe the pain : ac hing? burning'! constan t? int erm itt e nt ? For exa mpl e, venous ulce rs are not very painfu l and th e pat ie nt may find relief from e leva ti on of th e leg. A rt eria l ulce rs a re ve ry painful because o f the lack of c ircu la tio n. Keep in mind that th ere arc a lways except ions. The patient may have a combina tion o f arte ri a l and ve no us disease. The pmien t can have dia bet ic ncuropat hy and have a n arteria l ulcer wi th ou t a ny pain . Pain o n the plantar as pec t of the foot usually s igna ls a diabetic neuropat hic fool. Art eri al res t pa in is fo und on th e dorsum of the foot and is us ually described as a b urnin g ache type of pain (like a toothache). Sometimes the patient will f ind so mc re li ef w ith depe ndency of the leg. Rcst pain indicates that the patient has s ign if ica nt arterial insufTiciency und w ill need intervention from a vasc ul ar surgeon to hea l the wou nd s. Cla udi ca ti on is exe rcise· induced pa in in th e major mu sc le grou ps th at is rcli eved wi th rest (usua ll y descri bcd as a cra mplikc pai n in the ca lf, th ig h, or b utt ock). Ifthc pat ie nt has a history of c laud icati o n, thi s shoul d guid e the cli ni c ian 's thinking that thc ul cer being eva lua tcd may havc an arte ri al et io logy.
In the pas t decade. many adva nces have been made in the diagnosis and treatm ent of vascul a r di sease. The key to pre-
ven ting deb ilitat ing circulatory prob lems is prevention and early diagnosis. Noni nvasive vascu lar eva luations are lIsed to detect th e presence o r absence o f arterial occlusive o r ve nous disease. They a re lIsed to eva luate the healing po ten-
tial of ul cers/wou nds. as an a id in determining wou nd care management plans. and as a guide in determinin g which patie nt s need refe rral to a vascula r surgeo n for fur-
ther eval uation. T he f irst stcp in a vascul ar eval uat io n is to obtai n 11 CO I11 plete medical his to ry from the patient. Thi s infonnation is imperative in th e overa ll assessment and trea tm en t of the patient's cond it ion. The patient's history prov ides a g uide in determ inin g the etiology of the wo und be ing evaluating. A carefu l. thorough history is th e key in vasc ular assess ment. Thc history shou ld incl ud e th e a reas discussed below.
O Il EF COMPLA I NT PAST ME DI CAL H ISTORY T he ch ief co mplai nt is the combi nat ion of symptoms that prompted the patient to seek med ica l attention. I Focus on the symp toms that co nce rn the pati ent and th en ask th e patient to describe those sympt oms in mo re detail. Spending time liste ning to the patient is as important as the phys ica l exa mination. A detailed pai n hi sto ry is essential in determinin g the urge ncy an d type of treatm en t th e patie nt will receive. Invest igate the pain. Where is the locati on of th e pain? Wh en did the pain start? Wh at factors aggravate o r relieve th e pain: e levation? depe ndency? wa lk ing? restin g? standin g? si ttin g?
Ex hibit 6- 1 lists a reas of mcdi cal hi story qucstio nin g used to ide ntify risk fac tors for vascu lar disease, bot h art eria l and ve no us. It goes beyond th e ge neralmcdical hi sto ry di scussed in C hapter I and focuses 0 11 spec ific vascu la r-re lat ed factors.
PH YS ICAL EXAM INATION A fler obtai nin g a co mplete history from the patient. the next step is th e physical exam. A carefu l phys ica l exa m used
125
126
W OUND CARl
Exhibit 6-1 Past Mcdicai lli story
Risk Fuctors ror Peripheral Vascular Diseuse'
Cardi:.lc hi story
Concom itant illnesses (renal disease, co ll agen vascular disease. arthritis. pulmonary disease. mali gna ncy [type ormallgnancYI back [spine] problems. etc) Family hislOry or arterial disease
• lIeart disease (cardiac catheterization'! results?)
• Hcarl attack (dalc of last event) • Chest pain (note location of the pain. how is pain relieved? ollser!) • Stroke (date of event. nole location of weakness or speec h
deficit) Il ypertcnsion (severity, medications. age at onset, highest blood pressure reading)
Il ypcrlipidcrnia (iasl cholesterol leve l. medication. number of
Risk Faclors for Venous Diseu se Trauma (type. date) Deep vei n thrombosis (date. anti coagu lant s) Prolonged inactivity Pregnancies Family history or \e nous disease Obesity Clolling disorders
years)
Smoking history (number of packs per day x years smoked ... number of p:'lck-ycilrs) (For example: a patient smoking IwO packs per day for 20 years ha s a 40-pack-year smoking hi s-
tory.) (quit? year quit) Diabetes (number of yea rs. medi cations)
in conjunction with a thorough history can usually determine the etiology of the wound and determine the wound ca re plan or establish the need ror rurther vascu lar tesling. The rirst step to the physical exam is inspection of th e extrcmity. Note the presence and location orallY ulcers, wounds, or gangrene. Describe the wound : color. wound bed, drainage (color or drainage). size, and odor. Note Ihe presence or absence or swelling (compare both legs. and docul11ent the location orany swelling).Ask the patient how long the ulcer has been present. Look at th e skin color. Are Ihere any pigl11ent changes? Feel the tcxture of the patient's skin: dry? moist? Feellhe lemperature or ,he skin, comparing both legs. Using th e back of the hand to assess temperature. note the leve l at which the limb is cool or warm. Note the presence or absence or hair (legs. toes). NOle the appearance orthe loenails (thickened?). Check for the presence and distribution of varicose veins.
Pasl Surgical Hislory
or
Vasclliar surgery (date procedure. indicati on) Angiogram/venogram (dates, indi ca tion. interven ti on'!) Gelleral surgcry (date or procedure. indic:'ltion)
Clinical Wisdom: Severe Arteria/Insufficiency If arterial disease is severe, elevating the leg while the patient is supine will cause the patient's leg to become pale, which is known as elevation pal/or. The pale color is due to lack of blood flow in the patient's leg. If the patient then hangs the leg over the side of the examining table, the color of the foot will change to a deep red or purple color, known as dependent rubor. This is also due to the lack of blood flow and vasodi latation of the arterioles. Be careful not to confuse dependent ru bor with cellulitis. If the patient has cellulitis, the leg will not become pale with elevation. 1
VOl1im'll\'II'e I (/Sut/ar n'.\ li"X
Diffcn.'ntiation
hch~cc n
Arterial a nd Venous Ilisease
Patients \\ ith arterial in~ufriciency ha\e classic characterISllcs that will ennblt.! the eX(lJ11l1ler to distingUIsh easily bet\\ecn arterial and 'venous ulcers. Always remember that patienl!-o can have a comhinatlon of arterial and \cnou~ disease,. and Ihe \\ hole clinical piclure may not fll 11110 one speL'ific category. Usc the follmving lists of characterisllcs as a guide. C h 'lraCler i ~ l ic~
• • • •
PULSE EXA ,. The nexl ~tep in the physical c_xaminatlOn is the puIs£' IThe pulse exam mc1ude!-o locatmg and grading bi lat-
l!.HlUI.
erol femoral. popliteal. dorsalIS pedIS. and postenor tibial
artery pulses. The following system shou ld be used to grade pulses: () I+
t--.o pulse Barely felt
Diminished
of \ rtcr ia i llheao,c
Normal pulse (eaSily felt)
Bounding. aneurysmal r'pulse hils you in the
Pain (\\alklllg and'or at rest) I-oot cool or cold Weak or ab!-ocnt pulses :\bscnce of leg hair
face") Pu l1)C Tab le
• S~1I1 ,llIny. dry. pale
• Thickened toell,-lIls • Llcer location: usually belm... ankle (pressure arcas. toes) • Ulcer: m:crotic. 1111nitnal drainage • \nkle-brachlUl II1de\ (1\1l1) Ie" than 0.5 (11I1Ie' If dlabellc. can he greater than I.O) • Flcvation pallor dependent rubor • History of diabetes. hypertension . smoking. claudication • llistory of foot trauma (tight shoes. toenails cut too short. object falllllg on foot)
Clinical Wisdom: Trophic Changes Trophic changes are skin changes that occur over time 1n patients with chronic arterial insufficiency. TrophiC changes Include absence of leg half; shiny, dry. pale skin; and thickened toenails. These symptoms are due to the chroniC lack of nutntlon from a good blood supply to the extremlly. Some of these changes occur naturally in elderly patients.
Cha ractrri'ilic, of \ cnous Oiscas('
• • • • • • •
root \\ arm Edema Brawny :-,kin pigment challge~ Varicose \eill~ Llcer location usually abm,e ankle (l11edI3Imallcolus) Venous ulcer, gcncrally not painful Llcer: granulating. drainage
• I\HI greater than 1.0
• II i~tory of trauma. deep \ CIIl thrombosIs. \aricose \ eiIlS. malignancy
127
\·cllloral
Poplltcal
Dorsal!,
Po~tcrior
I)cdl~
Tibial
RLI III
The pulse exam algorithm (Figure 6 I) is the clinicians gUide to triage patients for appropriate pathways for examination. referral and patient teaching. The lower extremity pulse exam can accurately assess ror the presence, absence. and location of arterial disl':ase. The patient should be supine \\ ith head and legs adequately SllPported. The commoll/('''lOrul urler" (eTA) is easily palpated with the second third and fourth fingers in the groin below and medial to Ihe inguinal ligament. If the patiellt is obese, the CFI\ pulse m"y be difTicult to palpate. If the pulse is
diminished or absent. the palient may have aortieiiliac disease. Figurc 6 2 indicates the location of artcries to palpate and to u~e for malll probe sltcs \\ hen taking Doppler readIngs (described later). The poplileal arIel''' is the most difTicuh to palpate. The artery is located midl1l1c bchll1d the knee 111 the popliteal fossa . 11,,\e the pallent slightly !lex at the knee. Il ave the
clinician place both hands behind the patient's knee in a cupped fashion and ,,110\\ the pu"e to bounce back Into the clll1lcian's hands. \'ore Irthe popliteal pul~c is ca . . y to pa l-
pate. this could indicate a popliteal aneurysm, and fur ther Il1\esligl:ltion is nceded from a vascular lab. The dorsalis pedis p/llse is examined by sitting or standII1g facing the patient. Using the second and third finge rs. palpate the dorsum of the fool. Place the thumb on the plan-
tar surface oflhc foot to anchor the.:: hand. Do not press hard because thc prc!ssure can occlude the artery. Use a light touch. The posterior lihialarle/:\" is palpated at the level of the ,.!Ilk Ie (medial and posterior). While facing the patient, lise the sec-
128
W OUND CAR l
r
Pulse Exam
[
Diminished (1+ , 2+) or absent pulses
Perform ASI and Iranscutaneous partial pressure of oxygen (tcpO,) measurements
ASI :>1.0 tcpO, : > 30 mm Hg (- diabetes)
I
Wound care (debride if needed)
Patient teaching: 1. Wound, foot care 2. Risk factors 3. Orthotics
Fi~u"c
6--1 Pulse exa m.
1
ASI : <1.0 tcpO, <30 mm Hg
ASI : >1 .0 IcpO, <30 mm Hg
(- diabetes)
(+ diabetes)
l
Referral to vascular surgery (vascular lab)
Palient teaching: 1. Wound, foot care 2. Risk factors 3. Orthotics
l
1
I Referral to vascular surgery 1
l
(vascular lab)
Patient teaching: 1. Wound, foot care 2. Risk factors 3. Orthotics
NOllilll'asive Vascular Testing
LOCATING ARTERIES
ThcASJ measures the systolic blood press ure in the ankles and provides objcctive information as (0 the prcsence and severity of arterial occ lusive disease:' 1t is so mctimes called the ank le prcss urc index (AP I). The equipment needed to obtain an AB I is a Doppler probe (ultrasound stethoscope), blood press ure (BP) cuff, and ultraso und gcl (Exhibit 6- 2). The Doppler works on the principle that ultraso und waves that strike a moving object (blood) at one frequency a rc reflected back at a different frequency. Figure 6 3 illustrates the procedure for performing AS!.
( 0 " ' _ .Iioo; CHIotI)' •
1n"'t\Ol ,1;00;
OIMI)'
[,.,.rnoIl1Ioc 0,1.1)'
129
7
COMMON
fEMOkAl "UUY
o..p IPfolwndol ""'0101 CHl.1')'
P'O¥\HEAL ""UY
Significance of ABI Values AB I va lucs arc predictors of healing (Table 6 I). Wounds wi ll heal if the ABI is 0.8 or greater; an AB I of 0.5 to 0.8 means high risk for a nonhealing limb, which need s perfusion. If AB I is be low 0.8 wounds should not be debrided because of high ri sk for necrosis and infection or treated with compression.
P.,_'ol1'ry POSTUIOR T\tlAL A.'UY
~"!:~~::; DOUA"S nOls A~IfIY 10"'01
pio.IlOI • .....,.
~0fI101 011.. 101 ..
<"
o.r",I-..oIOl.o/.,..,;.. Mtdool pIoftlDr DlItr)t
AHl11101
VI~W
o
POtU_lOt VllW
1N0tCA1U MAIN I'106l slIn
•
Exhibit 6-2 Ankle-Brachial Index Procedure Figun' 6--2 Locating arteries . Courtcsy of Il unticigh Diagnostics Ltd., Cardin: United Kingdom .
Ankle-Brachial Index Procedure
1. Lay patient !lat. 2. Apply I3P cufTaroun d the patient's arm (above e lbow). 3. Apply ultrasound gel.
ond and third fingers to palpate the pulse. Place the thumb on the lateral malleolus to anchor th e hand . The other hand ca n be used to support the patient's heel .
NONINVASIVE VASCULAR TESTING A fter completin g th e hi story and physical exam. the cl inician may already know the etiology of the patient's ul cer or wound. If more information is needed, the patient will require noni nvasive test ing. If th c paricl1t ha s a ve nous ulcer and has 3+ 110rmal pulses. it is possible to safely trea t the ul cc r with wound care. compression, and debridcmcnt. If the patient has decreased pul ses and has an arterial or venous ulcer, an ASI will need to be performed and, ifavaiJablc, a tcp02mcasurement should bc obtained.
4. Hold Doppler probe at a 45° angle and place ovcr brachia l pulse. 5. Identify the arterial signal and innate the culT until the sig nal disappears. 6. Slowly de !late the cufT until the arterial sou nd returns. The first sound that is heard is the systo li c brachial pressu re . 7. Obtain brachial pressures in both upper cx tremiti es. 8. To obtain ankle pressures. place the cufTabove the ankle and place Doppler probe over the dorsalis pedi s or the posterial tibial artery. 9. Repeat steps 3 to 6.
Calculatin!!, rhe If 81
ABl =
Hi ghest anklc Doppl er pressure Il ighest brachial Doppler press ure
130
WOUND CARF
Dopplex' Ankle Pressure Index Guide leg uken or. commonly treated UIU\Q compn!lmon therapy bondogt,_ ,kxk'ng, Of ~ Interm,ltenl Compt'.u~ II n \tuonttOllo .PobIIJ, lions of wfflC1enl orteno' lUppIy p"Ot 10 "'''no compreu.an "*"OP7'.100 enobItng Ihe moll Dpptopt'l(lte treotmMl The Dopf~. AnUfI PreuUfflloo.., (API) gvld. will OUI,I yov 10 q,-"ckty and .HK,nnliy lden'lfy any
under~ng
problem,
.
loy patlenl Rot, alloy onx~ ood enc.ounlge ,eiwtohon • (n"'''8 ornbtenl
• ~e ~ cuff around arm • AppIygol " • Hold DoppI., j>'obo be-. I.,,",,~ and .nUmb , of 0 "05' angle and p&oc. oYef btodual ~HI • • InRote cuH unhl Oopp&er tOUncf dlloppeon. dowfy deflo. cuff un'" W)Und relVtnJ • Thu II me 8RACliIAl SVSTOUC PRESSURE • RlICOrd prelWfe readmg
me
me
• PI.co 'f'hyg cuR wound log ,v" 01,.,.. ankle Apply gel and Ioc:ot. donol •• pod.I or posJeriof"
•
hl),O( pul .. ~Ing ~
probe
• Inflo.. cvff unhl DoppIet .ound dlMllPf*H'J SIowfy defk,,. cuff unhl the toI.H'Id 'MImi thiS" the ANKl£ SYSTOUC PIIESSURE
• RecClf'd pte,Wf'. r-OOlng To coblloto {lee wkulol'Ot on (oYefM
INOeX • d,Y!de !he onkle prOUUt. ,GOding by the bnJchlOl p'.uure reodlng Ilde) Normal API.,.cpJOI to Of gr.otet than I oo.w+.n If I, JOf.IO apply ~ ItIerOpy
WARNING: Do no! apply ccmp'... ioo therapy 10 a I,mb wolf> on APt 1o .. lf1on 0.8.
AT RISK: Polienh who oro ""y old, diabolIC, hype.1en ...., """"en APt 10 .. If10n 1.00 "'IJ9O'b orIerioI d. ...... • Comp"'_ therapy .t.ouId be uMd wolf> _ Tho Ioww the APt the 9'...... the orionoI 'mpo,nnonl
Fi g ure 6- 3 Proced ure fo r pe r fo rmin g ABI. SO llrce: Reprint e d wi th pe rmi ss io n from . Moffatt , The C ha ri ng Cross Approach to Ve nous Ulcers. Nursing Standard, Dec 12.5. No. 12 . pp. 6 9. c 1990. ROY'll College of' N urs ing.
NOllim'(lsil'f! Ih.\'('u/ar Testing
131
Table 6-1 Table of ASI Values
Dopplex · Ankle Pressure Index (API) Guide - _ _ - __ ~__ 10 15-40 045 50 55 ~.6.5 "0 75 80 85 9Q·9.s:l(X)')051101151iOl2jllO~~.J~_~~Z51801!!..!-90195'200 180 16 19 22 2.S 27 30 II 36 J8 .(\ "' j...o .5Ol52 55 58 61 63+66 69" n 75 n eo 8:.3 So 19 n 9.( 9'>' 00 180 17517 20 22:2S:28.j-31.'~:l?:40~4~~~t48:5~ • .s.t~5(~62:6S~·68r.71>" n--<'-80 e;; 85 M f2~. 91.UIO ~:I!.' _ 11(.17 1O.2].26t29~J2 35.~;"ltCA "7..L...so.52,S5 .. 5B.61.~ 61t.1O_n.76. 19. 81 85 ~9 1,1. t;. 97100 1~ ::r.16Slle~~1 2A~27.. JO 13 36.39 ... 2 • .c5tA8.o-~.1._~? 6Q.63.66~69 ..?2~1~7tI 81 .. ~ 87 ~ VA ~6.100 1~ E IUI011~ 2!.15.28~Jlt~.J' .tOl"~+-46~50-1-5J __ 56...:S~:62.65,68..-71-+75.-'R 81 U 87 90 93 1;0100 ~~ t ..s.,\S.$1912. 25.29-+-J2 J5 18."I_~tA8 51-tSA.58 61 ... 6ot.07JO .... 7ol.7C 80 8J ill 9() 9~ Q61.00 ~ 150 '2O~21:26 lO 3J:16.eo 4J 46 .sot'SJ.56 6Ot63~66"70 n 76 80 e, 80 90 9) ~cl00 ISO ~ '145 20 2.. V"Ji'3A 3'" .1' ", "' A8 t"S\t'.ss' .,58'i2 t 65 69-n'75"]9'&2 &6 ~I 9J 961.(X) .1.t5 r § t1.a 21125+28;-32""-35 ... 3'7.....42.46 5O Sl:57: IIJ' 61" 67;7\ 'J5 78)2 8..' ali "'1 Cfll(X) ,1M) :: ~'15 n 16.-29 lJ 31 .to .... ..a 51t-.ss .!Ii9 02 66.70 .. 7 .. " III 8S 88 91 oe.IOO GREATER ~I~ 2 !'XI 13 .. V ... Xl::u. 3B .12.46 .5O:-S1.571.61 6.S 69 131-" 80 SA 88 f2 tol(x) THAN 1.00 ~_)l -5 12$ 2.. ,1S 321-'36.40 ...... .a,S2 f 56.60 64 68.nI-76J SO 84 58.'1 90100 .'25 120 25 29,..J3 11 .to &5 .50 54 58 r 62 66 10 75 J9 II~ S7 91 95100 1'20 t al 115161"11) 34 J9 .t3 4' 52 56~ 6O 65- 6" 7.. "'788286 91 95100 115 11 27'".31"'36"'40 A5·5C)·5.a"'S9to"t"'68"n·n"'81~86t9C 95100 110
r
~
________
.. ___Ank"'Pre ..ure(mm~ _ _ _ _ _ _ _
I
I".'
e
1
10511+])'38 ... ..247-5251"'6166 71 76' 8O"a.s Q()"'95 100 'OI?l...lO.-.~ 40_45_50 5.5_60_65_70 75 eo as 90 95100
.......Ieogh ~,o""Orld J.od,.,g ~ r.J poO..I ~ ~ orI ... IW\' ..... ~ Q......d. '0I'IQI0 01 ~~ probes Jo,- ~ \IOKVb- crJ ~t( lIJIPoCatoonl
..lOS 100 ~
CJl be do,~ P(d.~ Oapp/eor,.,.i. y,waI Ro-O"od
I'QIII
dnpb,.
~
WARl'a'IG. FoI~ I,;gh ~;,..". becbbNod .. ,.,......,.. a.Ior..d.,.,..,.. _ ..... ~_ ~ """'" July ::;.;." ...-~ 0iI1 [ ~ CoIcif..d ar1Inel may be ptDWlf pglMfth -*' hu...y of ~ ~i and
-
11'1
~
- -
Courtesy of Huntletgh Diagnostics Ltd. , Cardiff, United Kingdom.
Significan ce of Ankl e-Brachia l Index Va lues A I' I
::0.5
Referra l 10 vascu lar spec ialisl (compression therapy contraindicaled)
A PI
0.5 0.8
Referral to vascu lar specia list. Intermi ttcnt claudicant indicaring peripheral arteria l occlusive disease (compression therapy conlraindicaled)
A PI
0.8 1.00
Mi ld periphera l arlerial occlusive disease (compression therapy wilh caUl ion)
A PI
> 1.00
Referral to vascu lar specialist. Indicales ca lcified vessels ifdiabctic
Clinical Wisdom: Diabetic Patients
The ankle-brachial index can be falsely elevated in patients With diabetes. This is due to the calcification of the inner layer of the artery, ie, the cuff is unable to compress calcified distal vessel(s). This phenomenon is referred to as noncompressible vessels. Instead of ASI, proceed with transcutaneous oxygen testing if available. Another option is to take toe pressures,
Patients sometimes present with different occ lusive disease in the two legs. Thc following casc study example describes slIch a situation.
132
WaUNa CARl
are less likely to ca lcify and can be used to calculate a toebrachial index. The norma l toe pressure is approximately 80% to 99% of the brachial systo lic pressure.
Case Study: Ankle-Brachial Index Systolic Doppler Pressures
Posterior Tibial
Brachial
Dorsalis Pedis
RT
90
50
40
LT
100
a
100
Note: Always use the highest brachial pressure and
the highest ankle pressure to calculate the ABI. ABI = 50/100 =0.5 in the right lower extremity; the highest ankle pressure is 50. Using the highest brachial pressure (which is the left arm), divide the 50 by 100, which equals 0.5. ABI = 100/100 = 1.0 in the left lower extremity; the highest ankle pressure is 100. Using the left arm pressure again, divide the 100 at the ankle into the 100 brachial pressure, which equals 1.0.
Additional Doppler Pressures
Further diagnostic information can be ob tained by measuring the systolic Doppler pressures at ditTerent levels of the leg. Segmental Doppler pressures can identify the level of arterial obstruction. Blood pressure cuffs arc placed at
the high thigh, above the knee, below the knee, and above the ankle. Systolic blood pressure measurements are then taken as previously described. by innating th e cutTs consecut ively, starting at the ankle level. All pressure gradients should be less than 30 mm I-/g between cutTs. The high thigh pressure shou ld be greater than the brachial pressure. The segmental Doppler pressure study is usually performed in a vascu lar lab. Digital Plethys mograp hy Digital plethysmography (toe pressures) is anoth er study that is performed in a vascular lab with special equipment. Additional information can be obtained
by measuring the
sys toli c toe pressure. This study is very important in diabetic patients. ince the AB I can be unreliable in diabetic patients because of calcified vessels, this study can reliably assess the lower ex tremi ty circu lation. The digital arterics
Transcutaneous Oxygen Measurements Transcutaneous partial pressure of oxygen (tcp02) mcasures oxygen delivery to the skin ti ssue. This noninvasive measurement is very useful in predicting ulcer healing and amputation level. It is capable of documenting the hypoxemia charac teristic of ischemic ti ssue. This st udy is very si mpl e to perform and gives information that is very va luable in guiding th e wound care managen1ent plan.
Per/ormillg tl, e Ii:p01S(IIl/Y If a transcutaneous oxygen monitor is not available, this study ca n be performed in a vascu lar lab. The first step in performing the study is to ca librate the machi ne. There arc ditTerent models, and th e machines shou ld be ca librated according to the manufacturer's instructions. The small tcp02 sensor is applied to the sk in with an airtight self-ad hesive fixation ring. At the end of the (Cp02 electrode. there is a heating clement. This element heats the skin temperature above 41 °e. thus allowing oxygen transport from Ihe capillary level to the sk in surface. The sensor is left in place for 20 minutes and then the reading is taken from the machine. Choosing th e correct position for placement of the tcpO, electrode is a very important part of the study. The correct position depends on where the patient has the ulcer or wound that is being assessed. (fthe patient has a toe ulcer. the electrode is placed just proximal to the toe. Describe the area as " th e base of the toes."
Significance o/tI, e ( ('pO} Fillllillg The significance of tcp0 2 readings is that if the tcpOJ values are less than 20 mm I-Ig, th e ulcer/ wound wi ll not heal. If the tcpO, value is greater than 30 mm I-lg, healing will occur. If the tepO, reading proximal to the toes ( low clorsum) is grea ter than 30 111m I-Ig. then the wo und can be safely debrided and dressing changes may proceed. I f the patient has a gangrenous toe and it is being assessed for amputation healing, this toe amputat ion site would heal. If the I CpO ~ reading is less than 30 mm Hg at the low dorsum, do not debride the wound. Refer this patient to a vascular surgeon for further evaluation. If the patient has an ulcer higher up the leg. place th e electrode around the wound edge. I rthe reading is greater
VOllilll 'U \ i I '(' ' (ls("lIlar Test i IIg
than 30 mm Ilg. dduidt: tht: wound. If the patielll does 110t IKI\e enough blood Ih)\\ to h~al a wound and tht: wound IS still debrided th~ \\olllH.l \\ III necrose again and probably becomc inl~cted. The s"f~ thing to do if there is any doubt is 10 refer tht: patient to a vi.l:-.cular lab or vascular surgeon for further e\aluation. Ifthe \·ascular surgeon cvaluates thc patient and concludcs that there IS adequ:uc blood 11<)\\ In tht: cxtremity, \\(lund care management can illways be n;sullled for the pallent. If \:lscular testing is performed and the patient has good circlIlatuHl 10 th~ extremity but the wound \\ III not heal. this paticnt needs to be refern:d to a ytlscular surgeon for e\aluation There may be an infectum or malignancy that needs to be tre~l1ed. Remember. when III doubt. refer the patient out!
133
tOCA UNG VEINS
, ,.. ,,,01
...."
~OMM(,'j
'fMO'''~
'{[IN
K>f\:JfAt '{[IN
Af" rr~
~,bi
",III
, ......t~ •• · " It.,·
Clinical Wisdom :
I,b
...'
DoriO"I'.!!' ... ·n
Accuracy of tcpO, Measurements tepO measurements are not reliable in patients With swelling or Infection! Do not test these patients, The patient can be tested when the infection IS clear and the swelling is gone,
AIJDJ'lIO'lAL \ \SC l ILAR STUDIES There arc Ilumerous additional \ascular studies done in the \ascu lar lab 10 assess thl' arterial circulation. SOI11C of "ll1Ch IIlcludc duplcx scannlllg and \ clocl ty "il\·cform analySIS. Thesc studies complcmcnt the Information obtalllcd in thc history and physical c\am. but an.: 110t necessary in diagnosing the etiology oflhl' patlcnt's ulcer.
~UItIC)'
ANlItIQll YIIW
o
"HI
VIIW
·Alt~I,U,'HJIt(·U~I'f~
Fij.!urc 6--4 L.m:allng \CII1S. Courtcsy uf lIuntlcigh Dlagnoshcs l.td .. Cardlfr. unlled KlI1gdol11
care management and d~tcrl11l1lc which paticnt~ need prompt rcferrnlto a \·ascultlr surgcon (sec Figure 6 5).
\O"'II\' \SI\ ' E \ EI\OllS I ES lI NG Vcnous c\aluatlons arc lIsuall) performed to rule out deep \ein thrombosis IDVT). Thl.!)" arl.! also uSl.!d to e\aluatl.! for superficial and deep \ l'l1(lliS In sufficiency In patients \\ ilh se\cre \·arico~c \ eins or \ l'llOUS ulcer~. Venoll~ Dopp lcr ultrasonography is a 1l011111\i.\SI\e Imaging study thal is performed 111 a \·ascular lab. The ullrasollnd can \ isuallie thc vcms \\·ithlll the leg. thus diagno~lI1g incompl'lcnt \enous vahcs or clot \\ithin the deep \enous sys tcm (sec Fl gun: 6 4).
CO \ CL lSIO,", Thc nonll1\
R EFE RRAL CRITERIA The followlIlg indicators guide refcrral geon or the vascular lab:
10 1.I
vasc ul ar sur-
• Ankle-brachial index greater than 1.0. I CpO~ mcasurement greater than 30 mill Il g: se l11lurgent va:..cular appointll1l'nt • Gangrene pr..:scnt; urgcnt vHscular appointl11en t
• ABI: I, Grcater than O.N: routinc vascular appointlllcnt 2, Between 0.5 and O.N: sel11lurgcnt vascu lar appOI llt ment 3. Belt)\\ 0.5: urgent vascular appOlllll11Cnt
History
Claudication Diabetes Hypertension Smoking Cholesterol
Varicose Veins OVT Trauma
Ul cer Assess ment
Arterial
Venous • • • • •
• Warm foot, edema • Brawny skin • Located usually medial malleolus • Some pain when foot dependent, relieved with elevation • Size: usually large • Wound bed: exudate • Granulating
• • • • •
-
Foot cool or cold Absence of leg hair Shiny skin, dry, pale Nail deformities Ulcers below ankle (toes. pressure area) Elevation pallor, dependent rubor Pain w!elevation Size: usually small Wound bed: dry, necrotiC Slow capillary refill
Pulse Exa m
-
3+ (normal) pulses
3+ (normal) pulses
1
I
OK to treat venous ulcer With compression and wound care Debride if needed
Patient Teaching : 1. Wound Care 2. Foot care 3. Hygiene 4. When to notify MO
FiJ!.u rc 6-5 V
OK to treat arterial ulcer with wound care: MO's choice
Patient Teaching: Wound Care Foot care Control risk factors OrthotiCS When to notify MD
1. 2. 3. 4. 5.
NOl1jm'Qsil'e Vascular Tit.wing
• Exposed bone o r tendo n at base of ulcer: urgent vasc ular appoi ntmcnt • Gross in fce tion or ccll ulitis: urgcnt vasc ular ap po inlI11CI1l
• Ankle-brachial index less than 1.0 wit h diminished o r abse nt pu lscs: sc miurgent vascular appoi ntment • Nonhea lin g wo und s des pite 3+ pul ses and good wo und carc: se miurge nt vascul ar appointmcnt • When in do ubt. refer to vasc ul ar lab for further cva luation SELF-CA ll E TEAC HI NG GU ID E LI NES
135
• Do no t wear tight shoes. • Test bath water with a hand o r thcrmomc ter «98° F) to avoid burns. • Do not walk barefoo t at
Self-Care Teachin g C uid elines Speci fi c to Ve nous Insuffi cie nc),
Thc key to prevcntion of vasc ula r di seases is patient educa ti on. Education is the key to prcventing debilitating ci rculato ry problc ms. Pat ients must learn th e co rrect way to avoid addcd stress o n thcir c irc ulato ry systcm and when to no tify their phys ician ift hcrc is a problem . Self-Care Teachi ng G ui de lines S pecific to A rt e r ial
Insuffi ciency • Do not smoke! Even one ciga rette a day ca n decrease c ircu lation. • Foll ow physici an's directions for co ntroll ing blood prcssure, diabetc s, a nd hi g h c holestero l. • Inspcct legs a nd feet daily and report any sig ns of redne ss, pain. or ulceration immediatel y. Be SUfC to inspect bctween toes. • Wash and dry fcet cvc ry day. • Lubricate skin to avoid cracks. • The fi rst th ing to go into the shoe in the morning should be a hand . Check to make s ure thcre a re no foreign objects th at co uld injure the foo t. • Cut toe nai ls st raight ac ross. If possible, have a podiatri st c ut th e toe nails.
Do not smoke! Wear s uppo rt stock in gs as prescribcd. Avoid crossing legs. Elevate legs when silting. Inspec t legs and fect daily. and repon any increased swe ll ing, new or large r ul cers. increased pain, redness. or infection . • Avo id trauma to legs, s uch as bumping o r sc ratching. • Keep legs and feet clea n. • Eat a well-balanced nutriti o na l die t that is low in sodium .
• • • • •
RHERE:-I C ES I. Fahcy V. l'fuel//aY N,lnil/g. 2nd cd . I)h il adcl ph ia : WB Sa unders: 1994:53 55. 63 66. 2. Young J. Graor R. Olin J. Bartholomc\\ J. Periphl'l'(li HnCllfar ellses. SI. Louis. MO : Mosby-Yearbook 1991 :443 456.
f)j\'-
3. Dickson C. cd . l't,scu/(lr Surg{" ) ' COli/hat Mallual. Napcr\ illc. It : Wt Gore & Associ;nes: t996:4 I\. 27 37. 4. Rutherford R. /(HCIIllIr Surgery. 3rd cd. Philadelpll1a: WI) Sau nders:
t989: t:6t 91.
II
P A RT
Management by Wound Characteristics Barbam M. Bales-Jel/sen
The Bates-Jensen rules for wound therapy arc as follows:
Management of necrotic tissue involves wound debridement by one offour methods: mechanical, enzymatic. sharp.
is discussed. The definition and significance of wound infection arc presented. Misdiagnosis of wound infection occurs frequently in clinica l practice. Differentiation ofinfection and colonization of the wound is not a simple ta sk for most cli ni cians. Comparing charac tcristics of the infected wound with the inflamed wound reveals significant simi larities as well as some key differences. Onc of the primary methods of differentiating between infection and inflammation is by wound culture. Bates-Jensen provides background and discussion on wound cultures with tissue biopsy, needle aspiration. and quantita tive swab techniques. A procedure for each type of wound culture technique is included. The rising incidence of resistant organisms is presented with refere nce to methicillin-resistant Staphylococcus uureus. One method of management of exudate and infection is wound cleansing. Wound cleansing and irrigation are discussed in relationship to use of antimicrobia l cleansers. and specific cleansing procedures for variolls wOllnds are presented. The usc of topical antimicrob ials (antibacteria ls. antifunga ls. and ant iseptics) is presented with discussion on management of exudate with moist wound dressings completing the management interventions. Outcome measures for eva luating exudate management in terms of amount and type of exu-
and autolytic. Each debridemelll method is presented with
date arc presented. The chapter ends with self-care tcaching
indications for use, contraindicati on, advantages, and disadvantages of the method and procedures for implementation. Outcome measures based on the color and amount of necrotic tis sue in th e wo und arc presented as too ls to measure the effectiveness of debridement interventions. The
gu idelines for use with other health care workers. family caregivers, and patients. Chapter 9 focuses on the managemcnt of edcma. Wiersema-Bryant presents discussion of the etiologies associa ted with edema and strategies directed toward the management of edema. Management of edema includes a description of the procedures for managing edema and the parameters to measure in determining outcomes of interve ntions. Edema assessment and measurement of edema and edema control are presented as two primary categories of
!frlle wound is dirty. clean if. /flhere is leakage. manage il. If there is a hole. fill it. Ifit is/1m. protect it. Ifit is healed. prel'l!II'il.
Understanding Ihe impact of wound charac teristics on
treatment options provides a template for intervention. Often the physical appearance orthe wound is the driving force
behind treatment options. Management of wound healing by examination ofphysicaJ characteristics commonly observed in wounds is presented in Part II. The wound characteristics of necrotic tisslie. exudate and infection, edema, and the
clean. proliferating wound require specific interventions by the clinician . Pari II begins with a chapter on management of necrotic tissue. A description of the significa nce and pathophysiology of necrotic debris in the wound bed opens the discussion. Specific necrotic tissue characteristi cs of consistency. color, adherence. and amount are described. The characteristics of necrotic tissue in various wound types are described. The clinical presentmion of the two types of necrosis. slough
and eschar, is described.
chapter concludes with self-care teaching guidelines for other health care workers. family caregivers. and patients. Chapter 8 reviews management of exudate and infection.
The significance and pathophysiology of wound exudate are presented. Common wound ex udate for various wound types
137
qu antitative and qualita tive findings. Quantitati ve ly, Icg ci rc umfe re nce and leg vo lume ca n be meas ured to give a reference range o fl eg size, a nd, with care, pitt ing edema ca n also be meas ured and qu antified. Procedures and guide lines for de te rminin g leg circ um fe re nce, leg vo lume. a nd pitt ing edema a re included . Q ualitati ve assess ment includes ge ne ral appea rance of the sk in and leg and pati ent stateme nts about th e edema. Elimination and co nt ro l o f edema may be accomplished through leg e leva ti on, exe rcise. and the use o f co mpression the rapy. Leg e levat io n fac ilitates th e remova l of flu id th ro ugh utili zati on of g rav it y in ass isting ve nous re turn . Compression th erapy works with exe rc ise to fac ilitate th e move ment o f excess fluid from the lowe r ex tremity. Included as appropriate for cdema managemcnt are leg e levat ion. clastic wra ps. tubul ar ba ndages. paste ba ndages. gradu ated compress ion stoc kings, inte rm itt ent sequcllIial co mpression dev ices. and exercise. A di sc ussion o f each method o f edema ma nagement includes a definitio n o f the l11 eth o(~ th e indi ca ti ons and contraindicHiions for usc. adva lllages and di sadva ntagcs of th e me th od. a nd procedu res fo r impl e mc nt ati o n o f th e mcthod. Ex pec ted out comes re la ted to edema co nt ro l with each method and he lpful hints for using the me thod make these procedu res ve ry use r frie ndly. The chapte r co ncludes with seve ral ease studi es emphas izing the princ iples of edema manageme nt and. fin all y, self-ca re teac hing gui de lines. includin g a sa mpl e pati e nt co ntrac t. The final c ha pter in Part II exa mines wo un d manageme nt of the clea n wo und. Geo n'rey Sussman prov ides di sc ussion of topical wo und care products fo r moist wound hea ling. Disc ussion includes ine rt and pass ive products such as gauze. lint and fiber produ cts, and modern mo ist wo un d dressings. The features o f an "i deal" wo und dressi ng a re presented.
Generi c wo und product ca tego ri es of film dressi ngs. fO<1 ms. hydrocollo ids. hydroge ls, alginat es, hydroacti vc dressings, and co mbination/miscellaneo us dressi ngs are th en presented. Each wo und catego ry includes a de finit io n of th e prod ucts. th e compositio n and prope rti es o f th e dress ing. indicati ons and contrai ndi cati ons for use. procedu res for app licat ion and remova l of the dressings. and ex pected out co mes for each ca tegory. Discussion of wo und clea nsing and usc of top ical ant imi crobials is presented in relati on to th e clea n wound. The c hapte r concl ud es wi th a table of all dressing categories for easy refe re nce by the clinic ian. The chapters on wo und ma nagement by wO llnd characteristi cs in Pa rt II a ll include too ls sllch as proced ures for specific interventi ons. self-ca re teac hing guidelines. and gu idelines for measuring outco mes. The procedures and guidelines included in th ese chapters provide the cl inician wi th a " toolbox" fo r da il y prac ti ce in wo un d management. Each chapter foc uses on simpli fy ing the o nen-co mplex task of determin ing whic h inte rve nt io ns arc appro pria te for the pati ent with a wound . As such. eac h follows the simple rul es for therapy stated at the beginning o f thi s part int rod uction. If the wound is dirt y. if necroti c debris and infec ti on are presen t, clean the wo und. Debri de the devitalized tissue and identify and treat infecti on. If the wo und is lea ki ng excess ex udate or edema is prese nt. ma nage th e drai nage. Co ntrol th e edema and cont ain excess ex udate. Provide for a moist wo und envi ronm ent. not a wet wound environment. If there is a hole, if signifi ca nt ti ssue has been lost at the wou nd site. provide fo r ti ss ue re place ment with a wound dressing. or fill th e ho le . If th e wo und is n at, in th e p rocess of ree pith e lia li zati on, protect it from ex tern al trauma. Fi nall y, if th e wo und is hea led, preve nti on of future wo un ds is criti cal.
CHAPTER
7
Management of Necrotic Tissue Barbara M. Bales-Jensen
SIGN I FICAI'':CE OF :>IECROTIC TISSUE
As ti ssues die. they change in co lor, consistency. and adherence to the wound bcd. As necrotic tissue increases in
sc\'crity. the color progresses from white 'g ray 10 tan or ye llow and finally to brown or black. Consistency of the necrolic ti ssue changes as th e ( is~ lI CS desiccate or dry. Initially consistency may be mucoid with a high wale r content. Later the material becomes morc cl umpy and stri ngy in nature. Eve ntuall y the tisslies appear dry. Icmhcry. and hard. The level of tissue death and the \\-'Qund etiology influence the
clinica l appearance of the necrotic tissue. As subcutaneous fa! tisslIes die. a collection of stringy. yellow slough is formed. As muscle tisslies dcgcncn1tc. the dead tissue may be more thi ck or ten acious. Histologic stud ies of human ski n during pressure.:: sore development del1lonMrate that as the in ~lI lt to the tissue prog resses the level of necrosis deepens. l.~ liard black eschnr represents full-thickness destruction. possibly occurring from prolonged ischemia and anoxemia or a sudden large vesse l disruption from shearing forces. 2 Fat and dermal necrosis and the formation of a slough may be compounded by infection from previous contamination by normal sk in nora. I.l J The debris may appear as ye ll ow slough or a mucoid substan ce.J < Prolonged ischem ia may cause necrosis of underlying tiss ues and ll1an ifest as a gray area. blueness of the ski n. or white devitali/cd tiss ue. U.... Tiss ue co lor \ aries as necrosis worsens. from \\ hile/gray nonviable tissue to ye llow slough and finally black esc har. Co"si.\'lellc.:r refers to the cohesiveness of debris (ie. is it thin or thi ck? strin gy or clumpy'!). Consistency also varies on a continuum as necros is deepens. The terms slough and e.\char refer to di fTerent le\els of' necrosis and are described nccording to color and consistency. I I The term slo ugh is
described as yellow (or tan) and thin. mucinolls, or stringy; eschar is described as brown or black, so ft or hard. and representing full- thi ckness ti sslic dest ructioll . I •1 The more Wtiter content present in thc necrotic debris. the less adherent the deb ri s is to the wound bed. Adherence refers to the adhesiveness of the debris to the wound bed and the ease with which the two are se parated. Necroti c ti ss ue tends to become mo re adherent to tile wound bed as the level of damage increases. Clinica lly. eschar is more firm ly adherent thun ye llow slough. The boxed table on the following page refers to color plates for necrotic tissue assessment. Plate captions give more information. The amount of necroti c tissue retards wound healing because it is a mcdium for bacterial growth and a physical barrier to epidermal resurfacing. contraction. or granulation.' 'I The marc necroti c ti ss ue present in the wound bed. the more severe the insult to the tissue and the longer the time required to hea l the wound. l ln the process of treating the necrot ic wou nd the amount of necrotic tissue prese nt leads to mod ificat ion of trealment and debridement techniques. In addition. determining the severit y of the tiss ue insult may be postponed if' the amount of necrotic debris is sufTicient to obscure \ isualizatioll of the tot<11 wound. Necrotic ti ss ue may be obsencd in chronic wounds with various etiologic factors. Ar terial/Isc hemic \ Vo u mls ecrotic debri s in the ischemic wound may appear as dry ga ngrene. It may have a thi ck. dry, or desiccated, black/gray appearance. It is usuall y firmly adherent to the wound bcd . It may be surrounded with an erythematous halo (see Color Plates -15
139
lIlId
47).
140
W",
Nil
C'RI
Assessment of Necrotic Tissue Types
Color Phlfes
Color
Black brown eschar
Tan yellow slough
Yello\\ fibrinous
White. gray
MOisture content
liard
Sofilsoggy
Sofl'stringy
Mucinous
Ad herence
Firmly attached base and edges
Attached base on ly
Loosely attached
C lu mps
Color Plate(s)
7.20.2 1.25.29,46
1,30
3
27, 28, 30
Neurotrophic ""oullds
Discussion of advantages and disad\'antagcs of each debridement intervention follows .
Neurotrophic wounds lIsua lly do not present with ne-
crosis but often 11<.1\'c hyperkeratosis surrounding the wound. Th is hyperkeratosis looks like callus formation at
Mechanical Debridement
the wound edges. The wound edges need to be dccalluscd or
Mechanical debridement Itwo lvcs the usc ofsomc outside force to remove the dead tissue. The most common types of mechanical debridement are wet-to-dry gauze dresslIlgs, wo und Irriga tion (using syringe and needle), and whirlpool (sec Chapler 20). The advantages of mechanical debridement Include the following:
saucerized frequent ly (sec Chapter 15, Figures 15 99. 15 9C,and 15 14). Venous Disease \-\ounds Venous disease wounds may have either eschar or slough present. Orlen venous \\-'Dumts will appear with yello\\ fibrinolls material covering the wound. Eschar may be attributed to desiccat ion orthe \v'ound and the necrotic debris (see C%r Piale 50). Pres~urc
• Mcchanical debridclncnt uses treatment options tha t arc familiar to most health care professionals. • Wound irrigation can effec ti vely decrease the bacteria l burden on the wound when done correctly, and it can be used in conjunction with other treatment options.
Sores
The nccrot ic debris that occurs in pressure sores relates to the amount of tissue destruction. In the early stage of pressure sore formation. the tissues may appear hard (indurated) with purple or black discolora tion on intact skin. This is indicative oftissliC death. and the necrosis appears as the wound demarcates. exhibit 7 I presents a critical thinking model. or guide line. for assessment of necrotic tissue and may be helpful in determining the best intervention choice. TERVENTIONS
The therapcullc Intervcntion for necrotic tissue presenting III thc \vound is debridemcnt. A \ariety of debridement choices are a\'ai lable to the clinician. Debridement choices often hinge on the wound appearance, the type of wound and the type and amount of necrotic debris present in the wound. Some general guidelines may be helpful. Appendix 7 A presents debridemen t choices for a variety of wounds and necrotic tissue types. There are four main types of\\'Ound dcbridcment : mcchanical. eillymatic, sharp, and autolytic.
The disadvantages of mechanical debridement relate primarily to use of wet-to-dry gauze dressings and outweigh potential benefits: they include the following : • Mechanical debridemcnt is nonselective. It removes healthy tissue in addition to dead tissue. • Wet-to-dry gau?e dressings are rarely applied correctly. • Wet-to-dry gaule dressings may cause pai n on removal. • Wet-to-dry gauze dressings may be morc costly III terms of labor and supplies. Proccdures for each type of mechanical debridement are presented for reference and lise. A.fecllan;ca/ Debridement Procedures Prm:edure: 'Vet-Io-Dry Gall:.e Dre.\.\ illg.\ Equipment Needed'
• Steri le normal saline • Gaule (rolled or 4 x 4-lnc h squares)
A1anagemenl oj NeclV tic Tissll e
14 1
Ex hibi t 7- 1 NecrOlic Tissue Assessment G uideli ne
IDENTIFICATI ON OF NEC ROS IS Is wou nd bed viable (pink or red )?
r
YES Wound clea n. no nec rosis Refe r to C IHlpt er 10
1' ll EDOMI NANT CO L O R O F WOUN D7
Black brown esc har
Ta n/yellow slough
Whi te/gray
Ye ll ow fibrinous
MO I STU RE C ON T ENT'!
Soli/soggy
li ard
Soft/stringy
Mu ci no lls
A DH ER ENCE?
Firmly attac hed base an d edges
Attac hed base o nl y
Loose ly attac hed
C lumps
I'E RCENTAGE O F WO UN D COVE R ED wlnl NEC ROS I S'!
50°11 100° 0 Covered
25%- 50% Cove red
<25% Covered
I)R EDOM I NANT TY P E O F NEC ROS IS? (ge nenl chara cteristics of ea ch type)
I:,·.\·c/wr
Slougll
Fib,.;"
Ilyperkeraros;s
Gangrene
liard Soli, soggy
Soft, soggy
So O. soggy SoO, stri ngy Muc inous Yel low/white Att ac hed base Loosely attac hed Cl umps
li ard
li ard Soft . soggy
White/g ray Fi rmlya llac hed
I3l ack/ brown Firm ly att ac hed Attac hed base
50% 100% Covered 25% 50% Covered
S urrou nd s wound edges
100%) Covered 50% 100% Covered
llIack/b rown Firm ly attached Attached base
100° (, Covered 50° '0 100% Covered
So ft. stri ngy Mucinous Yel low/ tan Fi rmly attac hed Attac hed base Loosely attached Clu mps 100% Covered 50°1, 100% Cove red 25 u (j 50% Covered
• Cover/topper sponges
•
terile gloves (o ne pair)
• Clean gloves ( two pai rs) • Paper ta pe, tras h bag
Preca/lfioll: Pmient may need premedicat ion for pai n at
the time of dressing change. Pmcedure: I. Ex pl a in dress in g a nd procedure t o pa ti ent and
Freqllellcl': Ap ply eve ry 8 hours for wet-I o-dry (sec Chapter 10 for WC l-{o·moist ga uze dressi ngs). /lIdjca!iolls: Mo ist necroti c wo unds (nol effective on dry eschar). Cowrah,dictlliQlls' Do not use on clea n wounds because
the hea lthy tissue wi \1 be "debrided."
caregIve r.
2. Wash hands. 3. Pre pare dressing suppl ies. 3.
Open gauze and m o iste n w ith no rm al salin e.
b. Open cover sponges. c. Tear tapc.
142
W OUNI) CARl'
4 . Apply clea n g loves (to pro tect fro m cross-co ntam inati on), 5. Remove dirty dress in g and d ispose o f in tra sh bag. 6. Remove g loves a nd di spose of in trash bag (gloves have bee n co ntamin ated wi th th e dirt y dress in g). 7. Apply clean g loves (to pro tec t fro m cross-co ntaminati on). 8. Eva luate wound (see C hapter 3 fo r more o n wound evaluati o n). 9. C lea n wound. a . Usc 35-mL syri nge a nd 19-9a uge needl e to apply wound clea nse r d irectl y into wo und. b. Usc normal saline or a Ilollionic surfactant wo und c lea nse r. c. A ntimicrobial solut ions such as povidinc· iodine destroy hea lthy wo und ti ssues and should be used
cautiously- fo r shorf-term Ireafmelll.jol' appropria te hac/erial flora Ollly! (Sec Chapter 8 for morc on wound cleansers and infecti on.) 10. Remove g loves and app ly steril e g loves (to prevent
introdu ctio n of new bacteri a into th e wo und ). (When wo und care is being carri ed out in th e home or 1011g-
II .
12.
13. 14 .
15.
term ca re se ttin g, the procedure may be perfo rmed usi ng o nl y c lean g loves.) O pen th e mo istened ga uze, Ou ff, and p lace in the wo und loosely. Be s ure to place so me of the dress in g in unde rmin ed o r tunn e led a reas. Cover th e wo und with th e cover o r to ppe r s po nges. Use o ne cove r s po nge fo r eac h gau ze 4 x 4- in ch square used in the wo und o r each 6 to 8 in ches of roll er gauze used in th e wo und. Sec ure th e dressi ng with pa per lape, writ e the date and time, a nd initia l the tape. Dispose o f th e trash bag and wash hands. Rev iew procedure w ith patient and ca reg iver.
Procedure: IJlo ulld Irrigatioll Eallivmellf Needed:
• • • •
Steri le no rm a l sali ne Goggles. if s plashing is anti ci pated C lea n g loves (o ne pai r) 35-mL sy ringe and 19-9a uge needl e o r a ngiog ra phic catheter • Ir ri gati o n tray • Tras h bag • Gau ze s po nges (4 x 4- ine h squa res o r Kerl ix s upe r s ponges ) cove rlto ppe r s po nges
"r
Erequellell ' Apply with each dress in g cha nge.
ludiclIIions.' All wo unds.
CO ll lmilldicalio llS: Use "geOlle" irri gat io n o n c lean wo unds and mo re vigo ro us irri gati o ns o n nec rotic wo unds (sec C hapter 8). Procedure:
I. Ex pla in procedure to patient and careg iver. 2. Was h ha nds. 3. Prepa re suppl ies. a. Ope n gauze o r cover s po nges. b. Fill syringe w ith irri ga nl. ( I ) Use no rma l sa line o r a no n ioni c surfactant wo und c lea nse r. (2) Antimi c ro bia l so luti o ns such as povidine-iodin e des troy he alth y wo und ti ss ues a nd s ho uld be lIsed caut io llsly- fo r short-term
treatment. fo r appmpriate bacterial flo ra ullly! (See C hapt e r 8 fo r more o n wo und cleanse rs and infecti o n.) 4 . Appl y gogg les a nd c lea n g loves (to protect fro m splashing a nd cross-conta minati o n). 5. Re move dirty d ress in g and di spose o f in tras h bag. 6. Re move g loves, di spose o f in trash bag, a nd apply c lean g loves (to protect fro m cross-co ntaminati o n). 7. Eva lu ate wo und (see C hapter 3 for mo re o n wo und eva luatio n). 8. Flus h wo und with irrigan!. Ho ld needle/ca theter I to 2 inches fro m wo und bed. a . Irrigate forcefu lly to debride loose, necroti c tissue mec hani ca lly. b. May att ac h a 14-French stra ig ht catheter to irrigate tunne ls and la rge underm ined areas. c. Irri gate gent ly if wo und is c lean o r free of ncero ti c de bris. 9. Dry s ur ro und ing skin w ith ga uze o r cover spo nges. 10. A pply prescribed dress ing accordin g to procedu re for dress ing.
E nzy matic Debridement Enzy mati c de brideme nt invo lves the use of enzy mati c oi ntl11c11ls or so luti o ns to remove the dead ti ss ue. A phys ic ian 's o rd e r is required, a nd ma n ufac t ure r's g uid e lines sho uld be fo ll O\ved. Enzymati c o intmcnt s arc not acti ve in dr y e nviro nm e nt s and arc no t inte nd cd fo r usc o n dry eschar. Esc har mu st be c ross- hatched with a scalpe l and the wo und s ur face ke pt mo is t fo r the pre parati o ns to be sll ccessful. Th e most comm on types o f enzymati c preparati o ns a rc shown in Appendi x 7- 8. T he ad vant ages are th at enzymati c dcbridement is selecti ve. wo rkin g o nly o n necroti c ti ssll e, and is e ffecti ve in co mbinati o n with o th er debride-
A1al/agemel/( {~lNecrolic Tiss/le
ment techniques. suc h as sequential sharp debridement and autolytic debridement. The disadvantages include the following: • Onen enzymatic use is prolonged more than necessary. It should be stopped when the wound is clean and free of necrotic tissue. • Enzymatic debridement can be slow to achieve success: it may take from 14 to 30 days to achieve a clean wound bed. Procedures for enlymatic debrideme nt are included for refere nce and lI SC.
Enzymatic Debridem ent Procedures Procedure: Ell zymtllic Prepartlliolls £tlUipmellf
• • • • • •
Needed'
Enzymati c preparation Gauze (4 x 4-inch squa res) or cover/topper sponges Clea nsing solution Sterile gloves (one pair) Clea n gloves (one pair) Paper tape. trash bag
Frequel/ev,' Follow manufacturer's guidelines. Illdicaaol/.\" All necrotic wounds; moist necrotic wounds are best. If the wound has dry eschar. cross- hatch the eschar
to improve healing. It is usefu l to match type of necrotic ti sslle to actions of enzyme activity, but no t essent ial. For example, a ve nous disease ulcer wi ll have more fibrin associated with the necrosis. and an enzyme that works on fibrin might be more effective. COlllraindicatioll.\': Do not use on clean wounds, dry gangrene, or dry ischemic wounds un less vascular consultation or ankle-brachial index (see Chapte r 6) has been obtained and circulatory sta tus determined. Procedure' I. Explain dressing and procedure to patient and caregiver. 2. Wash hands. 3. Prepare dressing supplies. a. Open gauzc or cover/topper sponges and moisten with norma l sa line (mosl of the enzymatic ointments require a moi st dressing for maximum effectiveness). b. Tear tape. 4. Apply clean gloves (to pro tect from cross-co ntamination). 5. Remove dirty dressing and dispo se of in trash bag.
143
6. Remove gloves and dispose of in trash bag (g loves have been contaminated with the dirt y dressi ng). 7. Apply clean gloves (to pro tect from cross-contamination). 8. Evaluate wound (see Chapter 3 for more on wound evaluation). 9. Clean wound (follow manufacturer's guidelines on use or cleaning sol utions). a. Use 3S-mL syringe and 19-9auge needle to apply wound cleanser directl y into wound. b. Use normal saline or a non ionic su rfactant wound cleanser. c. Avoid antimicrobia l sol utions suc h as povidinciodine, which de stroy cl17ymatic activity in the e nzyme preparations. 10. Remove g loves and app ly sterile g loves (to preve nt introduction of new bacteria inlo the wound). (May lise a dressing other than ga uze or cover/ topper spongcs as appropriate lopicalthcrapy as the secondary dressing for the wound. When wound care is being carried out in the home or long-term care se tt ing. the procedure may be perform cd usi ng on ly clean gloves.) I I. Apply the enzymat ic ointlllent with a tongue blade or colton-tipped applicator to wound bed. As an alternative. the e nzymatic ointment may be applied directl y to the gauze dressing to be app lied to the wound surface. 12 . Open the moiste ned ga uze. Ouff. and place in the wound loose ly. Be sure to place some of the dressing in undermined or tunne led areas. (May use a dressing other than gauze or cover/topper sponges as appropriate topical therapy as the seco ndary dressing for the wound.) 13 . Cover the wound with the cove r or topper sponges. Use one cover sponge for each ga uze 4 x 4-inch square used in the wound or each 6 to 8 inc hes of ro ller gauze lIsed in the wound. (May use a dressing other than gauze or cover/topper sponges as appropriate topical therapy as the secondary dressing for th e wound.) t 4. Secure the dressing with paper tape, write the date and time, and initial th e tape. IS. Dispose of the trash bag and wash hands. 16. Review procedure with patient and caregiver. Sharp Debride me nt Sharp debridement may be performed as a one- time debridement or as sequential ins trum ental debridem e nt. Onetime surgical debridement is rapid and effec tive and may convert the chron ic wound to an acute wound. Laser de-
bridement may be considered a form of surgical debridecandidates for the operating room. Sequential instrumental debridement involves removal oflaose avascular tissue with sterile instrumen ts and may be performed by a variety of health care professionals. Both registered nurses and physical therapi sts may perform sharp debridement for wounds in most states. Check state practice acts before proceeding.
bridement) unless the clinician is certain of collateral circulation by vascular studies or an adequate ankle-brachial index is present. Pressure ulcers on heels that present with black hard eschar may be left intact provi ded they are inspected daily: if signs and symptoms of pathology develop (redness. sogginess, or mushy feel to th e area or frank purulent drainage). they should be debrided immediately. Procedures for sharp debridement are presented for reference and usc.
Clinical Wisdom : Licensing Issues
Clinical Wisdom: Safe Sharp Debridement
Registered nurses and physical therapists (PTs) may perform sharp debridement. Nurses must (and PTs should) complete an education course on wound debridement and competency validation of wound debridement skills. Competency validation involves per-
A key to successful, safe sharp debridement is knowledge of anatomy and assessment. The threepart Sharp Debridement of Wounds video series, Introduction and Technique, Anatomy and Assessment of the Torso, and Anatomy and Assessment of the Lower Extremity , is a training tool available to teach anatomy of common wound locations on the torso and lower extremities, assessment of necrotic tissue. instrument techniques, and procedures of sharp debridement. 10
ment and may be effective on those patients who are not
forming debridement skills on a wound model such
as a pig's foot and demonstration of debridement skills on patients with a qualified mentor to document competency. Some states do not allow nurses or PTs to perform sharp debridement, so it is wise to check with the state board of registered nursing, the state nursing practice act, and the PT licensing agency for vali-
dation of practice requirements for performing wound debridement.
Sharp Debridement Procedure Proc:el/ure: Sharp, Sequelltial/llstrume"t Debridemem
Of course. the main advantage of sharp debridement i s the speed of converting a necrotic wound to a clean wound. When sharp debridement is performed as a onc-time operative proccdure the chronic wound may convcrt to an acute wo und with resultant wound closurc. Sharp dcbridement is a selective form of debridement when performed properl y. Sequential instrumental debridement is effective in combination with enzymatic, mechanical, and autolytic debridement and can speed th e removal of necrotic debris when used in combination with other techn iques. The disadva ntages of sharp debridement include the fo llowing: • Sharp debridement requires a level of experience or skill and specific education. • There is often questionable reimbursement when sharp debridement is performed by nonphysic ians (nurses). Reimbursement depends on individual state practice acts for nurses.
There arc specia l indications for sharp debridement in relation ship to pressure ulcers. Sharp debridement should be performcd when gross necrotic tissu e. sepsis. or advancing cell ulitis is present. Ischemic wounds should not be debrided (by any means, but most certainly not with sharp de-
Eauipmelll Neelleli:
• Silver nitrate sticks , Gelfoam, or hemostatic dressing (optiona l) • Sterile normal sa line • Gauze or cover/topper sponges • Instrument sc t • No. 10 and No. 15 sca lpel and blade • Wound dressing of choice • Clamp (Ke\1y or mosquito) • Suture removal se t • Sterile gloves (one pair) • Clean gloves (one pair) • Paper tape, trash bag • COllon-t ipped applicators • Sc issors (sma ll. fine. serratc(l and large with or without serrations) • Forceps (Adson with or without teeth- or AdsonBrown) Frequel/cP' Perform according to clinica l judgment and physician's orders. /lIliiclIIioIlS: Allnccrotic wounds: moisLnecrotic wounds are best. Irthe wound has dry eschar. autolytic or enzymatic
A4allagemelll oj Necrotic Tissue
debridemcnt may be used first to soften necrosis and facilitate sharp remova l of debri s. COl!traiudi(·(lfiol/.\" Do not pcrform if you don 't feel comfortable or don't know what you arc cutti ng! Do not perform on cleH n wounds; dry ga ngrenc, or dry isc hemic wounds unl ess vasc ular consultation has been obtained and circulatory status determined . Procedure: I. Veriry phys ician orde rs. 2. Explain procedure to patient and caregiver. 3. Premedicate patient for pain and re laxation. a. Topical: lidoca ine (Xylocaine) spray or solution or benlocaine (J-Iurricainc) spray. Lidocaine spray can be used as <.1 gauze compress directl y to the wound site for 10 minutes for effective topical anesthesia or may be locally injected. b. Systemic: oral. intramuscular. or intrave nous as a preoperative/predebridement regimen . Administer approximatel y 30 minutes prior to therapy to increa se patient tolerance and compliance wi th procedure. 4 . Assemble equipment. 5. Arrange for an assistant. 6. Provide ror adequate lighting. 7. Position patient. 8. Wash hands. 9. PrepHfe clean field und equipment. 10. App ly clean gloves (to protect from cross-contamination). I I . Rcmove dirt y dressi ng and di spose of in trash bag. 12. Clean wo und (follow manufacturers guidelines on usc of cleaning solutions). Warm solution to 96° to 100°F ror patient comrort, irpossible. a. Usc 35-mL syringe and 19-9auge needle to apply wound cleanser directly into wound. b. Usc normal saline or a nonionic surfactant wound clea nser. 13. Evaluatc wound (see Chapter 3 for more on wou nd cvaluation). 14 . Remove gloves and di spose or in trash bag (gloves have been contaminated with the dirty dressing). 15. App ly sterile g loves (to preve nt introduction of new bacteria into the wound). (When wound care is being carried out in th e home or long-term care setting, th e procedure may be perrormed using on ly clean gloves.) 16. Using the pickup rorceps, lin th e dead ti ssue or eschar that you arc trying to debride and Cllt it with scalpel or scisso rs. Grasp dead ti ss ue and hold it taut so that the linc of demarcation is clearly visualized. Cut it with care and try to take it down in layers to prevent removal of hea lthy tissue. Pain and bleeding are signs of healthy ti ss ue.
145
17. Re move as much nonviable ti ss uc as possiblc, but limit procedure to 15 to 30 minutes. a. Request reevaluation when any of the following arc present : ( I ) Eleva ted temperature or patient is on downhill course (2) No wound improvement over several weeks (3) Cellulitis or gross purulence/ inrection (4) Impending exposed bone or tendon (5) Abscessed area (6) Extensively undermined areas b. Aggressiveness o r debridement should be guided by the ro llowing: ( I ) The amount of necrotic ti ssue prese nt (2) Patient pain tolerance limits (3) Time sc hedule and limits to avoid patient and provider ratigue (15 to 30 minutes) 18. Stop debriding when the rollowing occur: a. There is impending bone or tendon . b. You are close to a fascial plane or othe r named structure. c. You get nervous. 19. Provide postdebridcment care. a. C leanse wound with normal saline. b. Apply wound therapy or choice. c. Document procedure. 20. Secure the wound therapy with paper tape if necessary, write the date and time, and initial the tape. 2 1. Dispose of the trash bag and wash hands. 22. Review procedure with patient and caregiver. (See Exhibit 7- 2 for more information on self-care teaching guidelines for wound care wi th necrotic tissue.) Autolytic Debridement Autolytic debridement refers to the breakdown of necrotic ti ssue provided by the body's own white blood cells. Autolysis may be accomplished by use of any moisture-rete nti ve dressi ng. The moist wound surface promotes rehydration of th e dead ti ss ue, and the wound nuid contains whi te blood cells and enzymes that break down the nec rotic tissue. Autolysis is facilitated by cross-hatching if the wound is cov· ered with dry escha r. Autolysis is usually perrormed using one or the rollowing dre ss ing choices: • Transparent film dressi ngs (best for dry eschar; because they arc nonabsorptive Ihey rapidly create a nuid environment) • Il ydrocolioids (best ror moist wounds with necrosis because they provide some aso rpti vc capacity whi le maintaining a moist wound environmen t) • Hydrogels (promote auto lys is by maintaining a moist wound environmen t)
146
Wot lJ\D
C\RI
E~hibit
7 2 Self-Care Teaching GUidelines
Inslruclions Chen (Date/l nitials)
Self-Care Guidelines Silecific 10 'iecrolic Tissue
Dcmonstration or I~c\ ic\\ of M1l1crial (Date/l niti:lls)
Rcturn Dcmonstralion or Vcrbalizes lndcrslanding (Dale/l nilials)
I Type of Wlllllld and reason for necrotic tissue 2. Significance ofneerosls .1. Topic.1I themp) care roullne:
a Clean
\\'(llilld.
h. Apply ell7.ymatic preparation (ifappropriatc). c. Apply autolytic dressmg or hydrogel
transpnrenl film. hydrocolloid.
d. Apply secondary dresslIlg If using enzymatic preparation. 4. I'requency of drc,:,;slng changes 5. I '
III
wound appearance during dcbru.lcmellt
6. When to notify the health care provider: a
Signs and symploms of infection
h. hulurc 10 Impro\e c. I: '" alenee of undermining d impcnding bone o r joint II1vohement
7 Imparlance of follow-up with health care provider
The advantages of autolysis are that debridement is fast (there should be significant progress within 6 days). selective. 10\\ cost. and effec ti ve in combination with sharp debridemcnt techniques. Disndvantages include the caregiver education required to prepare for the wound appea ra nce wit h autolysis: the odor and exudate under the dressing also may be disturbing. Procedures for autolysis using scycra l dressings arc presented for reference and usc.
Autolytic Debridement Procedures
Proce{/ure: Autolytic Debrhlemellt- Trallsparellt Fi/m Dre.·,,\·;llg
Equipment Needed: • Steril e normal sa line • Skill sealant • Tmnsparcnt film dressing
FrequetlCr: Apply every 3 to 5 days . Always change dressing when drainage leaks out. IndicatiQns: All necrotic wounds. but most bcncfictal for dry esc har: may cross- hatch esc har to fac il itate autolysis. ConrrajmJjcqtions; Do not usc for dry gangrcne or dry ischcmic wounds unless vascular consultation has been obtained and ci rculatory status determined . Pmeet/lIre · 1. Explain dressing and procedure to patient ~lI1 d caregiver. 2. Wash hands. 3. Prepare dressing supp lies. a. Open transparent fi lm drcssll1g. b. Be surc dress lI1g SIIC is at least 2 inches larger than wound area to be covered. 4 . Position patient oITafTccted area. 5. Apply clean gloves (to protect from cross-contamination).
Management qlNecrofic Tisslle
6. Remove dirty dress ing and dispose of in tras h bag. (There is likely to be an odor. a nd th e wound drainage may appear quite di sturbing.) 7. ReIllove gloves and dispose of in trash bag (gloves have been contami nat ed wit h the dirty dressing). 8. App ly clean gloves (to protect fro m cross-co ntamination). 9, Eva luate wound (see Chapter 3 for more on wound evaluation). 10. Clean wound (follow manufacturer's guide lines on use of c leaning so lut ions). a. Usc 35-mL syringe and 19-9auge needle to apply wound cleanser d irect ly into wound. b. Use normal saline or a Ilonionic surfactan t wound cleanser. c. A\'oid antimicrobial so luti ons sLich as povidineiodine. which destroy healthy wound tissues and shou ld be used cautiously- for short-term treatmelll. Jor applVpriate bacterial flora only! (See Chapter 8 for more on wound cleansers and infection.) I I. Remove gloves and apply sterile gloves (to prevent introduction ofncw bacteria into th e wound). (When wound care is being ca rri ed out in the home or longterm care se ll ing, the procedure may be performed using only clean gloves.) 12 . Apply skin sea lant to skin surroundi ng the wound and allow to dry until skin looks shiny (skin sealan t protects the skin surrounding the wound from macerat ion and stripping during dressing rcmoval). 13 . Apply the tran sparent f ilm dressing acco rd ing to manufacturer's guide lin cs. a. When treating lesions in the sac ral/coccygcal area it is best to apply the dressi ng in a crisscross, overlapping fashion using strips of the dressing. b. Avoid tension and wrink ling of the dressing. 14. Secure th e dressing, write the date and time. and initi althe dressing. 15 . Dispose of the tras h bag and wash hands. 16. Review procedure with patient and caregiver.
Procedure: Autolytic Debridement- Hydrocolloid or J-1ydrogel lJ'(lfer Dressillg.\· Eallipmelll Needed.' • • • •
Sterile normal saline Hydrocolloid dressing or hydrogel wafer dressing Skin sea lant (op tional) Paper tape
PrealleIlCl" Apply evcry 3 to 5 days. A Iways change dressing when drainage leaks out.
14 7
/Il dicmioll.\" A ll necrotic wOllnds. Dry eschar may benefit from cross-hatching to facilitate autolysis. This procedure is particularly effective in moist necrotic wounds with moderate amounts of exudate. Comrailldicatiolls' Do not lise for cellulitis, documented wound infection, dry ga ngrene, or dry ischemic wounds unless vascular consultation has been obtained and circu la tory stat us determined. Procedure '
I . Exp lain dressing and procedure to patient a nd caregiver. 2. Wash hands. 3. Prepare dress ing supplies. a. Open hydrocolloid/hydrogel dressing. b. Be sure dressing size is at least 2 inches larger than wound a rea to be covered. 4. Position patient ofT affected area. 5. App ly clean g loves (to protect from cross-co nta mi nation). 6. Remove dirty dressing and dispose of in trash bag. (There is likel y to be an odor, a nd the wou nd drainage may appear quite disturbing.) 7. Remove gloves and dispose of in trash bag (g loves have been contaminated wi th the dirty dressing). 8. Apply clean gloves (to protect from cross-contamination) . 9. Evaluate wound (sec Chapter 3 for more on wo und eva luation) 10. C lean wound (follow manufacturer's g uide lines on usc of c lean ing so luti ons). a. Use 35-mL syringe and 19-9augc needle to apply wound cleanser directly into wound. b. Use normal sali ne or a nonioni c surfacta nt wou nd cleanser. c. Avoid antimicrobial sol uti ons such as povidineiodine, whi c h destroy healt hy wo und tissues a nd shou ld be used cautiously- jor sltort-ferm freatmelll. for llpplVpriate bacterial flora OIl~\I! ( ee C hapter 8 for more on wound cleansers and infection .) II. Remove g loves and app ly sterile glovcs (to prevent introduction of new bacteria into the wound). (W hen wound care is being carried out in the home or longterm care setting, the procedure may be performed using on ly c lean gloves.) 12. Peel backing off th e hydroco ll oid or hydrogel wafer dressing and appl y according to manufacturers guidelin es. a. Apply strips of tape to the wafer edges in a picture-frame manner; usc of a skin sea lant under the tape is advised to protect from strippin g.
148
W OUND CAR'
b. Avoid use or skin sealanls under hydroco lloid and hydrogc l dressings. 13. Secure the dress ing, write the date and time. and ini-
I
2
ti al th e dress ing. 14. Dispose orthe ,rash bag and wash hands.
3
15. Review procedure with pati ent and caregiver.
4 5
OUTCOME MEASUI{ES Outcome measures are too ls lIsed to eva luate the effective ness o f therapy. Three appro pri ate c haracteri stics fo r
cvalwuing the effecti ve ness of debri dement ra kc n fro m the Pressure Sore StallisTooIs 1lo12 are the amount of necrotic ti sSlie in th e wo un d. th e type of necrotic ti ssue in th e wo und. and th e adherence of th e necroti c ti ssue in th e wound. The
Sussman Wound Hea ling Too l uses the presence or absence of necrotic tiss ue as a predi ctor of healing and a way to monitor heali ng (sec Chapter 5).11 Changes in necrotic ti ssue are intermediate outcomes: the fi nal outcome measure is healing.
None visible White/gray nonviable tissue ancVo r nonadhcrcnt ye1\ow slough Loosely adherent yellow slough Adh erent, soli blac k eschar Firmly adh erent. hard black eschar
Adherence of Nec rotic Tissue
Adherence of the necrosis should decrease as debridement proceeds. Initially the necro,ic tissue may be rirmly attached to the wo und base and all wound edges. As debridement proceeds the necros is begins lifting and loosens fro l11the edges of the wound and eventually disengages from the base of the wo und as well. Adh erence is best evaluated lIsing a ra ting scale similar to that for types of necrotic tissue. General guidelines for length oftimc for de bride mcnt arc presented in Tab le 7- \. REFE RRAL C RIT ERIA
A mount of Nec roti c T iss ue
The amount of necrotic ti ssue should dimini sh progressive ly in the wo und if therapy is appropriate. The amount o f necrotic tiss ll e call be measure d by linea r measurements (measuring the length and width of the necrotic debri s), by determining the percentage of the wo und bed covered. and by photography. To determine the percentage of the wo und bed covered usc a transparent measurin g device wi th concentric circles. Draw a hori zo ntal and a ve rtical ax is th ro ugh the ci rcles and usc 'he device 10 help j udge the percentage of the wo und involved. A rating scal e similar to the following may be used to quantify amount of necrotic ti ssue:
2 3 4 5
NOlle visibl e <25% or wo und bed covered 25% to 50% or wo und covered >50% and <75% or wound covered 75% to 100% or wo un d covered
Type of Nec rotic Tissue The type of necrot ic tiss ue should change as the wound improves and heals. As the necrotic tissue is rehydra tc(L the appearance wi ll change fro m a dry, desiccated eschar to a more soggy, so rt slough, and finall y to a mucinous, easil y dislodged ti ssue. The color usua1\y changes as the necrosis is debrided. The blac klbrown eschar gives way to yellow or tan slough. Usuall y escha r improves to slough material. Rating 'he type or necro,ic tissue is best acco mpl ished by the lise of a scale similar to the follow ing:
Debridement in arterial/ischemic ulcers is cont rai ndicated un less, and unt il. adequate circulatory status has been determined. If yo ll don't feel comfortable or have limitcd or no ex perience in debridement, youl11ay wa nt to rere r to a hea lth care prov ider wi th more ex perience. The fo llowing patients may wa rrant referral to the physician or an advanced practice nurse: • Dry ga ngrene or dry ischemic wounds should be routinely referred for vascul ar consultation for circ ulatory status determination. • Patients with elevated temperature or those on a downhill course should be evaluated rurther. • Patients with no wound improvement over several weeks should be eva luated further. In this case. thc nurse may want to consult other health care practitioners (physical therapists. dietitians. wo und care nurses, ET nurses, and physicians). • Patients with evidence of celluliti s Of gross purulence! infection. • Patients with impending ex posed bone or tendon present in the wOllnd. • Pati ents showing evidence of an abscessed area or patients with extensively undermined areas present in the wound should be eva lua,ed rurther. SE LF-CA RE TEACH INC CU IDELI NES Pat ient and caregive r instruction in self-care must be individualized to the topica l therapy care rout inc, the individual
Table 7- 1 Debridement Time Frames Necrotic TIssue Type
Eschar
Debridement Choice
Autolysis
Expected Outcomes
1. Eschar nonadherent to wound edges
TIme Frame GUide
14 Days
2. Necrotic tissue lifting from
Notes
Depending on type of dressing used for autolysis, may proceed at more rapid rate.
wound edges 3. Necrotic tissue soft and soggy 4. Color change from black/brown to yellow/tan Eschar
Eschar
Enzymatic preparations
Sharp
1. Eschar nonadherent to wound edges 2. Necrotic tissue lifting from wound edges 3. Necrotic tissue soft and soggy 4. Color change from black/brown to yellow/tan 5. Change from eschar to slough
14 Days
1. Removal/ elimination of eschar if done one time or significant
Immediate jf one time,
be effective.
7 days if sequential
Autolysis or enzymatic preparations
1. Necrotic tissue lifting from wound base 2. Necrotic tissue stringy or mucinous 3. Tissue color yellow or white 4. Change in amount of wound covered-gradual decrease to
If sequential sharp debridement used in conjunction with
enzymatic preparation or autolysis, may expect clean wound base in 7 days.
change in amount and adherence if sequential
Slough or fibrin
Requires compliance on dressing changes in order to
14 Days
Will require moderate amount of exudate absorption and protection of surrounding
tissues from maceration.
,..
~ ~
~§
wound predominantly clean
Slough or fibrin
Sharp
1. Removal/elimination of necrotic slough if done one time or
significant change in amount and adherence if sequential
Immediate if one time,
7 days if sequential
If sequential sharp debridement used in conjunction with enzymatic preparation or autolysis, may expect clean wound base In 7 days.
~
~
~
'~"' ;:So
3l
" """ ~
150
IV""", ('.,.,
patient"s wouluL the individual patient's learning style and cop ing mechanisms. and the ability of the pariclll.icarcglvcr
to perform procedures. These general self-care
te~lching
guidel in es must be indh'iduali/cd for each patient and carcgl\'c r. E,h ibil 72 presents sci f:'carc teaching guidel illes related to necrotic tissue management.
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Appendix 7- A Debridement Choices for Chronic Wounds
151
V>
'" Wound Type Pressure sores
Tissue Type Black/brown eschar
Consistency Hard
Adherence Firmly adherent ,
attached to all edges and base of wound
Amount of Debris
Debridement Choices
Rationale and Notes
75%-100% Wound
1. Autolytic-best choice is
covered
May use hydrocolloid or hydrogel; score eschar with scalpel for more rapid results. 2. Enzymatic ointment with
1. Transparent film dressings trap fluid at the wound surface with no absorp-
transparent film dressing.
secondary dressingmust score eschar with scalpel.
tive capabilities , providing
for more rapid hydration of the eschar and facilitating autolysis. Hydrocolloid/ hydrogel dressings have an absorptive capacity and may require more time for autolysis. 2. Enzymatic ointments
effective against collagen and protein may be most effective.
Black/brown eschar or Yellow/tan slough
Soft, soggy Soft, stringy
Adherent, attached to wound bas~,
50%-100% Wound covered
mayor may
not be attached to wound edges
1. Autolytic-best choices are hydrocolloids and hydrogels; composite dressings may also be beneficial. 2. Enzymatic ointment with secondary dressing.
3. Sharp, sequential, or one time-may be used alone or in conjunction with any
of the above methods.
1. Hydrocolloids and hydrogels provide for absorption of mild to moderate amounts of exudate while maintaining a moist wound environ-
ment to facilitate autolysis. 2. Enzymatic ointments
effective against collagen and protein may be most effective. May need to protect intact skin from enzyme and excess exudate.
Yellow/ tan slough
Soft , stringy
Adherent, attached to wound base; mayor may
not be attached to wound edges or loosely adherent to
Less than 50,¥> wound covered
1. Autolytic-best choices are hydrocolloids and hydrogels.
2. Enzymatic ointment with secondary dressing. 3. Sharp, sequential, or one
time-may be used alone or in conjunction with any of the above methods.
1. Hydrocolloids and hydrogels provide for absorption of mild to moderate amounts of exudate while maintaining a moist wound environment to facilitate autolysis .
wound base
continues
:E
c c z
"n>c:
Wound Type
Tissue Type
Consistency
Adherence
Amount of Debris
Debridement Choices
Rationale and Notes 2. Enzymatic ointments
Pressure sores
effective against collagen and protein may be most effective. May need to
(cont.)
protect intact skin from
enzyme and excess exudate. Yellow slough
Mucinous
Loosely adherent to
wound base, clumps scattered throughout wound
50%-100% Wound covered
1. Autolytic-best choices are hydrocolloids and hydrogels. 2. Enzymatic ointment with secondary dressing.
1. Hydrocolloids and hydrogels provide for absorption of mild to moderate amounts of exudate while maintaining
a moist wound environment to facilitate autolysis. 2. Enzymatic ointments effective against collagen and protein may be most effective. May need to protect intact skin from enzyme and excess
exudate. Should be discontinued when wound is predominantly clean.
Venous disease ulcers
Black/brown eschar
Hard
Firmly adherent, attached to ali edges and base of wound
50%-100% Wound covered
1. Autolytic-best choices are hydrocolloids and hydrogels. 2. Enzymatic ointment with secondary dressing.
1. Hydrocolloids and hydrogel dressings have absorptive capacity, which helps prevent maceration of surrounding
tissues and promotes autolysis. 2. Enzymatic ointments
effective against fibrin may be most effective.
-..
"-
~ ~
~
~ -5'., <: ~
Q
~
continues
;::;-
..., -, '"~
~
'-" w
'"". Wound Type
Venous
TIssue Type
Consistency
Adherence
Yellow slough
Soft, soggy, or fibrinous
Firmly adherent, attached to all edges and base of
disease ulcers (cont.)
Amount of Debris
50%-100 % Wound covered
wound
Debridement Choices
Rationale and Notes
1. Autolytic-best choice are hydrocolloids and hydrogels. 2. Enzymatic ointment with secondary dressing. 3. Sharp, sequential, or one time-may be used alone or in conjunction with any of the above methods.
1. Hydrocolloids and hydrogel dressings have absorptive capacity, which helps prevent maceration of surrounding tissues and promotes autolysis. 2. Enzymatic ointments effective against fibrin may be most effective. May need to protect intact skin from enzyme and excess exudate. Should be discontinued when wound is
predominantly clean. Yellow slough
Fibrinous Mucinous
or
Loosely adherent Clumps scattered throughout wound
Any amount of wound covered
1. Autolytic-best choices are hydrocolloids and hydrogels. 2. Enzymatic ointment with
secondary dressing.
1. Hydrocolloids and hydrogel dressings have absorptive capacity, which helps prevent maceration of surrounding tissues and promotes
autolysis. 2. Enzymatic ointments
effective against fibrin may be most effective. May need to protect intact skin from enzyme and excess exudate. Should be discontinued when wound is predominantly clean.
continues
~
c z
~
f)
>
~
~
Wound Type
Artenal ischemic ulcers
Tissue Type
Black/brown eschar
Consistency Hard
Soft, soggy
Adherence
Amount of Debris
Debridement Choices
Flfmly adherent, attached to all edges and base of wound
50%-100% Wound covered
1. Autolytic-best choices are hydrogels. 2. Enzymatic ointment with secondary dressing.
Adherent, attached to wound base; mayor may not be attached to wound edges
50%-100% Wound covered
1. Autolytic-best choices are hydrogels. 2. Enzymatic ointment with secondary dressing. 3. Sharp, sequential, or one time.
Rationale and Notes Must be certain of
circulatory status prior to initiatmg debridement. 1. Hydrogel dressings have absorptive capacity, which helps prevent maceration of surrounding tissues and promotes autolysis. The amorphous hydrogels are nonadherent and require a secondary dressing. 2. Enzymatic ointments: may need to protect intact skin from enzyme and excess exudate. Should be discontinued when wound is predominantly clean.
1. Hydrogel dressings have absorptive capacity, which helps prevent maceration of surrounding tissues and promotes autolysis. The amorphous hydrogels are nonadherent and require a secondary dressing. 2. Enzymatic ointments effective against protein and collagen may be most effective. May need to protect intact skin from enzyme and excess exudate. Should be discontinued when wound is predominantly clean. continues
".
§ ~
"" ~
~
~
"
.;:. <:
""S'. ;:::.
3i
" u. u.
v-
aWound Type
Neurotrophic/ diabetic ulcers
Tissue Type White/gray
Consistency
Hard
Adherence
Hyperkeratosis, callus formation at wound edges
Amount of Debris
Involves all/ partial wound edges
Debridement Choices 1. Sharp, sequential, or one time-saucerization or callus removal. 2. Autolytic-best choices are hydrocolloids and hydrogels.
Rationale and Notes
1. Saucerization may be required at each dressing
change. 2. Hydrocolloids and hydrogels soften the callus formation , and this may facilitate removal as the dressing is removed.
!' ~
n := ~
Appendix 7-8 Enzymatic Preparations
15 7
v.
00
Name
Action
Dose
Duration of Action
Notes
Elase and ElaseChloromycetin (fibrinolysin and deoxyribonuclease)
Attacks DNA and fibrin of blood clots and fibrinous exudates
Santyl (collagenase)
Digests collagen , lysis of collagen in necrotic tissue, and collagen fibers anchoring necrotic tissue to wound base
1 Time/day
24 Hours
• pH range is 6-8. • Can be used with triple antibiotic to treat infection. • Detergents, antiseptics, and heavy metals will inactivate the enzyme. • Petroleum-based-remove completely before electrical stimulation.
Panafil and Panafil-white (papain and urea; Panafil also contains chlorophyllin copper)
Enzyme debrider and emollient; keratolytic
1 Time/day
24 Hours
• pH range is 3-12. • Can be used under pressure dressings. • Hydrogen peroxide, detergents, antiseptics, and heavy metals will inactivate the enzyme. • May experience transient burning on application. • Petroleum-based-remove completely before electrical stimulation.
Granulex spray (trypsin 0.1 mg, balsam of Peru , castor oil)
Proteolytic pancreatic enzyme; capillary bed stimulant and emollient
2-3 Times/day
Variable
1-3 Times/ day
6-8 Hours
• Hypersensitivity for people with bovine sensitivity. • Superinfection with chloromycetin. • More effective if applied more frequently rather than in thick layer. • Available in powder and can be used to pack wounds, but very expensive in this form. • Petroleum-based-remove completely before electrical stimulation,
• Do not use on fresh arterial clots. • External use only. • May experience transient burning with initial application. • Petroleum-based-remove completely before electrical stimulation. • Not powerful enough to debride heavy amounts of debris.
!E
~ ~
I')
> ~
C HA PTE R
8
Management of Exudate and Infection Barbara M. Bales-Jensel/
out of the open ti ssue. This fluid is se rou s or serosanguineous. Evaluation or the wound type, the number and type or organi sms present, and the condition of the patient arc important in determin ing risk for infection. Eva luation of wound type includes assessment of acute versus chronic wounds and necrotic versus clean. nonhealing wounds. The number and type of organisms present in the wound are evaluated for burden on the wound possible bacteria-produced toxins, and pathology of the organisms. Patient condition relates to immune function and local host defenses. In the infected wound, the exudate may thicken , become purulent. and continue to be present in moderate to large amounts. An example of exudate character changes in infected wounds is the presence of Pseudomonas organisms, which produce a thick. malodorous, sweet-smelling, gree n drainage,oI or PlVlelis infection, which may produce an ammonia odor. Wounds with foul-smelling drainage are generally in fected or filled with necrotic debris. and healing time is prolonged as tissue destruction progresses. 5 Wounds wit h significam amounts of necrotic debris will often have a thick, tenacious, opaque, purulent, malodorous drainage in moderate to copious amounts. True wound exudate should be differentiated from necrotic ti ssue sloughing off the wound secondary to debridement efforts. Exudate rrom sloughing necrotic tissue is common ly attached to or connected wi th the necrotic debris. However, frequent ly the only method of differemiation is adeq uate debridement of necrotic tissue from the wound. The solubization of necrotic tissue occurs most often as a result of enzymatic or autolytic debridement. Often the removal of the necrotic ti ssue dramatically reduces the amount and changes the character of the exudate. Wounds can become edematous when excessive amounts of plasma proteins leak from damaged capi llaries and per-
Wound exudate (also known as wound fluid and wound drainage) is an important wound aSSCSSI11CIll feature because
the characteristics of the exudate help the clinician diagnose wound infection. evaluate effectiveness of topical therapy, and monitor wound healing. Wound infection retards wound
healing and mllst be treated. Proper assessment of wound ex udate is also illlportaill because it afTirms the body's brief. normal. inflammatory response to tissue injury. Thus, accurate assessment of wound exudate and diagnosis of infection arc critica l components of effecti ve wound management. SIGN I FICANCE OF EXUDATE The healthy wound normally has some evidence of mois-
ture all its surface. Healthy wound fluid contains enzymes and growth factors, which may playa ro le in promoting reepithelializa tion of the wound and provide nceded growth factors for all phases of wound repair. I The moist environment produccd by wound exudate al lows efficient migration of epidermal cell s and prevents wound desiccation and further injury.~ J In acute wounds healing by primary intention, exudate on the incision line is normal during the first 48 to 72 hours. After that time, the presence or exudate is a sign or impaired healing. In fection and serom3 arc the two most likely causes. In chronic wounds, increased exudate is a response to the inflammatory process or infection . Increased capillary permeability causes leakage of fluids and substrates into the injured ti ssue. When a wound is present, the tissue fluid leaks
Nou~ :
The contributions ofNa ncyA . Stot ts, MN, EdD,arc gmtc-
fully acknow ledged.
159
160
WOLNIJ CARl
vade the wound cnviron mcllI. The fluid of wound edema contains proteolytic en7ymcs. bacteria and bacterial toxins.
CooperO suggests estimating the percentage of exudate in
prostaglandins. and necrotic debris, a ll of which contribute
the wound exudate is thick and can be observed in the wound bed. When wound exudate charactcr is more serous in nature, clinica l observation of the wound alone is insufficient to quantify the amount of drainage. For thinner wound exudate, the amount of drainage is estimated by noting the number of dressings saturated during a period of time. Although not part of exudate assessment. evaluation of the wound dressing provides the clinician with valuable data about the efTcctiveness of treatment. Eva luation of the percentage of the wound dressing involved wi th wound drainage during a specific time frame is helpful for clinicalmanagelllent that includes dressings beyond traditional gau7c. In cstimating thc percentage of the dressing involved with the wound exudate. clinical judgment is quantified. as the clinician must put a number to visua l assessment of the dressing. For example. the clinician might determine that 50'. orthe hydrocolloid dressing was involved with wound drainage over a 4-day wearing period. Based on the above data, the clinician might
to prolonged chronic inflammation. Exudate also drains valuable and needed substrates, slich as growth factors. from the wound bed and impairs the healing process. Excess exudate losses drain substrates and energy that could be used ror wound healing processes:'
Asscssmcnl of\Vo und Ex udate C hara cteristics of exudate arc color, consistency. adherence, distribution in the wound the presence of odor, and the amount prcscnt. lI The color and consistency of wound exudate may vary depending on the type of wound degree
of moisture in the wound the wound recovery cycle. and the presence of organisms in the wOllnd. Table 8- 1 presents \iuiOliS types of \'v'Ound exudate and associated characteristic!'!. Color Plale serie.\ 40 ItJ 45 (reading the dressing and wound exudate characteristics) will help the clinician identify exudate types and make an appropriate assessment of significance. Estimating the amount of exudate in the wou nd is diITicu lt because of wound si7e va riability and topica l dressing types. Certain dressing types interact with or lrap wound nuid to create or mimic certain characterist ics of exudate, such as color and consistency of purulent drainage. For example. both hydrocolloid and alginate dressings mimic a purulent drainage upon removal of the dressing. Preparation ofthc wound site for appropriate exudate assessment involves removal of the wound dressing and cleansing to remove dressing debris in the wound bed. Then cvaluate the wound for true exudate.
the wound by clinical observation. This approach \\orks ir
quantiry judgment for this type or dressing, length or dress-
ing wear time, and wound et iology 3S n "minimal"' amount of exudate. Cli nical judgment of amount of wound drainage requires somc experience with ex pected wound exudate output in relation to phase of wound healing and type of wound and knowledge of absorptive capacity and normal wear lime of topica l dressings. One problem wi th assessment of exudate amount is the size of the wound. What might be considered a large amount of drainage for the sma ller wound may be considercd a small amount for the larger wound, making clinically meaningful assessment of exudate more difficult to obtain.
Tabl e 8-1 Wound Exudate Characteristics Color
Exudate Type
Consistency
Significance
Sanguineous/bloody
Red
Thin, watery
Indicates new blood vessel growth or disruption of blood vessels
Serosanguineous
Light red to pink
Thin, watery
Normal during inflammatory and proliferative phases of healing
Serous
Clear, light color
Thin, watery
Normal during inflammatory and proliferative phases of healing
Seropurulent
Cloudy, yellow to tan
Thin, watery
May be first signal of impending wound infection
PurulenVpus
Yellow, tan, or green
Thick, opaque
Signals wound infection ; may be associated with odor
A/altagemellf (?r EXlldal(' anti /II/i.!ction
Appropriate wound c.xudatc assessment requires consideration of wound etiology. Independent of exudate differences related to etiology of the wound certain characteristics of exudate indicate \",ound degeneration and infection. If SIgns of celluhlls (erythema or skin discoloration. edema. pain. induration. and purulent drainage) arc present at the \\-'ound site. the exudate amount may be copious and seropurulent or purulent in character. The amount of exudate remains high or increases in amount and character may change to frank purulence wl,h further wound degeneration . Wound IOfecllon must be considered 111 these cases regardless of etiology.
161
As the \'enous ulcer heals. edema is lessened and the wound exudate increases . The excess nUld takes the path of least resistance. which in this case is the wound bed! Often venous wounds will appear with yello\\ fibrinous material covering the wound which must be differentiated from true exudate. Pre.\ .\UI"e So,.e!tl
Venous disease wounds lIsually arc highly exudative bOlh on initial prest.!l1tation and throughollt the course of healing.
Pressure sores present \\ ith a variety of \\iOlll1d exudate characteristics and amounts. In parllal-thlckness pressure sores the \\'ound exudate is most likely to be serous or serosanguineous in nature and presents in minimal to moderate amounts. In clean full-thickness pressure sores the wound exudate is similar. with minimal to moderate amounts of scrous to serosanguineolls exudate. As healing progresses in the clean full-thickness pressure sore. the character of the exudate changes and may become bloody if the fragile capillary bed is disrupted and lessens in amount. For full-thickness pressure ulcers with necrotic debris, wound cxudate is dependent on the presence or absence of infecllon and the typc of therapy instituted. Exudate may appear moderate to large. but in fact be rclated to the amount of necrotic tissue present and the liquefaction of the debris in the wound. Typically. the necrotic full-thickness pressure ulcer presents with serous to seropurulent wound exudate in moderate 10 large amounts (Figures 8 IA and 8 (8). With appropriate treatmcnt. the wound exudate amount may also tcmporarily incrcase. although the charactcr gradually assumes a serous nature.
A
B
A rteria/I/.\ chem ito If ollm/.\
Exudate 111 the ischemic wound may vary in amount and character Arterial ischemic wounds arc often dry or have only a scant to small amount of serous exudate present. Veuropllthil' "olilld.\
Neuropathic wounds may present with very little exudate presellt. One pOSSible reason for decreased exudate is a limlied innammation response due to concomitant vascular disease and Immune status changes from diabetes. Generally. the exudate is mll1imal and usually serous or serosanguineous in character. J (!IIOll.\ Di.\(!u.\(! HOI/lid.,·
Fi~urc
8 1 \ :tnd B. Ob\ iou, "gns of mfectton
SIGN IFI CANCE OF I NFECTION
!\1ct h ici II i n-I{csista n t SllIp/ty/Ol'Ol'l'u.\ A II rell.\
Although bacteria colonize all chronic wounds, wound coloni7ation by bacteria is not the same as infection. When host and wound condi ti ons arc favorable. infection can occur. Wound infection extends inflal11matory response. delays collagen sYl1lhcsis. retards cpithclialil.ation. and causes more injury to the tissues as the bacteria compete with fibroblasts and other cclb for limited amounts of oxygcn.~ Large acule wounds generally reaci to bacterial burden in a way different from that in small chrollle ulcerative wounds. ACLIte \\o'ollnds arc marc susceptible lO bacterial invasion by skin flora. in particular those with prolonged inflammatory rcsponscs. ~ Wounds with loss of large amounts of surface area (15 11/0 of body surface area or greater) arc also at a higher risk for bacterial invasion. SufTicient number:; of skin flora organisms will cause acute \vounds like graBs and flaps to fall and, ifuntreated lead to sepsis while a chronic leg ulcer may remain unchanged for months or years with no signs of infection or sepsis with the same or largcr number of organisms presclll.lC Thc same organisms that pose serious threat of infection and sepsis in some acute wounds present entirely difTerent pictures in the sma ll chronic WOUJ1(l which may go on to heal despite the presence of these organisms. Chronic wounds arc oBen contaminated \\ ith skin flora. such as Emerf)cocclis. Stap/ty/ocOCCf/.\, Bacillus, or occasionally gram-negative organisms. 1I Distinguishing between contamination and infection in wound, is orten difTicult. The process of difTerentiating between a contaminated wound and an infected wound is important to better underMand treatment choices. Coloni/ation is the process of a group of organisms living together. whereas infection is the invasion of tissues by microorganisms. resu lting in a systemic reaction. Most clinicians will agree that IO~ to IO~ organisms per gram of tissue indicate wound infection. Some laboratories lise different references, so what Illay be considered colonization in one facility may be considered infection in another facility. In general. the o\-erall condition of the patient also enters into the diagnosis process. Infection is signaled by a systemic reaction to the microorganisllls. and contami nation signals the presence of microorganisms in the wound. II igh leyels of bacteria arc found in chronic wounds with necrotic debris. The number and density of aerobes and anaerobes are greater in necrotic wounds and those with undermining. s The presence of a foul odor is usually associated with anaerobic organisms. Sharp debridement of necrotic tissue virtually eliminates the anaerobic organisms (such as Ba c teroilif!s , Streptococcus, EIIIl'rohucter, and Escherichia coli) and decreases the aerobic organisms (such as Sraphy/ococclI\' lIUf'f!IIS) present in the wound . ~
Methicillin-resistant S lIllH'II\' (MRSA) presents special concerns for patients with wounds. SWphy/ococl"Il.\ lIureliS IS part of normal skill flora and IS on the Skill of approxImately 20 00 to 50°'0 of healthy adults and can persist in wounds.' Patients at highest risk for de\'eloplllg MRSA colonl/ation and IIlfecllon arc those wllh a 111story of injecllon drug abuse, the presence of chronic discase. prc\ious antimicrobial therapy. prc\iou:,,> hospltali/ation. admiss ion to an IIltensi\'e care unit. or a prolonged stay in a health care institution. ln All forms ofSt/un'lI\,. includlllg M RSA. can quickly ill\ade and infect breaks in skin integrity. making woulllb onc of thc most C0l111110n sites of ,\. allrew infection and a site commonly coloni/ed with S 1IIIH' II.'i or M RSA. In the early 1940s. pellicillll1 was found to be cfTectiH! against S 1I111'l'1I.\: howcver. soon after Ih IIlllial usc. some strallb of S (JItreliS began to produce the ell/yme penicillinase. \\ hich lIlacti\·atcs antimicrobial\ slu;h as ampicillin. other pelllcillins. and cephalosp0rlns. MethiCillin was the fir:">t penicillinase-resistant semisynthetic penicillin and was (and is) used to treat S 1I11rellJ infcctions. The late 1960s and early 1970s saw the emergence of MRSA \\ ith the first rcports of outbreaks in both ,lcute and long-term caJ'e facilities.'" In fections caused by MRSA cause conccrn bec~lUsc resistance to I11cthlCllI1ll IS associated \\ IIh resistance to other tlntlllllcrobials. A gene on the bacterial chromosome that codes for abnormal penicillln-biJ1(ilng protein (PI3P) carries resistance to l11ethlcllllll .'" ThiS abnormal PBP has il lower afl'inity for all peniCIllin. so ,cry little methicdlin blllds to It. Therefore. all pel1lcillins. \'vhich mllst bind to the PSP site 111 order 10 kill the bactena, arc incffccth'c. Some strains of MRSA mutate and become resistant to additIOnal anwnicrobials. Of special concern is the recent finding of the potcnllal for MRSA to acquire the gcne-conferring \·ancol11ycin resistance from yancomycin-resistant enterococci (VRE). leading to vancomycin-resistant S UUI'('II\.'l Since yancomycin IS the drug of choice for treating MRSA. resistance to \'
A/al1ogemem of Exudate and Infectioll
\Vound Contamination versus Infection Clean wounds are contam inated with bacte ri a but usually progress th rough wound healing uneventfully. The clinician should suspect bacterial overbu rden ifhcaling docs not occur in clean wounds wi th appropriate topical therapy. Failure of the wound to progress may indicate a "silent" infection w ith colony COllnts above 100,000 organisms per milliliter yet minimal outward signs of \vound infection and superficial invasion of tissues.
Clinical Wisdom: Bacterial Overburden The clinician should suspect high bioburden of bacteria in the clean wound if healing or improvement does not occur within a 2-week time frame and the patient is receiving appropriate topical therapy for the wound.
Wounds with continuing moderate to large amounts of seropurulent or purulent exudate and signs and symptoms of infection should be evaluated for infection. Local signs of wound infection include cryt hcma or skin discoloration, edema. warmth, induration, increased pain, and purulent drainage with or without a foul odor. Systemic signs of infection include e lcvated temperature, white blood ccll count. and confusion in thc older adu lt . Table 8- 2 gives local and systemic characteristics of wound infection.
Assessment of\Vou nd Infection Assessment of wound infcction involves assessmcnt of the patient'S overa ll condition, observation of the wound and surround in g tissucs to di fTerentiate wound inflammation versus the infected wound and wound cu ltures to determine colony count. C linical signs of innal11l11atioll arc one n mistaken for infection. Table 8 3 presents clinica l manifcsta-
Table 8-2 Characteristics of Wound Infection
Local Signs of Infection Erythema or skin discoloration Edema Warmth Induration Increased pain Purulent wound exudate with or without foul odor
Systemic Signs of Infection Elevated temperature Elevated white blood cell count Con fu sion or agitation in older adults Red streaks from wound
163
tions of both innammation and infection for compariso n. Immullocornprornised patients may fail to demonstrate any signs of infection or the signs may bc significa ntl y diminished. For examp le, in older ad ult s, confusion or agitation may be the firs t indicato r ofinfcct ion and eleva ted temperature occurs much later in the course of the illness. In so me cnses, the wound simply fails to progrcss without other obviolls signs of ill feet ion. In the il11munocompromised patient, identification of the organism may be crit ica l to treatment, in that the responsible organism may be opport uni st ic in naturc and nOl the typical cu lprit in wound infections. II 1111mUl1ocompromised patients Illay also exhibit signs of infection when the bacterial burden is less than th at req uired for producing in fection in immunocompctent patients.
Clinical Wisdom: Cellulitis and Wound Infection Advancing cellulitis indicates that the offending organism has invaded tissue surrounding the ulcer and is no longer localized . Advancing cellulitis begins as a small red or discolored area that is indurated, edematous, and warm to touch and progresses to involve more extensive tissues. Left uncontrolled and untreated, cellulitis can result in sepsis.
The COIllmon mcthod of confirming clinical infection is by colony count. The clinic ian diagnoses the infcction based on c lin ical signs a nd symptoms and obtains a culture to aid in determining the appropriate antib iotic therapy. For example. in outpatient c linics the usual scquence involves the clinician diagnosing the wound infection based on signs and symptoms present and obtaining a culture to confi rm th e correct sclcction of antibiotics for treatmcnt. For inpatients diagnosed wi th infection, antibiot ic th erapy is gene rall y initiat ed immediately and the culture reports arc used to adjust or modify th e antibiotic regimcn. Colony counts higher than 100.000 ( 10' ) are considered indicative of in fcc tion. A heavy bioburdcn (bncterial contam ination in the wound) o r compromised host resistance (fo r example. immunocompromised or diabetic patients) ca n both result in bacterial colony count s higher than 100.000 (10' ) organismsi mL, which is co nsidered confirmation of clinical infection. Chron ic woun ds do not have to be sterile in order to heal. Howeve r, when the bacterial burden in thc wound is over I 050rgan isI11s per gram oftissuc, wound hcaling is impaired or delayed. ~· 1 2 Wounds colonized with ~-hemolytie stre ptococcus can ex hibit impaired healing with colony counts less than IOO,OOO/mL. 7 There are a lso wounds that heal uneventfully in the presence of bacterial co lony counts of greater than 100,000i mL. It is c lear that the dctcnnination of infection involves c riti cal evaluation of the wouncL the patient, and the pathogcn.
164
WOUN I) CARl
Tabl e 8-3 Comparison of Wound Characteristics in Inflamed and Infected Wounds
Wound Characteristic
Inflamed Wounds
Infected Wounds
Erythema
Usually presents with well-defined borders. Not as intense in color. May be seen as skin discoloration in dark-skinned persons, such as a purple or gray hue to the skin or a deepening of normal ethnic color.
Edges of erythema or skin discoloration may be diffuse and indistinct. May present as very intense erythema or discoloration with welldemarcated and distinct borders. Red slripes or streaking up or down from the area indicates infection.
Elevated temperature
Usually noted as increase in temperature at wound site and surrounding tissues.
Systemic fever (may not be present in older adult populations).
Exudate: odor
Any odor present may be due to necrotic tissue in the wound, solubization of necrotic tissue, and the type of wound therapy in use, not necessarily infection.
Specific odors are related to some bacterial organisms, such as the sweet smell of Pseudomonas or the ammonia odor associated with Proteus.
Exudate: amount
Usually minimal; if injury is recent, should see gradual decrease in exudate amount over 3-5 days.
Usually moderate to large amounts; if injury is recent, will not see decrease in exudate amount-amount remains high or increases.
Exudate: character
Bleeding and serosanguineous to serous.
Serous and seropurulent to purulent.
Pain
Variable.
Pain is persistent and continues for an unusual amount of time. Must take wound etiology and subjective nature of pain into account when assessment is performed.
Edema and induration
May be slight swelling, firmness at wound edge.
May indicate in fection if edema and induration are localized and accompanied by warmth.
Source: Adapted from J . Feedar, Wound Evaluation and Treatment Planning , Top ics In Geriatnc Rehabilitation, Vol. 9. No. 4, pp . 35-42 . 0 1994 , Aspen Publishers, Inc.
Eva luation of the pathogen occurs by colony count and provides thc documcntation of infection. Documentation of infcction is bascd on thc amount of the bacteria present in the wound ti ssue. The level of bacteria in the wound tissue is dctcrmined in order to document the presence of a wound infection. As traditionally performed swab cuhures detect on ly surface
contaminants and may not renect the organism causing the tissue infec tion. I,\ Quantitative wound culture is recommended for determination ofinfcction.According to Stotts. 1" if a standardit:cd techniquc is lIscd, a quantitativc swab tcchnique can accuratcl y documcnt thc bactcria l burden in wounds. The technique for obtaining the culture specimen shou ld mirror bacteria in the wound ti ss ue, not simply bacteria on the wound surface.
Quantitati ve Wound C ulture Tissue biopsy, needle aspiration. and the quantitative swab tcchnique are the most frequentl y used methods of quantita-
tivc wound culture. Each has an important place in clinical practicc. Tisl'lI e Biop!O'
Tissue biopsy is removal ofa piece oftissuc with a scalpcl or by punch biopsy. Before performing a tissue biopsy for
wound culture, the area is cleansed with sterile solution that does nOI contain antiseptic. The area may be treated with topical anesthetic or injected with local ancsthetic . The biopsy is performed and pressure applied to the area to control bleeding. The biopsy ti ssue is promptly tran sported to the
laboratory, where it is weighed, named to kill surface contaminants, ground and homogenized, and plated in various mcdia in varying dilutions. Findings are expressed in number of organisms per gram of ti ssue .' ~·'6
Needle Aspiratioll Needle aspiration invol ves insertion of a needle into the ti ssue to aspirate fluid that contains organisms. I? Intact skin
Management oj Exudate and Injection
next to the wound is disinfected with a substance such as povidone- iodine and allowed to dry. Using a I O-mL disposable syringe and a 22-gauge needle with 0.5 mL of air in the syringe , the needle is inse rted through intact skin; suction is achieved by briskly withdrawing the plunger to the 10-mL mark . The needle is moved backward and forward at different angles for two to four explorations. The plunger is gen tly returncd to the 0.5-mL mark, the needle is withdrawn and capped, and the specimen is tran spo rted to the laboratory. In the laboratory, the fluid aspirated is diluted in broth and plated. Data arc expressed in colony-forming units (CFU) per volume of fluid . If ti ssue is extracted by this technique, the weighing and grinding described for tissue biopsy processing also need to be done and, in thi s case, the data generated are in number of organisms per gram of tissue.
Clinical Wisdom: Performing Tissue Biopsy and Needle Aspiration Physical therapists are not allowed by physical therapy practice acts to perform tissue biopsy or needle aspiration procedures. Physical therapists must work coliaboratively with nursing to obtain these samples as recuired.
Quamirlll;,'e Swab Tec:llIIiqlle The swab technique often has been c ritici zed as a method that produces information about co lonization of the ulcer surface rather th an in the ti ss ue. One of the problems with the rOllline swab technique for culturing a wound is that it has been performed in a variety of ways. and therefore cannot be relied upon 10 address the issue of bioburden in the tissues. There is controversy on how 10 obtain a swab cu lture. Some recommend culturin g the exudate in the wo und prior to wound clea nsi ng. UI, 19 Others recommend that after cleansing of the wound is complete, the culture is obtained using a Z techniquc (side to side across the wound from one edge to the other).20.l ' Others suggest irrigation of the wound with sterile water or sal ine and pressi ng the swab against the wound margin or ulcer base to elicit fresh exudate. 22 The recolllmended method of quantitative swab cu lture involves cleansing the wound with a solUlion that contains no antiseptic solution . The end of a sterile cotton-tipped applicator stick is rotated in a l-cm 2 area of the open wound for 5 seco nds. ll Pressure is applied to the swab to cause ti ssue fluid to be absorbed in the cotton tip of the swab. The swab tip is inserted into a sterile tube containing tran sport medium and transported to the laboratory. The end of the applicator that is not sterile is not inserted into the tube for culture. Serial dilutions of the organisms are made on agar plates. A swa b moistened with normal saline without prescr-
165
vative provides more precise data than lise of a dry swabY Results are expressed as organisms per swab or C FU per swab or in a semiquantitative manner, such as sca nt, small, moderate. and large ( 1+ to 4+) bacterial growths. Tissue biopsy, needle inspiration, and the quantitative swab technique are used 10 evaluate the bacte ri a present in wo und tissue rather than on the surface of the wound, in the exudate, or in necrotic tissue. They are used to examine ti ss ue for aerobic and anaerobic organisms. They also can be lIsed to obtai n a specimen for Gram's stain, a mcthod recogni zcd as a rapid diagnostic technique of in fection. 2ul For a Grams stain, the tissue fluid is placed on a slide. treated with various stains and viewed under the microscope. In wounds where swa bs yielded less than 105 organisms. the Gram's SUI in is considered to show no bacteria. Data show that the ti ssue biopsy, needle aspiration. and quantitative swab techniques are comparable in terms of sensitivity. specificity. and accuracy. I" The following de sc ri bcs how the procedures are performed.
Procedures/or Qualltitative ,rollnd Cu/illre Eqllipmel1l Needed: • • • • •
Gloves (clean and sterile) Sterile saline (nonbacteriostatic) Container to tran sport specimen Lab req ui sition Appropriate dress ing mate rial s
e U/lUre Technique Specific Equipmenf Needed:
• • • • •
Punch biopsy/scalpel Wound culture swab Anaerobic medium if required IO-mL syringe with 22-gH uge needle Cork
Procet/ure Preparation-For A ll Alethotls I. Wa h hands. (Reduces transmiss ion of microorganisms.) 2. Don clean gloves (gown ifnccessa ry) . (Maintains uni versa l precautions.) 3. Remove soiled dressings and di scard in plastic bag. Then remove and di sca rd gloves. (Prevents contam ination and spread of microorganisms.) 4 . Clean wound and surrounding skin with normal saline. (Cleaning removes contaminated debris.)
Procedure: Swab Methotl I. Don sterile gloves and rcmove swa b from culturette tube, taking care not to touch swab or ins ide of tubc.
166
WOUNI> CARl
(Ma intains universal precautions and asept ic tech-
nique. ) 2. Swab wound area I CI11~ with sufficient pressure to obtain wound nuid . (Ensures collection of a good specimen .) 3. Use separate swabs if taking more th an onc specimen.
Swab only a I-em! area of wound with each swab. (Ensures good culture specimen and prevents cross-con-
lamination. Care must be taken to swab the wound instead of the wound edges to prevent conraminatioll by skin nora and contaminated debris.)
4. Carefully place swab into culturelte tube without touching swab. inside. outside, or lOp of container. (Prevents con tamination and keeps those areas free of pathogens
Ihat could be spread to others who handle the tube.) 5. Crush ampu le of medi um in culturcttc and close se-
curely. making surc swab is surrounded by medium. (Keeps speci men from drying out and provides supporting mediulll.) Procei/llre: A llilerobic Swab Culture Methoi/
I. Ifcollecting a specimcn for anaerobic cuilurc. take care to kecp anaerobic transport culture tube in an upright position to prevent carbon monoxide frolll escaping. Close contuiner securely after swab is placed in tube. (Maintains anaerobic environment.)
nation. Biopsy is usually performed by a physician or advanced practitioner.) 2. Place specimen in sterile container. (Prevents spread of microorgani sms.) Procedllre: Fil/{If Steps- All Methotls I . Remove and discard gloves in plastic bag. (Reduccs
transmission of microorganisms.) 2. Wash hands. 3. Don sterile gloves and apply sterile dressing to the wound. (Dressing absorbs drainage and immobilizes and protects the wound.) 4. Label specimen container(s) with patient name. room number, date. time. and exact source ofspecimcn. (Ensures proper identi Cication of specimen. Propcr source of specimen is important for laboratory to rule out norlllal nora from location.) 5. Place container in clean pia tic bag. and have spec imen transported to laboratory as soon as possible. (P lastic bag prevents spread of microorganisms. Immediate transport prevents overgrowth of microorganisms that can occur if specimen is len at room temperature for an extended length of time.) 6. Dispose of soiled equipment into approp riate receptacle. (Maintains universa l precautions.) 7. Wash hands. (Reduces transmission of microorganisms.)
Procel/llre: Syringe ft1elh (){/
I. Disinfect intact sk in with antiseptic and allow sk in to dry for I minute. (Anaerobic speci mens are obtained from deep inside wounds.) 2. Place 0.5 mL orair in 10-mL disposable syringe with 22-gaugc needle and insert needle into intact sk in adjacent to wound. Withdraw plunger to achieve suction and mOve the needle back and forth at different angles. (Prevents contamination at needle withdrawal site.) 3. Return the plunger gently to the 0.5-mL mark ; do not insert drainage into the tissues. (Ensllres good specimen and prevents contamination from sk in flora . Syringe method is used when large amounts of pus or drainage are present or for co llecting tissue.) 4. Cork needle to send syringe/needle to laboratory as one unit-containing speci men . Do not recap or attempt to di sconnect needle from syri nge. (Maintains univerSell precautions. Prevents injury from needle stick and spread of microorgani sms.) Procei/u re: Tissu e Biopsy
I. Don sterile gloves. Obtain a biopsy specimen using a 3- to 4-mm dermal punch or a sca lpel. (A llows ror determination of tissue level of micro organ isIII contami-
MANAGEMENT OF EXU DATE AND I NFECTION
Management of exudate and infection includes wound cleansing: usc of topical antimicrobials. antiseptics. Hnd antifungals: and management of exudate with topical dressings. ,"Vo und C leansin g
Effective wound cleansing removes debris that supports bacterial growth and delays wound healing. Wound cleansing delivers cleansing solution to the wound by mechanical force, aids with separation of necrotic tisslle from heallhy wound tisslles, and removes bacteria and dressing residue from the wound surface. The process of wound cleansing involves selecting a cleansing solution and a method of deli vering the sol ution to the wou nd. Ex hi bi t 8- 1 presents the Agency ror Health Care Policy and Research (AHCPR) panel's recommended guidelines for pressure ulcer cleansing. Cleansi ng of all wounds can be performed using these principles. The cleansing solution chosen must be effective and safe to the wound. Isotonic normal sa li ne is preferred as a soll!-
\/al1l1?,<' IIU! l1t (J{Enu/uu!
tion because II IS physIOlogic. nontoxic, and inexpensive. Saline docs not contain preservatives and must be discarded 24 to 48 hours aOer opening.:~Commercial wound cleansers are avai lable to assist in wound cleansing for wounds requiring more cleansing capacity to remove adherent debris from the \\.'ound surface. These wound cleansers contain surfactants that act to lower surface tension and to loosen matter from the \!"uund surface.:!~ Nonionic surfactant wound cleansers are recommended as safe to the healing wound.
Clinical Wisdom: Normal Salme for Wound Cleansing
lind
lujectioll
167
E\hibiI8-1 AII CPR RccoJnmenlh.!u CiuuJclLnes for Pressure
Ulcer CleanslIlg I. Cleanse wounds 1I111ially and al e.tell dressmg change 2. Usc IllJnllnal mechanical force whl.!l1 clc:IIl . . lIlg. ulcer \lvtth gau/c. dOlh. or sponges. 3. Do nol clean wounds" tth s!..1Il cleansers or antiseptic agenls (povidone-Iodme. sodium hypochlorite sulution. hydrogen peroxide. and acellc aCid). 4. Use normal salme for cleansing l110slulcers 5. Use enough Irrigation pressure to enhance wound cletlnsIIlg Without causlIlg trauma 10 the \\ound hed. S4.ltC and clTccti\c ulcer Irrigation pressures range from'" to 15 pSI.
Two useful strategies for obtaining normal saline for wound care in the home setting: 1. Saline can be made at home by adding two teaspoons of table salt to 1 L of boiling water. Be sure to discard after 24 hours. 2. Another useful strategy IS to use pressurized saline commonly used for contact lens wearers. This preserved saline may be used for a longer duration, and the pressure from the canister is not sufficient to cause wound trauma.
For healthy clean wounds, cleanse with normal saline and do not usc antimicrobial solutions or skin cleansers. Clean wounds do not need to be cleansed with antimicrobial solu-
6. Consider 'lvlmlpool tn:atmenl for cleansing ulcers that contain thick ~xudatc. slough. or necrollc tlsslle Dlsconllnue \\ hirlpool when ulcer IS d:an Soltrn!: Reprinted from \ Berg ... lrom, M.A Bennell, (" I Carlson. el .11 .. Tn'al/lll'lIi 0/ Prl'IWr,· tken. ('llllIc;11 Pral.:llce GUldclll1c No. 15, December 191)4. U.S. Depanmt.'nt uf Iteillth and Iluman Scn ices. Public I Icalth Scr\lcc. Agency Ic.lr Ilealth Clre Policy and Rc~carc h. :\I[CPR Puhlicalion 95·0(,52.
'0.
for antibiotic usc, that IS. for a short duration. Antimicrobial agents used as cleansing agents in the debris-filled wound shou ld be used for 10 to 14 days ond rinsed thoroughly from
lions as the goal of care is to clear low levels of contami-
the wound with saline. Rinsing the \!"ound \\ Ith saline aOer cleansing with antimicrobial ~olutlOns decreases the cytotoxic etlccts in the wound. The antimicrobial cleanser should
nants from the wound. In facl. they are harmful. Solutions such as pO\'idone-iodinc. acetic acid hydrogen peroxide, and
or \\ hen the wound is clean and debris free.
be discontinued aner the course of therapy (10 to 14 days)
sodium hypochlorite (Dakin's fluid) are toxic to fibroblasts.
Use of ant lillie robia I agents is contraindicated in the healthy prollferati\c wound because of the damage to the healthy tissues.' :,,' In general. most skin cleansers are not approprime wound cleansers as they hm;e been de\eloped for use e.'tcrnally. not 1Iltcrnally. as is the case with a wound. What is appropriate for cleansing the skin is not appropriate for open wounds because an open wound lacks the protection of intact epidermis and pro\ides direct access to internal body structures. For hc~ilthy clean wounds. cleanse with normal sallllc. For healthy wounds do not use antimicrobial solutions or s~ in cleansers, For infecled wounds. cleanse with normal saline or use a 10- to l-t-day cleansing regimen with an antimicrobial solution, For infected wounds do not usc skin cleanser~ and do not prolong the use or an antimicrobial solution.Antimicrobial agents may playa mlllor role in wound cleansing for infected wounds. wounds with large amounts of necrotic debris. or those with large amounts of e.'lCudate. Use of antimicrobial agents is best handled in a manner similar to that
Cleallsillg Metllod
There are several methods for cleansing the wound including soaking. \\hlrlpool. scrubbing, and Irrigation . Soaking IS 0 l'arm of hydrotherapy (Includes a ,""ety of types from a bucket to a Hubbard tank) and mal be useful for re-
moval of gross contaminants and loosenmg necrotic tissue. The softening that occurs with the soaking helps to ease the separation of necrotic debris from healthy wound tissues. Wound !'oak ing is appropriate only for wounds \\ ith large amounts of necrotic debris. Once a wound is clean and proliferating. whirlpool and \vound soaking impede v..'ound healing and thus generally me not appropriate.' Whirlpool may be useful for more than Simply soaking and cleanslllg. as is the case with using \\ hirlpool to increase perfUSion to an area. (Sec Chapters 17 and 20 for informallon
011
pulsatile
lavage and whirlpool.) Antimicrobial agents should not be used in the whirlpool or wound-soaking solution because of wound tissue toxicity.
168
WOl '" C '"'
Scrubbing the \\'Ound involves usc of gauze or sponges in direct \\"ound contact with mechanical force to enhance reIllmal of debris and efficacy of cleansing solution lIscd.!<
Scrubbing C~lUSCS microabrasions in the wound and thus delays healing. Usc ofa l1onionic surfactant clcansll1g solution will limit the damage inflicted wi th scrubbing to the healing wound tisslies. Use of nonabrasive sponges will also help dccrca::.c the damage to the healing tissues. T he mo rc porous the sponge. the less damage inflicted on the wound surface. !~
Even
lISC
of non ionic surfactant cleansing solUlions and non-
abrasive porous spo nges will injure the fragile wound tissue. Thus. no scrubbing is recol11mended.
Clinical Wisdom: Shallow Wound CleanSing Procedure
Fig ure 8-2 IrngatlOn of \\ound
\~ Ith
synnge.
Cleanse from the center of the wound in a circular motion, working loward the edge of the wound and the surrounding tissues. Do not return to the center of
the wound after cleansing at the edge of the wound or the surrounding tissues, as this will recontaminate the clean wound center.
\Vound irrigalion can be performed using a \'ariety of inMrUIl1Cnts and eqUIpment. Wound irrigation is particularly
appro priate for c leansing deep wounds with undermining or tunneling present. Usc a calch basin and lowels (0 absorb and ncclIlnlllalC waste ma lcriab and irrigant runoff. Repeat
the irrigation procedure at each dressing change. Protect eyes. race. and clothmg of the clinician by lIsing uni\crsal precautions. Some newer irrigation devices include a splashguard to he lp protect the clinician.
Clinical Wisdom: Deep Wound Cleansing Procedure Use of a catheter or a syringe to irrigate wounds with undermining and tunneling will not injure the tiSsues and can effectively cleanse the tissues involved in the wound under the skin surface. Flush with copious amounts of irrigant solution, then gently massage the tissues above the tunneling to express the exudate accumulated In the tunnel. Repeat two or three times until the solution and fluids returned are clear (see Figure 8-2). After the wound cleansing the undermined spaces are usually packed loosely with packing materials such as roller gauze or alginate rope products to prevent infection from traveling up the tunnel (see Figure 8-3).
Figu re 8- 3 Packing wound \\ Ilh lIndcrnlllllng.
The amount of prcs\url.! LISCO for irrigation IS dctcrrlllnc<.l by the dl.!sin..: not 10 harm the healing wound tisslIes and 10 cleanse the \\QlInd ellettl\ ely. The prcssurl.! of dt.!li\cring the
irrigant is commonly descnbed as 10\\ or high pressure. Pressure force is dcscribl.!d in rounds pcr square inch (psi). Pressure force under -t psi is coml11only referred to as I()\\ pressure and can be obtained by lbC of bulb sYringes or Just pouring so lution mer the wound bed. ' Pn!ssure force between 4 and 15 pSI IS conSidered high pressun.: and can be achleH:d by using commercial dc\ ices. a 35-mL syringe attached to a 19-9auge needle or angiocatheter. pulsatile 1m agc. or \\ hirlpool therapy. IlIgh-pressure Irrigation lIsing any of these forms is a mcthod of debridement. loosening and soHcning
J\lfllnllgemellf of c"xuc/lIle lind Illfec lioll
necrotic ti ssue for easy se para ti on from healthy ti ssue. Pressuri zed irriga ti on removes bacteria and debri s more e ncctively than grav it y or bulb syringe irrigation. As such, highpressure irrigation is most effecti ve with an inflammatory process. Use o f hi gh-press ure irri gation is not the method of choice for the healthy, proliferating wound, as thi s can damage fragile blood vesse ls and new ti sslle growth. A number of availab le irri ga tion devi ces deli ver solutio ns with too mu c h pressure, thu s driving bacteria and irrigant solution deeper into wo und ti ssues. Pressures over 15 ps i can cause trauma to th e wound bed, forcing bacteria deeper into wound tissues. For example, lise of a Water Pik at th e middl e and high se ttin gs provi des 42 psi and more than 50 psi, respectfull y, both of which arc too high and will drive bacteria farther into the wound tissues. Irrigati on pressures between 4 psi and 15 psi are recommended . The clinical outcomes from wound cleansing are determined by the purpose of th e clea nsing and the wound assessmen t. For predominantly clean wounds with new ti ssue growth, clea nsing is used only to remove dressing residue. and ifany adJitional clcansing is nceded a low-pressure irrigation system should be used (such as pouring the solution over the wound or usi ng a bulb syringe or pi ston syringe to deliver th e irrigant). The goals of th erapy with low-press ure irrigation arc to di slodge wound dressi ng res idue, reduce wound su rface co ntaminants. and protect fragi le new ti ss ue growth. For wounds with necro ti c ti ssue or debris, a highpressure irrigation system should be used. Whirlpoolthcrapy and pulsatile lavage a rc not always availab le or appropriate for a ll patients. and other devices such as the 35-mL syringe
and 19-9auge needle or angioeathctcr Illay be the best choice. The goa ls of therapy are to loosen and soflen thc ncerotie de bris for easier se paration from healthy ti ss ues, reduce the bacterial burden, remove dre ssing remnants, and prevent undue wound trauma .
Research Wisdom: Wound Irrigation
Use of a 35-mL syringe with a 19-9auge angiocatheter or needle attached delivers saline at 8 psi and provides more effective removal of bacteria and debris than use of a bulb syringe.
Aseptic Tech"iqlle One of the co ntinuing dcbates in wound manage ment is what type of aseptic technique is necessary for wound ca re in va ri ous health ca re settings. Asepsis includes activities that prevent infection or break th e chain of infection . It is generally divided into two types: surgi ca l asepsis and medica l asepsis. Surgical asepsis, or steril e tech niqu e, is the method used in surgery where all instrum ents and materials used arc sterile and all health care providers involved wea r sterile gloves, caps, masks. and gowns. Medical asepsis, or clean technique, in vo lves procedures to reduce the number of pathogens and to decrease th c transfer of pathogens. In surgical asepsis. the nurse prepares a sterilc fi eld don s sterile gloves. and foll ows surgica l aseptic techniques in caring for the wound. Sterile and clean techniques are compared in the following display.
Sterile Technique
Preparation ofa
~ t er il e
field
Clettn Tcchni(IUe
Preparatio n o r clean fi eld
Clea n glO\ es
Cle~lI1
Decontamination of the \vounel and surrounding sk in \\ ith an antimicrobial cleanser
Cle<:lIl sing of the wound nnd sur rounding sk in
Change gloves: Ste ril e gloves
Change glO\ es: Clea n gloves
Use sterile
forcep~.
sca lpel. and sc issors
169
g loves
Use steri le forceps. scalpel. and sc issors
Allow only "sterile to stcrl le" cont
Prcvent direct con tamination of materials and supp lies, but no "steril e to ste ril e" rules apply
Apply sterile dreSSing
Apply clean dressing
170
W OUND CARl
There arc variolls viewpoints on which approach is most suitable for wound care patients. Some general guidelines may help to clarify usc of an aseptic technique. Sterile techniqu e is most appropriate in acute care hospital settings, for patients at hi g h ri s k for infection (advanced age, iml11unocompromised diabetic) and for certain care procedures such as sharp wound debridement. Clean technique is most appropriate for patients in long-term care settings, home care, and so me cli nic settings, and for patients not at high risk for infection and receiving routine wound care such as dress ing changes. Further research is needed lO determine outcomes with lise of clean technique. Table 8-4 co mpares general guidelines for clean versus steril e technique choices for wound care patients. Hand Washing alltlllllet'tion Control What is clear about infection management and wound care is the importance of hand washing by the health care practitioner. Hand washing is the single most important means for preventing s pread of infection. Use of universa l standard precautions and hand washing by the wound care clinician promote health maintenance for patients and caregivers and as such are critically important to include when instructing others in wound care programs. Along with hand washing, caregivers mu st be instructed in appropriate di sposal of infectiou s wastc products. such as used wound dressings. gauze used for wound cleansing. and instrum ents used in wound carc. In institutional sellings. sllch as hospitals and long-term care facilities. there are procedures for di sposal of contaminat ed materia ls in bags clearly identified as infectious waste (eg, double bagging out of isolation rooms and use of red biohazard tra sh bags). In the home care arena. disposa l of contaminated wastc becomes mo re problematic and the wound care clini cia n must address di sposal based on the area
served, local waste collection procedures, and agency protocols. In the homc care se tting, education of the caregiver regarding the procedures for waste disposal is essential for maintaining community health .
Topica l Ant imicrobials· The use of antimicrobia ls is confusing for cI inicians. Systemic antimicrobial drugs (those agents given orally or intravenously) are often superior to topical agents (ointments, creams, or solutions put directly on the wound surface) because of the better penetration or sys temic agents. However, topical antimicrobials are often effective in limiting surface colonization so thal ti ss ue defen ses can clean up without continual reinfection rrom s uperficial bacteria. Some superficial infections may respond better to topical agents and in some cases, it is wise to usc topi cal agents to avoid se ns iti zing the patient or creating resistant microorganisms. Some topical antimicrobials can damage healthy ti ss ue s, exacerbating tissue destruction or damaging ti ss ue defenses. The (efillS tllllimicrobial. tllllibiotic, al1!ibacterial. and allfiseptic are often used interchangeabl y; however, the definitions are sl ightly different according to the Food and Drug Adminisl.mtion (FDA). Exhibit 8-2 presents definitions of these terms for easy rererence. The three main classes of antimicrobials used for wounds include antibacterials. antiseptics. and antifungals. Understanding how antimicrobials are prescribed is helpful for · Thi s inrormatio n is adapted with permi ssio n rrom G. Gilman. cd. Topical Agellls for Open HVUllds: Amibacferials. Anfisepfics. Anti/llngals. Reviewed by G. Rodeheaver. 1. W. Cooper. D.R. Nelson. and M. Meehan. Charleston. SC: Hill -Rom Internationa l. Inc.: 1991.
Table 8-4 Clean versus Sterile Technique General Guidelines Factor
Sterile Technique
Clean Technique
Settings
Acute care hospitals Clinics in acute care facilities
Home care Long-term care facilities Community clinics Physician'S office
Procedures
Invasive procedures Sharp debridement
Routine procedures Dressing changes
Patients
Immunocompromised Advanced age or very young age Diabetic
Patients NOT at high risk for infection
Afallagemel1l ol Exudute lIm/lnte('lion
171
E,hibiI8-2 Definitions or Antimicrobial Terms
Term
Defi ni tio n
A nt im icrobia l A nt iscp til'
An agent that mlllbits or kills microorganisms A substance that pre\en ts or arrests the gmll'lh by preventing multiplication (bacteriostatic) (lr (1('11011 or microorganisms either by inhibiling their activity or by destroying or killing them (bactericidal). Applies to sub~tances lIsed on living tissues (eg. povidone-iodine) An organic chcmicnl substance produccd by a microorganism that has thc capacity in diluted solu tions to destroy or inhibit the growth or bacte ria and other microorganism s (eg. penicilllll) An agent that dcstroys or stops bacterial growth (cg, bacitracin) A wide "Iriely or agents that inhibit or kill rungi (eg. nystatin)
Antibi otic A nt ibaClcriul
Antifun gn l
SOlIlH' Adaplcd \\lIh pCr1ll1"~Lon from Topim/ AgellIs (or Open lI ollfl(l~ IlIfil)(l("/('I'ial.,. " IIli,\el)fic.~. '"il/lIl1gtl/\, G Gilman . cd. rC\lc\\\!d by G RodchCJ\cr. J \\ Coopcr. DR Nebon. and M. Meehan. L' t99t . Ilill -Rom [nlcrnatlonal
\,-"ound care clinicians. This is the process by which antimicrobials arc ordered. The proper use of any antimicrobial requires determination of clinical infection in the wound corrcct identification of the invading organism by cuhurc and Gram's stain Sl11ears prior to beginning therapy, and consideration of pharmacology and toxico logy when choosing the agent. Ifan agcnt l11uSt bc chosen prior to recciving laboratory results. make the decision based on Gram stain smears (either positi\c or ncgati\c), the 1110st likely pathogens involvcd in the disease process (for example. Escherichia coli for a fecally incontinent paticnt with a sacral pressure sore), and the efTicacy of the agent in similar situations.
s
Clinica l Wisdom: Factors Altering Response to Topical Antibacterials and Antiseptics Patient response to antibacterial and antiseptic agents may be altered by age, disease processes (such as diabetes), malignancy, neurologic disorders, immune dysfunction, pregnancy, allergy, or concomitant drug therapy.
Multiple factor~ innuence the transcutaneous penetration of antimicrobial agents including physiochemical properties orthe drug (polarity, stabililY. and solubility in base and lipids), nature of the pharmaceutical preparation (drug concentration. composition and properties of the base, and incompatible mi"(turc ~), method of application (inert delivery systems, til11c-relci.l~ed dclivery systems. application in conjunction with occlusion, polar compounds to increase absorption. and substances that damage the stralllm corneum to improve penetration). and naturc of the skin {integrity of the epidermis. variability in skin thickness. and age}. Problems
associated with topical antimicrobial use in "ound care arc related to absorption of chemicals into the body tissues through the wound bed. There arc cases whcre absorption of certain chemicals contained in an antiseptic through the lVound bcd has caused systemic health problems. For examplc. iodinc toxicity has occurred from usc of povido n e~ iodine in open wounds.
A nlih" clel'i" ls Antibacterinl agents arc chemicals thnt elttninatc living organisms pathogenic to the host or pallent. Some cxamplc~ of antibacterials arc bacitracin, gentamicin. mctronidaLole, mupirocin. and siher sulfadiaLinc. Thc u~c ofantibactcrials is common for most infcctions. In the elderly. thc primary sites of infection in order of frequcncy arc urinary tract, pulmonary systcm. and wounds. 1!(:!'o/ Broad-spectrum antibacterials arc useful for mixed infections "hen there is more than one pathogen present and quick identificatIOn of the organism is difficult. Antibacterial topical administration occurs in sma ll er drug doses, compared with systemic antibacteria ls. due to direct contact wi th the affected area. 'ij The same or bCller results may be achieved without thl.! risk of toxicity. Systcmic agents may be lIscd in combination with topica l agcnts, as in the treatment of impetigo. Topically administered drugs arc in more direct contact with orgalllsms so tha t problems ofabsorplion, distribution. and a\ailability to the infectcd site arc reduced. Frequently, topical agents arc used in conjunction with one another to gi\c broader co\erage, thereby increasing the rate of bactericidal action against a large spcctrulll of bacteria. III Topical anlibacterials may be u;cd prophylactically. When used properly, thcy can be efTecli\e c hemical barriers that may impede the entrance of pathogenic organisms and diminish the local or systemic morbidity associated with in-
172
WOUND eMI
reeted wounds. When using topical antibacterials prophyresistant lactically. there is always a danger of overgrowth
or
organisms; therefore, use of antibacterials for prevention requires good clinical judgmenl for optimal efTcClivcl1css. -1U
Clinical Wisdom: Wound Healing and Antimicrobials
No antibacterial agent, whether bactericidal or bacteriostatic, will be curative when used in isolation. Attention to nutritional factors, management of underlying pathology, and relief of causative factors are also required.
ride, both of which are known to be occasional sensitizers. Oinuncl1(s may be confused with creams, particularly with the introduction of synthetic bases that claim to have the pmI'M erties of both creams and ointments, Lotions are preferable 10 greasy applications for areas thai rub against each other, for example. groin areas and in between the loes. Lotions are usually less occlusive than ointments. Appendix A contains an index of antibactcrial agents. The index provides a listing of commonly lIsed antibacterials and individual entries for each antibacterial. Individual antibacterials are presented with a description of the agent. the action, indications for usc. precautions. directions. and packaging information. A ftliseptic,'\
Topical antibacterials lIsed in a viscolls vehicle provide a wound healing environment facilitating epithelialmi-
l110ist
gralian. 11 The indications for topical antibacterials include
significant bacterial infection diagnosed or sllspecte~ and an indication for prophylactic use due to the patient's underlying disease and/or the patient's increased risk of infection resulting from surgical procedures. viral or metabolic diseases, chemotherapy or radiation therapy. and prolonged corticosteroid administration. Contraindications relate to the excessive lise of antibacterials for minor infections and for nonbacteri~ll pathogcns. -'Il I nappropriate usc of antibacterials subjects the palient to risk of drug toxicity, risk of allergy, superinfection with resistant organisms. and unnecessary costS.1U,12
Clinical Wisdom: Routine Use of Topical Antibacterials Routine use of topical antibacterials is strongly discouraged because of the frequent development of resistant organisms. This is particularly true of mupirocin. as it is effective against methicillin-resistant Staphylococcus aureus (MRSA) and, if used inappropriately, will not be effective when most needed.
The base, or vehicle, is the form in which the antibacterial agent is available. In general. it is best to lise a lotion or a paste for application to weI or weepy skin and wounds and a greasy ointment for application to dry, cracked skin. Crcams arc convenient since to some extent they can be used for \vct or dry surfaccs and arc easier to usc, Many ointments contain lanolin or wood alcohols, and patients can readily develop contact sensitivity to these substances, Creams less often contain lanolin. but usually contain a preserv
Antiseptics are a group ofwideJy diffcring chemical COIU M pOllnds possessing bactericidal (kills bacteria) or bacteriostatic (prevents bacterial multiplication) properties, Some examples of antiseptics are povidone-iodine. acetic acid, hydrogen peroxide, and hypochlorites. They are employed in medical practice with the object of preventing or combating bactcrial infection of superficial tisslIes as well as for sterili7ulion of instruments and infected material. Chemically, antiseptics may be inorganic or organic. Oxidizing disinfectants liberate oxygen when in contact with pus or organic substHllces. DifTerent bacteria are sensitive to difTerent antiseptics. For example, acetic acid is commonly used against infections caused by Pseudomonlls aeruginoslI. Antiseptic agents are applied directly to tissue to destroy microorganisms or inhibit their reproduction or metabolic activity. By reducing organisms, it is believed antiseptics may hasten wound healing and diminish local or systemic morbidity associated with \\'Otllld infection.n Ilowever. many commonly used antiseptics are cytotoxic and actually inhibit wound heal ing; therefore. caution is recommended. ~hThe major lIses of antiseptics are as hand scrubs. cleansers. irrigants, and protective dres:-;ings. It is important to remember that the skin cannot be sterilized and that approxilllHiely 20% of the skin's normal resident flora are beyond the reach of antiseptics. 2'i Excessive antiseptic lise subjects the patient to risk of allergy. risk of drug toxicity. superinfection, unnecessary costs and pose significant public health concerns due to ecologic pressure fnvoring selection of bacteria resistant to antiscptics. B Antiseptics. regardless of type. damage the healthy wound and impair wound healing. ~7 Appendix A contains an index to nntiseptics. The index provides a listing of COIllmonly used antiseptics and individual entries for each antiseptic. Individual antiseptics are presented with a description of the agent, the action. indications for lISC, adverse reactions (with special attenlion to effects on wound healing). dosage. and packaging information.
ManagemeJlt oj Exudate and Injection
All/ifllllgal.,
173
Topical Dressings fo r Management of Ex udal e
Fungi comprise five widely difTering classes of primitive
flora .Thus, antifungal agents include a wide variety ofchemica l types of a rather narrow antifunga l spectrum. Some ex-
amples of anlifungals include nystatin. ketoconazole, and miconazole nitrate. Not all antifungal agents are fung icidal; many are only fungistati c. and certain ofthcm may owe their efficiency to a keratolytic action.
Broad-spectrum antifungal agents in general arc toxic irritants, as expected from their nonselectivity; however, many of th ese have limited absorption through the epidermis and so may be used in dcrmatologic preparations.29 The indications for an antifungal are a significant fungal infection diagnosed or strongly suspected and an indication for prophylactic antifungal use due to th e parient's underlying di sease or the patient's increased ri sk of fungal infection resulting from invasive procedures or environmental exposure (diarrhea, diaphoresis. poor hygiene. diabetes, etc). The major contraindication for ant ifungal use is known allergy to ingredients. Antifungals must be used for the prescribed time to eliminate the infection fully. Some areas are more difficull to treat and some fungi are more difficult to eliminate because of the patient's underlying disease process. External factors may affect the alllifungal agelll's abi lity to penetrate the skin, including temperature, ambient water vapor pressure, and drying agents such as powders. which reduce the excess moisture in the skin folds and may aid in efficacy of anti fun gals. Nonsporing anaerobes are a significant pathogen in ulcers with a fou l smell and exposure to feca l contamination. 29 Metronidazole has been shown to be effective in eliminating or decreasing the odor associated with these wounds Y 31 Appendix A contains an index of antifunga l agellls. The index provides a listing of commonly used antifungals and individual entries for each antifungal. Individua l antifungals are presented with a description of the agent, the action. indications for use, precautions, ava ilable vehicle, dosage, and packaging information .
~
Research Wisdom: Treatment of Malodorous Wounds
Topical metronidazole has been shown to be effective in resolving odor in foul-smelling wounds. Use of
a 1% solution or 0.75% gel (Metrogel) applied twice daily reduced or eliminated odor in 80% to 90% of wounds in 4 to 7 days. Odor was significantly decreased in 2 days. J.4~7
Effective management of exudate requires knowledge of absorptive capacity of dressing materials and attention to fragile wound margins. Excess exudate on the wound edgcs can lead to maceration and destruction of the critical wound edge. Use of petrolatum products or other hydrophobic ointments around the wound can provide some protcc tion for the wound edges. Use of a topical dressing that adequately absorbs the wound fluid will also protect the wound edges.
Clinical Wisdom: Caution about Petrolatum Around Wound Edges If petrolatum products are being used and the patient is receiving physical therapy, nurses must notify the physical therapiSt. The therapist should be informed because petrolatum products interfere with PT technologies and are hard to remove from the patient's skin prior to PT interventions.
The choice of a dressing for a wound in many cases is dependent on the amount of drainage present in the wound and Ihe expecled drainage from thc wound. For example, a wound that has been recently debrided of yellow necrotic ti ssue may have a hi story of moderate to large amounts of drainage; however. the amount of expected drainage post debridement is less, usually minimal to moderate amounts. The topical dressing may also become not only the treatment but also the method of determining efficacy. For examp le, evaluation of the dressing upon remova l from th e wound allows the clinician to judge what percentage of the dressing material has interacted with wound drainage. Eva luation of the amoun t of dress ing used by the wound exudate onen determines whether treatment will continue with the same dressing or whether a new dressing will be applied. (See Color Plale series 40 to 45, readin g the dressing, for detcrmining the effectiveness of topical dressings in management of wound exudate and how to distingui sh exudate from the wound versus material from wound fluid and dressing interaction.) Table 8- 5 presents the generic product categories with notes about the absorptive ability of each dressing type. This information may be useful in choosing dressings for the exudative wound. How to choose a wound dressing to manage exudate is explained in detail in Chapter 10, Management of the Wound Environment. The type of wound under treatment also affects the choice of dre sing for exudate management. An example is the venous disease ulcer under appropriate managcment with compression therapy and topical dressings. For the venous
174
WOl lf\ll)
C \RI
Table 8-5 Topical Treatment-Wound Dressings
Wound Dressings: Generic Categories
Not Absorbent
Low to Minimal AbsorptIon
Minimal to Moderate AbsorptIon
------------------------------------------Skin sealan ts
x x
Composite dressings Tran sparent film dressings
x
x x
Gauze-woven Gauze-nonwoven Gauze-impregnated
Moderate to Large Absorption
X
---
x
Calcium alginates
X
X
Exudate absorbers-beads, pastes, powders, flakes
X
X X (when used WIth other forms of dressings)
Hydrocollolds-regular, thin, pastes, granules
x
X
Hydrogels-sheets, wafers, amborphous
X
X
X
X
Lubricating stimulating agents
X
Foams Hydroco lloid-hydrogel combinations
disease ulcer in the init ial cOlnpression therapy stagcs. exudate amount will increase as edema in the extremities is being managed. Sometimes exudate amount will remain copious for se\ era l \veeks as the edema is brought under control. In ge nera l. the exudate amount can be expected to rcm
X
exudate in the wound the typc of C\lH.lme 111 the wound and the im;ol\cmcnt of the wound dressing \\ith the exudate present in the wound. Measurcment of exudate is an IIltcrmediate outcomc measure; healing IS the final outcome. Amount of [\udate
The amount of c\udate should dimlillsh progrcssi\c1y in the wound if therapy is appropriate. The amount or C\Udate can be measured by lIslng clinical judgmcnt to c\aluate the distribution of moisture in the wound and thc illteraction ofc\udme \\lIh the wound drcsslng.A rating scale similar to thc folh.)\\ IIlg may bc used to quantify ~11110UI1I of c\udate:
2 3
OUTCOME MEASURES
Outcome measures arc lOob used to c\a luatc the results of therapy. Appropriate characteristics to assess in cvaluatmg the results of exudate management arc the amount of
X
4
None wound lJssues tlr) Scant \vound tissucs moist. no measurable c\udate Small wound tissues wet. moisturc c\ enly t.llstribuled In wound, dr3lnagc imol\'lxt ~ 25°o of wound dressing Moderate wound lJs ~'illes saturated dralllagc mayor may not be c\cnly distributed in \\ount.L drainage 111\olved '25()(l to ,75()u of wound dressing
A1allagemelll oj Exudate and IlIjection
5 = Large = wound tissues bathed in nuid drainage freely expressed mayor may not be evenly di stribut cd in wound drainage involved >75% of wound dressing
phase of wo und heal ing. serous drainage should become more serosa nguineous and then sanguineous in nature. As infection or necrosis is resolved, the exudate type should also renect improvement. Foul purulent drainage should become
merely purulelll and then seropurulent , and finall y scrous
Ty pe of Ex ud ate The type ofcxudate should c hange as the wound improves and heal s. As th e wound passes through the inflammatory
and se rosa nguineous in character. Measurement o f type of ex udate is best accomplished by the lise o f a rating scale. A
scale similar to the followi ng may be helpful:
Ex hibit H- 3 Se lf-Care TI.!3ching Guidelines
Se lf-Cltre G uid elines S peci fi c to Ex ud a te a nd Infect io n M a nage ment I. Type of \\ound and reasons for exudate
2. Significancc of c'{udate and infection J. Topical thcmpy ca re routine: a. C le,lIl wound . b. Apply absorptive dressing (note appeanlllce of dressing when it interacts with wound drainage and on remova l) .
c. Manage wound edges to prevent mace rat ion. d. App ly secondary or topper dressing as appropriate.
4. Frequcncy of dress mg changes 5. Expected clmnge
111
\\ound dra inage duri ng hea ling
6. When to notify the hcalth care provider a. Signs and symptoms of infection
b. Failure to Improve
c. Presence of odor d. Pus or purulent drainage
c. Copiolls mnOlillts of drainage f. Elevated temperature or signs of confus ion in the o lder
patient
7. Uni ve rsal precautions a. Il and washing b. Usc of g loves during care procedures
c. Disposa l of contami nat ed materials
8. Antibiotic regimen a. Oral medIcation usc
b. Topicall1ll!dication u))c
c. AntImicrobia l cleanser use 9.
175
Impo rtance of follow-up with health ca re pro\ ider
In stru ctio ns G ive n ( D:ll e/l nit illl s)
Demo nsl ra ti on or Rev iew of Materi a l (Da telf nit ia's)
Itelurn Demo nstra li o n or Ve rbalizes Und erslandin g (Da telf nili a's)
176
WOUND CARE
I ~ Bloody 2= 3= 4~ 5=
~
thin, bright red
Serosanguineolls = thin, watery, pale red to pink Scrous = thin , watery. clear
Purulent
teaching guidelines in Exhibit 8- 3 provide a model of information to teach and shou ld be individualized for each patient and caregiver.
= thin or thick, opaque tan to yellow
Foul purulent = thick, opaque yellow to green with offensive odor
REFER ENCES
[.
REFERRAL C RITERIA
WysockiAB. Wound nuids and thc pathogenesis of chronic wounds. J Itbwul Ostomy Continence Nllrs. 1996:23:283 290.
2.
Winter GD. Formation of the scab and the I"Jte ofrcepithelia [ization of superficial wounds in the skin of the young domestic pig. Natllre. [965 : 193:293 -294.
management requires adequate assessment orlhe patient with
3.
attention to evaluation for possible referral . For example, the following patients would warrant referra l to the physician
Kerstein MD. Moist wound healing: the c1mical perspecti\le. Os· lomy /Hnwd Manage. [995:41(supp 7A):37-45.
4.
Stotts NA. [mpaircd wound hcaling. In : ClIrrieri·Kohlman VK. Lindsay AM. West eM, cds. Pathophysiological Phenom('llon in Nurs· illg. 2nd cd. Phi[adc[phia: WB Saunders Comp:my: 1993:343 366.
5.
Sapico FL. Gmunas VJ. Thornhil1-l1yones M. et a1. Quanlltative microbiology of press lire sores in difl'crent stages of heal mg. Dtagll Bio/lnject DiJ·. 1986:5 :3 1-38.
6.
Cooper OM . The physiology of wound healing: an over\liw. In : Krasner D. cd. Chronic Ubl/fu/ Cure. King of Prussia . PA: lIealth Management Publications. Inc: 1990:1 II.
7.
Robson Me. Di sturbances of wound healing. A/II/ Emerg Med.
8.
Thomson PO, Smith OJ . Wh:1I is Infection"
Determining whether a patient is a candidate for wound
and/or an advanced practice nurse for either a medical evalucHion or immediate intervention or referral to another health
care professional for consultation. 1. The perso n with a wound exuda te that is copious, mal-
odorous, and pro longed should be eva luated further for infection, ce llul itis, abscess, or progressive degen-
2.
3.
4.
5.
eration. In this case the advanced practice nurse may choose to manage the patient initially. If the condition worsens or the patient fails to improve over a 2-week time frame, the physician should be consulted. Patients with an elevated temperature or those on a downhill course should be evaluated further. Intervene as in No. I. PUliel1l s with no wound improvement over severa l weeks should be evaluated further. In thi s case the advanced practice nurse may want to consult other heahh care practitioners (physical therapists, dietitians, wound care nurses or ET nurses, and phys icians). Patients with evidence of cellulitisor gross purulence! infection should be evaluated further. Intervene as in No. I. Patient s with impending exposed bone or tendon present in the wound should be evaluated further. Intervene as in No.3.
1988: t 7: t274 t 278. t994: t67(supp
SELF-CARE TEACHING GUIDELINES
Pottinger JM . Methicillin-resistant Slllphy/ococCII\' mlrf!U\ in aster· nat wound. In : Sou le BM. Larson EL. Presion GA. cds. Injections and Nllrsillg Practice. SI. Louis, MO : Mosby Year Book. Inc:
10.
Boyce JM . Methieillin·resistant Staphylococcus UI/reus: detection. epidemiology. and con trol measures. I,,(ect Dis Clin North Am.
[I .
Mosiello Gc. Tufaro A. Kcrstein MD. Wound healing and eompli· cations in the immunosuppressed patient. IIolllllls. 1994 :6(3) :
t995:240 245. t989:3:90t 913. 83 87. 12 .
Daltrey DC. Rhodes B. Chmt wood JG . Investigation into thc microbia[ nora of healing and nonhcaling decubitus ulcers. J CIi" Putllnl. [981:34;701 705.
[3.
Bergstrom N. Bennett MA. Carlson CEo el al. Tretl/mem of Pressure Ulcers. Clinical Pmctice Guide[ine No. 15. AH PR Publica· tion No. 95·0652. Rocb illc. MD : Agency for lIealth Carc Policy and Research. U.S. Public Hea lth Service. U.S. Dcpanment of t lealth and l1uman Services; Dceember [994 : [5 -22.
14.
Stotts NA. Determination of bacterial burden in wounds. Adv II(Jllnd Care. [995:8 :28 52.
IS.
Robson Me. lIcggars JP. Bacterial quantification of open wounds. Milil Met!. [969:134:1924.
16.
Wood GL. GutlerrezY. Diagnostic Path%gyoj lnjectiolls Du('uses. [>hiladelphia : Lea & Febiger: 1993 .
17.
Lee P, Turnidge J. McDonald JlJ. Fine-need le aspiration biopsy in diagnosis of soft ti ssue infections. J e/ill Mihrobiol 1985:22:80
Patient and caregiver instruction in self-care must be indi-
vidualized to the topical therapy care routine, the individual patient 's wound the individual patient's and caregiver's learning style and coping mechanisms, and the ability of the patient/caregiver to perform procedures. The genera l self-care
Alii J S,lrg.
t t.
9.
6. Patients with evidence of an abscessed area should be eva luated further. Intervene as in No.3. 7. Pmients with extensively undermined areas present in the wound should be evaluated further. Intervene as in No.3.
HA):7
83. 18.
Morison MJ. A C%ur Guide to rite N/lr.~i"g Management of Ilbunds. Oxford Eng[and : l3[ackwe[[ Scientific I>ublications: 1992.
19.
l)ag:lIla KD, Pagana TJ. Mosby's f)iagno stic a"t! La/Jortlwry Test Refe rence. SI. Louis. MO : Mosby Year l3ook; 1992.
A1al1agemellf (~r EXlIdare am/Injection
20 21.
22.
23.
24. 25.
CII7c11 JI rhe right w:ly to culture a wound. Am V/lr.v. 1993:93:48 50. Al\nrclO. ROlillt J. Mcchan ~,1. Principles of moist wound heal· ing: IndiCallOI1\ for chronic \\ounds. In : Krasner D. cd. Chronic 11(111",1 Can'. King of Pru ~sia. I'A: lIealth Management Publ ica· tion~; 1990. Levine NS. Lindberg RB. M.lson AD. I)rultt BA. The quantitative swab culture and \l1lcar: :1 quick simple method for determining the number of \ iublc aerobic bacteria on open wounds. J Tl"Cll/ma . 1976:16(2):89 94 Gcorgiudc t\G. Lucas MC'. O'FallOI1 WM. O!)tcrhout S. A compari · :o:.on of method!) for the quantification of b:lcteria in burn wounds. Alii J CIIII Pat/wi. 1970:53:35 39. Duke WI. Robson Me. Krilek TJ. Civi lian wounds: their bactcri:ll nom and rail! oflllfection. Surg FfJl'/lI11 1972:23:518520. Barr JE . Pnnclples of wound cleanslIlg. O\'roIllY lI owul Manage.
1995A1('''pp1 7A ): 155 225. 26. 27. 2ft
LlIleawea\cr W Cellular and bacterial tOl(iCllies of topical antimi· crobials. Phlll RecOIH'" SUI'g. 1985:75:394 396. RoochelIlg diagnoses related to physi· ologlcal :lllcrJtions: In : Malleson l·...IA. t-. lcConnell ES. Linton AD. cds. Geromological Nursing: COIlet'pH (//,,/ Proctice. 2nd cd. Phila· delphia : WB Saunders: 1997
29.
177
Gilman G, cd. TopiclIl Agelllv ji)I' Opelt /I()lUIl/\ ,llttihClcfel'iaf:.J. Allfiwplic.\. Alllijlmgal:> Rc\ie\\cd by Rodehea\cr G. Coopcr JW, Nelson DR. Mceh.m M. Charleston. SC- Iltll-Rom Internal ional, Inc: 199\.
30.
Coopcr BW. Antimicrobial chemotherapeutics. In: Soule 13M , Larson EL. Preston GA. cds. /n/l!C"lio//\ lIlItl \/lniIlK PIY/i'rice: PreI 'C'I/NOII (lnd COII/I"o[. SI. LoUIs. MO: Mo~b) . 1995.
3 1.
Speight TM. AI'el')''' Dnlg TIl'Mlltt'lII. Pl"ltt("Jjl/e\ ami PIY/clice of C1ittical Plwl'mllcology lIlI(l 71ll'l'llpeJJli("\. 3rd cd. 1l.llIirnore: Williams & Wilkins: 1987.
32.
Leaper OJ. Prophylacti c and tllcr.lpeutlc rolc of an ti biotics In wound care. Am JS/lrg. 1994:167{.suppllA):15~S 19S
33.
Crow S. Planchock t\ Y. Il cdrick ",. Antlscp'm. disinfection and ster· ilization . In : Soule 13M . Lar!)on EL. Preston GA. cds. Illfeclhms lIlItI VI/I" ...·ing Praclice : P'"el·elllio/l (/1/(1 CO/llro/ SI. LOlli'>. MO : Mosby: 1995.
34.
Poteete
\~
Case study: Elulllnatmg odor... from \\ollnds. f)ecII11II1J'·
1993:6(4):43-46. 35.
McMullen D. Topical mctrOllldazolc. pari II
O\fOIllI·
II(J/Jlld
MlllI-
age. 1992:38(3) :42-48.
36.
Jones I~ Willis A. Ferguson I. Treatment of anucroblc:.lly infected pres:.ure sore:. with topical metron idalolc. I..wll·('I. I'J78: I :2 14.
37.
Gomolin I. Br.tndt J. Topical therapy for prC1>),Ufe )'orcs in geriatric patients. JAm G"rillll' Soc. 1983:31'7 10 712
CHAPTER
9
Management of Edema Laurel A. Wiersema-Bryanl
INTRODUCTION
cations, especia lly th e ant ihypertensive age nt s. may ca use leg edema. T hese medi ca ti o ns inc lude calcium c ha nn e l blockers, clo nidine. minoxi dil . guanethidin e mo nosulfate, hydra laz in e , ra uwo lf ia d e ri va ti ves, m e th y ld o pa . a nd di azox ide . l Managi ng a clie nt with mo rbid abe ity requ ires the ass istance of the tea m in directing the clie nt to appropriate exercise and weight manage ment strateg ies. Fitting these clie nt s w ith co mpress ion therapy is a cha ll e nge; in these indi vidua ls we are asking for mult iple li fes tyle adju stm ents to be made to reduce the we ig ht a nd manage the edema. Increased inte rstiti a l vo lume is a noth er reason fo r ede ma. These c li ent s may suffer from a protei n-l os ing entero pathy, li ve r c irrhos is, rena l fa il ure, and/or prote in-cal ori c malnutriti o n. Ca re must be taken to ma nage the frag ile skin. a nd edema manageme nt becomes a s uppo rti ve th era py as the unde rl ying med ical pro ble m is add ressed. A nother category of edema is th at re lated to drug therapy w ith hormo ne replaceme nt. Ho rmo nes in thi s ca tego ry include corti coste ro ids, estrogen, testosterone. and progesterone. Clients ex perie nci ng edema secondary to hormo ne therapy generally respond we ll to leg elevat ion and exerc ise. If compression stoc kings are req uired, the low co mpressio n usua ll y wo rks we ll. Client s with primary lymph edema require aggress ive management and ge nera ll y require compressio n at much hi gher levels than the indi vidua l w ith primary veno us hyperte nsion. Comprehensive management o fl ymphedema is not addressed in thi s chapte r. The reader interested in thi s to pic is enco uraged to obtain info rmati o n from the Nati ona l Lymphedema Netwo rk o r oth er so urces avai lable to th em.:!
In this chapter. the reader w ill f ind a di scussio n of the etiologies associated wi th edema and stra teg ies directed to-
ward the manage ment of edema. Management of edema includes a desc ript ion of the procedures fo r managing edema
and parameters to measure in determining outcome. Emphasis is placed o n th e steps the cl ie nt needs to tak e in o rder to care for himselfo r herself beca use th e manage mcm a nd control of edema requires a n investm ent of lime, energy, and dedi cati on on the part of th e client. At the end of th e chapter two case studi es are d isclissed in an e tTort to appl y th e as-
sessment. management plan, and outcome evaluation of the chapter content.
OVERVIEW OF THE PROBLEM Venous disease w ilh ul cers occ urs in approximatel y 1% of the genera l po pulati on and 3.5% o f pe rso ns ove r the age of 65 years. Edema in the c lient w ith ve no us di sease occurs as a res ult o f sustain ed inc reased ve no us pressure. This ve nous hypert ension may occur primaril y in the dee p ve in system (femora l, popliteal, and tib ial ve ins) o r the supe rfi cial system (t he g reat er and lesse r sapheno us ve ins or the perforator ve ins th at join thc dee p and s uperficia l syste m). These problems may occ ur in isolati o n o r in combinati o n. Respecting th e underlying pathology is criti cal in the man age ment o f these client s. Increased ve no us pressure may be a res ult of chronic venous insuffi c ie ncy (as described above), ca rdiac disease. pe lvic tumors th at place increased pressure on or occl ude veno us a nd lymph atic return , o r mo rbid obesity in whic h the weight of the abdo me n may restri ct venous and lymph ati c return. In clients with ede ma seco ndary to cardi ac disease , manage ment of edema needs to be accomplished in co ncert wi th the ca rd iologist. A number of medi-
TESTS AND MEASUREMENT Meas ure men t of edema and edema control ca n be di vided into two primary ca tegori es of q uantit ati ve and qualit ati ve find ings. Q uant itatively, leg c ircumfe rcnce a nd leg vo lume
179
can bc mcasu red to give a reference range of Icg siL.e: with ca re, pilling edcma can also be measured and quantified. Mcasurin g leg circumference is an easy tool for c linica l usc; mcasuring leg \'olumc is less ··friendly" clinica ll y. but it is a good mcas ure of leg volume. Leg circumference can be measu rcd with a disposable tape. obtaining measures of the calf 10 c m belo\\ the IIlfcrior rim ofthc patella. at the \isually largest portion of the calf ( if different fro m the first measure). and 5 cm above the superior rim of thc lateral mallcolus. These measuremcnts, plottcd over time. pro\ide a refere nce range for leg size and progress toward edema con trol. Leg \01u1l1c measuremcnt requircs a large cylinder. which wi ll hold the c li ent's leg. and a basin to hold the water that is displaced. The cylillder or chamber is filled with water and the clicnt's lower leg is placed in the chamber. allowing th c excess watcr to be displaced O\"cr the top and contained in the reservoir. The volumc of water is then measured: the amo unt displaced will decrease as leg \'olume (ede ma) is dccreascd. Leg circumfercnce is measured wc!ek ly o r with eac h clinic/n ursing \'isit. Measurement of pitting edcma is onen dcscriptivc~ howcver. edema can be quantified by using a simp lc grading sca le as out lined be low:
o to L4-inch pitting ti .. to t/2- inc h pilling t/2 to I-inch pitting > I-inch pitting
I + (mild) 2+ (moderate) 3+ (sc,cre) 4+ (very se,ere)
Clinical Wisdom: Improper Bandagmg of Edematous Foot The foot shown in Figure 9-1 shows pitting at the arch where the bandage was wrapped. This indicates that the bandaging was started up too far on the foot. Bandage should have been started at the toes.
Qualitative measures to follow include the general appearance of the leg. the shi niness of the skill. the amount of drainage frol11 the uiccr(s). ifprcsent. and the client's sense of the heavi ness or \veight of the leg. It is also important to docllment the appearance of the Icg when the \HapS arc rCl110vccl loo king for areas of ridging and bu lging between the layers o r above the level ofthc wrapping. Clients may a lso identify changes ill how their clothing and shoes fecI.
Figuf1.' 9- 1 Pllung ctll.!ma. Source Rt.:pnnlcd \\ IIh rcrnm.... ion from
R.B. Chmnhcrs and N. Unman. Orlhnllc Management Mlhe Neuropathic anrJDY"'''Jsculaf P'lllcnl. 111 Irlu.\ 01"0,.,110.\0 cllld.h.,i.\fII"(, Dnin'.\. 3nl cdnion. 11 Goldberg and lD, 'hu. cds .. p, 450. ( 1997. ,\.lnshy- YC
therapy. II is often necessary to uuii/t: a combimllion ofthcsc therapies to achic\ e the de:-.ircd control of !.!dcm
Leg MODES OF INTERVENTION A'ID PIWCED URES FOR I TERVENTIO'l Elimination a nd control of edema may be accomplished through leg CIC\'3t10n. exercise. and the lise of compression
Eh~\ntion
Leg ele\'alioll facilitatcs the rCl11o\al of tluid through utili7allon of grmity in assistlllg \,cnou.., return. h.lr leg clevation to be sliccessfui. the legs must be elc\;1ted higher than the heart. Simply placll1g the feel on a stool IS of no benefit. To faclli tatc leg cIC'"'Hion. the client may find it hclpful to
Managemem of Edema
place one or two bricks under the foot end of the bed which results i n the legs being elevated higher than the heart during sleep. It is helpful to demonstrate thi s wi th the client by utilizing the exam table or bed to elevate the legs while reclining on the surface. The client should be encouraged to exercise the feet and ank les while elevat ing the legs. It is important to stress thm leg elevati on can be intermi tt ent and that total bed rest is not recommended . Interm ittent leg elevation during the day for 20 to 30 minutes at a time for a total of at least 2 hours a day is a reasonab le goa l.
181
A cl ient with dependent edema who is unable to work the ca l f musc les w ill not tolerate thi s level of compression and a lower leve l of compression, Class 1 or Class 2, should be considered. The fOllf classes of compression used are as follows:
Class I : Class 2: Class 3: Class 4:
14-18111 111 18- 24 111m 25- 35 mm 40- 50 mill
Hg Hg I-Ig Hg
Compression Therapy Compression therapy wo rks with exerc ise to facilitate the movemenl of excess nuid from the lower ex trem ity. Several options are avai lable for vascu lar support during compression therapy. depending on need (Table 9- 1). The level of compression needed for edema secondary to venous di sease, for examp le, is approxil11a1cly 40 mm I-I g. It must be emphasized here that compression of 40 mm Hg is recommended for the client who is able 10 wa lk and wo rk the ca lf muscles.
Research Wisdom: Guidelines for Safe Compression Warning: Do not apply compression therapy to a limb with an ankle-brachial index (ASI) less than 0.8. Consult Chapter 6, Noninvasive Vascular Testing , for ASI testing and significance. An ASI less than 1.0 suggests arterial vascular disease.
Table 9-1 Vascular Support Options Level of Support
Examples
Recommendations for Use
Light support (8-14 mm Hg)
• Fashion hosiery • Jobst • Sigvarus
• Edema prevention for persons engaged in activities/wo rk that require standing/sitting without much activity; examples: beautician, cashier, factory worker, some nursing positions
Antiembolism stockings (16-18 mm Hg)
• Anti-EM/GP (Jobst) • TED stockings
• Deep vein thrombosis prophylaxis • Nonambulatory clients with edema
Low compression (18-24 mm Hg)
• Relief (Jobst) • Elastic wraps • Paste bandage
• Nonambulatory clients with edema failing 16-18 mm Hg stockings • Clients with dependent edema
Low to moderate compression (25-35 mm Hg)
• • • •
Fast-Fit (Jobst) Custom Fit Double reverse elastic wrap Four-layer bandage
• Edema secondary to venous insufficiency • Edema in client able to participate in exercise rehab
Moderate compression (30-40 mm Hg)
• • • •
Ultimate (Jobst) Custom stocking (Jobst, Sigvarus) Sequential pump Four-layer bandage (Profore, SurePress)
• Edema with/without ulcerat ion • Edema that persists in spite of lower- level compression options • Ulcer that failed to heal after 6 months
High compression (40-50 mm Hg)
• Vairox (Jobst) • Custom stockings (Jobst, Sigvarus) • Sequential pump
• Edema secondary to lymphedema
182
WOUND CARl
Elastic bandages are relatively easy to apply, inexpensive, and easi ly removed. As with all compression garments/devices, it is best to apply the bandages within 20 minutes of waking and placing the feet below the level of the heart. Most compression wraps giving at least Class 2 compression are removed at night. Bandages do require practice to apply correctly and the sk ill needs to be taught to the client and
caregiver. Manufacturer's guidelines should always be followed when applying the elastic bandage. The most common app lication technique is the spiral ; an alternative is the figure-or-eight. Figure
9- 5 shows the fou r- layer bandage
being applied in spiral fashion. Several types of bandages are now available with printed rectangles thai , when stretched to squares. apply th e co rrect level of compression. These
bandages faci litate correct wrapping of an extremity (see Figure 9- 2).
fig ure 9- 3 Tubular bandages. Courtesy of Convatcc. Skillman, New Jersey.
Tubular Bandages
Tubular bandages are also avai lable to provide li ght compression (Figure 9- 3). One should be careful to select bandages that arc tapered at the ankle. Straight tubular bandages provide compression that is higher at the calf than at the ank le; these are not as usefu l for the client with edema.
Paste Bandages Paste bandages such as the Unna boot are widely used in the treatment of leg ulcers (such as that shown in Figure 9-4A) and as a result in the contro l of edema. The boot was developed in the 1880s by a German physician, Paul Gerson Unna, and consists ofa fine gauze impregnated with
zinc oxide. ge latin. and glycerin (some varieties also include calamine). The gauze is app lied without ten sion in a circular fashion from the foot to just below the knee (Figure 9-48). Paste bandages do not provide compression; however, as the boot dries and stiffens. the leg cannol continue 10 swell. Application ofa compression wrap over the boot (Figure 9-4C) will enhance compression and protecl the client 's clothing from the moist paste of the boot. A paste bandage is routinely changed every 4 to 7 days.
Clinical Wisdom: Dressing Application before Paste Bandage Venous ulcers are dressed before applying the compression bandages. They are often very large and exudative. Size may exceed that of standard dressings available. Two dressings such as the hydrocolloids illustrated in Figure 9-48 can be used and then covered with the paste boot. ,
Four-Layer Bandage
Fig u rc 9- 2 Shon-stretch bandage . Councsy of Conva tec, Skillnmn. New Jersey.
An alternative to the pas te bandage is the four-layer bandage developed at Charing Cross Hospi tal in London. The four-layer bandage provides graduated sustained compression through the application of a series of layers providing protection, padding, and compression (Figure 9- 5). The dressing is removed weekly.
A/allllgemelll (~r Edema
183
A
B
Figure 9-4 A. Large .. enous ulcer. 11, l\vo overlapping dressings. C, Application of paste bandage o,er drcsslIlg.
c
184
WOl
~() c.\lU
Craduated Compression Stockings Graduated compression stockings assist vcnotls return,
thereby reducing edema (Figure 9 6). The client should be measured and fitted for compression stockings when the
edema is absent or minimal. These stockings are then applied before the client has gOllen out of bed or at least within 20 minutes of rising. Stockings may be difficult to get on. and devices are available to assist III donning. A nonambulatory client does not need moderate or high compression and will likely better tolerate a lower compression
(18 to 24 mm Hg) stocking. Stockings do wear out and need to be replaced at the frequency recommended by the manufacturer. Many clients prefer
(0
order two stockings (or two
pairs) to prolong the life of the indl\ idual stocking and allow for laundering.
Clinical Wisdom: Check Joint Range of Motion and FunctIon at the Hip and Hands A Joint range of motion and functIonal exam at both the hip and the hands should be performed to determine the patient's ability to don compression stockIngs. Fi~ure
9-5 four-layer band"lgc.
Fil-!Url' 9 6 Cnl11pr~ss\(lIl SllH:kll1g. ('nurt~sy of BClcrsdorf·Jobsl. Inc .. Charlulh':. Nnrth ( .. Tolllla
Managemel1f of Edema
Co mp ress ion Pump The ra py Sequ enti al co mpression therapy has gained popularit y for the management of lower ex tremity edema. The leg sleeve (ei ther knee high or th igh hi gh) is di vided into a 3-, 5-, or IO-c hamber style with peak press ures of 45 to 60 mm Hg at the ankle (Figure 9- 7). The sleeve inflates first at the ank le, followed 2.5 seconds later at the calf chambers, and 3 seconds later at the thi gh cha mbers. Eac h successive chamber inflates less, and th e Io ta I inflati on is sustained for approximately 5 seconds, followed by co mplete defl ation. The cycle repea ts eve ry 7 to 8 seconds for the prescribed treatment period, which may range frol11 I to 2 hours twice per day. Clients should be encouraged to follow treatment with either application of a fitt ed stoc king or compression bandage to maintain edema control. Use of compression therapy at night while sleeping is not recommended. Clients with congesti ve hea rt di sease should be monitored closely fo r to lerance of the extra intravascular fluid burden with compressio n th era py. Medicare G uid elines for Sequ entia l Co mpressio n T hera py
2. Postirradiati on fibrosis 3. Malignant spread to lymph nodes with obstructi on 4. Scarring of lymphatic c hann els 5. Milroy's disease 6. Co ngenital ano malies • General quali fying criteri a I. Treatment for edema with custom-fabricated pres-
sure stock ings used without success 2. Scarri ng of lymph ati c c hann els 3. Signi ficant ulcerati on of lower ex tremities b. Seve ral unsuccess ful trea tm ent s wi th clas tic wraps or pressure stockin gs unsllccessful c. Ulcers that have failed to heal afl er 6 months of continuous trea tment • Auth ori za tion I. 3-Chambe r: no ulce rs 2. 5-Chamber: ul cers present 3. I O-Chamber: onl y afte r a 5-chamber has been used with min imal or no success or physician requests and doc um ents co nditi on acco rd ingly PROCE DURES FOR MANAGEMENT OF EDEM A
I The fo llowing are the Medi ca re guidelines at the time of this publi cati on. Check with du rable medi cal eq uipment suppliers to make sure that the guidelines are still as listed. • Types of lymphedema pumps I. 3-Chamber 2. 5-Chamber 3. 10-Chambc r • Quali fy ing di agnosis: refractory lymphedema I. Lymph node re moval/surgery
185
Leg Elevation and Exercise
D~allitiQII: The legs are elevated hi ghe r th an the level o f the heart , with or without foot and ankle exercise, to allow gravity to assist in the remova l of nuid from the legs. Adva " la~es .
• No costs are assoc iated with the procedure. • Effective when used regularly in combination with other form (s) of co mpression bandagi ng or stoc kin gs . • No special equipment is requ ired.
Figure 9- 7 Co mpression pump and sleeve. Counesy of Progressive Medical Technology, Inc., Lansi ng. Mi chiga n.
186
WOUND
C ·\R/
• Involves client in active participation in edema reduction. Disa(/t'al1111ges:
• Requires consistent performance in order to be of benefit. • Some clients may be unable to elevate legs higher Ihan the heart. such as those with morbid obesity. congestive heart failure, or orthopaedic limitation s. • Selling may not be conducive to reclining with legs c1-
Clinical Wisdom: Leg Exercise
• Use of a kitchen-type minute timer is useful for ensuring an adequate amount of time. • Encourage the client to work up to 20 to 30 minutes time if that is too much when starting out • Encourage the client to be creative at work in looking for opportunities to get the exercise in.
cvmed.
Comp,.essioll Wrllp.·j (Ellistie Ba",It'ges)
• May be ineffective in some forms of edema.
Equipment Needed: • Clean surface upon which to recline • Minute timer (optional)
Frequel/C)" Elevate legs for 20 to 30 minutes every 2 to 3 hours during the day for a total of approximately 2 or more hOllrs per day. Indicatiolls: Edema of the lower extremities secondary to impaired venous return. COI1/ra i "diclI! iOlls:
• Morbid obesity • Clients with arterial occlusive disease and ischemic pain with leg elevation • Clients with congestive heart failure limiting ability to recline in a horilontal position • Other medical conditions limiting client ability 10 recline in a hori70ntal position
Procetlure: Leg Ele"lItioll
II"" Exerl..:ise
I. Recline horizontally on a clean. comfortable surface. 2. Elevate legs approximately 30· so that the feet arc higher than the heart. Rest feet against the wall or footboard of the bed. 3. Set timer for 20 10 30 minutes (optional). 4. Wi th one leg at a time, flex and extend foot against wall or footboard, then make circles (rotate) the foot! ankle. Do 5 to 10 repetitions with each foot, then rest and repeat until timer goes off. 5. Remove compression bandage and rewrap Icg if compression bandage is being used. Expected Outcome: Edema and corresponding discomfort is relieved with leg elevation.
Definition: A compression wrap is a short-stretch elastic bandage that when applied to the leg applies :mfTicient external compression to cause mQ\crncnt of excess Ouid from the extremity. A c/wlII/lIf:es: • • • •
Wraps are incxpcnsive. Wraps are readily available. Wraps are easily removed. Wraps involve clients in active participation of edema reduction.
Disoth 'll 11 laves: • Requires practice to apply bandage correctly. • Care must be taken to 3\'oid unc\,cn tenSion when wrapping. • Wrap may telescope and fall down the leg \"l1h acti\ity and will require reapplication. • Client may be unable to comfortably reach the toes in order to wrap from the fOOl to below thc knee. • Client must bc committed to application and wcaring of thc elastic bandage for it to work sliccessfully.
Equipmem Needed.' • Short-stretch clastic bandage(s), or a width to accommodate fOOl and leg size (3- or 4-lIlch bandages arc the most common sizes selccted) • Cotton padding or combination ABD type dressings (optional)
FrelllieJlC\': Apply wrap daily within 20 mimllcs of rising. Reapplication is required if wrap tclescopes or slides dO\\·n the leg.
Managemellf of Edema
187
Indicatiolls·
Clinical Wisdom: Leg Bandaging • Edema of th e lower extremi ti es secondary to impaired venous return o Clients physically able to apply elastic bandages • Clients who require edema reducti on prior to fitting wi th compress ion stockings • Clients who require low to moderate compress ion for the management of edema COni rai I1dica! iOlls:
o Ankle-brachial index <0.8 • Clients unable to wrap legs independently and have no caregiver able to ass ist o A llergy to any component in the elast ic bandage (for example, latex)
o The index finger should be able to be slipped under the bandage if the dressing has been wrapped with the correct tension; if too tight, remove and rewrap. o If the toes become numb and tingle, remove the bandage and rewrap. o Encourage the client to walk for 30 to 60 minutes after wrapping, then remove and rewrap the bandage for correct compression. • To maintain compression for a longer period, advise the client to walk after wrapping as above, then rewrap with a double-layer elastic bandage. Segin as above, holding the roll in the right hand, and wrap from toe to knee; then wrap again beginning with the roll in the left hand, wrapping from toe to knee. Layering anchors the wrap, and it stays in place for a longer period of time.
Procel/ure: Compression 'Vraps
I . Wash lower leg and foot and dry thoroughly. 2. Apply topical agent i f ordered. 3. Apply wrap. a. Begin wrapping th e bandage at th e base of the toes using two layers around the fOOl to anchor th e bandage. b. Continue wrapping from roe to knee in a circu lar fashion by stretching th e bandage approximately 50% of capacity or, if using imprinted bandages, unti l th e rectangles become squares. c. If the leg is champagne bottle-shaped, pad the ankle area with cotton padding or ABD type dressing to minimize the shape disparity of the leg. d. With each turn around th e leg, the wrap should overlap th e previous layer by approximately 50%. 4. When the wrapping is complete, assess to make sure that wrap is not too tight by attempting to slide the index finger under one layer of th e wrap. Assess skin under the anchoring clips (i f used) to be certain the ski n is not pinched. Expected Oll1come·
• Edema is decreased as evidenced by a decrease in ci rcumference of the calf and ankle. • Cl ient/caregiver is able to provide a return demonstration correctly wrapp ing the leg. o Clien t arrives at follow-up vi si t(s) with leg(s) correctly wrapped.
Paste Bandage /2i1illjrjOIl: A paste bandage consists of a roll of gauze that has been impregnated with zinc oxide, gelatin, and glyceri n (some have calam ine added). The bandage is applied to the leg from th e toe to the knee and left in place for 4 to 7 days. The bandage should be applied when th e leg is without edema; as the bandage dries, it becomes resistant to additiona l swelling. AdvlIlIlllge£: • It is useful for clients unable to comply wi th other mo-
dalities or con tribute to self-care. o It eliminates daily dress ing changes. Disadvantages:
• Client is unable to shower while bandage is in place. • Client's ownersh ip of the problem is tran sferred to th e health care provider. • Odor may be a factor when it is time to change th e bandage. • I fthe bandage is not wrapped correctly, new ulcerations may develop. Equipmelll Needed:
o Pre-packaged pas te bandage (review manufacturer's guidelines that accompany the bandage)
I SS
WOUND CARl
• Gauze (3- or 4-inch wide roll) • ompression wrap (Coban or elastic bandage) • Gloves (clean)
• Scissors • Receptacl e to contain old dressing • Soap and water to wash leg • Wound care supplies. if indica ted
Frequ ency: Apply eve ry 4 to 7 days; morc frequent changes may be necessary if exudate is particularly heavy. Change immediately if the client ex peri ences severe pain, excessive drainage. or foul odor. Indications: • Clients unable to comply with other modalities directed toward edema co ntrol
9. Smooth paste bandage and assess for wrinkles or folds, which should be removed. 10. Wrap from the toes tojust below the knee with a single layer of gauze to fac ilitate drying and protecti on of clothing. I I . Remove gloves. 12. Apply an elasti c bandage or short -s tretch se lfadherent wrap (Coban) from the base of the toes to the kn ee (Figures 9- SE and 9- SF). Overlap 50% with mild to moderate tension.
Ex()ected Outcollle: • Wrap stays in place without compli ca tion for 7 days . • Leg edema is controlled, as evidenced by measures of circumference.
• Clients physically unable to wrap legs independently on a daily basis
• Clients awaiting custolll-fitted compression garments
Clinical Wi sdom: Paste Bandages
who need interva l assistance with edema control
CmUm;" d i(.'(1 Ii () II S" • Clients with poor personal hygiene • Clients with significant arterial occlusive disease (anklebrachial index < O.S) • Clients with frail, friable skin • Clients with active celluliti s
• Clients with infected ulcers Procedure: Paste Bandage I . Apply gloves. Remove old bandage by unwrapping or ca refull y cutting with bandage scissors as boot is lifted from the skin . 2. Wash foot and lower leg well. Use a so ft brush to remove dry sca ly skin. 3. Dry foot and leg well (Figure 9- SA ). A moisturi zing cream may be appl ied. 4. Se lec t paste bandage. Open all supplies. 5. 8 egin wrapping at the base of the toes (two revolutions) without appl yi ng ten sion (Figure 9- S8). Client should keep the foot and leg at a 90° angle. 6. Continue wrapping in a circular fashion around ankle and ellclosillg the heel (Figure 9- SC). 7. Overlap each turn by 50% as you continue to wrap up th e leg to just below the knee (Figure 9- SD). A paste boot can and should be cut as often as necessary to avoid any folds, pleats, or wrinkles that may become pressure areas as the boot dries. S. Stri ve for two to three layers of the bandage on th e leg.
• Client may wi sh to remove paste bandage immediately prior to clinic/ nursing visit to allow time for showering. Leg must be elevated or an elastic bandage applied after showering if more than 20 minutes will elapse before new dressing can be applied. • Some products recommend a figure-of-eight method of wrapping whereas others recommend a circular overlap; check the package insert. • Cast padding may be used to absorb heavy drainage. • If boot feels too tight after client has been up and active for several hours, encourage client to elevate legs higher than the heart for at least 30 minutes. • Paste boot can and should be cut frequently during application to avoid pleats, folds, or wrinkles that may cause damage to the skin as the boot dries. • Assess client for allergies prior to application. Clients allergic to calamine should use a calamine-free bandage. • A client with a narrow ankle and large calf (champagne bottle) may need to have the ankle padded with ABO type dressings or cotton batting to avoid overpressurizing the calf.
I Four-Layer Bandage Definirioll : The four-layer bandage consists of a wound contact layer and four bandages for sequential application to the leg. Correc tly applied, the four-layer bandage system provides 40 mm Hg pressure at the ank le, decreasing to 17 mm Hg at the ca l f.
A1allllgemenl (~r Edema
189
c
B
o
Figure 9-8 A 10 F, Procedure for putting on a paste bandage. Source for 9 SA. B, and F: Reprinted with permission from R B Chambers and N. Elfiman, OrthOlic Management orthe europathic and Dysvascular Patient. in Atlas o/Orthoses alldA.'l ~'isr"l'e Del'ices. 3rd. edition. B. Goldberg .nd J . ~. IIsli. cds .. pp. 450. 451. c', 1997. Mosby- Ye., Book. Inc.
190
WOINI) ( '"I
Figure 9- 8 contlllllcd
F
E
..I!/I'lI11IllVes:
• It IS useful for clients unable to comply \\ tlh other modalities or contribute to self-care. • It eliminates daily dressing changes.
ElIlli{Jmelll
Needed:
• Four-layer bandage system (Profore) • Gloves (ciean)
• Scissors • Receptacle to contain old dreSSing • Soap and water to wash leg
D/.\'{uh 'al l/ages :
• Client is unable to shower while bandage is in place. • Cltent's owne rship of the problem is transferred to the health care provider. • Odor may be a factor when It is tlllle to change the bandage . • I fthe bandage is not \'vTappcd correctly. new ulcerations may de,elop.
1~J!{{lIelJ(,\" Apply e,ery 4 to 7 days; more frequent changes may be necessary if exudate is particularly heavy. Change immediately if the client experiences severe pain, excessive drainage. or foul odor.
Illdicatiolls .
• Clients unable to comply \\ IIh other modalities directed toward edema control
Nf{wagemelll of Edema
• Cl ients phys ica lly un able to wrap legs independently o n a dai ly basis • Clients awai ting custom-fitted compression garments who need interval assistance with edema contro l
eollfmillcijcatiolls '
• Clien ts with poor personal hygiene
• Clients with signi ficant arterial occlusive disease (anklebrac hial index < 0.75) • Clients with active cel lulitis
• Clients with infected ulcers
4.
191
M easure ankle and cal f ci rcum fe rence.
5. Ope n fou r-layer bandage system and prepare s uppl ies. Review package insert for directions if not fa mili ar
with the system. 6. Cover wo und (if present) w ith contac t dress in g. 7. Wrap cott o n padd in g layer w itho ut te nsio n fro m th e toes to j ust below the knee (F igures 9- 9A and 9- 98 ). 8. Wrap a lig ht , conform ab le ba nd age ove r the cotto n padd ing laye r, aga in wi th out tensio n (Fig ure 9- 9C). 9. Wra p a li g ht compress io n bandage. Wrap fro m toe to knee (Fig ure 9- 9 0 ). 10. Wrapping in the di rection of the first two layers, wra p
the cohesive compression bandage with 50% stretch Pro('edure: Four-Layer Ball dage I . Apply gloves. Remove old ba ndage by un wra pping or carefu lly cutti ng with bandage scissors as bandage is li fted fro m the sk in. 2. Was h foo t and lower leg we ll. Use a so ft brush to re move dry scaly skin . 3. Dry foot and leg we ll. A moisturizi ng cream may be applied.
A
Figure 9- 9 A and B, Padding under four-layer bandage .
fro m th e toes to just below the kn ee using a fig ure o f eight (Fig ures 9- 9E and 9- 9F). I I. Remove g loves and disca rd. Expected Ou tcome' • Wrap stays in pl ace without complicat ion fo r 7 days.
• Leg edema is controlled, as evidenced by measures of circumference,
B
192
WOU~DCARr
Figure 9- 9 co ntinued
c
o
F
Fi gure 9- 9 C, Light. conrormabl e bandage covers padding wi thout tension . O. The third layer is wrapped at 50°0 and in a figure orclghl from the toes to just be low the knee. E and F. T he cohcsi",c comprl!SSIOn "rap 1:0. \\ rapped with modera te tension 10 di rection of first IwO layers: wrap is from toes to bel ow knee.
A'fallllgement of Edema
193
Equipmelll Needed: Clinical Wisdom: Four-Layer Bandages • Clien t may wish to remove bandage immediately
prior to clinic/nursing visit to allow time for showering. Leg must be elevated or an elastic bandage applied after showering if more than 20 minutes will elapse before new dressing can be applied. • If bandage feels too tight after client has been up and active for several hours, encourage client to elevate legs higher than the heart for at least 30 minutes. • A client with a narrow ankle and large cal f (champagne bottle) may need to have the ankle more heavily padded with the cotton padding to avoid overpressurizing the calf.
Compression Stockillgs
Defillition' Compression stockings are garments measured and fitted to the clien t that will provide external compression to the leg at a prescribed level. Stockings are available th at wi ll provide all levels of compression from light sup-
port to high compression. Individual needs can be mel
through special order and a wide variety of ready-fit garments. Stockings arc available knee. thigh, and waist high. Alil'(JIllm,'es '
• Stockings provide graded compression. • Stockings last from 4 to 9 months, depending on the manufacturer. • A variety of types is available. including custom made for the difficult-to-fit client. • Stockings are cosmetically acceptable.
Disadwllllages; • Stockings may be difTicult to get on client s who are disabled, have arthrit is. or are elderly. • The cost of stockings is not universa lly covered by insurance providers. • The client must adopt a positive self-care atti tude and be consistent with wearing the garment. • Stockings arc not recommended for clients with extensive leg ulcers or circumferential wounds.
• Rubber gloves • Stockings as ordered FreqlleIlQ'· tockings should be applied before getting out of bed in the morning and removed just before going to bed at night.
ludications: • Venous disease • Lymphedema
COlltl1liudiCllliollS· • Clients with arterial occlusive disease wi th ankle-brachial index < 0.8 should use any stockings with caution . • Clients with allergy to latex should not use stockings made with latex .
Procedure: Compression StockillGs I . Wash leg and foot and dry completely. 2. Measure ankle and calf circumference. 3. Apply loti on to the leg and foot if needed; refer to manufacturer's guideline for type of lotion, as many products break down the fibers in the stocking, shortening the stocking wear life. 4. Turn stocking inside out, holding the heel portion. so that the stocking is pulled back over the foot portion (Figure 9- IOA). 5. Place stocking over the foot and place heel in the heel portion of the stocking (Figure 9- 108). 6. Pull stocking back in place over the foot and to below the knee (Figure 9- 10C). (Procedure is the same for thigh-high stockings. Waist-high pantyhose type must be applied without invert ing the stocking.) 7. Smooth stocking to eliminate wrinkles (Figure 9- 1OD).
Expected Ou/come ' • Client/caregiver is able to apply stocking with minimal difficulty. • Client arrives at office visits wi th stock ing in place. • Edema in leg is kept under control, as evidenced by clinical improvement and a decrease in leg circumference.
194
WOL~O
C.\RI
A
c
o Fig ure 9- 10 ApplYing compression stocking. A, Turn stocking inside OUI. A liner makes pulling on siocking casier. (Note dressi ng under the Immg. The liner keeps the dressing positioned correctly). B. Work stocking gradually up leg. smoOlhmg out all wrinkles. (Stockings are avadable with or without tocs.) C. Knee·high stocking ha lfway up showing zipper rear closure. 0 , Slocking extended to below the bend on the knee. Patient is positioning slocking. SOllrce: Copyright c' Evonne Fowler, MN. RN. CETN.
Afallagemelll (~r Edema
Clinical Wisdom: Stockings
195
I
• Clients should be measured for stockings when there is the least amount of edema in the leg-early morning or after using a sequential pump for 1 to 2 hours. • Clients arriving for their appointment with stockings in a bag for you to put on do not understand the need for edema control. • Review teaching . • Inverting the stocking over the foot portion facilitates donning. • Order two pairs at a time to allow one pair to be worn while the other is washed. • Follow manufacturer's guidelines for washing. • Stocking butlers are available as a device to assist a client in donning a stocking (see Figures 9-11 A and 9-118). • Stockings are available in a variety of fabrics and colors. Cotton stockings are available from several manufacturers.
Clinical Wisdom: Tubular Bandage as Alternative to Compression Stocking
A
A tubular bandage may be used as an alternative to compression stockings (Figures 9-12A to 9- 12C). For some patients it is easier to don than compression stockings.
Sequential Compression Pump Definition: The sequential compression pump is a device that consists of a programmed pump and leg sleeves, which the client puts on. The pump is programmed to build and sustain compression rrom the lower leg/ankle to the thigh over a set period of time. then dcnation occurs and after a brief rest the process start s all over agai n. Leg sleeves can be ordered ror one or both legs. Ad\'{lIltages '
• The pump provide s true g raded comp ression that
"milks" the edema from the leg. • The pump is used intermittently during the day.
• Studies have shown the therapy to be effect ive in clients with venous disease and ulcerations. • The pump is easy to use. Disadval1wges :
• During pumping, the client is restricted to chair or bed.
B figure 9- 11 A and B, Using a stocking butler. Source: Copyright Evonne Fowler, MN, RN, CETN.
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A
B
c
f ig ure 9- 12 A to C, Us ing lubul ar ba ndage alternative. Courtesy of Conva tee, Skil lman, New Jersey.
Managemenf o/Edema
• Pumping may be too aggressive for clients with congestive heart fai lure.
• The client will still need compression therapy of some type when not using the pump.
Equipment Needed ' • Sequential compression pump, as ordered by physician
• Sleeves for one or both legs
197
Clinical Wisdom: Compression Pumping • If client is taking a diuret ic, he or s he should be ad vised to take it before pumping so that the peak effect will be realized as fluid is being pumped o ut of the leg(s). • Clients who work may want to use the pump while at work. An extra pair of sleeves may be ordered so
that only the pump travels back and forth , or a second pump may be obtained.
Freqllencv .· Use for a 1- to 2-hour session tw ice during the day, preferably mornin g and late afternoon or evening.
Indication,\': • 3-Chamber: edema, no ul cers I . Treated with custom pressure stockings without success 2. Several treatments with ela sti c bandages without success • 5-Chamber: edema, lower ex tremity ulcers I . Severa l treatmen ts wi th elasti c bandages wi thout
healing 2. Treatmen t with custom pressure stockings unsuc-
cessful • IO-Chamber: only afte r 5-chamber used without success COllfrajlldic{Jtiol1s'
• Untreated congesti ve heart failure
• Inabil ity to obtai n slecves that fit • Cellulitis • Ac ti ve wo und infection
Procedure: Sequelltial Comp ression Pump
RE f[ RRAL C RIT[ RI A When working wi th the client wi th periph eral edema, it is critical to kn ow when to refer the client for additional eva luation and treatment. Knowing that there are many potential rea sons for the edema and that many of these require a mu ltifaceted approach to management , th e practiti oner needs to be aware of parameters that guide the mak ing of referrals.
The list below is to be co nsidered as a guide only. In your practice, you may elect to accept, reject, or add add iti onal
parameters depe nding on the type of client seen and re ferra l opportunities ava ilable. • Physical assessment revea ls indicators of arterial occlusive di sease, including pain and cramping of the calf
wi th wa lking, absent peri pheral pulses, locali zed lack
of hair growth , th ickening of toenails, and delayed capillary refill. • The client has persistent edema fo r I month despite compression wrapping, leg eleva tion, and exerci se. • The client develops new ulcerat ions or there is an in-
crease in size of ex istin g ulcer(s). • The client has pain wi th leg elevati on and exercise.
I. Client should be in a comfortable reclining chair or in bed. 2. Pump should be plugged in with the co ntrols (on/off) wi thin casy reach of th e client.
3. Remove stockings or elasti c bandages (if possible). 4. Don and secure the sleeves. 5. Turn on pump. M ost home units have an automatic "o fT " in 2 hours; if this feature is not on the pump, an
alarm should be set for th e prescribed time. 6. Remove sleeves when prescribed time interva l has
passed, rcapply compression wraps or stockings. 7. Clean sleeves peri odically according to manufacturer's recommendations.
Where To Refe r Wh ere and
(0
whom the client should be referred needs to
be established in conjunction with the medical dircctor of the faci lity in which you practice. Some of th e therapies require a physician's order (sequential compress ion pump) to receive reimbursement and therefore require th at a physician see the client. Other circumstances are not quite so clear. It is also criti cal to take into considerat iolllhe client 's insurance plan, as it may in fac t dictate a particular path for the referral process. Some of the potential referra l directi ons
include the fo llowi ng:
Expected Outcome'
• Client tolerates procedure for 2 hours twice daily. • Edema is relieved from extremity.
• Interna l medici ne physician for general medica l problems, including hypert ension, congestive heart failure, and other conditions
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• D ermat o log ist for ven ous derm atiti s, ul ce r w ith
un certa in path ology, non healing ul cer, and other co nditions • Vascular surgeon for indicators of arteri al occlusive disease • Wo und healin g c linic/ce nt e r for nonh ealing wo un d, refrac tory edema, comprehensive evaluati on, and th e
like
• Rehab specialist for a client with need for exercise th era py and re habilitati on • Lymphedema network for a client with lymphedema and
need fo r speciali zed management and care • Bariatric speciali st for a client wi th obesit y complicating management of the edema • Home health care for assistance with and tolerance of applicati on o f co mpression dev ices
ELF-CA RE TEAC HI NG GU ID ELI NES Teaching th e cl ient with edema th e tec hniques for selfmanagement is criti cal to the management o f edema. In most
cases the edema does not represent a temporary, short -term probl em. Therefore, management of edema requires that the clie nt ad opt lifestyle changes for a lifetime. II is important that the health care provider and th e cl ient respect that the problem of long-term edema management is owned by the client, not the practit ioner. A clie nt contract (Ex hibit 9- 1) may be o f benefit in assisting th e client to a position of ownership. For many clients, thi s may take some encouragement and effort because most clie nts come to the hea lth care provider for a treatm ent and cure, not for the provider to instruct th e clie nt that he or she owns the problem and is key to its successful management. In selecting a plan for managing th e edema, ownership and res ponsibil ity need to be co nsidered . Bandages/wra ps that require th e client to return for dressing changes, such as paste bandages and the four- layer sys tem, may be a startin g point for many. These systems, however, do not requi re acti ve participation on th e part of the cli ent. Th erefore. it is important to keep thi s in mind and move th e cli ent to an increasingly acti ve role in his or her care as soon as possible. Several examples of edema management prog ram s are illustraled by the two case sludies th at foll ow.
Ex hibit 9- 1 Sample Cl ient Cont ract for Management of Venous Disease
li ent name: _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ __ 1. 0 . num ber: _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ __ StarT member: _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ __ Date of' goa l-setting in terview: _ _ _ _ __ Interva l for reassessment: _ week ly _ monthly
_
quart erly
other
I. , unde rsta nd that I have a problem with the ve in s in my leges). In order to take ca re of my leg(s). I understand that lhere are some th ings I must do. I agree to take ca re of my leg(s) as desc ribed below:
Cli ent Signature/ Date
Staff Member SignaturefDate
Mal/agement of Edema
199
I Case Study 1: A Case for Elastic Bandages R.A. is a 68-year-old man with a multiple-year history of swollen legs and ulcerations. The edema at the time of initial evaluation was severe with pitting (3+) to just inferior to the knee. A large irregular ulceration was present on the medial aspect of the left lower leg with irregular borders and minimal periwound ery1hema. R.A. reported a heavy drainage from the leg, which prompted him to "try again" to get help for the problem. His past medical history was significant for a deep vein thrombosis (DVT) 15 years prior to this evaluation. Now retired, client had worked in a position that required long periods of standing with little walking. Medications were felt to be noncontributory. The client's legs initially were wrapped with elastic bandages in a circular fashion. He was found to
have the bandages wrapped correctly when returning for appointments: however, after 3 weeks, little progress had been made. A 5-chamber sequential compression pump
was added to the regimen, with significant progress in edema management over the next month. The client was felt at this time to have minimal edema and was fitted with 40 mm Hg compression stockings, and sequential pumping was to continue twice daily. At a I -month follow-up, the client was found to have increased edema with deterioration of the ulcer. The client felt that he did better with the wraps. The stockings were discontinued
and R.A. resumed wrapping his legs with elastic bandages wrapped in a circular fashion, and a second layer coun-
terclockwise to the first was added. He has continued to be followed every 3 months with this regimen and is doing well. R.A. wraps his legs daily and has decreased use of the pump to once per day. Edema has been kept under control with this combination, and the client is com-
mitted to the program.
Case Study 2: Combination Therapy with Sequential Pump and Class 1 Stockings An 89-year-old woman presented to the clinic with more than an 18-year history of ulceration to the left lower extremity. Her history was significant for DVT in the left leg years earlier; the right leg was without significant change
given a diuretic and the pump interval was increased to
or edema. On assessment , the client 's left leg was swollen, and the skin was shiny. There was a circumferential
gan to resolve . Subsequently, the client was recom -
wound measuring 15 cm long anteriorly and 13 cm laterally; the drainage was clear yellow, and the wound edges were hypertrophic and scarred. The client is independent and refused home health nursing more frequently than twice per week. A sequential compression pump was ordered to be used for 1 hour twice daily, along with leg elevation every 2 hours. The client was able to do this herself and had been taking care of the wound without assistance. She had a family member raise the end of her bed with bricks. Wound care was directed toward keeping the area free of infection and the drainage con-
REfERE"CES Gerj(l/rjc~_
1993:48(5 ):34-45.
2. Nationa l Lymphedema Network. 22 11 POM Street. Suite 404. San Fran· cisco. C A 9-1 115. (41 5) 92 1· 1)06: Fax (41 5) 92 1-4284: hotl inc (800)
54 1-3259.
tained. After 6 weeks of pumping, the leg was softer to the touch, but there was little change in the measurements. In collaboration with her internist, the client was !y, hours twice daily. With this regimen , the edema be-
mended Class 1 stockings, which she was able to apply herself between intervals on the pump. At present, the wound has shown progress toward healing, with a de-
crease in length by 1.5 cm on the lateral side and 1.2 cm on the anterior surface. The skin of her leg is less tense and shiny, and the circumference of her calf has decreased by 1.5 cm and the ankle by 2 cm. The mounded hyperkeratotic tissue has reduced in bulk and the client feels that her leg "has lost some weight." The client is able to continue this program and maintain her independence and church activities.
SUCC t:STED READINGS
I. Ciocon JO. Fcrnandcl BB. Ciocon DO. Lcg edema: cli nica l clues to the d1fferential d1agnosis.
I
Airaksi ncn 0 , Partancn K, Kol3ri PJ, So imakallio S. Intermittent pncu· matic compress ion thempy in posttraumatic lower limb edema. Anll Phys Med Rehabil. 199 1:72 :667670. Ciocon JO. Fernandez BB. G3l indo·Ciocon D. Leg edema in the elderly: a prJctica l diagnostic approach. Compr Tiler 1994:20:586 592 .
W()L~1) C\RI
200
Ciocon JO. Galindo·Ciocon D. Galindo OJ. Raised leg exercises for leg cdcmOl III the elderly. ·Ingiology_ 1995;46: 19 25.
Deatey C lilt' Puhlicallon~;
("(lI"I.'
of IIollml.\ Oxford England Blackwell Scientific
1994
(lulm k L\I. Lo\ rien rc An algorithm for C\alu3ting swollen cxtrcllutlcs In
,I commumty hospital: rccollllllcndalioll::' and results. SOIllIl Dakota
,H etl 1995AR(3):93 94
LH!hr
I~
Todd B.
Rm~sl
M. Culligan M. FITccl of\cnous support on edema
and leg pain in pallcnh ancr coronary artery bypo'is graft surgery. Hellrl I.ullg 1992;21:{) II
Lippmann Jll, Fishman LM. Farrm RH. Bernstein RK. ct al. Edema con· Iro1 in the management of disabling chronic venous insufficiency. .1r(:h Phl'.~ MedRehllhiJ 1994;15:436-441 Moffatt CJ, Franks Pl. Oldroyd M. Bosanquci N. ci al Communlly clmics ror leg ulcers and lmpaci on healing. Br Ah·d J 1992 ;)05:1389
1391. Struckmann J. The pathophysiology of venous ulccrmion Scope Phlehol LympllOi. 1995:2(3):12 16. Zmk M, Rousseau P. lIollow'''y GA LO\l.. cr extremity ulcer:.. In: Bryant RA. cd. Acute lIlId Chmllic 11<11111"-5 .IVllrsillK \ftlllagemellt. SI. Louis. MO Mosby·Year Dook; 1992 : 164 212.
CHAPTER
10
Management of the Wound Environment Geoff;'ey Sussmall
changing the loading of paraffin in Ihe base and by Ihe use
INTRODUCTION Dressings provide the appropriate environm ent for heal-
of e mulsified forms of paraffin slich as Adaptic r M . These dressi ngs in ge neral prod uce a waterproof paraffin cove r ove r
ing by both direct and indirect methods together with the prevention of skin breakdown. The hi story of the develop-
llcts, li ke ga uze. may not allow wa te r va por and ex ud ate to
the wound, which may lead 10 mace ration because fiber prod-
ment and use of dressings has seen an evolution th rough many
pass through and may be tra pped within the wo und. These products are permeable to bac teria and are known 10 adh ere
centuries from inert and passive products such as gau ze, lilli, and fiber products to a dazzling range of modern moist wound
the wound, ca using trau ma on re moval. The ir use is limited to simple. clea n, su pe rficia l wo un ds and minor burn s. They are also used over ski n grafts. They need to be changed frequ ently to avoid dryi ng'o ut a nd always require a seco nda ry dressing. 1 10
dress ings.
INERT WOUND DRESSINGS In examining the continued use of pa ssi ve products as
described by Turner,1.2 particularly gauze, it is c1eartha! there arc a number of negati ve aspects in the use of gauze. Ga uze, being a fibrous material , tends to shed very readil y and as such will contaminate the wound. Gauze is hi ghly absorbent and as a primary dressing willtcnd to dry the surface of the wound rapidly. Ga uze is permea ble to bacteria, and moist
IDEAL DRESSING The properties of a £oood or ideal dressi ng have bee n desc ri bed as fo llows l : • Will re move excessive ex udate fro m th e wo und but will no t allow the wo un d 10 dry out so as to mai nt ain a moist environment • Will allow gaseo us exchange so th at oxyge n. watcr vapor, and carbon diox ide can pass in to and out o f the dress ing • Will be th erma lly insula ting so as to mainta in th e wound co re tempera tu re at approxi mately 37°C • Wi ll be impermea ble to mi croorga nisms to minimi ze co nt amin ati on o f the wound fro m outside th e wound • Will be free from either part ic ul ate or tox ic co nt aminati on • Will bc no nt rau mat ic and will not ad here 10 th e wo und so that on remova l no damage is done to granul atin g ti ss ue
gauze tends to be an environment for the growth o f bacte ri a. This would risk penetration and ultim ate contamin ation o f the wound. Gauze is also adh crent a nd will traumati ze thc wo und further on removal, ri skin g damage lO granulatin g ti ssue and pain. In add ition to ga uze and lint, th ere are avail able oth er si mpl e, modifi ed abso rbent pads cove red with a perforat ed pl asti c film to prevent adheren ce to a wound, such as th e trade name produc ts Me lolin and Te lfa, whi c h arc used as both primary and seco ndary dressings. They are used in min or wound s and wo unds with low ex udati on. Paraffin (petrolatum ) ga uze dressings were amon g th e earli est mod-
ern dressings developed by Lumiere in the First World War. Many va ri ati ons have bee n devel oped ove r the years by
201
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In addition, the following properties should be co nsidered when selecting the appropriate dressing: • • • • • •
Will Will Will Will Will Will
provide the environment for healing be user friendl y (to ensure compliance) have ease o f application and removal simplify treatment (minimal changes of dressing) be cost effective (ie, total management cost) be compatible with th e wound
• Will have minimal need for secondary dressings • May be suitable for combined use with compression
therapy
• May be used in infected wounds • Will remain in pl ace
MODERN WOUND DRESSINGS Film Dressings
Descriptio" alld Effects Film dressings arc thin membranes coated with a layer of acryl ic adhesive. They are moisture vapor permeable and oxygen permeable; these properties vary from brand to brand, but not significantly. They arc impermeabl e to microorgan-
isms and moisture. Film dressings are nexible and allow easy assessment of the wound because they arc transparent. They do not have the ab ilit y to absorb any ex udate. The latest films
being developed, however, have a very high moisture va por permeability and as such wi ll allow th eir use on more highl y exuding wounds. Film dressings arc elastic and exten siblc.".s The effects that make these dressings use ful include the followin g: • Provi ding a moist environment • Enabling autolytic debridement • Providing protection from chemicals, friction, shear, and microbcs • Tran smittal of oxygen into and carbon dioxide and watcr vapor oul of the dressing • Functioning as a secondary dressing Ifldielltion .~ for
Use
Film dressings are indicated in the management of minor burns and simple injuries (eg, scalds, abrasions, and lacerations) and as a postoperative dressing over suture lines. They are also used as a protective layer over intravenous catheters and for the prevention and treatment of superficial pressure areas."·1 A film dressing enables autolytic debridement and provides a moist wound healing environment.
Ifldieatiolls [or Discontifluation An increased level of exudation that causes pooling und er the dressing may lead to maceration of both the wound and the surrounding skin. The dressing also should be di sco ntinued should th e wound become clin ica lly infected.
Method ofApplicatiOl' An appropriate size piece of film should be chosen to cover the wound and provide an overlap of at lea t 4 to 5 cm from the edge of the wound. It is important to ensure that the ski n around the wound is dry and free from oils or cream, as these may reduce the capacity of the product to adhere to the skin. The boltom backing paper is removed, and the film dressing is carefully applied over th e wound while maintaining light but firm stretching of the edges of the film to prevent it from sticking to itself. Once the dressi ng is in place the upper cover is removed. Film dressings are also used as a secondary dressi ng over hydrogels and alginates and may be used as an alternative to tape for holding a dressing in place.
Removal Film dressings may remain in place for 1 week or even longe r. Changing of the dressing wi ll depend on the position, type, and size of the wound. It is important to remove film dressings with care. The correct method is not to pull the dress ing back across itself. This may cause a breakdown of intact skin particularly in the elde rly and in those with fine and dry skin. The film should be carefully pulled away from itself while applying light press ure to the ce nter of th e film dressing until it has been entirely removed.
Preca utiolls alld COlltrailldicatiolls Care should be exercised in app lying fi lm dressings to damaged or frai l skin because of the ri sks of further damage on removal. Film dressings are not recommended for use over deep cavity wounds, full-thickness burns, and wounds showing signs of c linical infection .
Outcomes Expected Fi lm dressings provide a transparent, flexible, waterproof, and breathing dressi ng that will protect simple wounds and encourage healing. They can be left in place for I week or more and are cost effective in that on ly one application of the dressing may be needed to manage the wound. When they are used postsurgery over sutures, they can remain in place until the sutures are removed.
Mal/agemell/ oj the WOllnd EllvirolJmelll
COMPARISON OF MOISTURE VAPOR PERMEABILITY OF DIFFERENTWOUND DRESSINGS
temperature of the wound, maintaining a moist environment. They are useful as both primary and secondary dressings, The effects of foam dressings include the fo llowing: • Providing a moist environment
C up Upright glm'/24 hours
Cup Inverted glm'/24 hours
Opsite™
839
862
Biociusive'·M
547
605
• Providing protection and cushioning • No produc ti on of re sidue
Ensure™
436
436
• Nonadherency
OpraflexTM
456
477
• Providing thermal insulation • Transmitting moisture vapor out of the dressing
Derma fi 1111™ TegadcnnTM
422
472
• Requiring no secondary dressings
794
846
Dressing Brand
• Providing high absorbency • Conformability to body shape
FOAM DRESSINGS
The moisture vapor permeability tcs~ is done under the
conditions specified in the 8rili,,11 Pharmacopoeia /980, In this test. the cup is either placed upright so that any loss of
203
Main
Dressing Brand
Constituent
Form
fluid is by evaporation or is inverted so that the liquid comes
in contact with the membrane. It should be noted that the loss of water vapo r from intact sk in is 240 to 1,920 glm'/24 hours and the water vapor loss from an open wound is abo lit 4,800 glm'/24 hOllrs, Combillutioll Film Dressillgs
Ventex™ combines a vented film dressing and an outer absorbent pad, The vented film is applied directly over the wOllnd, allowing 2 to 3 em greater than the wound size, and then the absorbent pad is stuck around the outer edge of the film, The pad remains in place until it is saturated with exudate . Then it is changed for a new pad without removing the vented film covering the wound. Viasorb™ also combines a vented film and absorbent pad, but they are not separate so
AllevynT>'
Polyurethane
Three layers Filmlhydrophilic foam/plastic net
Curafoamn . ,
Polyurethane
Single uniform structure
Hydrasorb™
Polyurethane
Single uniform structure
LyofoamTM
Polyurethane
Two laye rs Hydrophobic foam/ hydrophilic contact layer
Lyofoam
Polyurethane
Extra
th e entire dressing is changed. These dressings are indicated for use in exuding wound ul cers, pressure wounds, abrasions, and minor burns.
Three layers Fi 1m/ Hydrophobic foam/hydrophi Iic contact laye r
'"dicatiolls/or Use Foam Dressings
Descriptio" a"d Effects
Foams are indicated for a wide range of minor and major wounds, including exuding wounds (both superficial and cavity types), leg ulcers, decubitus ulcers, and sutured
Foam dressings are produced from polyurethane as soft,
wounds, They can be used over sk in grafts, donor sites, and
open cell sheets and may be single layer or multiple layers, They are also available impregnated with charcoal and with
minor burns. They may also be lIsed as a secondary dressing over amorphous hydrogels. Foams improve the functioning of amorphous hydrogels by removin g excess exudate from the wound and raise the core temperature of th e wound. This assists with autolysis. Foams may also be used around tracheostomy tube s and other drainage tubes and catheters.!! 10
a waterproof backing.4 Foam dressings meet many of the standard require-
ments of the ideal dressings, They absorb exudate protecting the surrounding sk in from maceration, and rai se the core
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flll/icaliolls lor Discolltinuatioll
classes of polymers are swollen extensive ly in water, but they do not di sso lve.
Foam dressi ngs shoul d be di sco ntinued when th e level of exudation cannot be absorbed into the dress ing in less than a 24-hour pe ri od.
linked stru ctures formed fro m hydroph ilic homopolymers or copolymers. Hydrogels are of two types. The firs t type is
Methot! ofApplicatioll
amorphous, being a nonfixed, three-dimensionalmacrostruc-
The foa m dressing is placed over th e wo und, allowing at least 3 to 4 em grea ter Ihan th e size of the wound . Th e dressing should be kept in place wi th one of the fo llowing: • In I. 2. • In I. 2.
pat ients with fi ne or easily damaged skin Light weight co hesivc bandage Tubular band age olher patients Adhesive tape (hypoallcrgeni c) Tubu la r or lig htweig ht co hesive band age
Hydrogels are three-dimensional, water-swollen, cross-
ture consisting o f hydrophilic polymers or copolymers. The
polymers absorb water, progressively decreasi ng viscosit y. They are free n owing and will easily fi ll a cavity space. These are amorphous gels. The seco nd type is a fixed, three-di-
mensional macrostructure usually presented as a thin nexibl e sheet. These gels swell , increasing in size until the gel is satu ra ted; they do not change their physica l fo rm as they abso rb nu id. Many also contai n propyle ne glycol, and all cont ain a hi gh proporti on of wa ter- up to 90%.' The table
below shows a comparison of wa ter content of some amorphous hydrogel prod ucts.
The dressing ca n be used under compression bandaging and as a seco nda ry dressi ng fo r amorphous hydroge ls and alginatcs. In th e case ofa cav ity device, se lect th e appropriate size device to fit comfo rt abl y into th e cavity and insert it inro the wound. It may remai n in pl ace for 1 to 4 days or
unt il saturated with exudate. A shee t foa m dressing can remain in place for up to 7 days or until the exudate has saturated to th e edge of th e dressi ng.
PrecllutiollS
Foam dressi ngs are of little val ue on dry wounds with a scab or eschar. Cavi ty dressings sim ilarly should not be used on their own in a dry cavi ty, but they may be used with an
Properties Hydroge ls are a moisture donor to a dry wo und but are also able to absorb a ce rtain amount of nuid. They have the following useful effects:
• Prov iding a moist environment • Aiding in auto lyti c debridement • Conform abi li ty to body shape
• Nonadherence • Prov id ing bo th moisture do nors and mois ture absorbers
amorphous hydrogel. COli trailltliclltiolls
WATER CONTENT OF SOM E AMORPHO US HYDROGEL PRODUCTS
There are no speci fic cont ra indications ror the use of roam dressi ngs. The a uthor has cli nically ex perie nced a local re-
Dressing
action causing erythema, but thi s may have been due to an
Brand
all ergic reactio n or to the increased blood now ca used by th e thermal effec t of th e dressing.
Carrasyn™ gel
Outcomes Expectet/
Foam dressings provide a satisfactory primary and secondary drcssing fo r a wide range or wounds. They will aid in the removal of exudate, ra ise the core temperature of the wound, and protect the wound rrom ex ternal irritati on. They
95%
ca rbomer 940. sod ium chl ori de
DuoDerm™ gel
wi ll also pro tec t the healthy sk in aro und the wound from
Sod ium carboxym-
8 1.5%
ethylce llulose, pec tin, propylene glyco l
Intrasite™ gc l
Modified ca rboxymethylcellulose, pro pylene glyco l
78%
Solugel'"
Propy lene glyco l,
75%
Hydrogels
Descriptioll alltl tjlects
having a high wa ter content- from 30% to 90%. These broad
Triethanolamine,
Water C ontent
acemannan,
becoming maceratcd by the wound exudate.
Hyd rogels a re a gro up of co mpl ex orga ni c po lymers
Chemical Type
sa line
Mal1agemem a/rile Wound EnviIVnmellt
205
Illdicatiolls/or Use
PreculItiollS
Amorphous hydragels in general are indi cated for dry and sloughy wounds to rehydrate the eschar and to enhance rapid debridement by autolysis. They are used on leg ulcers. pressure wounds. extravasation injuries, and necrotic wounds. They facilitate granulation and epithelialization by preventing th e wound from drying out. They are used on simple and partial-thickness burns and on pressure wounds. Gels arc used to prevent the drying out of ti ssue such as tendon . Gels are also a use ful carrier of topica l drugs to be applied to wounds, such as metronidazole and proteolytic enzymes. Hydroge ls are suitable for use in infected wounds. Amorphous hydrogels are also used for management of the lesions of chickenpox and shingles. 6•11 14
Sheet hydroge ls should not be ap plied to wounds clinically infected without coverage with systemic antibio ti cs.
IIIdiclIfiomj for Discoll1i IIl1atioll Amorphou s hydrogels should be di sco ntinued if the exudate from th e wound is excessive. It is genera lly considered that sheet hydrogels should be stopped if the wound is cli nicall y infected.
Method ofApplicatioll Amorphous hydroge l should be applied to a wound to a minimum thi ckness of 5 111m and covered with a secondary dressing. Th e choice of secondary material will depend on the type and posi ti on of the wound and ava ilabi lity and cost. The au thor has found that foa ms are the most satisfactory secondary dressings by virtue of their properties of absorption of ex udale. thus maintaining the integrity of the gel for a longer time, protectin g the surrounding skin from maceration, and raising the core temperature to aid in autolysis. Other products may be used such as film dressings, hydrocolloids, and simple nonadherent dressings. Gauze is also a suitable secondary dressing. Hydrogels can remain in place with a clean wound for up to 3 days and then removed by irrigation with water or saline. When used for the lesions of chickenpox they shou ld be app lied four or five times a day. The sheet hydrogels arc placed over the wound with at least 3 to 4 cm coverage greater than the wound. They are held in place with either tape or a light cohesive bandage, dependin g on the sk in of the patient. In difficult areas they should be held in placc with a retention sheet such as Hyparix, Fixol11ull, or Medipore. The sheet hydrogels do not ca use maceration of the surrounding ti ssue. The sheets are left in place. depending on the wound type and th e amount of exudati on. but generally should be removed alier 3 to 4 days. For some superfici al burns they may remain in place for up to 7 days. When removed they ca use no di scomfort and leave no residue on th e skin.
COli trllilldicatiollS
Amorphous hydrogels containing propylene g lyco l shou ld not be used in patients known to be sensit ive to propylene glycol. Sheet hydrogels should not be applied over small deep cavity wounds or clinically infected wounds. They should also not be used in highly exuding wounds.
Outcome.. Expectel/ Hyd rogels will aid in the rapid removal o f necrotic tissue and rehydrate dry wound s, ass istin g in granul ation and reepitheliali zation. In burns they reduce the heat and pain . The thicker sheet hydrogels, when used in the managcment of superficial pressure wounds, wi ll also assist in the reducti on of pressure by reducing friction and shear forces. Hydroco lloids
Descriptio" alld Effects Hydrocolloids a re a combi natio n of gel-form ing polymers with adhesives held in a fine suspension on a backing of film or foam . Hydrocolloid dressings are co mposed of a backing of either polyurethane foam or film and a mass containing in most cases sodium carboxymethy1cellulose and oth er gel- forming agent s such as pectin, gelat in, and elastomers. These form a self-adhesive mass;' These products are also avai lable as granules, powder, and paste. When placed on a wound the exudate combines with the polymers to form a soli gel mass in th e wound. They were originally introduced as Stomahesive to protect good skin arou nd ileostomies and colostom ies. They vary from being occlusive to being semipermeable. When removed, the gel remaining is yellow and malodorous but not infected. TIle presence ofbacteria under hydrocoll oid dressings does not retard healing. When applied to an exuding wound the dressing absorbs exudate from the wound and forms a gel. This gel wi ll vary in viscosity, depending on the brand of dressing. The dressing does not adhere to the wound itself, only to the intact ski n around the wound. Hydrocolloids have the foll owing efTeets I S.16 ; • • • • • •
Providing a moist environment Aiding in autolyti c debridement of wounds Conformability to body shape Protection from microbial contamination Providing a waterproof surface Requiring no secondary dressing
The following table shows a comparison of so me hydrocolloid products.
206
WOUND CARE
COM PA RI SO
Dressi ng Bra nd
O F HYDROC O L LOID DRESS ING PRO DUCTS
Mai n Compone nt
Bac king
for ms
Comfcel™
Sodium carboxymethyl cellulose
Polyurethane film
Standard, thin
Duoderl1l™
Carboxymethyl cellulose
Polyurethane foam/ film
Standard, thin
Tcgasorb™
Polyisobutylene
Polyurethane film
Standard, thin
11l(lica/ions/or V ,lie Hydrocolloids are indicated in the management of superficial leg ulcers, burns, donor sites (when hemostasis has
been obtained). and pressure wounds. They may be used in
small cavity wounds in combination with hydrocolloid paste, powder, or granules. Thin versions of these dressings are
waterproof. They require no secondary dressing, and help to appose wound edges by distribution of tension at the suture line across the surface area of the dressing. Prec(llitiollS (III(/ COllfrtlilldictiolls
Hydroco lloids should be discontinued on surface granulation of the wound or if hypcrgranulation occurs.
Care should be taken in using these dressings on patients with thin and fragi le skin. as they may cause further damage on removal. There are no absolute contraindications for use of hydroco lloids. l-IydrocolJoids are not indicated for use in very heavily exuding wounds or in clinically infected wounds. They are also not considered suitable for deep cavity wounds.
Meth od ofAppli<'utiO//
Outcomes Expected
Hydroco lloids on a superficial wound should be applied to the wound with at least 3 to 4 Col of product greater than thc wound size. The ski n should be dry to ensure good adhesio n, and it is preferable to place one third of the dressing above the wound and two thirds below the wound; this wi ll prolong th e wear time of the dressing. The dressing may remain in place for 5 to 7 days or until strikethrough has occurred, that is, exudate has migrated to the outside edge of the dressing. The dressi ng should be carefully removed and the wound irrigated with warm saline before applying a new dressing. In the case ofsm311 cavity wounds. ifrelatively moist the cavily should be filled with hydroco lloid powder or granules and covered with a sheet of hydrocolloid dre ssing. With a low 10 moderately exuding cavity, hydrocolloid paste should be inserted carefully and the wound again covered with a sheet of hydrocolloid dressing. The dre ss ing should be changed after 3 or 4 days by irrigation of the cavily with warm saline and gentle removal of any remaining product before applying the new dre ss ing. Thin hydrocolloid dressings are applied after suturing of a surgical wound, and in most cases, can remain in place and be removed at the time of suture, clip, or Steristrip removal. These dressings have the advantages of being flexible and
Hydrocolloids should help remove necrotic tissue and slough from the wound and encourage angiogenesis and granulation of the wound. The presence of colonized bacteria in the wound does not contraindicate the use of these dressings.
indicated as dressings over sutures in both minor and major surgcry.6... .ll III
ludications for Dh.coll timlllt;oll
Algina tes
Descriptioll alld Effects Alginates are the calcium or calcium/sodium salts of alginic acid and are composed of polymannuronic and guluronic acids obtained from seaweed- mainly the genus LamilJaria. When applied to a wound the sodium ions present in the wound exchange for the calcium ions, producing a hydrophilic gel and provid ing calcium ions into the wound. This is part of the mechanism by which alginates act as a hemostat. Alginates are gelling polysaccharides. They are prese nted as either calcium alginate, a mixture of sodium and calcium alginate in textile fiber sheets. or as a loose packing ribbon. Alginates combined with activated charcoal arc also available. Alginates are combined with so me hydrocolloid dressings 10 aid in the fluid handling properties.
'l/allugemt!l1t
Sodium alginate has the empi rical formula CIl H.,OIlNa with a molecular weight in the range of 32.000 to 200.000. Sodium alginate has a complex structure consisting essentially of two monic acids. D-polymannuronic acid and L-guluronic acid. The ratio of these isomers will vary depending on the species of seaweed from \\hich the alginate is extracted and the method of production. Gels rich in polymannuronic acid form soft amorphous ge ls that partially dissolve or disperse in solutions containing sodium ions. Aiginates rich in guluronic acid tend to swell in the presence of sodium ions while retaining their basic structure:t.~ Alginates have the following useful errects: • • • • • •
Providing a moist environment Providing a high absorptive capacity Conformability to body shape Protection Providing hemo~tatis Nonadherence
The following table shows a comparison of the chemical composition of different alginate products.
COMI'AIUSON OFALGINATE CHEMICAL COMPOSITION
Dressing Brand
Guluronic Acid (%)
I>ul) mannu- Calcium Sodium Aiginaic Aiginaic ronic (%) (%) Acid (%)
Algiderm™
58
42
100
Curosorb™
68
32
100
Kaltostat™
66
34
80
20 20
Kaltocarb™
66
34
80
Sorbsan™
34
63
100
Tegagcn HGTM
40
60
80
Tegagcn IIITM
40
60
100
Algosteril™
58
42
100
20
o/rhe Ifhmu/ EIlI'irtJlIIIU'11I
207
Illdicatio".\ for Di.'·Colltillllatioll Aiginatcs should bc discontinued if thc level of exudation is insufficient to cause the fiber to gel. Alglnates shou ld not be premoistened with sa line before application to a wound.
I'del/wd ofApp/iclIlioli Sheet algll1ates should be placed in the wound to the shape of the wound and covered \\ ith a sccondnry dressing such as a foam. or a nonadhercnt dressing and held III place with tape or a light cohesivc bandage. depending 011 the condition of the patient's skin. I f the wound is highly exudative, an additional co\"ering with a simple absorbent pad is appropriate. In the case of a cavity \vound, rope or packing alginate matenal should be placed gently in the ca"ty. taking care not to pack the material tightly into the space. When used 011 a donor site. the sheet alginate should be :lpplicd to the donor area after harvesting of skin and covered \vitll a film dressing or foam. This will aid 111 rapid hemostasis and provide the environment for reepithelialization of the skin. The dressing in general should remain in place in c lean wounds for no longer than 7 days or when the gel loses its viscosity (thIS will vary depending on the level of exudation from the wound). Wounds clinically infected should be changed daily. The alginate is removed by simple irrigation of the wound or canty with warln saline.
Precautioll' aud COlllraiudi£'atiolls Wounds clillically infected should be changed daily with consideration for the concurrent lise ofsystcmie antibiotics by the prescriber. There arc no known contraindications to the lISC of alginates. They are not suitable for lise ill dry \vOllllds or wounds with thick black eschar.
Aiginates will absorb exudate and provide the moist environmcnt for granulation. They are sUitable for usc in infected \vounds and arc very effective in the management of bleeding. in particular in postnasal surgery and \\hen applied to donor sites. They will provide a comfortable dressing. Rnpid healing of the skin is expected.
Indications/or U.\e Aiginates are used in exuding wounds such as leg ulcers, cavity wounds. nnd pressure wounds, and at donor sites as a hemostat postsurgically and other bleeding sites. They may be used in infected wounds."·IU.~1 ~"'
Combination Alginates Manufacturers ha\"c combined algll1atcs \\ Ilh other prodlIcts to enhance cffects of each.
208
W OUND CARE
Calciutll/Smlill'" A lginDle Combinatioll
Kaltocarh.™ Kaltocarb™ is a combination of calcium and sodium alginate in a fiber sheet bonded to a layer of acti-
vated charcoal and an outer layer of viscose. This product is a highly absorbent dressing with the ability to absorb odor. It is indica ted in infected malodorous wounds, fungating neoplasms and ulcers, and superficial pressure wounds. The sheet should be applied to the surface of the wound, ensuring that the alginate white layer is in contact with th e wound and the dark charcoal layer is on the outside. The product is covered with a secondary dressing and held in
place with tape or a li ght cohesive bandage. The dressing should be changed every few days, depending on the leve l
of exudate and the extent of infection . The use of systemic antibiotics in clinically infected wounds is indicated . The dressing is easily removed; removal may be assisted by irrigation with warm saline. Thi s dressing. as with other alginates, is of no value in a dry wound with thick dark eschar.
A Igilllllelfly drocolloid Combillatioll Curaderm™ {lII d COlllfeel PIUS™. The combining ofhydrocolloids and algi nates in one dressing enhances the properties of the dressi ng and allows their use in more high ly exuding wounds. They present in sheet form similar in appearance to standard hydrocolloid sheets. They are used in a manner similar to that for hydrocolloids; however, they can remain in place for a longer time because of the better absorptive properties.
Hydroactivc Dressings Descriptioll alld Effects I-Iydroactive dressings have some si mi larities to hydrocol loids; however, they are not gel- fomling products. They act by absorbing exudate into the structure of the dressing. and swelling as the amount of exudate is absorbed. They maintain a moist environment at the interface of the wOllnd. I-Iydroactive dressings are multilayered dressi ngs of highly absorbent po lyme r gel with an adhesive backing. These dress-
ings are composed of an outer polyurethane film membrane combined with a polyurethane ge l and other absorbents (eg, sodium polyacrylate). They are semipermeable and are adhesive to the skin. They are available in a number of forms. including cavity fille rs, foam , and thin types.' Hydroactive dressings have the following useful effects: • • • • • • •
Providing a moist environment High absorbency Waterproof surface Regaining shape when stretched Aiding in autolysis Leaving no residue Semipermeability to moisture vapor
!tlilkatiolls for Use Hydroacti ve dressings are indicated for use on exuding wounds including leg ulcers, pressure wounds, minor burn s, and exuding cavity wounds. They are of particular use over joints slich as the elbow, knee, fingers, toes, and ankle because of their ability to expand and contract without causing constriction. 2.S 27
Iltdieatiolts fo r Discolttillllatiolt Hydroactive dressings shou ld be di sco ntinued for the wound with little or no exudat ion or if the dressing is unable to absorb the level of exudate being produced by the wound.
Meth od ofApplicatioll The application of hydroactive dressings will vary depending on the type of dressings used. Tielle'" is placed overthe wound so that the centra l island of dressing completely cov· ers the wound. Allow 2 to 3 cm greater than the wound size, and then adhere to the surrounding skin. Cutinova™ is applied directly to the wound, allowing 3 to 4 cm of dressi ng greater lhan the wound size. It is preferable to warm the edges of the dressing slightly with the hand to aid in adhesion of
A1al/agemellf oJthe Wound Environmellt
the dressing. Cutinova CavityTM, because of its ability to abso rb exudate and ex pand. should be placed ca refull y into th e cavi ty, not occu pying more than 33% of the space. The outer wound shou ld be covered wi th a sui table dressing such as
Cutinova Thin™ or Hydro™, These dressings may remain in placc fo r up to 7 days depending of the level o f exudation. Care should be taken on removal in pati ents with thin or eas-
ily damaged skin . When removed, they will leave no residue from the dressing; however, it may still be necessary to irrigate the wo und wi th warm sa line if there is exudate present on the surface of the wo und before redressing. Precautions and COlltraill dicotiollS Hydroactive dressings arc not co nsidered suitable for usc on clinica lly infected wo unds or nonexuding wounds. There arc no known contra indica tion s; however, ca re should be taken when using these products on fine and easily damaged sk in. OIlICOllle~'
Expected
Hydroac ti ve dressings will absorb exudate and provide a
209
AQUACELTM is a nonwoven , 100% sodium carboxylmethyl-cellulose spun into fibers and manufactured into sheets and ribbon dressing. This product mirrors th e properti es and actions of alginate dressings: however, it differs in that it rapidly absorbs exudate vert ica lly and can also absorb laterally. It reta ins Ouid within the stru cture of the fiber. The sodium carboxymethyJcellulose fibers swell and convert into a gel sheet. This product is ind icated in heavily exud ing wounds such as leg ulcers. pressure wounds, cavity wound s. minor burn s, and donor sites. The dressing is appl ied to the wou nd, a llowing 2 to 3 c m greater than the wound size or wound cavi ty. The dressing will remain in place for I to 3 days depending on th e ex udate leve l a nd when the product is saturated. CombiDerm is a multilayer absorben t pad combi ning a se miperm eable hydrocolloid border with absorbent padding of hydrocolloid particles and a nonadherent cover against the wound. This product is highly absorbent and is able to hold the ex udate within th e dress ing preventing maceration to the surrounding skin . It mainta ins a moist environmen t. It is indicated on highly exuding wounds, pressure wo unds, leg ul cers, and surgical wo unds. It may be used as a secondary dressing over cavity wounds.
moist environment for granulation and epi thelialization. They
wi ll provide a comfortable dressing that will re mai n in place and have a good wear time.
Miscel laneous Dressings With constant research and development, new products have entered the market that do not fit into any of the standard groups melllioned. These products have properti es resembling ex isting groups, but are composed of different material s. Exu-dryTM is a nonadherent absorbent pad composed of an outer layer of perforated polyethylene-laminated rayo n and an inner layer of absorbent rayon/polypropylene blend with a cellulose backing th at wicks wound ex udate and ho lds large quantities of Ouid. It is indicated in highly exudative wounds and in particular in burn s.28
DRESS ING C HO ICE Wounds are dynamic and as such the choice of dressing wi II va ry and change as th e wound changes. The product you may commence treating the wound with initially will in many cases change as the wound itself changes.The choice should be based on th e three major aspects of any wo und : color, depth, and ex udate (Table 10- 1). The color wi II va ry fro m pink (epithelia li zing), to red (granu lating), to ye llow (s loughy), to black (nec rot ic). The depth will incl ude superficia l, shallow, and deep cavity; the ex udation will be none, minimal, moderate, or high. The ot her aspects that will need to be considered are the presence of infection , the tissue surrounding th e wound, the need also to apply grad uated compression, the fragilit y of the skin, and any medical condition that may have an impact on the dressing choice.
Management of the Wound Environment
SECONDARY DRESSINGS The choice of secondary dressing wi ll depend on the na-
ture. position. and level of exudate. In general terms. film dressings and nonadhcrcnt dressings arc suitable for low exudaling wounds but not for high exudating wounds. Foam dressings are useful over amorphous hydragels and a lginates.
The usc of gauze as a secondary dressing is limited, especially over hyd rogel s or algi nates, as the gauze will reduce the ability of the dressing to function at its optimum level. The olher consideration is the method of dressing retention.
If the surrounding sk in is good, the dressing may be held in place wi th good-q uality tape. If the skin is poor, a tubular bandage or a lightweight cohesive bandage is suitable. Sec Appendix B. Resources for Wound Care Products. THE USt: OF ANTISEI'TICS IN WOU 'OS
Antiseptics arc an essential part of modern clinical practicc. Their va lue as a hand-washing procedure prior to an
aseptic procedure or for the preparation of the patient's skin prior 10 su rgery is clearly documented. Studies have shown that the bacteria on the skin, whether resident or transicnt , arc reduced by lip to 95%. There is not, however, a considerable amount of research on the effects of antiseptics on open wou nds. There wi ll always be microorgani sms present in a wound 10 H grcHtcr or lesser extent. It has been argued that one of the most prolific researchers and publishers in the area of antiseptics and healing has said that antiseptics for this purpose may in fact be harmful in that they damage healing tisslie. thus allowing infection to gain a foothold .29 1J It was Alexander Fleming in 1919 who sa id that it is essential in the estimation of the value of an antiseptic to study its efTects on the tissues rather than its efTect on bacteria. Unfortunately, Fleming's wise counsel of so many years ago has tended to be ignored in modern practice. It is known that the surface of open wounds docs not need to be sterile for healil1g to takc place. Equally, there is no evidence to support that dressing changes pcrformed once or twice a day with antiseptics guarantee protection from invasive infection. The concern with antiseptics is their toxicity. A number of studies, particularly with the hypochloritcs, havc shown major problems. Brennan and Leaper, m ill their study of the effects of antiseptics 011 hea ling wounds. used a devised rabbit ear chamber that was irrigated with a number of products. The efTect on microcirculation was measured using laser Doppler. This study clearly showed the effects of various an tiseptics on the microcirculation. In particular, Eusol was shown to occlude permanently the microcirculation after a I-minute exposure with no change in mcasured flow after 24 hours. 10
21 I
Apart from the wound cell toxicity and the depression of collagen synthesis, hypochlorites may cause localized edema, hypernatremia, hyperthermia, and burns. It has also been reported that cases of renal failure associated wi th topical application of chlorinated solutions to pressure sores have occurred. This has been attributed to the release of a toxic lipid from bacteria, causing the bacteremia or endotoxic shock called Schwartzman's reaction. '" Hypochlorites as a chemical entity arc chemically unstable. have a short shelf-life. are rapidly deactivated by organ ic material , and really are not cost effective, requiring frequent changes of dressing. And after al l. sodium hypochlorite is a bleach. A further study by Brennan et al. " showed that in particular hypochlorite retards the deposition of co llagen, an essential element in the matrix for the healing of wounds by secondary intention. The common ly used antiseptics fall into the di guanide group, one example being chlorhexidine, which is a bactcricidal agent with gram-positive and gram-negative acti vity. It is ineffective against acid-fast bacteria, bacterial spores, fungi, or viruses. Skin sensitivi ty is reported, and ch lorhexidine is incompatible with soap: the presence of blood and organic material also will decrease its activity. Antimicrobial activity is best at neutral or slightly alkaline pH . Chlorhexidine is used mostl y as a hand or skin disinfectant. The second antiseptic group contains the quaternary ammonium compounds and the re arc a number of these, cetrimide being one example. Quaternary ammonium compounds are oOen used in combination with the chlorhexidinetype preparations, an examp le of which is Savlon. These arc also bactericidal against gram-positive and gram-negative organisms. They are relatively ineffective against bacterial spores. viruses, or fungi, and some strains of Pseudomonas aerllg;nosa and A1ycohacterillm wberculosis arc resistant. They can also cause hypersensitivity. The third most commonly used antiseptic is povidone-iodine, an organic comp lex of iodine with polymers. It is a polyvinylpyrrolidione. It is bactericidal and sporcidal and is active against fungi and viruses. Local irritation and sensitivity may occur, and it may cause burns if applied to denuded areas. It should not be used on patients with goiter. Its absorption may also interfere wi th thyroid function tests. It is incompatible with alkalis and is used as a sk in preparation and as a disinfectant. The topical application of an antiseptic wi ll reduce the level of bacteria on the surface of the wound but will not penetrate into infected tissue .JS If a wound is clinicall y infected, the lise of systemic antibiotics should be considered as the most appropriate. Dr. Chri s Lawrence considers that antiseptics and to some extent certain antibiotics, if used wisely, afTord excellent antibacterial prophylaxis in a vari-
212
WOUND
CARL
ely of skin wounds. Unwise use of antibacterial agents, however. especially antibiotics. can create further problems. Dr. Lawrence. as do a number of other investigators. considers that convincing comparative clinical tfials concerning the possible value of antiseptics arc lacking. There is. however, sufficient in \llra evidence that would indicate that a problem exists with the prolonged usc of antiseptics in chronic wounds. lh In general the usc of topical antiseptics in chronic wounds
is con,idered 10 be oflillie beneril and may in racI be injurious to the tissue. The exceptions arc patients with major arterial circulation deficiencies. such as diabetics and
is clean wilh lillie or no residue rrom Ihe dressing, a simple irrigation with water or saline is the most appropriate. If there is dressing residue, slough, or dry or scaly lissue, Ihen in addition to water or saline the use of a skin wash wi th surraclanl properties wi ll aid in the remo,al orlhe debris. The most important aspect is to minimize the direct contact with the gra nulating wound. It is considered best to use the cleansing malerials al body lemperalure, as Ihe app licalion or a cold solution will reduce the temperature of the wound and may affeCI blood now. The use or antiseplic cleansers is or little valuc in chron ic \vounds; however. they are of benefit in the init ia l cleaning of an acute wound.'~n
immunocompromiscd, neutropenic patients. A decision
should be made for the individual patient, taking into account all the posllive benefits and risks.
REFERE'ICES TurnerTD ProdUWi and theIr development in wound managemenl PltHl Sllrg 1Jt.:rmawl ASJI('("t\. 1979:75 84
ANTISEPTICS A 'ID ACUTE WOUNDS
The use or lopical antiseplics and anlibiolics ror acule wounds is enlircly different from that for chronic wounds. In a traumatic wound the risk of infection from contamination at the lime of \vounding is very high. Also. in the case of major burns, the presence of necrotic tissue is a focus for infection. and it is mandatory to use topical management. The aim ofusing anlisepltcs and anlibiolics prophylaclieally is to rl:ducc the level of bacteria in the wound and allow the body's own mechanisms to destroy the rest. The use of povidone-iodine. chlorhexidine. and chlorhexidineicetrimide products is appropriate in the early management of acute traumatic wounds. The use of products such as si lver sulfadiallne cream III burns is part of the early management of Ihis Iype or wound.
2.
the drug tanl) H'1/Iml \lllIwgt'
3.
Thomas S Pain and wound management: community outlook .'\"/In Ttm('\ 19RQJt5(suppl):11 15.
4
Thomas S. Ifwlt/blHlA 0/ II(mml Orns,ng\ London: Macmillan;
5.
Thomas S, Lovcless P. lIa)' NI' Comparau\'c revle .... of the proper· tie~ of six semIpermeable film drcsslngs. Pllllrm J. June I K.
6
Gollcdgc CL Ad . . ance ... May 1993;42 47
7.
Myers JA. Ease ofu~c ofl\\o sellu·permeable adhc!iI\e mcmbranes compared. Plwrm J Dccemher I. 191'14;233:6K5 686.
8.
Loitcrman DA. Bye .... PI!. [treets of a hyt.lrocellular polyur~thane dres'img on chronic \ienotls ulcer healing. lI;mm/v. Septcmbcr Oc· tober 1991;3:178 IXI
9.
Mycrs JA Lyofoam a \crsall ic polyurcth:lllc fO:lm surgical mg. Phurm J Augu~1 31. 19X5;235:27()
1994 19HH:240785 788 III
wound managcmcnt Mot!\h·t! AIl.\l
dr~s ..•
10
I-"ostcr AVM. Grcenhlll MT. Ldmont.ls MI· Companng two dres .. · ing~ III the trCiltmcnl of diabetic fOOl ulcers. J 1f()lIml Cart' July 1994;3:224 22M.
II
Sussman GM lIydrogeb:
it
rcne.... Primtln" Inlt'''titm Fcbruary
1994:2:6 9 12
Srnlth RA. Rusbournc J. Thc use of So luge I 10 the closure of wounds by secondary intcntion. Prinwrl" IlIft'nliml Mily 1994;2
13
Thomas S. Joncs II Clime .. 1e'penenccs \\-Ith a new hydrogel dres ... · ing. J Hlllllll/ Cart'. March 1996:5:132 133
14
Thomas S. Comparing two drcsslIlgs for wound debndemcnt J UOl/m/ C/lrt!. September 1993;2:272 274
15
Thomas S. LO\ieless P A compar.:ttl\C study of the properties of si .. hydrocolloid dres ... /Ilgs. Plltlrm J No\embcr 16. 1991 :247:672 675 .
16
Rouo;seau P. Niecestro Rt-.·' Compari,on of the physicochemical propcrtles ofvariou .. hydrocollOId dresslllgs 1I')llIItI,. J
17.
\1arshall r J. Eyers A. The u~e of a hydrocollOid dre ... slng (Comfccl transparent) as a wound closurc dressing follow 109 lo.... cr bowel surgery. Prim"IT In/t·llfUlII August 1994;2 :39-40
14 17
V.OUNIl CLEANSING
CleanSing ora wound at the time of dressing changes will depcnd 011 the nature of the \vOt1l1d. In general. if the wound
III
1991:14 6.
ANTIBIOTICS
The lise of topical antib iotics in chronic wounds should also be based on a genera l principle Ihat lopical usc or anl ibiotics is not recommended because of the development of rcsistHl1CC Hnd scnsitilation. However. in surface anaerob ic contamination of some \vounds. especially fungating wounds. thc use of metronidalole gel is appropriate. and there have been cases of methicillin-resistant Staphylococcus Clllreus where topical mupirocm has been used. The other topical antibiotic used in clinical practice is si lver sulfadiazine cream in ~ollle infected ulcers where Pseudomonas has been found to be present. 17 "" Appendix A has additiona l information on antiseptics and antibiolics.
Turrn.:r TD. SurgIcal dreSSings
.1 1ullugelllelll
I N.
Banks \: Bale SI·. lIardlllg KG Comparing I\~o dressmgs for cxudlng pn:ssurc sores 111 communlly patlenh, J Jl(lIIm/ Om' June \1)<)4;3: 175 171<
29
Sh~i!!h
or,"e
H(ml/{ll:.~m·im1l1m'l1f
2 13
J\\. Linter SPK IIM;lrds Ill' hydrogen pem\ide IIr \ft'cI J 17Utl.
19~5;291
10
Thomas SS, L.m'rencc )C. Thomas /\. huluation of hydrocolloids and tupic.1I medication 111 minor burns J IHnmd Care. M:ly 1')95;4:2IN 220.
Brennan SS. LC;lper DJ The Cn'cl:ls or .L11t l ~erlH.:~ nn the hC;llIng wound a study u ... tn£ the rabbll ear chamber Ilr.l .\'lIrx
JI
20
Thomas S. OhscnatlollS un the fluid handlm£. propertlcs of alginate dressings. Plwrm J June 27. 1992;141'1:1'150 X51
Lmrence (1. Dressll1g'o alld wound IIlfcclion IIJ1J4.167(suppl):2IS 24S
32.
21
SU'i'iman (iM Aigmatcs 19\)6;411 J7
Brennan SS. IlIsh:r ".11-. l.e;1lll'r DJ /\ntl,>eptu: 10\1\;11) III \HlUnds he.lled by sec(lndi.lr~ nllentlon J 1/11\1' 11I/t'd 19X6;X:26J 2(17
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I,caper I)J. AntlseptlC'i ;Ind thelre llcet on healing II ...... UC . ~\;lIn "limt'\ May 19it
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r-..1organ ()/\ ('hlonnaled sulutlllns (I.) u...elul or (e) u . . cle ... s. P"arm ./ /\ugu'>l II), 19!N;24J:2J1) 22()
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t.;1\\ reno'! J( The dc\elupmcnl of an In \ llro wound model and Its application to the usc of topi( In : Pmtn'dillgl fI/lht'
19
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19X5;71:7X07X1
rc",ie". Pnmllr\' IlIlelllioll February
Miller L Jones V. Bait: S The u...e uf alglll:t1e packing III the management Ill' deep 'iItlUSCS ./lIiJltlld Cart'. September 1993;2:262 26.~
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Thomas S Usc of;\ t:alciul1l algUlille drc'i'iing. PJ/fIr", J /\ugU'it 10.
24
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l 'lnl 1:'/11"01'("(111 ('oll/"/WU'(' OIl , Iliml/('('I III
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Achtcrberg VB. Welling C. Meyer- Ingold W lIydro:lcli\'e dressIngs and serum protein: an III \llIro study. ./ lIillmd Care. Fehnmry
1X
27.
Collier J /\ I11ms! oduur-free Cn\lronl11en l. Pml !Vur\e September
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llr(mn-I-.tns M. Snulh JA. Pascen I~ runehello M Case sludies: conSidering Jrcs~ing option.. OI/otlll' IIllUnd\lunaXe. June
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1(1)2;X04 X07.
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\Vound infection ./ IImll/li Can' September
11}9J;2:277 .2XO
Willialll'i (' Treallng;1 pauellt\ \cnous ulcer wnh a foamed gel drcsslllg. J 11(1/11111 Clu'(" September 11)1});2 :264 265.
1994;4(J54~
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1996;5:79 X2.
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I,e J I/mp 111/('1'1 191(4;5 :6 1) 73. )(HII1£ JB, DubrJ'anslo.l S. I)rcssurc sorcs epidellllology anti I;urrcnt managcment com:epls, f)rI/.I!.\ ,·Ij.!/Ilg 1992;2:42 57. Brown CD, Ilte1li J/\ " rc\ic", of topil.'al agent .. for \\'OUI1(1\ and methods of woundlllg . ./ IkrllWfof SlIr.1! Ol/wl J (1).1; J 9
H27.n 4()
Din: JD. \\el ... h ,\P. A clllllpariMHl of wound Irrlgatiun solution used the emergency department '"" Emt'l".I!, .\It'd June 11}90; 71)4 71)7
111
P A RT
III
Management by Wound Etiology Barbara M. Bales-Jensen
Determining the cause or etiology of a wound is a critical element in creating a co mp rehe nsive trea tm ent pla n for pati ents with wounds. The chapters in Part III foc liS on management by wound etiology. Specific attention to acute surgical wounds, pressure ulcers, vasc ular ulcers, and neuropa thi c ulce rs is prese nted in the chapters in Part III. Em phasis is placed on understanding the pathophysiology involved in the wound type, assess ment methods, and prevention and manage ment of spec ific wound types. Improving and expanding knowledge of wo und eti ology empowers
cli nicians to provide quality comprehensive care in clinical practice. In Chapter II Bates-Jensen and Wethe present management of the acute surgica l wound. Th e chapter begins by defin ing the acu te and chro nic wound. When does an acute woun d become a chronic wound? The easiest and perhaps the least controversial defin ing characteristic of the acute wound tha t becomcs chronic is fa ilure to follow the normal wou nd hea ling tem poral sequence. Better understanding of ac ute wou nds im proves ability to monitor and treat all wounds. Types of surg ical wound healing- primary intention, secondary intention, and tertiary intention- are presented. Extrinsic factors that affect wound hea ling during the preo perati ve, intrao perative, and postoperati ve time periods are described. Surgical wound class ifications are presented and reviewed. Interven tio ns fo r managi ng hypovole mi a. thermoregul ation strategies, and meth ods o f optimizing tissue oxygen perfusion are described. In tri nsic factors affecting hea ling of the acute surgical wo und are those that innuence the person systemically. Examples of intrinsic factors incl ude age, concurrent conditions, nu trit ional stat us, and oxygenation and tissue perfusion. Each intrinsic factor is disc ussed with special attention to the patie nt with diabetes. Examination of the surgical in-
cision includes evaluation of wou nd characteristics such as incision locatio n, length , presence of hea li ng ridge, type and amount of exudate. type of wound closure materials. and approx imation of wound edges. The incisional examination forms the basis of acute surgica l wound assessment and is presented by phase of wo und heal ing (i nflammatory, pro li ferati ve, and remodeling). Management of the surg ica l incision includes atte ntion to factors that affect wound heali ng as addressed in Chapter II , as well as dressing care. The surgical dressing includes the primary and secondary drcss ing. Di scussion inc ludes types of dressings lIsed for pri mary and seconda ry dressings. Wound healing in secondary intention and tertiary in tention wo unds is discussed and cont rasted with pri mary intention incisions. Outcomc measures for eva luati ng heali ng in incisional wounds following the phases of wound hea ling are presented and described. Thi s sectio n includes examples of approp riate documentation of the healing incision. Chapter II concludes with a case study for review of material and self-care teaching guidelines for use wi th other health care prov iders, famil y caregivers, and patients. Chapters 12 and 13 descri be issues related to managemcnt of pressure ulcers. Chapter 12 is devoted to pathophysiology and prevention of pressure ulcers. Pressure ulcers arc areas ofl oea l tissue tra uma that us uall y develop where soft tissues arc compressed betwee n bony prominences and any external surface for pro longed peri ods. Chapter 12 begi ns with a definition of pressure ulcers and an extensive rev iew of the pathophys iology of pressure ulcer development. The re lationship between time and pressure in the deve lopment of pressure ulcers is presented. Clinica l presentatio n of pressure ulceratio n and the 1110st preva lent locations fo r pressure ulcer development are covered. Specific information is i112 15
2 16
W OUND CARE
el uded o n assess ment or the dark-skinn ed ind iv idua l for risk o f pressure ulcera ti on. Pressure ulcers are commo nly classified according to g rading or staging sys tems ba sed on th e depth of ti ssue destructi on. The sta ge is dClCfmincd on initial assessment by noti ng
the deepest layer of tiss ue involved. The history of stag ing systems and th e c urrent system recomm ended by the Age ncy
for Hea lth Care Policy and Research and the National Pressure Ulcer Ad visory Panel are described . The issue of pressure ulcer assess ment and the usc and misuse of staging classi fi cation systems are a subject of debate and cont roversy. Pressure ulcer develo pment docs no t necessa ril y occur fro m
one stage to the nex t, and there may be different etiologic factors f'or va rio us stages. Chapter 12 reviews this issue. Di scussion of press lire ulcer pathophysiology and etiology would not be complete without mention of other interac ting facto rs. Pressure ul cers are phys ica l ev idence of multiple causati ve influences. Factors that contribute to pressure ulcer developmcnt can be th ought of as those that afTcct the prcssure fo rce over the bony prominence and those that affect the tolerance of the tissues to press ure. Mobility, sensory loss, and ac ti vity level are related to the concept of increasing pressure. Ex trinsic factors such as shear, fri ction. and moisture, as well as intrinsic fac tors sllch as nutrition, age. and arteri olar pressure relate to the concept of tissue tolerancc. Each of thc factors is presented and discussed. Particula r attention is given to immobility or severely restricted mobility because it is the 1110st important risk fac tor for all populations and a necessary condition for the deve lopment of pressure ulcers. The most common risk assessment tools, Braden·s Scale for Predicting Pressure Sore Risk, No rt on's sca le. and Gosnell 's scale, are all presented and di scussed. Preve ntion strategies are ta rgeted at reducing risk factors present. Appropri ate prevention intervent ions can be focused on eliminating spec ific ri sk fac tors. Thus, earl y intervention for pressure ulcers is ris k factor- spec ific and prophylactic in natu re.The preve ntion strategies arc presented by risk factors. begi nning with general informat io n and ending with speci fi c strategies for a particular ri sk fac tor. Chapter 12 includes speci fi c information on the use of support surfaces with de finiti ons of pressure-reduci ng and pressure-relieving dev ices, pill ow bridgi ng, and pass ive repositioning. Extensive discussion on nutrition interve ntions and management of incontincnce is included. Skin hygiene interventions and sk in maintcnance interventions round out the prevention strategies. Chapter 12 concludes with outcome measures for eva luating thc success of a pressure ulcer prevention program and extensive sc lf~ca re tcaching guidelines for other health care prov iders. fa mily caregivers. and patients. In Chapter 13, Rappl continues the di scussion of support surfaces that began in Chapter 12. Rappl provides a look
at therapeutic posit io ning for pressure ulcer prevention. Persons who become sitting dependent more than a m~ bu latory and those who use the lying-down or the sitting position for the majorit y of their day are at high risk of skin breakdown. And for the patient with an ex isting pressure ulcer, proper positioning in the most acti ve and fu nctional position possible. both in sitting and in recumbent positions, improves the healing rate of the ulcer and mini mi zes the likelihood of developing new ulcers. Chapter 13 provides an overview of therapeutic positioning kn owledge. The areas the clinician should exam ine in order to determine the need for intervention arc presented and described. The bas ics of therapeut ic positioning and a di scussion of how therapeutic positioning affects body system impa irments is presented. The chapter includes a ta ble on fun ctional diagnosis and relationship to prognosis. interventions. and out comes related to therapeuti c posi tioning. The idea l sitting position is described, and basic seating principles re lated to pelvic co nt ro l, th igh cont ro l, scat dept h, and footrest arc di scussed . Finally, spec ifics in pos itioning the patient with an ex isting ulcer both in sitting and in lying down are described. An extensive di scussion of methods of determining appropriate wheelchai rs and sitt ing pos ition and proccdures for recumbent posit ioning for patients is presented. Donayre provides an in-depth analysis of the diagnosis and management of vascul ar ulcers in Chapter 14. The chapter begins with a review of ge neral anatomy and physiology of the circulatory system and pathophysiology related to lower extremity ulcers. Thorough hi story and physical assessment are essential for the patient wi th a lower leg ulcer, and Donayre prov ides this information for each ulcer type; in addition, risk factors for arteria l/ischemic, ve nous, and diabetic ulcers are discussed. Donayre describes presentation and assessment of common find ings related to lower leg ulcers, such as intermittent claudication, rest pain . altered an kle- brachial index, edema. and tissue changes. Associated diagnostic tests for the lower leg arc described. Differential diagnosis for leg ulcers is a key fac tor in determining appropriate treatment. Treatment that is appropriate for a ve nous ulcer may be contraindicated for an arterial/ischemic ulcer. The presenting clinical manifestations, diagnostic tests, and differential wound assessment are presented for each lower leg ulcer type. Medical and surgical manage ment related to arteria l/ischemic, venous di sease, and diabetic ulcers is described. Special attent ion is given to diagnosing osteomyeliti s in the diabetic and describin g pathophysiology of edema related to ve nous di sease with indications for clinica l manage ment . Part III concludes with Elfiman 's presentation of the neuropathic foot. Chapter 15 opens with a disc ussion of the necessit y of interdisciplinary coll aboration in the management
Par/III
of neuropa th ic ulcers. The neuropat hi c patient ofte n has dysvasc ul ar components Ih at muSI be add ressed by a m ed i ~ ca l tea m ra th er Ih an one specialty. The trineuro pal hy assess ~ ment with allen tion to senso ry, motor, and a ut onom ic neur-
opathy is explained. Gradua l and sudden-onset peripheral neuropa thy are compared for easy differential diagnos is. Diabeti c neuropathy is th e major foca l point of Chaptc r 15. Common infections and derma tologic changes are prese nted. T he definitions of wet and dry ga ngrene are prese nt ed, and the two conditions are compared. Footwear assess ment guidelines and interve nt ions based on th e Wa gner ul cer g rade is
explained. Chapter 15 includes in-depth exp lanatio ns of sensory, pressure, vi bra tory. and root de formit y eval uati on.
Charcot's deformi ty is explained and the method of assess-
2 17
mcnt described . Managemcnt wilh orth otic devices is explained. Specific instrll cti ons for procedures. such as how to make a foam toe se parator are incl uded. Interve nt ions to decrease pressure, such as tota l-contact cas ting. use of splints and insc rt s, and ncurowa lke rs are all di sc ussed. T he chapter concl udes with self-care teac hin g g uide lines ror usc wi th patie nt s and family caregivers and doclimentation req uirements for ne uropath ic ul cers. Although similarities exist in th e treatment ora ny wo und, treatment ap proach va ri es depcndi ng on wo und eti ology. The c hapters in Part III form a foundation on knowledge o f wounds of va ri olls eti ologies. This fou nd ation should provide c linicians with a stron ger and more indi vidualized ap~ proach to th e person with a wou nd .
CHAPTER
11
Acute Surgical Wound Management Barbara M. Bales-Jensen and James WeIhe
ACUTE SURG ICA L WOUND DEFINITION
Acu te wounds arc defined as disruptions in the integrity of the skin and underlying tiss ues that progress through the healing process in a timely and uneventful manner. The acute elective surgical wound is an exampl e of a healthy wound in
which healing can be maxi mi zed. However, not all surgical wounds are uncomplicated, with maximal healing potential or the possibility of uneventful healing. For example, acute surgical wounds can occur in unhealthy tissues, in a compromised host, or as a res ult of unexpected or significant trauma. Surgical wounds may be allowed to heal by one of three methods : primary intention, secondary intent ion. and tertiary intention (Table 11 - 1). Wounds healing by primary intention are wounds with edges approximated and closed. Secondary wounds are wounds left open after surgery. Secondary healing wounds heal wi th scar tissue replacement in the ti ssue defect. Tertiary wound hea I ing, or delayed primary closure, involves aspccts of both primary and secondary wound healing. In tcniary wo und healing the wound is left open ini tiall y and afier a short period of time the edges are approximated and the wound is closed. Wound healing by secondary intention or dchisccd wounds may not follow a timely and uneventful healing course and thus may be considered "chronic" wounds by some clinicians. I When does an acute wo und become a chronic wound? The easiest and perhaps the least controversial defining characte ri stic of the acute wound that becomes chronic is failu re to follow the normal wound healing temporal sequence. In general, the acute surgical wou nd should complete the proli ferative phase of wound healing in 4 weeks. For example, th e wound should have filled with granu lation tissue and be resurfaced with
epithclial tiss ue. Acute surgical wounds that progress at a slower pacc or fail to progress can be considered chronic. The surgical inci sion healing by primary intention might be described as the ideal wound for healing. The wound is controlled with attention to ti ssue handling and proper use of surgi ca l instruments by the surgeon. and the wound edges are apposed and aligned immediately to decrease the risk of infection. The acute surgi ca l incision wound healing by primary intention is the focus of thi s chapter. FACTORS AFFECTING HEALING I N ACUTE WOUNDS
Healing in acute surgical wounds involves the interaction of extrinsic and intrinsic factors. Extrinsic fac tors relate to those agents outside the person , whe reas intrinsic factors are those influencing the person internally or systemically. Extrinsic Factors The physical environment before and during surgery, the surgical preparation , the technique of the surgeon, and types of sutures are all examples of extrinsic fac tors aficct ing acute wound healing. Thus for the surgical woun(~ evaluation of the perioperative period is indicated, as it plays a role in the wound outcomc. Wound infection is the major cause of surgical wounds ' fai lure to progress through th e healing process in a timely and unevcntful manner. Operat ing room protocols, attention to instrumentation, and appropriate surgica l technique are all means of decreasing the risk ofinfecti on and ensuring optimal healing from the outset for the surgica l wound.
219
220
WOUND CARE
Table 11 -1 Types of Surgical Wound Healing Wound Healing Type
Definition
Primary intention
Wound edges approximated and closed at time of surgery
Secondary intention
Wound left open after surgery and allowed to heal with scar tissue replacing the tissue defect
Tertiary or delayed primary closure
After surgery, wound left open initially and after a short period of time the wound edges are approximated and the wound is closed
Preoperlllive I'er;or/ The length oftimc the patient spends in the hospital prior
to surgery innucnccs the rate of surgical wound infection. As the length of hospital time increases prior to surgery, the
risk of wound infection incrcascs. 2 Prcparation orthe operative site also innucnccs the risk of wound infection. Showering immediately prior 10 surgery. lIsi ng a hexachlorophene soap. has been shown to result in a decrease in infection rate, compared with not s howering . ~ Shaving the operative area and the method used to shave the area have also been impli-
cated in surgical wound infection.
Research Wi sdom: Operative Site Preparation
Use of an electric razor, clipping hair, and not shaving the operative area are all associated with wound infection rates lower than those with use of a nonelectric razor to shave the operative area. 2 0espite the research, however, most preparations still include nonelectric shaving, most commonly performed in the operating room. The poor implementation of the research may be due to the absence of electric razors or clippers in the operating room.
contaminated wounds are procedures wherein the gastrointestinal (G I) tract or respiratory tract is entered without signi ficant contamination. A contaminated wound is one in which a major break in ste rile technique or gross spillage from the gastrointestinal tract occurs. Procedures in which acute bacterial inflammation or pus is encountered with devitalized ti ssue or contamination are classified as dirty or infected wounds. Increased length of time for the operative procedure increases the risk for wound infection significantly. One study found that th e infection ratc doubled each hour the surgical procedure continued.:! Strict adherence by operating room personnel to a protocol ha s also resulted in decreased wound infection rates. 4 The surgeon must be concerned with wound tension , vascular supply, and proper surgical technique. If the wound ca nnot be closed without a significant amount of tension or if the vascular supply is poor, there is increased risk of dehiscence and infection.~ Suturing technique can assist with optimal wound healing outcomes. Use of buried sutures ca n improve primary wound healing by decreasing potential dead space underneath the incision, giving ten sile support for 4 to 6 weeks while the wound is still weak. and decreasi ng tension on the apposed wound edges. ~ Surface sutures may provide additional concerns for optimal hea ling because they provide additional "wound s" to heal alongside the incision.
ill frtlOperllfi l'e Periol/
po:,·toperlllive Perioci
Limiting the infection rate intraoperatively is largely under the control of the surgeon . Sometimes infection co ntrol is hard to obtain. For example. the surgeon has limited power over the nature of the problem for which the surgery is performed the operative si te. and the general condition of the patient ; all arc more complicated factors that are not easily controlled. The type of surgical procedure influences the risk ofinfcction. Surgical procedures are classified according to the ri sk of infection .1 Table 11 - 2 prese nts wound classification s for s urgery. Clean wounds are those nontraumatic injuries in which no innalllll1ation is encollntered during the procedure and there is no break in sterile technique. Clcan-
The stress response associated with surgery has also been implicated as a cause of impaired wound hea ling. The stress of surgery is known to stimu late the sympathetic nervous system with a resultant sympathetic nervous syslemmediated vasoconstriction. The effect of high levels of circulating catecholamines in the immediate postoperative period causes the resulting vasoconstriction with factors leading to the trigger of the sympathetic nervou s system, including hypoxia, hypothermia, pain, and hypovolemia.b ln the immediate postoperative period measures of subcutaneous ti ss ue/wound oxygenation arc lower after major operations
Acute Surgical Wound Nlcmagemel11
22 1
Table 11 -2 Surgical Wound Classifications Surgical Label
Definition
Clean
• Nontraumatic injuries • No inflammation found during procedure • No break in sterile technique
II
Clean-contaminated
• Procedures involving GI or respiratory tract • No significant contamination
III
Contaminated
• Major break in sterile technique • Gross spillage from GI tract
IV
Dirty or infected
• Acute bacterial inflammation found • Pus encountered • Devitalized tissue encountered
Wound Classification
and correlate wi th extensive. morc complex surgica l procedurcs.b Attempts to restore ti ssue and wo und oxygen defi cits re late to minimi zing the risks of hypoth ermi a. pain, hypovolemia, and hypoxia si multaneously in the immed iate postoperative period.
Clinical Wisdom: Maximizing Wound Healing Critical measures to maximize wound healing in the immediate postoperative period include all of the following . Keep the patient • Warm • Well hydrated, intravenously or orally • Pain free by use of patient-controlled analgesia if possible • Well oxygenated by use of supplemental oxygen if needed
Thermoregulatory responses are diminished in the surgica l pat ient because th e prolonged exposure to thc co ld
or
Correc tin g hypovolemi a wi th adequate fluid infusion preven ts continuing vasoconstri ction caused by hypovo lemia . Fluid replacement occ urs si multaneollsly with rewarming efforts. Assessment and management of pain and ti ssue perfusion are also recommended to ensure optimal wo und healing.6 Additional factors crucia l to opt imal surgical wound hea ling in th e postoperati ve period are intrinsic factors that can be controlled, which are discussed in th e following sect ion.
In trinsic Factors Intrinsic factors affecting hea ling of th e acute surgica l wound are thosc that influcnce th e person systemically. Intrin sic factors include age, concurren t conditions. nutritional statu s. and oxygena ti on and ti ssue perfusion. Age The physiologic changes that occur wi th aging place the older individual at higher ri sk for poor wound hea ling outcomes. Decreased elastin in the skin and differences in collagen replacement innuence healing in older adults. 7 A de-
operating room environment. Pati ent s treated with active rewa rming by usc of hea ted bl ankets during the recove ry
period respond wi th a faster return of normal tissue/wound oxygen levels th an do those allowed to return to normothermia without rewarming intervcl1tions. 6Routine use of me asures to warm th e patient actively during the surgical procedure, slich as warming blankets and th e lise of warmed intravenous nuids along with active monitoring during sur-
gery, hclp prevent thermoregulatory problems. It is casier to prevent therm oregu latory problems than to remedy th ermoregulatory problems.
Clinical Wisdom: Risk of Delayed Wound Resurfacing in the Older Adult The delay in wound resurfacing puts the older patient at risk for wound infection. Daily wound assessments and use of topical dressings for protection are required for a longer period of ti me than necessary for younger patients.
222
WOuND CARl
creased ratc ofreplaccl11cnt of cells affects the rate of wound healing and. in particular. rccpithclialization of the skin.1 Immune system function declines with age. and this may
Clinical Wisdom: Urine Glucose Levels
account for increased ri sk of infection in o lder adults. The microorganisms proliferate in the wound before they can be removed due (0 the diminished immune response. Older adu lts present with chronic discases. circulalOTY changes. and
Urine glucose levels are not sensitive enough to provide good glucose control because of the high renal threshold for glucose (approximately 180 mg/dL) . The use of blood glucose monitoring for more definitive management is a critical assessment strategy.
nutritional problems. which increase the risk for poor or delayed wound healing. Decreased mOlor coordination and di-
minished sensory function increase the potential for injury. \\,ound complications. and rcpealed wounding at the same
site. COII ('lI rrellf Couditiolls
The presence of certain discases, conditions, or treatments can innuence \.,,'ound healing outcomes. Diabetes mellitus is one condition that interferes with wound hea ling. Diabetcs is associated \\ ith small vessel disease. neuropathy. and problems specific 10 glucose control- all of which predisposc
the person to impaired wound hcaling. Diabetic wound healing problems include increased ri sk of infec tion, delayed epitheliali73tion. impaired or delayed collagen synthesis. and
slowed wound contraction and closure. ~ Hyperglycemia can arrect the cellular response to wounding. There may be a delayed response or impaired functioning of the leukocyte and fibrobla st cell>. both of which are essential for \\ound
repair." The eOcct of surgery on the diabetic patient can bc dramatic. The diabetic responds to the stress of surgery by releasing a series of hormones: epinephrine. glucagon. corti sol. and growth hormone. The stress hormones reduce the amount of ci rculating insulin while increasing circulating glucose. Ele\'ated glucose levels can reduce the errecti\cness ofneutrophils' phagocytotic function and alter the deposition of collagen by fibroblasts, leading to a decrea se in
wound tensile strength .MElevated glucose leyels can also lead to cellular malnutrition. as insulin is the key for allowing nutrient usc in cells. Because glucose is not able to be used as energy, proteins and fats are used as fuel , depleting necessary substrates for wound hea ling. The ability to control the glucose level in the postoperative period is probably advan-
tageolls for positive wound healing outcomes in the diabetic. Maintaining serum glucose levels below 200 mgldL is recol11mended for patients with wounds. ' In the immediate postoperati\e period c lose monitoring of blood glucose and insulin supplements as indicated are required for adequate wound healing. Careful attention to blood glucose levels can assist significantly in positive outcomes and prevent an acute surgical wound from becoming a chronic wound.
Other conditions also affect wound healing. Cardiovascular di sease presents risks for wound healing because of the associated perfusion alterations. impaired blood flow, and vascular disease. Atherosclerosis is a common cause of inadequate perfusion of wounds." Immullocompromi sed patients are an additional group at fisk for poor healing outcomes. The immune system plays a significant role in wound healing, and any impairment (eg. aging. malnutrition. and cancer) can have serious sequelae for the patient with a wound. Treatments that affect \VOlllld healing include steroids. antiinflammatory drugs. antimitotic drugs. and radiation therapy. Steroids inhibit all pha ses of wound healing, affecting
phagocytosis, collagen synthesis. and angiogenesis. The effects of steroids can be reversed with the usc of topical vitamin A. The vitamin A is applied directly to the wound and acts as an inflammatory agent. Vitamin A is approprinte to apply to open wound beds. Wounds healing by primary in-
tention. closed with edges well approximated may not be appropriate candidates for topical \ itamin A.
Clinical Wi sdom: Vitamin A Use for Wounds The usual dose of topical vitamin A is 1,000 U applied three times a day to the open wound bed for 7 to 10 days.
Other anti-innamrnatory dru gs also inhibit wound healing. with errects seen predominantl y in the inflammatory phase. Cancer therapies. antimitotic medications. and radiation therapy work by impeding the normal cell cycle in rapidly dividing cells. The antimitotic activity interferes with new tissue generation in the wound. In addition. radiation therapy has both acute efTects on cellular fun ction and longterm sequelae for healing. The long-tcrm efTects of radi ation therapy on wound healing arc caused by hypoperfusion of
Acute Surgical Wound Manageme"t
ti sslles in the irradiated fi c ld . Hypope rfu sion induced by irradiation is due to damage. deterioriation. and fibrosis of the vasculature. 1
NlIIritiollll/ Statlls Adequate nutriti on is esse nti al fo r wou nd healing. In the hea lthy surgica l patient malnutriti on may no t be an iss ue. Howeve r. with the populatio n aging and more procedures bei ng perform ed on older adults. nutritional statu s is a conccrn for wound healing. Adeq uatc amounts of ca lories I proteins. fa ts. ca rbohydrates. vitamins. and minerals arc all required for wou nd repa ir. Inadequate am ount s of a ny nutri CIll S ncga tive ly influence wo und healin g.1t) Pro tein s are necded for ncovascul arization. fibroblast prolifera ti on. coll agen synthesis, and wound remodelin g. Amino ac ids are the struct ural co mpon ent s of proteins and an.! csse nt ia l paris of deoxyribonuc le ic acid (DNA) and ribo nuc leic ac id (RNA). DNA and RNA provi de the panern for cell milOsis and enzy mes required for ti ss ue generation. Protein malnutrition results in loss of bod y stores of amino acids and insufficient substrates for wound repair and new tissue growth. Carbo hyd rates and fa ts provide necessary energy required forccllular fun ction . When th ere are inadequate amounts o f carbo hydrates and fats (ca lo ri e malnutrition ), the body uses ca tabolism to brea k down prote ins in order to meet energy requircments. G lu cose balance and ava ilable esse ntial fally ac ids are esse ntial substrates for wo und healing. Vitamins and mineral s play an important ro le in wound heal ing. Several vitamins a nd mineral s have specific functi o ns for wound healing. Vitamin A is ~I fat-soluble vi tamin and is responsible fo r suppo rting epithel ia li zation , ang iogenesis, and collagen formation. It is a lso important for th e inflammator y phase of wou nd healing. The wa ter-soluble B vitami ns are co facto rs in enzymatic reaction s. Vitam in C has been associated with wound healing. Vitamin C is essential for an giogene sis and collagen sy nethesis. Vitamin C al so supports fibrobla st function an d is critical for leukocyte functi on. For pati ent s w ith wound s, infection. or significant injury, suppl emental vitamin C is often provided to ass ist in meeting the incrcased metaboli c nceds and wound healing needs. Co nse nsus o n s pecific guidelines for appropriate supplemental doses of vitamin C is not available: howeve r. megadoses of vitamin C have not been proven beneficial. ViUlll1in C usc and elimination increase w ith exercise, stress. injury, increases in metabo li c rate. and smoking. Vita min 0 is requi red for bo ne healing and abso rption of calc ium. wh ich is important in enzyme system s. Vi tam in K is necessary for coagulation and hemosta sis. Vitamin E is used for fat mc-
223
taboli sm ; excess amo unt s are not beneficial to wo und healing.
Clinical Wisdom: Vitamin E and Wound Healing Many people think that vitamin E has healing properties. In fact, vitamin E delays healing and fibrosi s. 1o It is the delay of fibrosis or scarring that may be responsible for decreased scar format ion at the injury site.
Mineral s also playa role in wound hea ling. usually: the minerals of co ncern arc zinc and iron. Zinc plays an esse ntial role in enzy me systems and immune system function and is a cofacto r for co ll age n sy ne th es is. Zinc defi ciency contrib ut es to di srupti on in g ranulati o n ti ssue formation. diminished ten sile strength. dehiscence, and ev isceration . 'o Low levels of z inc are found in o lder adults and low- inco me patients, with losses associated with d iarrh ea. re na l failure, diuretic and la xative use, and paren teral and ente ral nutri tion. 11 lron is a cofactor in coll agcn synthesis and acts to transport oxyge n. Iro n dcficiency may be prese nt in those with c hanges in eat in g habits, intestinal damage. o r inc reased metabolic need s.
Oxygellatioll and Perjilsioll Adeq uate wound oxygcnati o n is essen tial for wound healing. The initia l injury causes hypoxia. and th e resultant growth factor release s upports initial c(lp illary budding. Oxygen is influc l1l ia l in angioge nesis, fibroblast function , e pithe lial ization, and resistance to infccti o nY 14 Ti ssue perfusio n is intertwined with ti ss ue oxygenation . Sati sfactor y ti ss ll c perfusion is essential for oxygenati o n. Ample ci rc ulating blood vo lume ca rri es oxygen- ri c h hemogl obin to the ti ssues. Tiss ue perfu sion a lone, however, does not g uarantee wo und oxyge nation. Probl ems related to tissue perfusion and oxygenati o n may be due to cardiovasc ular or pulmonary disease as well as other conditi ons sllch as hypovolemia. Thus, ma inlaining vascular vol um e is crit ical for ensuring adeq uat c ti sslle pe rfusion. The c linic ian mu st ba lance fluid rep lace ment to prevent both underhydration and overhydrati o n. Excess hydration ca n lead to hypervo lem ia and edema, wh ich may decrease ti ssue oxygenatio n. To optimize oxygenation in the presence of adequate ti ss ue perfusion, use of pulmonary hyg iene interventions, assessment and monitoring of tissue oxygen levels, an d low-fl ow s uppl eme nta l oxygen may be warra nted . IS Pulmo nary hygiene, inc luding incentive spirom-
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amount of time postsurgery, since the hea ling progress of the wound can be measured against the standard time expectations for acu te wound repair. Knowledge of the wo und healing process provides a critica l foundation for assess melll of the acute surgical incision. During the inflam matory process, assessment focuses on identification of signs and symptoms of in flammation, eval ua tion of wound closure materials and wo und dressings. and appraisal of epithelial resurfacing. The central point during the proliferation phase of wound healing is evaluation of collagen deposition. wound exud31e, and tissllcs surrounding the incision. Assessment during the remodeling phase is directed toward exami nat ion of collagen remodel ing at the incisional sitc.
etry, deep brea thing and co ughing, and postura l drainage,
improves the pulmonary toi let and increases the likelihood of adequate oxyge nati on of the wound. Low-now oxyge n cun saturate hemoglobin so that the supply to the ti ssue is
ample. Promoting activity such as repos ition ing and early 3mbulation ca n also be beneficial for periphera l tissue per-
fusion and Qxygcnation,l' Oxygcn3tion and perfusion arc vital to wound hea ling. and postoperative intervent ions (0 improve the ci rculatory and oxygen-carrying capaci ty of the tissues or blood (the oxygen saturation of tissues) can enha nce wound
heali ng. ASSESSMENT OF THE ACUTE SU RCICAL WO UN D
IncisionalAssess ment during th e Innammatory Phase Assessment of the acute surgical wound invo lves physical
examination of the wound site and surrounding wound tis-
The major assessment finding in the first 4 days postoperati vely is the identification of inflammation . The surgical incision may fee l warm 10 the tollch. and there may bc surrounding erythema and edema at the incision site. Signs of inflammation are ex pected and normal during the first 4 days
sues in relation to the wound healing process (Figure II - I ).
Physical examina tio n of the wou nd and the surro unding tissues includes measurement of the incision: observation of the wound ti ssues wilh attent ion 10 epithelia l resurfac ing, wound closure, wou nd exudate, and surroundi ng wo und tissues; and palpation of the incision with attention to coll agen deposition and surround ing tissues. The linear measurement orth e length of the incision and the ana tomic location of the incision provide a baseline measure. Measure the length of the incision in centimetcrs. Observation and palpation of the incision line provides insight to the healing process that occurs in the underlying ti ssues. Healing proceeds in the surgica l inc ision as it does in other wou nds with inflammation- proliferation of new tissues and remodeling. In the surgica l incision the wo und healing processes are not always visible. Thus. the standard for assess ment of healing may be best based on time since the surgica l injury. It is important for clinicians to track the
postoperatively.
Clinical Wisdom: Signs of Inflammation
It is normal to observe signs of inflammation such as warmth, erythema or discoloration, pain, and edema at the incisional wound site during the first few days after surgery.
Pat ients wi th immune system compromise due to age, a disease process. or therapy (such as steroid treatments) may not be able to mount an elTective inflammatory process. thus
rf,
•
,
,.
Figure 11 - 1 Surgical inci sion healing by primary intention. Note the lack of wound edge approximation and no healing ridge at the posterior halfofthe inci sion . SUlures remain present along the posterior incision . Courtesy of Evonne Fowler. MN. RN. CETN. Banning, C'lli fo rni a.
Acute SurgicallVolilld Mallagemem
the signs of innammatiol1 aI the incision are not visible. The lac k of innammat ion at th e incision si te is an indi cat ion of immune system comprom ise. Thus. an ab normal finding during the first 4 days afte r surgery is an incision with no ind ication of innammation. The process of epithelia l resurfaci ng also occu rs during th e innammatory phase of wound healing. In th e ac ute surgical inc isio n, new epidermal ti ss ues are ge nerated quickly because of the prese nce of intact hair folli cles and sebaceo us and swea t gla nds and the short distance th e epi thelia l cells mllst trave l to resurface th e incision. The surgical incision is resurfaced with epithe lium within 72 hours poslsurgery. T he new epidermis provides a barrier to bacterial organisms and to a small degree external tra uma. The tensi le strength of the incision is rela ti ve ly weak and th e incision is not able to withstand force. The astute clini c ian ca n obse rve c hanges in th e new incisio n indicati ng the presence of new epithelia l ti ss ue. The incision is eva luated for the close approximation of th e wo und edges and co lor of the inc ision line. Wound edges should appear we ll aligned wi th no tension observed.
Clinical Wisdom: Incisional Color Changes As the new epithelial tissue migrates across the incision, the color of the incision may change from bright red to pink; although this is not observed in ali patients, it is a useful clinical change that demonstrates maturing epithelial tissue.
A wound dressing is no longer necessary to preven t bacterial contaminat ion of the incision once epithel ial resurfacing has occurred. However, the wo und dress ing has other benefits at thi s point. Some cli ni c ians suggest that the presence of th e dressing at thi s point may be a reminder of the wounds presence and th e need to use care in the wo und area. The dressing provides a physica l barrier to rough edges of clothi ng to limit local irritation , and th e dressing ca n hel p the patie nt to inc lude th e wound in a new body image by allowing gradual view in g of th e wound. Wound closu re materials are assessed for the reacti on of the surrounding incisiona l tissues. The lise of sutures. o f any type, to approximate the wo und edges creates small wo unds alongside the incision wo und. The wo unds frOl1) th e surures increase the innammation at th e wo und site and can ca use ischemia if th e sutures are pulled taut with increased tensio n, e ither from poor technique or wo und edema postoperat ive ly. The continued presence of sutures or stapl es provides additional tensi le strength for th e wound, but th e sutures can also ca use increased ri sk of infection and the potenti al for wound ischcmi a. Use ofSteri strip tapes for wo und
225
c los ure or early remova l of sutures with Steristrip tape replace ment ca n decrease th e problems associated with sutures. Re mova l of the wo und sutures or staples in a timely manne r is a proactive hea lin g intervention. Remova l of sutures in healt hy surgica l patients in 7 to 10 days postoperatively can be lIsed as a genera l gu ideli ne depending on surg ica l site.
Incisiona l Asscss mcll' du ri ng th e Proliferative I>hase Palpation of th e surgical incision rcvea ls th e underlying process o f co llage n deposition. The new coll agen tiss ues ca n be pa lpated as a f irm ness along th e incision, exte ndin g I em on e ither side of the incision: 4 T hi s firmness to the tissues ca used by new collage n deposition in the wound area is ca lled the hea ling ridge. The healing ridge should be palpable along the entire length of the inc ision between day 5 and day 9 postoperati ve ly.' If the healing ridge is not palpable within 5 to 9 days, th e wound is at risk for dehiscence or infec ti on. 4 Eva luati on o f surgical inc is ional wo und exuda te requires knowledge of what wou nd exudate is expected in the co urse of hea ling. The characte r and th e a mount of th e ex udate c hanges as wound heal ing progresses. The wound exudate immediate ly afte r surgery is bloody. Within 48 hours the wou nd dra inage becomes serosa nguineous in nature and finally the ex udat e is serous. The a mount of the wo und ex udat e shou ld gradua ll y decrease throughout the healing peri od. An increase in wound ex udate usua ll y indicates co mpromised wound hea ling ca used by infection. New drainage fro m a previollsly healed incision hera lds wound dehiscence, in fect ion. and in some cases fistula formation . The ti ssues immedia te ly su rround ing th e inc ision should be obse rved and palpated for the presence of ede ma and induration and for color cha nges. T he presence of edema retards the wound hea lin g process. as the excess nu ids in th e ti ss ues provide an obstacl e to angiogenesis and raise the potential for wound ischem ia. Skin color changes may indicate th e presence of bruising or hemato ma formatio n ca used by surgery. T he skin color will appear dark red or purple. Skin color changes may also indicate impending infecti on. Signs of eryt hema, wa rmth , and edema and inc reased pai n at the inc ision wo und a re indicators o f possible wou nd in fecti on. Evaluation of the heali ng ridge, wound exudate, and surrounding inc isiona l ti ss ues provides information on the progress of the pro liferati ve phase of wou nd hea ling.
I ncisional Assess ment d u ri ng th e Remode li ng Phase The remode ling phase of wound hea ling is best assessed in the surgica l incisio n by eva luation o f th e colo r of the incision. As th e sca r ti ssue is remodeled a nd organ ized str uctur-
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ally. th e color o f the tissue changes. The remodeling phase
of wound healing can last I to 2 years. The incision color changes throughout the first yea r, gradually changing from
Securin g the wou nd dressing is usually done with the use of tape. Premature and frequent dress ing changes can damage the tissues surrounding the incisional wound and nega-
bright red or pink to a sil very gray or white. The tensile
tively affect wound healing. Use of Montgomery straps, skin
strength of the wo und gradu ally increases over the first yea r,
sea lants. or hydroco lloid frames aro und the wound and underneath the tape can eliminate sk in stripping around the incision wound from frequent dressing changes. Frequent dressi ng changes are more likely to be a problem with wounds heali ng by secondary intention. tert iary intention. or draining wounds.
eventually ae hi eving approx imately 80% of the ori ginal
strength of the ti ssues. The main focus of int erventi ons at
this stage is to lim it force on the wound site. Interventions to lim it force and tension at the wo und site include teaching the patient to avoid heavy lifting. bending, or straining at the site. MANAGEMENT OF HIE ACUTE SU RGI CAL WOUND
SECON DARY AND TERTIARY INTENTION WOUND HEALING
Managemen t orthe surgica l incision includes attention to fHeloTs that affect wo un d healing as addressed earl ier, as we ll
Surgica l wou nds len open to hea l by secondary or tertiary intention have a reparative trajectory similar to that of chronic wounds. Secondary intention healing is allowing wounds to hea l without surgica l closure. Wounds healing by secondary intent ion must heal by scar tissue replacement. The tissue defect at the wound site must fill with new collagen tissue during the proliferative phase of wo und hea ling. The inflammatory phase of wound hea ling may be prolonged because of the contaminated nature of the wo und. Tertiary intent ion is a combi natio n of both primary and secondary intention wound hea ling. The wound is allov.led
as dressing care. The surgica l dressing includes the primary and secondary dressing.The primary. or first. surgica l dressing is the dressing in direct contact with the wound . The di rect wo und contact requ ires that the primary dressing be nontraumatic to the wound. The primary dressing provides absorption of drainage, ma intains a sterile wo und environment , and serves as a physical barrier to further wound trauma. The primary dressing shou ld be nonad herent to rhe wound si te. The tradi tional ga uze dressing becomes ad herent to the new incision and upon removal causes ncw ti ssue injury. Use of nonadhcrent abso rpti ve dressings c(tn faci li tate wound healing because the nonharm ful nature of the dressings allows wo und healing to proceed. The primary dressing absorbs wound exudate and wicks it away from rhe wou nd site, allowi ng the ex udate to be absorbed into the secondary dressing. Secondary wound dressings provide increased absorpti ve capacity or hold the primary dressing in place. Secondary wo und dressings are applied on top of the primary dressing and may be composed of the sa me materials as the primary dressing. The secondary dressing plays an important role for wo unds when increased amounts of wo und exudate arc anticipated. The secondary dressing absorbs drainage from the primary dressing and wicks the ex udate away from the wou nd bed and into the absorbent material of the dress ing.
Clinical Wisdom: Surgicallncisional Dressings The vast majority of primary intention surgical wound dressings continue to be gauze. Conversion to moist wound healing in the immediate postoperative period may facilitate wound healing and provide for patient com fort when changing dressings. Education of the surg eon on "better" primary wou nd dressings is also helpful.
to heal secondari ly and then primarily closed for final hea ling.' Tertiary wo und hea ling is designed for spec ialized
wounds in which primary intention is pre ferred but nOt possible at the time of wounding. The de lay in primary closure may be to clear infection. allow somc wound contracture. or creat\! a hea lthy gra nulation base for a gran. ~ Most surgical wou nds left to heal by secondary or terti ary intention are those in whic h the risk of infection is increased or the tissue loss is such that thc wound edges cannot be approx imated wi thout unacceptab le tension 0 11 the incision. Reversal of both conditions- in fec tion and extensive tissue loss-can be max im ized in the earl y wee ks following surgery. The ad mini stration of systemi c antibiotics. when appropriate, and careful wound observation and care can lessen infection risk. The process of wo und cont raction and proliferat ion of granulation tisslle occurs as the hea ling response attempts to decrease the IO tal surface area or the woundSand to decrease the ti ssue loss. The primary wo und dressing takes criti ca l importance in th e wo und hea ling by secondary or tertiary intenti on. Nonadherent, absorpti ve dressings optimize wound heal ing for secondary and tertiary intention wou nds. Assessment of the wound for signs and symptoms of infecti on includes
eva luation of the character and amount of wound ex udate and exam ination of the wo und and surroundin g tissues for eryt hema, edema, induration, heat, and pain. Wounds healing by secondary or terti ary intention should be evaluated
AClIIe Surgical Wound MlIllligemel1l
using the same parameters used for chronic wounds. Evaluate the wound size ..md depth. the presence or absence of necrotic tissue. the characteristi cs and amount of exudate, the condition of the surrounding tissues, and the presence of the healing characteristics of granu lat ion and ep it hel ia Iizat ion.
OUTCOME MEASURES Outcome measures for acule surgical incisio ns relate to healing progress according to time since injury. The outcome measures for incisiona l wounds are presented according to the time frame since surgery. Postopenlti\'e Day I t hrough Day 4
The following signs and symptoms represent measures of positive outcomes for acute surgica l incision wounds. The presence of an innal11l1latory response, inc luding erythema or skin discoloration , edema, pain, and inc reased temperature at the incision site during the first 4 days after su rgery is a normal healing respon se. The lack of innammation at the new surgical incision is a negative outco me . Wound ex udate should be bloody in character initially, and toward day 3 and day 4 change to serosanguineolls in nature. The amount of wound exudate should gradually decrease from a moderate amount to scant exudate by day 4. Many surg ical wounds have no exudate past day 2 or 3, especia lly facial wounds. Failure of the wound exudate to decrease in amount and to change in character from bloody to serosanguin eous is a negative indicator for hea li ng. Ep ithe li a l resurfacing shou ld be complete by day 4. The incis ion appears bright pink as opposed to th e initia l red co lor of th e incision. Lack of epithelial resurfacing of lhe surgical incision indicates delayed healing and less than op timal outcomes. One negative outcome that ca n occur at any time during the postoperative course of the patient is th e development of a hematoma (swelling or mass of blood usua ll y c l o tt e(~ confined in the tissues and ca used by a break in a blood vesse l). External evidence of hematoma formation includes swel ling or edema at the site, a soft or boggy fccl to the tissues initially, which may bc followed by induration at the site, and color change of the sk in (sim ilar to bruising). Postoperative Day 5 through Day 9
The major healing outcome in the surgical incision on days 5 through 9 is the presence of the healing ridgc along the entire length of the inc isio n. The healing ridge indicates new collagen deposition in the wound site. Lack of developmen t or incomplete development of the hea ling ridge may be prodromal to wound dehiscence and wo und infection. A defi-
227
Case Study: Lack of Inflammatory Response Postoperatively M.J., a 71-year-old Caucasian woman, was admitted for bowel surgery with resection of the descending colon and low anterior anastomosis. M.J.'s history included long-term steroid therapy for rheumatoid arthritis. On postoperative day 1 her midline incision primary dressing showed evidence of bright red bleeding. The wound edges were well approximated with staples as the closure material. Assessment of the incision on postoperative days 2 and 3 revealed no evidence of any edema, warmth, erythema, or discoloration at the incision site. Exudate was moderate and serosanguineous to seropurulent in nature. By postoperative day 4, the incision was not fully resurfaced with new epithelial tissue, and signs of inflammation, although now present, were diminished and the exudate remained seropurulent and moderate in amount. She showed signs of confusion and agitation (signs of infection in older adults); lab tests con firmed the presence of wound infection. In this case, the absent signs of inflammation were early warning signs of impaired healing and wound infection.
c ient or non existent hea lin g rid ge is a negative ou tcome measure for wound heal ing. \Vound exudate character should change from serosanguineous to serous and gradua ll y disappear over days 4 to 6. The exudate amount should diminish from a minimal amount to none present. Any increase in the amount of wound exudate during days 5 through 9 sho uld be viewed as a negative outcome and heralds probable wou nd infection . The suturc materials shou ld begin to be removed from the incisiona l site during days 5 to 9. Adhesive tape strips or Steristrips may be used to provide additiona l wound tens ile strength. Failure to remove any of the wound suture materi· a ls during days 5 through 9 may indicate a negative outcome for the wound. Continued signs of inflammation at the incision site during days 5 through 9 are indicative of delayed wound healing. igns of erythema or edema. extensive pain. or increased temperalUre at the inc ision wound during this time frame indicate that wound healing is not normal. Prolonged innammati on may occ ur as a result of under lying infection, immunoeompromise, or continued trauma at the wound site. Documentation of a ll characteristics of the incision a nd healing are important for continui ty ofeare throughout the wound recovery period but especially during this time frame. as the patient wi ll likely be changing health care settings. For examp le. the su rgica l patient is often discharged fromlhe acute care hospi tal to the home setting very soo n after surgery.
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Clinical Wisdom: Documentation of Incisional Wound Healing Documentation should include all of the following: • • • • • • • •
Time since surgery in days Location Size in centimeters Closure materials present Color of the incision Type and amount of exudate Presence or absence of epithelial resurfacing Presence or absence of collagen deposition or healing ridge • Actions taken for follow-up or referral as necessary • Primary and secondary dressing as appropriate
Posloperali ve Day 10 Ihrough Day 14
Example: Postop day 6 for a 12-cm midline abdominal incision with Steristrips present. Incision is completely reepithelialized with no exudate present. Incision is bright pink with healing ridge palpable along anterior 10 cm of incision. Posterior 2 cm of incision is soft and boggy to touch with no healing ridge palpable and erythema present. Physician notified of possible impaired healing. Dry gauze 2 x 2-inch dressing applied to posterior aspect of incision for protection of site.
A positive outcome measure at year I for the incisional wound includes lack of significant hypertrophic sca rring or wound
The major outcome measure for day 10 through day 14
is the removal of externa l incision suture materials. Internal or "buried" sutures remain in place. Failure to remove externa l suture material s during this time frame will prolong incision healing. Healing is delayed by increasing the risk of in feC Iion from the suture microwounds and the continued in sult to the tis sue s by the presence of the foreign
objects (the suture materials), prolonging the illnammatory response.
Postop erati ve Day 15 through I to 2 Yea rs
During the end of the proliferative phase of wound healing and throughout the remode ling phase. attention is directed toward the changes in the incisional scar tissue. The collagen deposiled alongside the incision is gradually re-
aligne(L restructured and strengthened. The outcome measure for this time period is predominantly based on the changes in the incisional Scar tissuc color. The color of the incision changes from a bright pink after the initial epithelial resurfacing. gradually fading to pink and eventually turning a pearly gray or si lvery white color. The noticeable induration and firmness associated with the healing ridge gradually soncns during thi s timc frame also. Negative outcomcs include reinjury of the inci siona l linc such as hcrniation orthe wound sitc and complications associated with scarring such as keloid formation or hypertrophic scarring. Functional ability with the scar tissue becomes a key outcome measure for many surgical incisional wounds during this time frame.
herniation, maximal functional abi lity with the Ile\v scar. and acceptable cosmetic results of hea ling with a si lvery white or gray scar line. Tables 11- 3 and 11-4 present the positive and negati ve outcome measures for time frames from the point of surgery to the end of remodeling. CONCLUS ION
There are many strategics clinicians use to optimize wound healing in the aCLIte surgical incision . The astute and attentive clinician may diminish risk of complications, ident ify delayed or impaired hea li ng. and provide for a supportive healing environmcnt. The key to sliccess ful intervention for the patient with an acute surg ical incision is knowledge of normal healing mechanisms and temporal expectations, knowledge of factors that impair wound healing. and vigilant aHemion to both . The case study at thc end of this
chapter helps to demons trate the interaction between knowledge of normal healing and thc timc seq uence associated with wound healing, and factors that interfere with normal healing.
REFE RRAL C RI TE RI A
Watchful assessment of the patient with an acutc surgical incision can innucnce prompt referral to the physician or advanced practice nurse for evaluation and intervention for complications of wound healing. The following critcria are helpful guide lincs for referral of the patient to an-
Acllfe Slirgical WOlilld A1allogement
229
Table 11-3 Positive Outcome Measures for Incisional Wound Healing
Outcome Measure
Days 1-4: Inflammation
Days 5-9: Proliferative
Days 10-14: Proliferative
Day IS-Years 1-2: ProliferativeRemodeling
Incision color
Red,edges approximated
Red, progressing to bright pink
Bright pink
Pale pink, progressing to white or silver in light-skinned patients; pale pink, progressing to darker than normal skin color in darkskinned patients
Surrounding tissue inflammation
Edema, erythema, or skin discoloration; warmth, pain
None present
None present
None present
Exudate type
Bloody or sanguineous, progressing to serosanguineous and serous
None present
None present
None present
Exudate amount
Moderate to minimal
None present
None present
None present
Closure materials
Present, may be sutures or staples
Beginning to remove external sutures! staples
Sutures/staples removed, Steristrips or tape strips may be present
None present
Epithelial resurfacing
Present by day 4 along entire incision
Present along entire incision
Present
Present
Collagen deposition (healing ridge)
None present
Present by day 9 along entire incision
Present along entire incision
Present
other level of health care and to other specialties for their expertise:
• The patient with markedly increased bloody drainage during the imlllediate postoperative period may be at risk of hemorrhage from undetected leaking blood vessels in the surgical rield. • Patients who exhib it a change in exudate characteristics. from bloody or serosanguineous to purulent, should be evaluated for wound infection or abscess formation and treated with appropriate antimicrobia l therapy. • Any increase in alllount of exudate after postoperative day 4 is indicative of wound infection or abscess formation and as above, requires primary care provider evaluation and appropriate antimicrobial therapy. • The absence of a healing ridge along the cntire length of the incision wound by postoperative day 9 indicates
impaired healing and, often, abscess formation. Prompt refcrra l to the primary care provider usually results in drainage of the abscess area. antimicrobial therapy, and a wound len to heal by secondary intention. • The patient wi th the presence of sig ns and symptoms of wound infection. including erythema, edema. elevated temperature, and increased pain along the incision after day 4, andlor signs of systemic infection. including elevated temperature. elevated white blood cell count. or confusion in th e older adult, requires evaluation. These signs and symptoms suggest a wo und infection. and the primary care provider should evaluate and treat appropriately. • The patient with a frank wound dehiscence or fistu la formation requires eva luation by the primary care provider. usually the surgeon, and may nced a referral to an cntcroslomal therapy (ET) nursc (special izing illl1lanagemcnt of draining wou nds) for management.
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Table 11-4 Negative Outcome Measures for Incisional Wound Healing
Outcome
Days 1-4:
Measure
Inflammation
Incision
Red, edges approximated but tension evident on
incision line Surrounding tissue inflammation
No signs of inflammation present: no edema, no erythema or skin
discoloration , no warmth, and minimal pain at incision site; hematoma formation
Days S-9: Proliferative
Days 10-14: Proliferative
Red, edges may not be well approximated; tension on incision line evident
May remain red ,
Edema, erythema, or skin discoloration;
Prolonged inflammatory response with edema, erythema, or skin discolora-
warmth, pain at
incision site;
progressing to bright pink
hematoma
tion ; warmth and
formation
pain ; hematoma formation
Day IS-Years 1-2: Pro/iferativeRemodeling Prolonged epithelial resurfacing, keloid or hypertrophic scar formation If healing by second-
ary intention, may be stalled at a plateau (chronic inflammation or proliferation), with no evidence of healing and continued signs of inflammation
Exudate type
Bloody or sanguineous, progressing to serosanguineous and serous
Serosanguineous and serous to seropurulent
Any type of exudate present
Any type of exudate present
Exudate amount
Moderate to minimal
Moderate to minimal
Any amount present
Any amount present
Closure materials
Present, may be sutures or staples
No removal of any external sutures! staples
Sutures/staples still present
For secondary intention healing, failure of wound contraction or edges not approximated
Epithelial resurfacing
Present by day 4 along entire incision
Not present along entire incision
Not present along entire incision, dehiscence evident
Not present or abnormal epithelialization , such as keloid or hypertrophic scarring
Collagen deposition (healing ridge)
None present
Not present along entire incision
Not present along entire incision, dehiscence evident
Abscess formation with wound left open to heal by secondary intention
SELF-CARE TEAC HI NG GUIDELINES The patient 's and caregiver's instructi on in self-care must be individualized to the type of surgical incision and the individual patient's wound, the specific incisional dressing man-
agement routine. the individual patient's learning style and coping mechanisms. and the ability of the patient/caregiver to perform procedures. The general sci f-care teachin g guidelines in Exhibi, 11 - 1 Illust be individualized for each patient and caregiver.
Acute Surgical Wound Monagemelll
I
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Case Study: Incisional Wound Healing PL., a 78-year-old African American man, was admitted for radical prostatectomy surgery for prostate cancer. PL. has a history of diabetes mellitus, hypertension, obesity, and peripheral vascular disease. His diabetes is managed with oral hypoglycemic agents and an 1800calorie diabetic diet (with which he is noncompliant). PL. lives alone on a small pension and fixed income and is a smoker. He was admitted with a random blood sugar of 198 mg/ dL.
Postoperative Day 9 PL. was discharged from the hospital to his home with home health care nursing follow-up . Upon discharge from the hospital, PL. 's incision was bright pink with no exudate present. The incision was completely resurfaced with new epithelial tissue present along the entire incision, and half of the staples had been removed . A healing ridge was palpable along the anterior 13 cm of the wound but not palpable at the posterior aspect of the wound.
Preoperatively
Postoperative Day 10 Assessment of PL. revealed several risk factors for impaired healing: uncontrolled diabetes mellitus, obesity, advanced age, hypertension, and peripheral vascular disease. Control of blood sugar level was identified as a goal in the preoperative period, and PL. was started on sliding-scale insulin therapy with blood glucose monitoring. PL. 's history of hypertenSion and peripheral vascular disease put him at risk for poor tissue perfusion; thus, in the immediate postoperative period (days 1 and 2) he was put on supplemental oxygen per nasal cannula to optimize tissue oxygenation. Obesity is a risk factor for excess incision wound tension, which increases potential for poor perfusion of the incision wound due to the presence of excess subcutaneous fat. Postoperative Day 4
p.L. 's 15-cm midline abdominal incision showed evidence of inflammation with edema, skin discoloration, and warmth at the site. There was evidence of epithelial resurfacing, and the incision line was bright pink. There was a continued minimal amount of serous drainage and staples remained in place. The primary gauze dressing was changed daily. Blood sugars ranged from 110 to 132 mg/dL on insulin therapy. Oxygen was administered the fi rst 2 days postoperatively at 2 L per nasal cannula.
The home health nurse evaluated PL.'s incision and found surrounding skin discoloration , increased pain, and edema present at the posterior aspect of the wound. No healing ridge was palpable at the posterior aspect of the wound, although collagen deposition was evident along the anterior 13 cm of the wound. Half of the original staples were still present in the incision line. The physician was notified, and PL. was referred to the physician's office for evaluation of the incision. Postoperative Day 12 The physician removed the remaining staples, performed an incision and drainage (I and 0) of the posterior aspect of the incision in the office, started PL. on systemic antibiotics, and left the posterior aspect of the wound open to heal by secondary intention, using moist saline gauze dreSSings. Postoperative Day 15 PL.'s posterior incision is 75% filled with granulation tissue and there is minimal serous exudate present. The anterior aspect of the incision is well healed and pale pink. PL. 's incision wound went on to heal uneventfully by secondary intention over the next 10 days.
232
WOl'N() ('.\RI
to: "hibit 11 - 1 Self-Care Tcaciullg GUldclim:s
Se lf-Care
G ui dc l i n c~
In st r uct io ns Ch·cn (Dale/) nili a ls)
Spec ific to Ac ut e Surgica l In cis io ns
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Return Oemonstration or Slates Understa ndin g ( Dal e!) nili a ls)
L Type or incislonal wound and specific C
formal Ion h, Showt!nng or bathmg area c, Importance of adequate nutrition for wound hcalmg
2, Slgnlflc.mee of wound exudate. inCISiOn wound tisslie color. surroundlllg tisslie condition. and prcst!llcc of hcalll1g ridge
3. Wound drcsslIlg care routine n. Wash hands, Ihen rCITIO\'c old dressing and discard
b. Clean wound wuh normal saline c. Apply primary
d
Apply
drc~~lIlg
to wound
~ccondary drc~slllg
if appropriah':
c. Secure dressing with tape
r
Unl\cNal precHlllions and dress ing disposal
g. Frequcncy of drcsslIlg changes 4
I"pecled changc in wound appearance during healing process n Scheduled removal of closure matenals b. IncIsion color change as wound heals (bnght red or pink to palc pmk and flllally to slh;cry whue or gray)
5. When 10 nOlify the health care provider H. Signs and ~yl1lptoms of \I,"ound IIlfection (erythema. edema. paUl. elevated temperature. change III exudate character or ;:Ull0Ullt. discoloration in tl"sues surrollndlng Incision wound) b. Absent or IIlcomplete healing ridge along incis ion aftcr postoperative day Q
1>. Importance of follo\\ -up \\ IIh health care pro\ ider
III:I'E II£ ~ (,£S
1 ;I/arus (is. Cooper DM. Kmghton DR. el al Defllut!ons and guillehllo.!s flU asscssment of , .. nunlls anll c\aluali(ln of healing. Anll /)c'''''/IIIO/' 19114.13():4XI1 493. 2.
Crllse rJl-. l'OIud I lhc cpldellllology of "OlIlU,I Infecllon a Icnye;lr prosrec;ll\-c study of 6:!.1139 wound,> SlIrJ.: Uin Sorl" -/m
J
Stolts r-;A Imp.urcll wuund healing. In C
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Cooper DM ACUh! surgical \\oumb In: IlrY;1nt RA. \!d, At'llfe till/I Chroll/(" lIiuIIU/I, Vun'"J: \/IIII/1~wmf'nt St LouIS. j\ IO: Mosby Ye;.r Book. 199:!:91 104
5
MllY LS, Management of acute \\ollluis. Of'mllllol Cit" 11759 766
6
\\c,>' JM Wound healing III Ihe ... uTglcal pallcnt inl1ucnec or the pcriopcr:ul\'C 'MCss responsc on rerfuslOn IICr\- Cltn /HI/I!~ 1990;1-595601
7
(iCNCIII AD. 1)llIlhp~ 1J. RlIgc~ (is. Glichrcsi BA Wound healing ,lIul aging. f)ermtJI,,1 ClIII 1993:1 I '749 757 .
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diabcte~
1993;
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Acute Surgica/llhIlJl(/\fa"agement
<)
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\\'clIlgartcn \IS, Oh ... tac!c!.tu \\ound healing. firwmll, 1993:5:23ts 244 Stoll ... N,"" W,hhlTlgton Dr Nutrlllon: a critical component of wound healing . lIe\ eli" 1\\I/n 1990;1;585 594
Wagner P'\ line nutriture
111
the elderl) Gena/rio
1985;
233
14
Knighton DR. Sihcr lA, lIunt TK. RcgubtlOIl of w{)ulHl·hcallllg angiogencsi!.: effect of oxygen gradient ... and ITl",plred o"'),gen con· centrallon. Sm1-wn- 198 I ;90:262 269
15.
Whitney JD. The influence orli~ ... uc oxygen and p..:rflhion on wound healing, ·HC\ Cit" lnlll'l. I 99f);j -578 5X4
4t1(J) III 125
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Jon ......OTl K. Jcn ...cn JA. Ciootbon WII. Hunt TK \'.-ound healing in ... uhcutancou ... ti ...... uc of ... urgical patients in relation 10 oxygcn a\'ail. ahllil) .\"/lrg /-il/"lllll 1986;J7:86 89.
Pai MP. lIullt TK.. I fleet of varying oxygcn Icn ... ion ... on hcaling or opcn \Hlund ... , .\/IIl{ Gnu'wl Obs/t.,/, 1972;135:756 758.
SUGGESTED
READ I ~G
Bryant RA, ed ·klllt.' mill Cllmni(" U()llIu/l\lIntnJ.! \/WIClJ.!(·",(·1/t St Louil>. MO \4o .. by Year Book; 1992. Mulder GD. Jeter KF. ]'airchild PA Cfiniciw/\ Pod.. cI (illitit' til Clmmil" "OUIIl' Rt'pdir Spartanburg. SC Wound Ilcahng Publica lions; 11)92
C H A PTE R
12
Pressure Ulcers: Pathophysiology and Prevention Barbara M. Bafes-Jensell
PRESSURE ULCER DEFIN IT ION
Pressure ulcers arc areas of local tissue trauma usually deve loping where sofl tissucs are com pressed between bony prominences and any external surface for prolonged lime periods. I.! A press ure ulcer is a sign of local tiss ue necrosis and death. Pressure ulce rs arc mos t comI11only found over
bony prominences subject to external pressure. Pressure exerts the greatest force al the bony tissue intcrf"lce; therefore. there may be significant musc le and subcutaneous fat tissue destruction underneath intact skin .
PRESSU RE ULCER l'ATI10P HYS IOLOGY
Press ure ul cers arc the result of mechanical injury to the ski n and underlying tissues. The primary forces involved are pressure and shea r.-1 7 Press ure is the perpendicular force or load exerted on a specific area. causing ischemia and hypoxia of the tissues. I-ligh pressure areas in the supine position are the occiput. sacrum, and heels. In the sitting position, the isc hial tuberosities exert the highest press ure and the trochanters arc affected in the s ide-lying position .-I·II As the amount of son tissue available for compression decreases. the pressure gradient increases. Likewise. as the tiss ue available for compression increases, the pressure gradient decreases: thus most pressure ulcers occur over bony prominences where there is less ti ssue for compression and the press ure gradient within the vasc ular network is altered. 1I Figure 12- 1 demonstrates this relat ionship. The changes in the vascular network allow an increase in the interstitial fluid pressure. which exceeds the venous flow. This results in an additional increase in the pressure and impedes arteriolar circulation. The ca pillary vessels collapse
and thrombosis occurs. Increased capillary arteriole pressure leads to nuid loss through the capillaries, tissue edema, and subseq uent autolysis. Lymphatic now is decreased, allowing further ti ss ue edema and contributing to the tissue necrosis. S.7.9 II Pressure, over time, occludes blood and lymphatic circulation, causing deficient tissue nutrition and bui Idup of waste products due to ischemia. I f press ure is relieved before a critical time period is reached, a normal compensatory mechanism. reactive hyperemia, restores tissue nutrition and compcnsatcs for compromised circulation. Ifpressure is not relicved bcfore the critical time period, the blood vessels collapse and thrombose. The tiss ues arc dcprived of oxygen, nutrients. and waste removal. In the absencc of oxygen, cells use anaerobic pathways for mctabolism and produce toxic byproducts. The toxic byproducts lead to tissue acidosis, increased cell membrane permeability, edema, and eventual cell death .'·' Ti ss ue damage may also be due to reperfu sion and reoxyge nation of the ischemic tissues or post ischemic injury. l~.1l Oxygcn is reintroduced into tis s ues during reperfusion following ischemia. Thi s tri ggc rs oxygen-free radicals known as superoxide anion. hydroxy l radicals, and hydrogen peroxide, which induce endothelial damage and decrease microvasc ular integrity. T ime a nd Press u re
Isc hemia and hypoxia of body tiss ues arc produced whcn capillary blood now is obstructed by localized pressure. How much press ure and what amount oftimc is necessary for ulceration to occur has been a subject or stud y for many years. In 1930 Landi s,I4 us ing single-capil lary microinjeetion techniqucs. determined normal hydrostatic pressure to be 32111111 235
236
W OUND CAR '-
/
,
I
\
BONE
!
I
/ = tissue damage
\
= e xternal pressure from support surfac e
\ SUPfORT SURFACE
\
\
Figure 12- 1 Pressure gradient at the bony prominence.
I-Ig at the arteri o le end and 15
111111
Hg althe venule end. H is
work has bee n th e cri terio n for meas uring occ lusion of ca pilla ry blood fl ow_Ge ne ra ll y, a range fro m 25 to 32 mm Hg is co nsidered norm a l capill ary blood flow and is used as the marker fo r ad eq uate re licfo f presslire on th e tissues. Press ure is the g reatest at the bony prominence and so ft
tissue inte rface and g ra d ually lessens in a co ne-shaped g radi ent to th e pe riphe ry.'-" -" Thus, altho ug h tissue da mage appa re nt o n the skin surface may be minima l, the damage to th e deeper structures ca n be seve re. In add it io n, subcuta neo us fa t and mu scle arc more se ns iti ve than the ski n to isc hemi a. Muscle and fa t tiss ues arc mo re meta bo lically acti ve a nd th us mo re vuln era ble to hypox ia wit h increased s usceptibility to pressure damage_ T he vulnerab ilit y of musc le a nd fa t tissues to press ure fo rces ex pla ins press ure ul ce rs where large a reas of muscle a nd fat tissue a re da maged wi th und ermining du e to necrosis, yet th e ski n ope ning is re lati ve ly sl11 a ll. lO
Intensity and Duration of I')ressure T here is a re lat ionship be tween in tensi ty and d urati o n of press ure in pressure ulcer deve lo pment. Low pressures ove r a lo ng period o ft imc arc as ca pab le of produ cing tiss ue dam-
age as hig h pressures fo r shorter periods of time:' Tissues can tolerate higher cycl ic press ures versus constant pressure. 11 Pressures di ffer in va ri ous body pos itio ns. Pressures are highest (70 mill Hg) o n th e buttocks in the ly in g posi ti o n, and in th e sitting pos itio n ca n be as high as 300 !TIm Hg over lhe ischi all ll berosi t ies.~·II These leve ls are we ll above the nonnal capillary c losi ng press ure and a rc capa ble of ca using tiss ue isc hemi a. When tiss lies have been co mpressed fo r prolonged periods of time, tissue da mage continues to occ ur even after th e pressure is relieved Y T hi s continu ed tissue damage rclatcs to changes at the ccllular levellhat lead to di fTic ult ies with resto ratio n o f pe rfusion. Figure 12- 2 shows the rclati o nship between timc, press ure, and tissue destructi o n. Fo ur levels of skin breakd owll occ ur dependi ng 0 11 the amo unt o ft imc ex poscd to unreli eved press ure . III Hype remia ca n be observed wi thin 30 minut es or less; it is mani fes ted by redness of the sk in a nd diss ipates w ithin I ho ur afte r press ure is relieved. Isc hemi a occurs a ft er 2 to 6 ho urs of continuo us pressure: the erythema is dee per in color and may take 36 ho urs or more to di sappear afier press ure is rel ieved _ Necros is is the th ird level and occ urs a ft er 6 hours of co ntinu o us press ure. The sk in may take o n a bl ue o r g ray color and beco me indu rated. Damage th at has progressed to thi s leve l disappea rs o n an indi vidua l bas is. Ulce ration is the
Pressllre Ulcers: Pathophysiology alld Prel'emiOIl
237
PRESSURE
SKIN
Cellular necrosis and tissue death
TIME
A
PRESSURE
Cellular necrosis and tissue death
TIME
B
PRESSURE
PRESSURE
normal tissue response reactive hyperemia
TIME C
Fig ure 12- 2 Relation ship of limc versus pressure . A. lIi gh pressures over a short period of lime. B. Low pressurcs over a long period oftimc. C. Intcrminent pressure .
238
W OUND CAR.
fourth and final level and may occur within 2 weeks aficr necrosis with potential infection: it resolves on an individual basis. In dark-skinned paticllIs it is often dilTicult to di scern red-
ness or erythema of the sk in . Redness and erythema may appear as a deepening of normal ethnic color or as a purp le hue to the sk in. 1<'!.20 Other manifestations in dark- sk inned
patients arc local changes in sk in temperature and skin texlure. The immediate response of innammation of the ti ssues can be seen by an increase in skin temperature. As the ti ssues become more disturbed, the temperature decreases, sig-
naling underlying tissue damage. Skin texture may feel hard and indurated, and observation of the sk in may reveal heightened sk in features or an orange peel appearance. 19.20 (See Chapter 3 for morc information on assessment of the darkskinned patient.) C LI NICAL PIl ESENTATIO ULCE IlS
OF 1' ll ESSUIlE
The clinical presentation ofa pressure ulcer is a predictable cutaneous chain of events. The first clinica l sign of pressure ulcer formation- blanchable erythema- presents as di scoloration of a patch or flat. nonraised area of the skin larger than I em. This discoloration presents as redness or erythema that varies in intensity from pink to bright red in ligill-skinned patients. In dark-skinned patients, the discoloration appcars as a deepening of normal ethnic color or as a purple hue to the skin. Other characteristics include slight edema and increased temperature orthe area. In light-skinned paticnts the severity of the ti ssue insult can be evaluated by testing for blanchability of tissues. Afler finger pressure is applied to the area, complete blanching occurs following by quick return of redness once the finger is removed. In darkskinned patients, it is difficult to discern blanching. Use of temperature is a more va luable assessment of the severity of the tissue damage in the dark-skinned patient. Initial skin trauma and discoloration will exhibit an elevated sk in temperature as compared with that of healthy tissues. The beginning clinical indi cators of pressure ulceration all relate to the signs of inflammation in the tissues. At this beginning stage of damage. if the pressure is relieved the skin can return to normal in 24 hours.21 If pressure is not relieved, the damage progresses. Nonblanchablc erythema involves more severe damage and is commonly the first stage of pressure ulceration . The color of the skin is morc intense. It varies from dark red to purple or cyanotic in both light- and dark-ski nned patients. Darkskinned patients exhibit deepening of nonnal skin color, a purple or gray hue to the sk in. and changes in skin texture with induration and an orange peel appearance. I IUO Skin temperaturc is now cool, compared with healthy tissllcs, and the
area may feel indurated . In light-skinned patients, nonblanchable erythema is detected by testing ror blanching of tissues. The damage to tissues is more severe and is indicated by the inability or the tissues to blanch. This stage of tissue destruction is also reversible, although tissues may take I to 3 weeks to return to normal.:!: 1 The resuh of further deterioration in the tissues is evidenced as the epidermis is disrupted with subepidermal blisters. crusts, or scaling present. If properly treated the situation may resolve in 2 to 4 weeks. 21 The early pressure ulcer renects continucd ti ssuc insult and progressive injury. The early ulcer is superficial with indistinct margins and a red shiny base. It is usuall y surrounded by nonblanchable erythema. If not dealt with aggressively, progression to a chronic, deep ulcer is inevitable. Superficialu\cers begin at the skin surface and progress to deeper laye rs. Deep ulcers do not originate at the skin surface; they begin at the bony prominence- son tissue interface and spread to involve the sk in structures. The chronic dee p ulcer usually has a dusky red wound base and docs not bleed easily. It is surrounded by nonblanchable erythema or deepening of normal ethnic tone, induration, and warmth, and possibly is mottled. Undermining and tunneling may be present with a large necrotic cavity. Eschar formation may be a result of larger vessel damage from shearing force and may be the result of large vessel damage below sk in leve!.:!: 1Eschar is the formation of an acellular dehydrated compressed area of necrosis. usually surrounded by an outer rind of blanchable erythema. Eschar formation indicates a full-thi ckness loss of skin . Location More than 95% of all pressure ulcers develop over five classic locations: sacra l/coccygeal area. greater trochanter. ischial tuberosity, heel , and lateral malleolus.' Common pressure ulcer sites occur over bony prominences and depend on the patient 's position ; areas with large amounts of son tissue between bone and sk in are least susceptible to breakdown. 11I Meehan," in a prevalence surveyor 148 hospi.als, found the sacrum the most common location of pressure ulcers and the trochanter the location of the Illost severe ulcers. Correct anatomic terminology is important in identification of the true location of the pressure ulcer. For example. many clinicians often document pressure ulcers as being located on the patient's hip. The hip. or iliac crest, is actually an un common location for pressure ulceration . The iliac crest is located on the front of the patient's body and rarely subject to pressure forces. The area most clinicians are referring to is correctly termed the greater trochanter. The greater trochanter is the bony prominence located on the side of the body. just above the proximal, lateral aspect of the thigh or "saddle-bag" area.
Pressure Ulcers: PlIIhophys;ology and Pre\'elllioll
The majority of pressure ulcers occur on the lower half of the body. The location of the pressure ulcer may have an impact on clinical interventions. For example. the patient with a pressure ulcer on the sacra l/coccygea l area with concomitant urinary incontinence wil l require treatments that address the incontinence problem. Ulcers in the sacral/coccygeal area are also more at risk for friction and shearing damage due the loc3tion of the wound. Figure 12- 3 presents the usua l locations of pressure ulcer development with correct anatomic terminology. Pressure ulcers co mmonly occur over bony prominences, but ulcers can develop at any site where tissues have been compressed causi ng ti ss ue ischemia and hypoxia. Patients with contractures are at special ri sk for pressure ulcer development beca use of the internal pressure of the bony prominence and the abnormal alignment of the body and its extremities. (Refcr to Chapter 13 on therapeutic positioning.)
Clinical Wisdom: Contractures and Pressure Ulcer Formation The compression of tissues may be greater in the presence of contractures, and the management of the contracture must be considered when assessing the patient for risk of pressure ulcer development. 23
PR ESSU RE UL CE R STAG I NG Pressure ulcers arc commonly classified according to grading or staging systems based on the dep th of ti sslle destruction . The stage is determined on initia l assessment by noting the deepest layer of ti ssue invol ved . The ulcer is not restaged
Sacrum
Coccyx
Trochanter
I.
Ischial Tuberosities
Medial Malleolus (ankle)
I, I,
I
Latera1 Malleolus (ankle)
1996, Applied Heal,h Science.
I ,I
'I
~w 'ff! I I I
Figure J2- J Anatomical locations. Source: Copyright
239
240
WOl'''' C '0'
unless deeper layers oftissliC become exposed.:~ Ilistorically. one problem III assessment was the lack of a universal slaging system for classifying the severity of pressure ulcers. Many of the staging systems available nrc based on Shea!.; initial 1975 articlc'\ describing a method of classi fying pressure sores. Shea believed that a r>athology-based classification system would simplify communication for health care prolessionals. pro\'idc a mechanism for identi fication of pressure ulcers. and suggest a broad guide for determining \'vhclhcr operatIve care was needed. Shea defined each grade of pressure ulceration by the anatomic limit of soft tisslie damage Ihal could be observed. I lis numeric classification system suggested an orderly evolution ofprc!;slIre ulceration.
The Nallonal Pres.ure Ulcer Ad,isory Panel (NPUAP), and the Agency ror l1calth Care Policy and Research (AIICPR)" recommend use of a lInl\crsal four-stage classification systcm to dcscribe depth of lIsSUC damage. The rccommcnded system is similar to Shea's original systcm with the major exceptioll belllg that of dcfilllllg stngc I lesions. [xhibil 12 I shows the staging system recommcnded by the AIICPR and NPUAP. Thc isslic of pressure ulccr assessmcnt and the lISC and misusc of staging classification systems is a subject of debate and controversy. Prcs!;ure ulcer development does not nccessarily OCCLIr from onc !;tage to thc ncxt. and there may be dificrent etiologic factors for various stages. Ulccrs do not henl by rcverse !;laging. Stagll1g systcms measurc only one characteristic of the \\-'Cund und should not be viewed
E~ h i b it
as a complete assessmcnt independent of other IIltilCalors and should not be thc solc critcria in dctcnmnillg trcatmcnt plans (sec Chapter 3 on wound assessmcnt). Siaging classification systems do not assess for cnteri:1 111 the healing process and hinder tracking of progress bccause of the inability of the staging system to dcmonstratc change ovcr timt:. The staging system docs not allo\\ for Illmement \\ itllill and between stagcs. Many clinicians ust: the staglllg system as a measure of healing. despitc the inherent difficulties associated with back staging or do\\ n staging (use of tht: stages in reversc order. for cxample. n wound mo\- IIlg from stage I V to stage II). Dctcrmining tht: stage of Ihe pressure ulcer is a diagnostic too l for e\aluatlllg the le\ el of tIssues exposed. Once the stage of destruction is dctermined the stage should not change. even as the wound heals. In a full-thickness pressure ulcer (stage II I or IV) the wound defect is filled with granulation l1ssuc as the wound hcals. The granulation tissuc does not replace the structural layers ofmllscle. fat. and dermis that were prescnt in the original l1ssucs. Back staging of pressure ulcers I:, lI1appropriatc usc of thc staging critena and docs not rencct physiologic healing phenomcna. The terms partia/thk/..II(>.\,\ and ./illl thickness arc COI11monly used to describe wounds of various skin dt:pths that heal by euher rcgeneration or scar fOfllH1tion. Partl3l-thickness wounds imolve only the epidermis and dermis. hlllthickness wounds invol\'c complcte destruction of the epidermis and dermis and extend IIlIO deeper tissues.
12- 1 Prl.!ssure Llcer Stagll1g Cnteria
Definiti on
Prcs \ure l lce r St:tge
erythcma or IIltacl ,>1..111; Ihe her:tldlllg lc"lon of skill uJccralloll. In II1lIl\lduals \\ IIh darker ... klO. dlscoloral1on of the S1..111. warmth. e(lcma. mdurJl1oll. or hardncs ... may also be indicators.
NOJ1blanchabl~
skin loss l1l\'ol\lng cpldcnl11s or dennis. or both. Thl! ulcer IS superfiCIal and presents clinically as all
St:tg(' II
Partial-tlllcknl!s~
Stage III
Full-tillcl..ness skl11 loss 111\01\· 111£ damage or Ill!crosis of SUhcutnlll!OllS tissue. which 11m} extend dO\\ 11 to but 1101 through undcrlY1l1g faSCia The ulcer pre"cnh c1il11eally as a deep crater w I1h or without undermllllllg of adjacent tisslie.
Stage 1\
lull-thiel..ness ~Ii.ln los'> wlIh extl!IlSI\C destruction. tissue portlllg structures (such as tendoll. j011l! cap ... ulc)
necro~ls.
or damagc III mu . . c1e hone or sup·
• The 1'I,i.1I101lal I)re~ .. ure Ulcer \d\ i~or) Pal1el ha~ recently cOIl!.ldcred an ahernall\e dcfllllliun urthe !.tage I pre ..... ure uk-er_ I he dcfllllliun under re\ ie\\ b ii' fi)IiU\h "\n ub ...cnahle rre .. sure-rdatcd aller.Hillll of intact .. 1-.11\ \\hosc Indicator... a .. comrMcd hl an atiJ'lcclllllr (lpfl(hltC arc.1 on the body. may Include ch,lItgc;, 11\ .. kin color Irc(l bilic. rurplc toncs) ... kin tcmpcralUre (\\;mnlh Of c(}{llm·'oS). .. kin !.IIITnc" (hardnc .. s. edcma). ,md or ..cn .... llon (pam)
Pressure Ulcers: Pathophysiology lIIId Prn'ellfioll
Supcrficial lesions in vo lving the epidermis and dermi s gc ncrally heal in days to weeks. Deeper lesions involving the subcutaneous tissues and musc le may require weeks to 1110l1ths to hcal. ~1! Tisslle trauma extending to bone or joim structures may result in osteomyelitis and further prolong healing time. Ulcers involving the subcutaneous ti ssue layers may be obsc ured by necrosis or eschar and additiona lly may presen t as areas o f both partial- and full-thi c kness ti ssue losses.
PRESSURE ULCER I'REDICTION: RISK FACTOR ASSESSMENT Discussion or pressure ulcer pathophysiology and eti ology would nOI be complete withollt mention of oth er interacting factors. Pressure ulcers are phys ical evidence ofmultip Ie causative innuences. Factors that contributc to press ure ulcer development can be thought of as those that afTect the pressure force ovc r the bony prominence and those that affect thc tol erancc of th e ti ssues to prcss urc. The concep tual sc hema of Bradcn and Bcrgstrom!'! divides factors into categori es according to the role played in eve ntual pressure ulcer development. Figurc 12- 4 illu strate s Braden and Bergstrom's co nce ptual framewo rk for press urc ulcer development. Mobilit y, se nso ry loss. and activity Ic\cl arc related to the concept of increasing pressure. Extrinsic factors (shear. friction. and moisture) as well as intrinsic (nutrition, age, and arteriolar pressure) relate to the concept of ti ssue tolerance. everal additiona l areas may influence pressurc ulcer development: emotional stress, temperature. smoking, and interstitial nuid now. 1U
24 1
Research Wisdom: Immobility ImmObility or severely restricted mobility is the most important risk factor for all populations and a necessary condition for the development of pressure ulcers.
Acti vity is the production of energy or motion and implies an action. Activity is often clinically described by Ihe ability orthe individual to ambulate and movc about. Those perso ns who are bed or chair bound and thus inactive. a rc more at risk for press ure ulcer dcvelopment. 26•J2 A sudden change in acti vity level may signal s ignificant change in health status and increased potential for pressure ul cer development. Sensory loss places patients at ri sk for compression of tissues and pressure ulccr dcvelopment because the normal mechanism for translating pain messages frol11 the ti ssues is dysfunctional..!4 Paticnts wi th intact ne rvous system pathways feel co ntinuous local press ure, become un comfortable. and change their position before ti ss ue ischemia occurs. Patients with spina l co rd injury have a hi gher incidence and prevalence of pressure ulcers. J3 .J4 Pat ients with paraplegia or quadriplegia are unable to sense increased pressure, and irtheir body weight is not shined, pressure ulceration develops. Likewise. patients with changes in mental status functioning are at increased risk for pressure ulcer formation . They may not feel the di scomfort from pressure, be alert enough to move spontaneously, remember to move, bc too confused to respond to commands to move, or be physically unable to move."
Extrinsic factors Slrelll'
Pressure Factors Immobilit y. inactivity. and decreased sensory perception all affect the duration and intensit y of the press ure over the bony prominence. Immobility or seve rely restricted mobilit y is the most important ri sk fac tor for all populations and a necessary condition for th c development of pressure ulcers. Mobilit y is the state of being movable. Thus the immobile patient cannot move. and fac ility or ease of moveme nt is impaired. Exton-Smith and Sherwin ' l demon strated that 90% of individua ls with 20 or fewer spon taneous nocturnal body movements developed a pressure ulcer. while none o f the persons with g reater than 50 movements a night developed a press urc ulcer. C losely re lated to immobility is limited activity levels.
Extrinsic ri sk factors are those forces that make the ti ssucs less tolerant of press ure. Extrinsic forces include shear, rriction, and moisture. Shear is a parallel force. \OVhereas pressure acts perpendicularly to causc isc hemia. shear ca uses ischemia by displacing blood vessels laterall y and thus impeding blood flow to tissues. " J7 Figure 12- 5 shows the erfect of shearing on the tissues. Shear is caused by the interplay or gravi ty and rriction. Shear is a parallel rorce that acts to stretch and twi st ti ssues and blood vesse ls at the bony tissue interface and. as such , shear affects the deep blood vesse ls and deeper ti ss ue st ructures. The most common circumstance for shea r occurs in the bed patient in a se mi-Fowler's position (scmisitting position with knees flexed and supported by pillows on the bed or by elevation or the head or the bed ; Figure 12- 6). The
242
W OUND CARE
•
Mobility
•
Activity
,
{
I /
I.
Pressure
} I
/
l
J/
Sensory perception
T
Pressure sore development
.
k
Extrinsic factors
r · Moisure
j
... Friction • Shear
r
Intrinsic factors
Tissue tolerance
I
1
l
• Nutrition • Age • Arteriolar pressure Other hypctheticalfactors: Emotional stress Smoking Skin temperature
Figure 12-4 Factors contributin g to the development of pressure ulcers. SOl/rce: Reprinted frol11 RelllIhiliflltioll Nflrs;ug, J.?( I). 9. wit h permi ss ion of the Assoc iatio n of Rehab ilitation urses. 4700 W. Lake Ave nue. Glenview. IL 60025-1485. Copyr i gh t ~' 1995. Associa tion o f Rehabilitati on Nurses.
Pressure Ulcers : Pathophysiology and Prevemiol/
Bony Prominence without Pressure
Bony Prominence
Body Tissue
No Compression of Tissue ----"o,"'~~,..,
Bony Prominence with Pressure
Bony Promlnenc:e Body Tillue Comprelled Between Promlnenc:e and Support Surfac:e
BodyTIllue
Support Surfac:e
Bony Prominence with Pressure plus Shear
Direction of Pressure
Direction of Shear Bony Prominenc:e Body nssue / . Body nllue Compressed
Tillue is Stretc:hed Forward 01 Shear
Fric:tIon Agaln.t Support Surfac:t Grab. Pallenr, Skin
II and Moved Latlfally
(Sheared) Between Prominenc:e and Support
Support Surfac:e
Figure 12- 5 EtTects of shearing and fri ction in conju nction w ith pressure on (he skin . COUrlcsy of RIK Medical, 13ou ld cr. Co lorado.
243
244
W OUND
CARE
Support Surface
Shear Effect of Raising the Head of the Bed Hinge Point of Hlp
The Greater the Distance Between Frame Hinge Point and Hlp Hinge Point, the Greater the Shear Effect of Raising
the Head of the Bed.
\
Direction of Shear
Hinge Point of Bed Frame
Bottoming Out Prominence Body Tissue Compressed Under Pressures of up to 100 mm Hg or more
Point of Bottoming Out
Figure 12-6 Semi-Fowler 's pos ition and sheari ng effect. Courlesy
or RIK Medical , Bou lder, Co lorado.
Bodynasue
Support Surface
Pressure Ulcers: Pathophysiology (llId Prel'elllio"
patient's skeleton s lides down toward the foot of the bed but the sacra l skin stays in place (with the he lp of friction against the bed linen). This produces stret ching, pinching. and occ lusion of the underl yin g vessels. producing ulcers with large areas of interna l ti sslle damage and less damage at the sk in surface.
Clinical Wisdom: Shear Injury Shear is the reason many pressure ulcers are much larger than the bony prominence over which they occur. In clinical practice this explains, in part, pressure ulcers with large undermined areas.
245
Fecal incontinence has an ad ded detrimental etTeet: the presence of bacteria in th e stool, which can contribute to infection as well as ski n breakdown . Fecal incontinence is more significant as a risk factor for pressure ulceration because of the bacteria and enzymes in stool and the subsequent effects on the s kin . ~·u~ In the prese nce of both urinary and fecal incontine nce, the pH in the perineal area is increased by th e fecal enzymes' co nve rsion of urea to alllmonia. The elevated pH increases the activity of proteases and lipases found in stool , which in turn cause increased permeability of the sk in. leading to irritation by other agents sllch as bile salts.40 4~ Inadequately managed incontinence poses a significant risk factor for pressure ulcer development, and fecal incontinence is highl y correlated with pressure ul cer d evc lopm ent. l~ "' l
Intrinsic Ris k Factors
Frktioll Friction and moisture. although not direct factors in pressure ulcer development. have been identified as cont ributing to the problem by reducing tol era nce of tis sues to pressure. 37 Friction occurs when twO surfaces move across one another (sec Figure 12- 5). Friction acts on the ti ssue tolerance to press ure by abrading and damaging the epidermal and upper dermal layers of the ski n. Additionally. friction acts with gravity to calise shea r. Friction abrades the epidermis. which may lead to pressure ulcer development by increasing the skin's susce ptibility to pressure injury. Pressure combined with friction produces ulcerations at lower pressures than just pressure a loneY Friction acts in conjunction with shear to contribute to deve lopment of sac ra II coccygea l pressure ulcers on patients in the semi-Fowler's position.
Aloistllre Moisture contributes to pressure ulcer deve lopment by removing oi ls on the sk in, making it more friable, as well as interacting with body suppo rt surface friction . Constan t moisture on the skin leads to maceration of the tis sues. The waterlogged tissues lead to softe ning of the ski n's connective tissues. Macerated ti ssues are more prone to erosion, and once the epidermis is eroded there is increased likelihood of further ti ssue breakdown. " Moisture alters the resi liency of the epidermis to ex ternal forces . Both shearing force and friction increase in the presence of mi ld to mode rate moisture. Excess moisture may be due to wound drainage, diaphoresis, and fecal or urinary incontinence. Urinary and fecal incontinence are common ri sk factors associated with pressure ulcer development. Incontinence contributes to pressure ulcer formation by creating excess moisture on the skin and by chemical damage to the skin.
Nutritioll There is some disagreement on the major intrinsic risk factors affecting tissue tolerance to pressure. However, most studies identify nutritional statu s as playing a role in deve lopment. Hypoalbuminemia. weight loss. cachexia, and malnutrition arc a ll cOlllmonly identifi ed as risk factors predisposing patients to pressure ulcer development. 44 -47 Malnutrition is associated with pressure ulcer development. 44 .4n Individuals with low sefllln albumin level s arc associated with both having a pressure ulcer and developing a pressure ulcer.
Age Age itself may be a ri sk factor for pressure ulcer devel opment, with age-related changes in the ski n and wound healing increasing the ri sk of press ure ulcer development. 4l1 The sk in and support structures undergo changes in the aging process. There is a loss ofl11l1scle, a decrease in serum albumin levels, diminished inflammatory response. decreased elasticity, and reduced cohesion between the denni s and epidermi s."'~·49 These changes combine with other changes related to aging to make the ski n less tol eran t of pressure forces. shear, and frietion."'11
A-'Iedic(t/ COllllitiollS (lil t! P!Jychologic Factors Certain medical co nditions or disease states are also associated with pressure ulcer development. Orthopaedic injuries, altered mental status, and spina l co rd injury arc such conditions Y·H,. j 7.so,S1 Others have examined psyc hologic factors that may affect risk for pressure ulcer development. ~1.~1 Self-concept, depression, and chronic emotional stress have been cited as factors in pressure ulcer development.
246
WOl'" CARl
Ri sk Assess menl Tools
increased risk. with a score of or belm\ 16 indic3t111g "onset of risk" and scores 12 and belm\ indicating high risk for
For practitioners to intcncnc cost effectively. a method of screening for risk factors is necessary. There arc several risk
pressure ulcer rorl11ation. ~~ Others have revised the Norton tool and de\'clopcd ~ldditional toob for asscssing risk such
assessment instruments available to clinicians. Screening tools assist in prevention by distinguishing those per~ons \\ho
as the Gosllelltool.
arc at risk for pressure ulcer development from those who
Gosllell:, SClile
aTC not. The only purpose in identifying patients at risk for pressure ulcer deve lopment is to allow for appropriate usc of
resources for prevention. The lise of a risk assessment tool allows for targeting of inlCTventiom. lO specific risk factors
for individual palients. Selection of which risk assessment instrumcnl lo lise is determined by reliability orthe tool for the intended rater•. predielive validity of the 1001 for the population. the sensitivity and specificity of the in~trull1cl1t under consideration. and the case of usc and time required for completion. The most common risk assessment tools are
NOrlon's Sca le. Gosnell's Scale. and Braden's Scale for Predicting Pressure Sore Risk.
Go~neJl based her scale on further refinement of the Norton Scale. Gosnell kept the original categories on the Norton Scale, changed the general condition category to nutrition, and renamed the incontinence category continence. 't>·~7 She added skin appearance. medication, diet and nlild balance. and intervention categories to the tool. along with detailed instructions for usc. Gosnell reversed the nUlllerical scaling so that thc higher the score the higher the risk of pressure ulcer development. so a Gosnell score of 5 is the lowest risk and a score of20 is the highest risk (sec F,hibit 123).
Brat/ell:\ SLoa te for Pre//iclillg l're.\slIre So,.e
Nortoll ~' Scale
Ri~k
The Braden Scale was developed in 1987 and
The Norton tool is the oldest rh.k assessment instrument
De,e loped in 1961. it consists of five subseales: physical condition. mental state, activity, mobility. and incontinence. q Each parameter is rated on a scale of I to 4 with the sum of the ratings for all rivc parameters yielding a total score rang-
ing from 5 to 20 (sec Exhibit 12 2). Lov,ler scores indicate
IS
composed
of six subscales that conceptually rencct degrees of sensory perception. moisture. activity. mobility. Illilrition. and friction and shear.!'UUAll subscales are ralCd from I to 4 except for friction and shear. whit;h is rated from I to 3.Thc subscales may be sUlllmed for a lotal score. with a mngc frolll 6 to 23 (sec Exhibit 12-1).
[), hibit 12-2 Norton's Scale
NO RTON RI SK ASSESSMENT SCALE P h ~sical
Me nta l Cond ition
Co ndit ion
Good ,""air Poor V. bad Name
Source
4 3 2
I
Alert
4 Aprllhcllc 3 Confused 2 Stupor I
Activit} Ambulanl Walk help Chalrbound IJed
Incontinent
t\lobilit~
4 3
2 I
full SI. 1II1lIIed V. limited Immobile
4 3 2
NOI
4
Occasionnl J Usually Urine 2 I Doubly I
TOTAL
SCORI
Date
Rcpnlllcd \\ IIh pcnni\~lon from D, Norton. R McLarcn. und A l'\ I 'tlln-Snlllh. 11I IlIl'n/iXlllltlfl III (jailll"/( - \'1If"\/IIg Pmh/(,,,,\ ill 1975. Churchill LI\ ing~tonc
1/0'l1l1tl/.\ RC-I~~uc'
Pre,\Sllrt! Lker\'_ ParllOphys;%gr CInd Pre\ 'el11;Ofl
247
E\hibil 12-3 Go:-.ocll\ Tool
GOSNELL SCALE-PRESSURE SORE RISK ASSESSME T I I). Agc___ Sex Ileight· _ _ _ _ _ _ _ _ 'hclght. _ _ _ _ _ _ __ Dale of Admission _ _ _ _ _ _ _ _ _ _ _ _ _ __
Medical Diagnosis: Pnmary Sccondar} _ _ _ _ _ __ Nur:-.mg Diagl1o,)I,)~
Date of Discharge Instruction s: Complete all categones willull 24 hours of admission and c\cry other day thcreaOcr. Refer to the accompanying gUlddines ror specific fatlllg details. \Ienlal
~taluS
I Alert
Continence
\Iobilit)
Acth il)
hilly Controlled 2. Usuali) Controlled 3. Mmimally Controlled 4. Absence of Control
I Full 2. Sllghlly
I. AmbulalOry
I. Good
2 Walks with
2. Fair
Llilliled 3 Very LlillIted 4 1I111110bi Ie
Asslslance 3. ehalrfast 4 Bedfast
3 Poor
I
2. Armthctlc 3. Confused 4 Siuporous 5. UnconscIous
IHTE
TOTAL SCORE
COLOR
2... -Jlour Fluid B
Vilal Signs Date
TII'IRIIlP I
I
Diet
Intake
I
I Output
'utrition
I 2. 3. 4 5 6. 7.
Pallor MOllied Pmk Ashen Ruddy Cyanotic Jaundice Other
~.
GENERAL SKIN APPEARAI\CE Moisture I Dry
TemlJeraturc I Cold 2. Cool 3 Warm 4. lIot
2. Damp 3. Oily 4. Other
Tc~ture
I. Smooth
2 Rough 3. Thin Transp 4. Scaly 5. Crusty 6. Other
Inlcnentiolls No
I
I Yes IDescnbe I
I
PRESSLIRE SORE RISK ASSESSMENT \IEDICATIOl\ I'ROFILE
~Iedicalion
GOSNELL SCALE-GUII>ELI'<ES FOR Rntin~
\Iental Statu'l: \n assessment (li" one \ le\eI of rcspon:-.e to Ius cm IrOlllncnt.
\lerl: Orienled tt) tlllle. place. and person. Responsl\e to all stimuli. and undcrst
Dosage
Frequcnc~
Date Begun
Route
Dale Discon.
lMERICAL RATII\G OFTIIE DEFI'<ED CATEGORIES
2
3
\1)1lthetic: Lethargic. forgelfuL drO\\'sy. passivc. and dull. SluggISh. depressed . Able 10 obey Simple commands. Possibly dlsonented to tll11e.
Conrused: Parllal and or Intermittent diSOrientation to TI>P Purposeless rcsponse to slImlih. Restle~s, aggn:ssi\ e, Irritable. anxiolls, lind may rcqlllfc tranquilizers or scdati\es.
4 Stuporou~:
Total dlsorlcntatiOIl . Docs nOI respond to namc. sllnple COOlmands, or vcrbal stimuli
5 Unconscious: Nonresponslvc to painful stimuli.
('olltillll(,.\'
E'\:hibil 12-3 contll1ued Rating
2
3
4
Continence: The amounl of bodily cont rol of Urination and defecalion .
full~
Controlled: Total conlrol of urine and feces
Usuall~
Controlled: Incontincnt of urine and 'or feces not morc onen than once q 48 Ius OR has Foley catheter and is incontinent of feccs.
Minimall) Controlled: Incontincnt of urine or feces at least once q 24 h",.
Absence of Control: Consistcntly incontment of both urine and feces.
Mobiljll: The amoun t and conlrol of movement of one's body.
Full: Able to control and move all extremities al will. May reqUire the usc of a device but turns. lifts. pulls, balances. and alia illS Slttlllg posillon at will
Slighlly Limited: Able to control and move all extremities but a degree of limitation is present. Requires assistance of another person to turn. pull. balance. and/or altam a SHtl1lg pOSH Ion at will but sclf-lIl1tiates movement or request for help to movc.
VCr) Limitcd: Can assist another person who must initiate movement via turning. lifting. pullmg. balancll1g. and, or atlailll11g a siltlllg position (contractures. paralysis may be present).
Immobilc: Does not assist self in any \.\.'ay to change position. Is unable 10 change pOSition wlIhout assistance. Is completely dependent on others for movement.
Activit,': The ability of an Individual 10 ambulate.
Ambulafor~
: Is able to wnlk unassistcd . Riscs from bed unasslstcd. With the use of a dc\ ice such as cane or walker is able to ambulate withoUlthe aSSistance of another person
\\'a lks nith lIelp: Able to ambulate wllh assislance of another person. braces. or crutches. May have 11I11It<1lion of stairs.
Chairfast: Ambulates only to a chair. requircs asslslance 10 do sO OR IS confined to a whcelchair.
Bedfast: Is confined to bed dUring entire 24 hours of Ihe dny.
Eats some food from each basic food category cvery day and Ihe majority of each meal served OR is on tube feeding.
Occasionally refuscs a meal or frequently leaves nl lea ... 1 half of a 111ea1.
Seldom eats a complcte menl and only a few bites of food at a meal.
Nutrition: The process of food I11takc.
Vital signs: Skin :'Pl1carance: Diet: 24-hour fluid balance: Intenentions: Medications: COlHmellts:
SO//I"('('.
Copyrighl
I"
5
The lemperature. pulse. respiration. and blood pressure to be t.aken and n:eordcd at the tll11C of every assessment rall11g. A deSCription of observed skin characteristics: color. mOisture, temperature. and texllIrc. Record the speci fic diet onJer. The amount of fluid Intake and output during the pre\ IOUS 24·hour period should be recorded . List all devices. measures. and or nursing care aCU\'Ity belllg used for the purpose of pressure sore prevention. List name. dosage. frequency. and roule for all prescribed medic::llions. If a PRN order. list the pattern for the period since last iISSCSSIllCI1t. Usc this space to add explanntion or further dewil regarding ;.IIlY of the pre\- iously rc.:curded dma. p:ilienl condition. ctc. OR Describe anythlllg ""hieh you belic\e to be of importance hut not accounled for prc\.lollsly.
19X}!. Da\ ina Gosndl
Pressure Ulcers: Pathophysiology lIl1d Pl'el'entiol1
249
Exhibit 12-4 Broden Sc::tlc for I>rcdlctlng Pressure ore Risk
Pa tient's Na me
( \'a lu a tor 's Na me
Dat e of Assess me nt
SENSORY I' ERCE I'TIO N abi lity to respond mcaningfu lly to prcssurc·rclatcd di scount
1. CO IllI)let ely Limit ed: Unresponsive (docs not moan. flll1ch. or grasp) to painfu l stimuli. due to dimini shed level of consciousness or sedation . OR limited ability to feci pain over most of body s urface.
2. Very Limit ed : Responds only to pai nful stimu li. Cannot communicate discomfort except by moaning or restlessness , OR has a sensory impairmcnt which limits the ability to feel pain or dISCOIllfort ovcr I '2 of body.
3 . Slig htly Limit ed : Respond s to verbal commands. but ca nnot always coml1lunicnte discomfort or nced to be turned . OR 11::Is some senso ry impairment \\hich limit s ability to fcel pain or discomfort In I or 2 c;~trcnllIlCS.
4. No Iml)airm cnl : Responds to ve rba l commands. II <1S no sensory deficit which would lunit ability to feel or ,oice pain or di scomfort .
MOI ST UR E degree to which skill is exposed to mois ture
1. Con s ta ntly Moi st: Skill is kept moist almost constant ly by perspinl ti on, urine . etc. Dampncss is detccted e\ery time patlcnt is moved or turned .
2. Ve r y Moi st : Skin is oOen. but not always moi st. Linen must be changed at least once a s hin .
J. O Cc II SiOll a ll)
4. Ra rely Mo is t: Skin is usually dry. linen only requires changing at routine interva ls.
ACT IV IT Y degree of physical activity
t. Bedfas t: Confined to bed.
2. C h a irfast : Abi lity to \\alk sc\'erely limited or none,istenl. Cannot bear own weight andlor must bc assisted into chair or wheelchair,
MOBILITY ability to change and control body position
I. C omplet ely Imm obile : Docs not make e,en s light changes in body or extremity posi tion \\ Ilhout assistance.
2. Vcr)l Limit ed : Makes occasional slight changes in body or extremity position but unable to make frequent or s ignificant changes indepcndently.
M oist: Skin is occasionnlly moi s t. requiring an extra linen change approximately once a day.
J. Wa lks
4. Wa lks
O cca sion a lly: Walks occasionally during day. but for very short distances. with or without aSSistance. Spends majority of each s hi fI in bed or chair.
Frequ e ntly: Walks outside the room at leas t tWice a day and inside room at lea!.t once vcry 2 hours during wOIking hours.
J. Slig htly
4. No Limit a tion s: Makes major and rrcquent changes 111 position without assistance.
Limit ed : Makes frequent though slight changes in body or extremity posi tion independently.
coli/miles
250
W OUND CARE
Ex hi bit 12-4 continued
NUT RI T ION lIsual food intake pattern
protein (meat or dairy products) per day. Takes Ouids poorly.
intake includes only 3 servings o f meat o r
Docs
servi ngs or less o f
FRI CTION AND Stl EAR
2. Proba bly
3. Adequ a te: Eats ove r half of most mcal s. Eats a 10la1 of 4 se rvings o f pro te in (mea t, dairy products) each day. Occa· sionally will refuse a mea l, but will
I. Very Poor: Never eats a compl ete meal. Rarely cats more than 1/3 of any food o ffered . Ea ts 2
take a liquid
In adequ a te: Rarely eats a complete meal and ge nerally ca ts only about \/2 of any food o ffered. Prote in
dairy products per
usuall y take a
dietary supplement . OR is N PO and/o r maintained on clear liqui ds or IVs for more than 5 days.
day. Occas iona lly wi ll take a d ietary s upplemenl. OR rece ives less than optimulll amount ofliquid diet or tube feeding.
supplement if o fTered. OR is on a tube feed ing o r TP N reg imen which probably meets most of nutrit ional needs.
I. Pro bl em: Requires moderate 10 maximum assistance in movi ng. Compl ete lifting wi thout sliding aga in st s heets is impossibl e. Frequent ly slides down in bed or chair, requirin g freq uent repos itio nin g with max imulll assista nce. Spasticity, contractures. o r agitation leads to a lmost constant fri ction.
2. Poten t ia l
3.
n OI
Problem: Moves feeb ly or requires min imum assistan ce. During a move sk in pro bably slides to some extent against sheets. chair. rest raints, or ol her devices. Maintains relati ve ly good pos ition in chair o r bed most of the lime but occasio nally slides down.
4. Exce ll ent :
Eats most of every mea l. ever refuses a mea l. Usua lly ca ts a to tal of 4 or more servings of meat and dairy products. Occas ionally cats between meal s. Does not requi re su pplementat ion.
o Apparent Problem : Moves in bcd and in chair independenlly and has suffic ient muscle strength to lift up com pletely during move. Main tai ns good pos itio n in bed or chai r at all times.
Total Score SOl/ret': Copyright ( 1988. Barbara
J. Braden and Nancy Bergst rom.
Lowe r sco res indi cate lower fun cli o n and hi g her ri sk for deve lopin g a press ure ul cer. The c utoff sco re for hospi tal ized adults is co nsidered to be 16, with scores of 16 and be low indi ca ting at-ri sk status. lO In o lder pati e nts some have found c utofT sco res of 17 or 18 better predictors of ri sk statll S. 46,s1l Leve ls o f ri sk are based o n the predictive va lue o f a positivc test. Scores of 15 to 16 indicate mild ri sk, with a 50% to 60% c hance of developing a sta ge I pressure ulcer; sco res o f 12 to 14 indicate moderate ri s k. wi th a 65% to 90%
chance of deve lo pin g a sla ge I o r II les io n; a nd scores be low 12 indicate hi gh risk , with a 90% to 100% chance of develo pin g a stage II or deeper pressure u lcer.#l·~9 The Braden sca le has been tesled in acute ca re and long -term ca re sett ings wi th several leve ls o f nurse raters and demon strates hi gh interra ler re liabi lity with registered nurses. Validity ha s bee n eSlablis hed by ex pe rt o pini o n . and pre di c ti ve va lidil Y ha s been studi ed in several acute care setlings with good se nsiti vity a nd speci f ici ty del11onstrated. 1o•46 Based o n the c urrent
Pressure Ulcers : Pathophysiology and PrevelltiuN
25 1
re liability and validity testing the AHCPR guidelines rec-
Regardless of the instrument chosen to eva luate risk sta-
ommend the use of either the Braden Scale or the Norton Scale.It!
tu s. th e clinical rel eva nce is threefold. First. assessment for risk status must occur at frequent interva ls. Monitor assess-
ment at admission to (he health care organi zation (within 24 hours), at predetermined interval s (usually weekly), and Clinical Wisdom: Quick Risk Assessment Screening The Braden scale activity subsea Ie can be used as a quick screening tool. Those patients who receive a score of 1 or 2 (indicating patients who are not bed or chair bound) may be considered at low or no risk, and no further assessment is required . If patients are bed or chair bound , they should receive the full Braden Scale assessment, and prevention interventions should be instituted specific to level of risk and individual risk factors present.
whenever a significant change occurs in the patient "s ge neral health and status. The second clinical implication is the targeting of specific prevention strategies to identified risk factors. The fina l clinical implication is for those patients in whom prevention is not sllccessful. For patients with an actual pressure ulcer, the continued monitoring of risk status may prevent further tissue trauma at the wound site and may prevent development of additional wound sites. The prevention interventions presented are based on the Braden Scale Risk Assessmcnt instrumcnt items. Figure 12- 7 presents an algorithm for determining when to perform ri sk assess ment
PATIENT ADMITTED TO ORGAN IZATION
Perform risk assessment with focu s on activity subscale score for Braden Scale
1 Does patient have hig h risk related to activity and mobi lity?
YES, perform full risk assessment
NO, no jitrther assessment needed at th is time
==:::::>- REASSESS WEEKLY
DOC'
====::>-::: REFER APPROPRlA TELY
DOC '
D ietary Phys ical TIlerapy
IN TERVEN TIONS based 011 idelltified risks Fig ure 12- 7 Whcn to assess patients for risk of pressure ulcer developmcnl.
252
WOUND
CARe
on patients and Exhibit 12- 5 present s a flow diag ram for determining prevention strategies based on ri sk factor assessment.
PRESSU RE UL CE R PR EVENT ION: EARLY INTE RVENT IONS
caregiver education and caregivcr-depcndcnt repositioning. The spinal cord- injured patient requires selr-ca re education and may be able to perfo rm self-reposit ionin g. Thus. the interven tion ror the risk ractor o r immobility is very different ror these two patients. Imm obilit y, Ina ctivit y, a nd Se nso r y Loss
Prevention strategies are targeted at reducing risk factors
present . Appropriate prevention interventions can be focli sed on eli minating specific risk factors. Thus, early intervention for pressure ulcers is risk-factor specific and prophylactic in nature. The prevention strateg ies arc prese nted by risk fac-
Patients with impaired ability to reposi ti o n and who cannot independentl y change body posit io ns must have local pressure alleviated by any orlhe rollowing inlerve nti o n s.N .26.~9
tors. beginning wi th genera l informarion and ending with s pecific strategies for a particular ri sk factor. The Braden Scale is the basis for these prevention interve ntion s. Prevention interventions should be instituted that are appropriate to the patient's leve l or ri sk and spec ific to indi vidual ri sk ractors . ~6 For examp le, the ri sk ractororimmobility is managed very difTcre ntly ror th e co matose patient ve rsus the spinal co rd- injured patient. The comatose patient requires
• Passive repositioning by th e careg ivcr • Pillow bridging • Use or pressure-re lier o r pressure- redu ction s upport surfaces fo r chair and bed In additi o n, meas ures to in crease mobility and activity and to decrease fri cti o n and shear should be institut ed. Overhead bed fram es wi th trapeze bars arc he lpful for pati ent s with
Ex hibit 12- 5 Flow Diagram for Determining Pre\ cm ion Strateg ies Based o n Risk Factor Assess ment
Pre.'iell ce o/tissue trim",,, Ol'er hOlty promilteltce'! (u.m a//o(·atiolls: .wl(·mV(·O(·qcea/. tmcllllllter. i.'ichial tuherosity. "",lIeo/us. heel) NO
YES. provide for wound assessment and treatment plus prc\icn tion strnh.:gics
Patie"t NOT clwir or hed bOlllld altd titus (It JlO or low risk'! (pmie", scores (I I or 2 011 Brat/elt Scale llct;" ily slIhsctllej NO. completc full risk asscssmcnt
YES, do not nced furth er risk assessmen t
Pressure ulcer risk fuctors preSt'III'! Illll1lobi Iit y
Inacti vi ty
Dcc reased Sensory Perception
utrition
Friction and Shear
Moi sture Urinary and Fccal Incontinence
Prel'elltiolt iuterl'elltiolls by risk fa("fors: Immob ilit y. Inacti vity. and Dccreascd Sensory Perception
Malnutritio n
Friction and S hear
Moi sture Incont inence
pass ive reposit ion in g. pillow bridging. pressure-rcducing/relieving su pport surfaces
provide nutrition suppl ement: protei n. ca lori e. vi tam in C. zi nc, iron
cornstarch, lubricants. pad protectors. tran sparent film. thin hyd rocolloi d dress in gs. turning. and draw s hcets
absorben t products. diagnosis o f inco ntincncc. gc neru l skin c:'lre
Pressure Ulcers: Pathophysiology alld Pre\'ellfioll
paraplegia, stroke pat ients wi th upper body streng th. and obese patients and may increase mobil it y and independence with body repositioning. Wheelchair-bound patients with upper body strengt h can be taug ht and encouraged to do whee lchair pushups to relieve pressure and a ll ow for rcperfusion of the ti ssues in th e ischial tuberosi ty reg ion. For patients who are weak from prolonged inactivity, providi ng support and assistance for reconditioning and increasing strcngt h and endurance wi ll he lp prevent future debi lity." Mobility plans for eac h patient sho uld be ind iv idua lized with the goal ofauaini ng the highest level of mobility and activity individually possible. Mobility plans are the responsibi lit y of nurses and physical therapists worki ng together in all health ca re se ttin gs. It is essential th at health care professiona ls train and obse rve home ca reg ivers in the mobility plan and. in particular. passive repositioning techniqucs. Careg ivers in the home arc often left to fend for th emselves for preve nti on interventions and Illay be fra il and wi th health problems th emse lves. A return demonstration of a repositioni ng procedure ca n be very info rm ative to th e health care providcr. The health care provider may need to coach, improvise, a nd think of creative strategies for caregive rs to usc in the home setti ng in order to meet th e patient's need for movement a nd tiss ue reperfusion.
P(u."Ih'e Repositioning by Cllregh'er Turni ng schedules and passive reposit ion ing by caregivers is the normal response for patients wi th immobility risk factors. Typically. turning sc hedul es a re based on time or event. If time based, turning sc hedu les are usually eve ry 2 hours for full body change of position and more often for sma ll shifts in position. Event-based sched ul es relate to typica l events during the day, for exa mpl e, turning the patient aller eac h meal. Fu ll body cha nge of position involves rurning the patient to a new lying position. for example, turnin g the patient from the right sidelying position to the left sidelying position or the sup ine position. When th e sidelying position is used in bed, avoida nce of direct pressure on the trochanter is esse nti al. To avo id placing pressure o n the troc hante r, po it io n the patient in a 30 0 laterally inclined position instead of the com mo nl y lI sed 90 0 s id c lying position , which increases ti ssue comp ression over the trochanter.6 °The 3~' laterally inc l ined position a ll ows for distribution of pressure over a greater area (see Figure 12- 8). Use of diagrams wit h c lock faces and body position of patient are he lpful in reminding staff when and how to position the patientbl (sec Figure 12- 9). Small shifts in position invo lve moving the patient but keeping thc sa me lying position.!:>:! for exa mp le, c hang ing the ang le of the right side lyi ng position o r cha nging the lowe r extremity position in the right side lying position. Both strateg ies are helpful in achieving repe rfusioll of co mpressed tis-
253
30' angle between hips and mattress
Figure 12- 8 Th irty-degree laterally inclined position . SOllrce: Copyright Barbara M. Bates-Jensen and Lynette Mcrrman.
sties but Dilly full body change 0/ position completely relieves pressure. T here arc techniques to make turning pati e nts easie r and less time cons umin g. Turn ing shee ts. draw shee ts, and pi llows are essential for passive movement of patients in bed. Turning sheets are useful in repositioning th e patie nt to a side lyillg position, and draw sheets are used for pulling th e patient up in bed and help prevent draggi ng the patient's skin ove r th e bed surface. Two-person repositioning is a s imple task with th e turning sheet and can be accomplished in a very sma ll amo unt of time with little ri sk of dragging the patient's skin across the bed li nens:
I. Positio n one person on eac h side of th e bed. 2. Bend th e patient's knees and fo ld the pati ent 's arms across the chcst. 3. Ro ll up th e draw sheet nex t to the pat ie nt 'S body and grasp fi rmly. 4. On a prearranged verba l cue. both perso ns lift th e pati e nt and move him o r her up in bed. 5. Nex t. o ne person pulls on th e turn sheet to ro ll th e patienl pass ively toward th e side. 6. The person on the othe r side of the bed immediate ly places pillows behind th e patient's bac k for s upport.
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CAR"
SUPINE POSITION
LEFT SIDELYING POSITION
RIGHT SIDE LYING POSITION
RIGHT SIDELYING POSITION LEFT SIDELYING POSITION
SUPINE POSITION
Figure 12- 9 Clock method of determining turn ing sc hedule.
7. Additional pillows are then used for easing pressure on other bony prominences. The recommended time interval for full change of position turning is every 2 hours, depending on the individual palienl profile. Simi lar approaches arc use ful for patients in chairs. Fu ll body change of position invol ves standing th e patient and re sitting him or her in the chair. Small shifts in posi tion for tho se in chairs might be changing lower ex tremit y position . For Ihe chair-bound patienl, il is also helpful 10 use a foolstool to help reduce the pressure on the ischial tuberosities and to distribute the pressure over a wider surface . Attention to proper alignment and posture is essential. Indivi dua ls at ri sk for pressure ulcer developmcnt should avoid uninterrupted sitting in chairs and shou ld be repositioned every hour. The rationale behind Ihe shorter lime frame is the extremely high pre ssures generated on the ischial tuberosities in the sCaled position . I Those patients with upper bod y strength shou ld be taught to shift weight cvery 15 minutes to allow
Clinical Wisdom: One-Person Turning
For one-person turning, the followiog procedure may be helpful: 1. First, remove the pillows previously used to position the patient. 2. Next align the patient's body in a central position . 3. Gently bend the right knee and position the right leg in a crossed position over the left leg , 4. Place the right arm across the body, as if the patient is reaching for the other side of the bed. S. Using the turn sheet from the opposite side of Ihe bed, gently pull the patient's body over to the left sidelying position. 6. Alternatively, from the same side of the bed, with hands on the shoulder and hip, gently push the patient's body over to the left sidelying position. 7. Position pillows at the patient's upper back area, between the knees, between the ankles, and under the feet if appropriate.
Pressure Ulcers: Pathophysiology and Pret'elllioll
for ti ssue reperfusion. Aga in, pillows may be used to help po sition the patient in proper body alignment. Physical therapy and occupational therapy can assist in body alignment strategies with even the most contracted patient. (See Chapter 13 for further di scussion on orthotic devices and sea tin g thempeutic s.)
Pillow Bridgillg Pillow bridging involves the usc of pillows to position patients with minimal tissue compression. The usc of pillows can help prevent pressure ulcers from occurring on the mcdial knees, the medial malleolus, and the heels. Pillows should be placed between the knees. between the ank les. and under th e heels.
Clinical Wisdom: Positioning Pillows
Five pillows can overcome repositioning pressure point difficulties. Use the pillows in the following positions: Pillow Pillow Pillow Pillow Pillow
1: 2: 3: 4: 5:
under legs to elevate the heels between the ankles between the knees behind the back under the head
(Use a small pillow for comfort under the arm in sidelying position .)
Pillow usc is especially important for reducing ri sk of development of hee l ulcers regardless of the support surface in use.!/I The best prevention strategy for eliminating pressure ulcers on the heels is to keep the heels off the surface of the bed. Use of pillows under the lower extremities will keep the heel from making contact with the support surface of the bed. Pillows help to redi stribute the pressure over a larger area. thus red ucing high pressures in one specific area.
Research Wisdom: Donut Pillow Devices
One type of pillow device is not recommended for use. Use of a donut type or ring cushion device is contraindicated . Donut ring cushions cause venous congestion and edema and actually increase pressure to the area of concern. 2iI
I
255
Use of Pressure-Relief or Pres.m re-Rel/u clioll Support Surfilces There are specific guidelines for the use of support surfaces to prevent and manage pressure ulcers. Ui1 .1t4 Regardless of the type of Slip port surface in use with the patient, th e need for written repositioning and turning schedules remains essential. The support surface serves as adjuncts to strategies for positioning and careful monitoring of patients . The type of support surface chosen is ba sed on a multitude of factors, including clinical condition of the patient, type of care se tting, ease of use. maintenance, cost, and characteristi cs of the support surface. The primary concern should be the therapeuti c benefit associated with the surface. Table 12- 1 ca tegori zes the types of support surfaces avai lable and th eir general performance characteri sti cs l ; Exhibit 12 6 presents ideal support surface characteristics. Table 12- 1 and Exhibit 12- 6 are presented as an overview to the remainder of thi s sec tion. The information on support surfaces is organized in the following manner: first. information on tissue interface pressure is presented: second information on pressure-reducing and pressure-relieving support surfaces is presented ; finally, thi s sec tion ends with information and guidelines on how to determine the appropriate surface for specific patients.
Tissue IlIlerface Pressures. Tissue interface pressures are common ly evaluated by using capillary closing pressure (genera lly considered 10 be 12 to 32 111111 Hg) as an indirect l11easure to label effectiveness of support surfaces. The lI SC of capillary closing pressures implies that skin surface interface pressure is equallo capillary closing pressures. Further, as ti ssue interface (skin surface) pressures approach capillary closing pressures (12 to 32 111111 Hg). the support surface is 1110re effective and less likely to occlude blood vessels ( less likely to cause pressure ulcer formation) . One of the difficulties with the use of capillary closing pressures is th e assumption that capillary closing pressures are absolute values. Capillary closing pressures may be more individualized than absolute values imply. Capi llary closing pre ssures assume that skin interface pressures renect pressure at the bony ti ssue interface. Some suggest that pressure on subcutaneous ti ssues may be three to five times higher than skin interface pressure. Interface pressure is a measurement obtained by placing a sensor between the skin and the restin g support surface. It i s usually obtained wi th sOl11e type of electropneumatic pre ssure sensor connected to an inn ation system and gauge. Typically, three or more readings arc obtained and the average of the readings is used as the reported va lue. Instrumentation (size of sensor, shape of sensor, and position of sensor) greatly affects values of pressure readings, so it is difficult if not imposs ible to make cornpari sons between studies.
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Table 12-1 Selected Characteristics for Classes of Support Surfaces
Performance Characteristics Increased support area Low moisture retention Reduced heat accumulation Shear reduction Pressure reduction Dynamic Cost per day
Air Fluidized (High Air Loss) Yes Yes Yes Yes Yes Yes High
Low Air Loss Yes Yes Yes
? Yes Yes High
Alternating Air Static Flotation (Dynamic) (Air or Water) Yes No No Yes Yes Yes Moderate
Yes No No Yes Yes No Low
Foam
Standard Hospital Mattress
Yes No No No Yes No Low
No No No No No No Low
Source: Reprinted from N. Bergstrom , M.A. Bennett, C.E. Carlson, at al., Treatment of Pressure Ulcers, Clinical Practice Guideline No. 15, December, 1994, U.S. Depanment of Health and Human Services, Public Health Service, Agency for Health Care Policy and Research, AHCPA Publication No. 95-0652.
Ex hibi t 12- 6 Ideal Suppo rt Surface C harac teristics
• • • • • • • • • •
Red uces/re li eves pressure under bony prominences Comrols pressure gradi ent in tissue Provides stability No interference wi th we ight shift s No interference with transfers Controls temperature a! in terface Co ntrols moisture at skin su rfn ce Li gh tweigh t Low cost OUnlblc
Source: Reprinted wi th permi ss ion from J. McLean. Pressure reduction or pressure relief: making thc right cho icc. Jot/mal of ET Nflrsillg, Vol. 20. 0 , 5. pp. 2 t I 2 15. (' 1993. Mosby YearBook . Inc.
Pressure- Relludllg Support Su rfilce..·. Pressure-reduction dev ices lower ti ssue interface pressures, but do not consistel/tly mailllain interface pressures below capillary closing pressures in all positions, on all body 10cations. 68 Pressurereducing support surfaces arc indicated for patients who are assessed to be at ri sk for pressure ulcer development, who can be turned, and who have sk in breakdown invo lving ollly onl! sleep slIrjace .N.26 Patients with an existing pressure ulcer who are determined to be still at risk for development of funher skin breakdown should be managed on a pressurereducing support surface. Pressure-reducti on devices can be classified as static or dynamic devices. SUllie devices do not move; they reduce pressure by spreading the load over a large r area. The easy definition of a static support surface is a device that does not require electrici ty to function, usua ll y a mattress overlay (lies on top of the standard hospital mattress). Examples of static devices
are foam, air, or gel mattress overlays and water-filled mattresses. When considering the foam mattress overlays, the health care provider should consider stifTness of the foam and the density and thickness of the foam. Indcntat ion load deflection (ILD) is a mcasure of the stiffness of the foam ; generally, the ILD should be 25% for 30 lb. The density and thickness of the foam relate to the fO<1m 's ability to defl ect the pressure and redistribute the pressure over a wider area. Typically, the density and thickness ofa foam product should be 1.3 Ib per cubic foot and 3 to 4 inches, respecti vely.' Foam devices have difficulties with retaining moisture and heat and not reducing shear. Air and water static devices also have difficulties associated with retaining moisture and heal. Dynamic support surfaces move. The easy defin ition of dynamic support surfaces is that they require a motor or pump and electricity to operate. Examples are alternating pressure air mattresses. Most of these devices use an electric pump to alternately inflate and deflate air cells or air columns, thus the term alternating pressure air mattress. The key to determination of effectiveness is the length of time that cycles of inflation and deflation occur. Dynamic support surfaces may also have difficulties with moisture retention and heat acc umulation. 1 Pressure-reduction devices can also be categorized as overlays or replacement mattresses. Mattress overlays are devices that arc applied on top of the standard mattress. Most overlays are pressure-reduction devices and require a one-lime charge, setup fcc, daily rental fee, or a combination of fees. Most are single-use items and may present environmental issues for disposal. When usi ng mattress overlays, the height of the bed is increased, so transfers and linen fit may be complicated. Mattress overlays may be static or dynamic. Some provide air move ment to reduce moisture buildup. Some examples inc lude foam. gel, water. or air-filled matt ress. alternating pressure pads, and l ow~ air- Io ss overlays.
Pressure Ulcers: Pathophysiology and Pr{!\'{!nlioll
Research Wisdom: Evaluating Studies Using Tissue Interface Pressures • Look for interface pressures stated as a percentage against a standard surface, usuall y a hospital mattress. Standard hospital mattress interface pressures for sacrum = 36 to 48 mm Hg and for trochanter = 62 to 97 mm Hg.65... For example, a support surface that reports tissue interface pressure readings of 25 mm Hg for the sacrum has approximately 30% lower pressures than the standard hospital mattress pressures for the sacrum (25 mm Hg/36 mm Hg x 100 = 69.44; 100 - 70 = 30% of hospital mattress pressures). • Look for standard deviations (SD) reported in the study-95% of measurements lie within 2 SD of the mean (average). So the larger the standard deviation , the less reproducible the pressure measurements and the more variable the results with the product. 65,61 For example, a study reports mean tis sue interface pressures of 25 mm Hg with standard devia tion of 8.2. So 95% of all the measurements were between 8 .6 and 41.4 mm Hg . This is not so bad at the 8.6 end, but what about the 41.4 mm Hg? That figure is far higher than capillary closing pressure of 32 mm Hg. • To interpret the study results , consider these is-
sues61 ; 1. Range and number of pressure readings obtained for each site. 2. Procedure used to acquire the pressure readings should be described . 3. Who was tested ? 4. How were they tested ? 5. How often was equipment recalibrated? 6. The equipment is fragile and subject to malfunction.
One additional concern when lIsing mattress overlays is th e bottoming out phenomenon. Bottoming out occurs when the pati ent 's body si nks down, the support surface is compressed beyond function, and the patient 's body lies directly on the hospital mattress. When bottoming out occurs there is no pressure reduction for th e bony prominence of concern. Boltoming out typicall y happens when the patient is placed on a stati c air maltress overlay that is not appropriately fill ed with air or when the pati ent has been on a foam mattress for ex tended period s of time. The health care provider can monitor for boltoming out by inserting a flat, outstretched hand between the overlay and the patient 's body part at ri sk. If the caregive r feel s less than an inch of support material , the patient has bottomed out. It is important to check for bottoming out when the patient is in va rious body positions and to
257
check at va ri ous body si tes. For example. when th e pati ent is lying supine. check th e sacra l/coccygea l arca and th e heels; when th e pati ent is sidelying. check the trochanter and 13teralll1alleolus. 1 Use of a stati c support surface is wa rrant ed if the pati ent can turn ofTthe pressure ulcer site without bottoming out. Replacement mattresses are designed to reduce interface pressures and replace th e standard hospit al mattress. Most are made of foam and ge l combinat ions. Some arc air-filled chambers and foam struc tures. All are covered with a bacteriostalic cover that can be maintained with standard cleaning. These mattresses involve an initial signi fi cant expense. and there are minimal data on long-term effec ti veness.
Pre.
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vided with repositioning. Most models include buill-in scales. Conscio us pat ie nt s may 11 0 t tolerate the movement o f the bed. The last cat egory o f support surfaces includes th ose designed for obese acco mm odatio n. These support surfaces are des ig ned to prov ide pressure reducti o n fo r the severe ly o bese patie nt and can acco mm odate ex tre me loading. as is the case wi th the obese pati ent. Obese acco mmodati on dev ices have
features similar to th e other support surfaces described. Gen-
erall y. the bed frame is large r and man y include the ca pab il ity of rai sing the patient to a standing position while positi oned in the bed . There a rc also c hair devices for the obese
patient.
S upport Sur/ace Selectioll. Determ inin g whi ch support surface is bes t for ind ividual patie nts ca n be co nfusing. The primary co ncern must al ways be th e effec tiveness o f th e surface for the indi vidual patielll 's needs. The AI-I C PR guidelines on preventi on a nd predi ctio n o f press ure ulce rs reco mmend the fo llowi ng criteria for dete rm ining how to ma nage ti ssue loading and support surfacc se l ccti o n . ~11 • Assess a ll patients wi th ex istin g press ure ulce rs (0 determine the ir ri sk for develo ping additi o nal press ure ul ce rs. If th e patic nt re ma ins at ri sk. usc a press ure-redu c ing surface. • Use a static support surface if th e pati ent ca n ass um c H va ri ety of pos iti ons without bea ring weight on an ex isting press ure ulcer a nd without bottoming out. • Usc a dyna mi c support surface if the patie nt ca nn ot assume a vari ety o f positions without beari ng we ight on an existin g pressure ul cer. if the patient fully co mpresses th e stati c support surface, or if th e press ure ulcer does not show evidence o f hea ling. • If a pati ent has large stage II I or stage IV pressure ul ce rs 0 11 multiple turn ing surfaces. a low-ai r-I oss bed or a flu idi zed air (hi gh-air-Ioss) bed may be indica ted. • When excess moisture on inlact skin is a potential source of macerati on a nd skin brea kdown. a support surface that provides ai r fl ow can be important in dry ing the skin and prevent ing add itiona l press ure ulcers. • Any indi vidual assessed to be at ri sk for devcloping pressure ul cers should be placed on a static or dynami c pressure-reducing support surface. Use o f an al go rithm can also be help ful in makin g clinical decisions. There are multiple decision trees and algo rithms avai lable. The algorithm recomm ended by th eA HC PR guideli nes (Figure 12- 10) is a lTered as one exa mpl e o f a clinieal decisio n-mak ing tree or trea tm ent al go rithm. I There a re addi tio nal co ncerns in choosing a support surface. Crit eri a for c hoosing support surfaces ca n be class ified as intrinsic and ex trinsic. intrinsic crit eri a include wound
burd en (ti ss ue hi story- prev ious ul cers. surg ical re pai r. stress. durat ion of press ure ul ce r. number of press ure ul cers prese nt ). body build (o bese, thin, co ntmctures present ), and th e magn itude and distributi on of interface pressures (locati on of hi ghest pressures. etc). t>5 The following case exa mpl es help illustrate how intrinsic cri teri a are used for detcrmin ati on of support surface: Pati ents who undergo specific surgical opera ti ve repai r o f the pressure ulce r may need to be placed on hi gh-ai r-Ioss or flu idi zed air the rapy postopera ti ve ly. Patie nts wi th mult iple ulcers invo lving more th an one turn ing surfacc also need to bc placed on press ure-reliev ing devices such as low-a ir-Ioss the rapy or hi gh-ai r-Ioss therapy. Pati ents with severe co ntrac tures may not req uire a su pport surface that has good hce l press ure readi ngs (wi th c011l racti on of th e legs, the heels do not reac h the bOll om of th e mattress). If th e bony pro min cnce of conce rn is the g reater trochanter, th en the support sur face chosen must adequately reduce press ure over the trocha nte r. Although an algorithm is a helpful too l in choosing a support surface. as th ese case exa mpl es illustrate. the clinician must also eva luate the individual pati e nt 's needs. Ex trinsic cri te ri a include all o f th e fo llowing: • The numbe r of hours spent on the support surface daily (Will prod uct be needed for short - or long-term use?) • Shcar and fri cti on e ffects • Enviro nm ent facto rs (temperaturc. hum idity. cont inence, a nd moistu re) • Li ving arrange ments (Will patient be in acute ca re.iongte rm ca re, or home care setting?) • Se lf-ca re de fi c its (I s the ri sk o rprcssure ulce r development likely to inc rease or dec rease?) • Ease of tran sition and weanin g to othe r products or ot her hea ilh ea re sellings • Ease of use a nd managea bility • Cost- re imbu rseme nt level • Service and warrant y • Availa bilit y of prod uct • Scie nti fic va lidityfl4,M Eva luati on o f ex trin sic criteri a requires the clinician to review the goa ls for th erapy. Fo r exa mpl e. the pati ent who uSeS the support surface onl y at night and spends mos t o rthe day in the chair will requi re an agg ress ive app roac h to sea ting support sur faces. and a lesse r support surface ca n be chosen for th e bed . If the pati e nt spend s most of th e day in bed th e support surface chosen will be difTere nt. For ag itated pat ie nts (parti cul a rly th ose wi th co nt inual body moti ons). the support sur face's a bilit y to handl e shea rin g and fri cti on may be cri ti cal, and good choices may invo lve evaluati on o f the support surface coveri ng. The ex ternal environme nt is also esse nti al to include in choosi ng a support sur-
PresslIre Ulcers: Plilhophysiology and Prel'enlion
.-----11 Appropriate patient positioning
-<>D
259
Key Yes-No Decisions Interventions
Yes
,-----{5 No specia surface needed
air across skin
No Dynamic overlay or mattress
Yes
Yes
Figure 12- 10 Management of tissue loads. Source: Reprin ted from N. Bergstrom, M.A. Bennell, C.E. Carlso n, et al.. Treallllellf of Pressure Ulcers. Clinica l Practice Gui deline No. 15. December. 1994. U.S. Department of Hea lth and II 1Iman Serv ices. Public Hea lth Service. Agency fo r lI ea lth Care Policy and Research , AI-ICPR Pu blication No. 95-0652.
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face. I r the patient is at home, with no air conditioning, is incontinent of urine, and lives in a humid environment, the breathabilit y of th e support surface and the ability to handle
moisture arc essentia l to positive outcomes. Likewise, eva luation orthe patient's prognosis is helpful in support surface choi ce. Is the patient ex pected to recover and improve? I fso, a pressure-reduction or lower-end support surface device may be very appropriate. However, if the pat ient is expected to decline in function. choosing a support surface that will meet
future. as well as present, skin care needs may be prudent. Throughout the decision-mak ing process one thought should
preva il: it is important to promote patient independence, not patient dependcnt bchavio r. Enco uragi ng paticnt movemcnt out of bed and thus ofT the support surface is important for those patients who are ab le. and th is must be considered by the clinician.
Clinic al Wisdom: Reimbursement of Support Surfaces Support surfaces are reimbursed in home care under Medicare Part B benefits. Medicare requirements for reimbursement include the following: • • • •
Must be stage III or IV pressure sore Must be located on trunk of body Must have current Medicare Part 8 coverage Must be in permanent res idence (own home, longterm care faci lity, etc.)
Clinical Wisdom: Teaching Wheelchair-Bound Patients Wheelchair-bound patients with upper body strength can be taught and encouraged to do wheelchair pushups every 15 minutes to relieve pressure and allow for reperfusion of the ti ssues in the ischial tuberosity region. Use of a watch with a timer device may be a helpful reminder. The use of a chair support surface can help lessen the burden of wheelchair pushups, but does not elimina te the need for reperfusion of the tissues.
both facility acqui red and those admitted with the conditi on.
Prevalcnce studies can be done on one day (o ne point in time) and requi re a team to review all medica l records and perform skin inspections of all patients in thc organization on that day. Incidellce is fhe lIlunber oj new cases delle/oping over a period oj time. Incidence includes only facili ty-acquired conditions and as sllch, re fl ects the efTectiveness of the prevention program in the orga nization . Inci dence studies are done over a period of timc (a month, a quarter, a year) and require eva luation of all new patients wit h the conditio n (mcdica l record review and skin inspcction). The eva luatio n tcam revicws all paticnts (bu t counts onl y those with ncw cond itions) at periodic intervals over the time period, for example. once a week for 4 weeks to determine monthl y incidence. Many times prevalence and incidence studies are combined. The team performs a prevalence study on I day
Selltillg S upport S urfaces. Support surfaces for chairs and wheelchairs ca n be catego ri zed as the support surfaces for beds. In ge neral, providing adequate pressure reliefforchairbound or wheelchair-bound patients is critical, as the paticnt at risk for pressure ulcer formation is at increased risk in the seated position because of the high pressures across the ischia l tuberosities. Most pressure-redu cing devices for chairs are static overlays, such as those made out of foam. gel, air, or some combination. Positioning chair-bound or wheelchairbound individual s must include consideration of individu al anatomy and body contours, postural alignment, distribution of weight, and balance and stability. in addition to pressure relief. Chapter 13 provi des additional informat ion on therapeutic positioning. El1alu atillg Outcom e.Y of S upport S urfaces. In ordcr to cva luate outcomcs from the support surfaces chosen for a particu lar health carc selling, baseline data IIllist he 1I1'{Ii/able 011 tlte prevalence and incidence of the condition in the sctting. Prevalence is the I1Il1llber ojall persons with the COIIditiun at Oll e particular poi11l ill time. Preva lence includes
and then cont inues to eva luate the population over a period oftimc to eva luate the incidence also. Incidence is the most va luab le of the two baseline stud ies because it reflects actllal occurrencc of pressure ulcer developmcnt in the fac ility. Over time. wi th an effective prevention program. includ ing availab il ity of the appropriate support surfaces, the incidence of pressure ulcer development in th e facility should decline.
Choosing support surfaces for cli ents based on algorithms (see Figure 12- 10) and predetermined crit eria (factors cho-
sen by the clinician. such as the support surfacc's abi lity to handle fric tion, cost, service. etc). use ofa multidisciplinary team to fi nal ize selections. and peri od ic reeva luation of products and patient/i nstitution needs based on baseline prevalencc and incidence data are the keys to efTective support surface lise. Fri cti on an d Shear
Measures to reduce fri ction and shear relate to passive or active movement of the ptuient. To reduce friction several intcrvent ions arc appro priate. Providi ng topica l preparations
Pressure Ulcers: Pathophysiology and Prel'elllioll
to eliminate or reduce the surface tension between the skin and the bed linen or support surface will assist in reducing friction-re lated injury. Use of appropriate techniques in moving patients so that skin is never dragged across linens will lessen friction-induced skin breakdown. Patients who exhibit voluntary or involuntary repetitive body movements (particularly th e heels or elbows) require stronger interventions. Use of a protective film such as a transparent film dressing or a skin sea lant. a protective dressing such as a thin hydrocolloid, or protective padding will help eliminate the surface contact of the area and decrease the friction between th e skin and the linens." Even though heel, ankle, and elbow protectors do nothing to reduce or relieve pressure, they can be effective aids against friction .
Clinical Wisdom: Reducing Friction
Sprinkling cornstarch on the bed linen or use of skin lubricants is helpful in reducing overall friction .
Most shear injury can be eliminated by proper positioning such as avoidance of the semi-Fowler's position and limiting use of the upright position {positions over 30° inclined}. Avoidance of posit ions greater than 30° inc lined may prevent sliding a nd shear-related injury. Use of footboards and knee Gatches (or pillows under the lower leg) to preve nt sliding and to maintain position are also he lpful in reducing shear effects on the skin when in bed. Observation of the patient when sitting is also important. as the patient who slides out of the chair is at equa ll y high ri sk for shear injury. Use of footstools and the foot peda ls on wheelchairs and appropriate 90° nexion of the hip (may be achieved with pillows. special scat cllshions, or orthotic devices) can help in preven ting chair slid ing.
Nutrition Nutrition is an important clemen t in maintaining healthy sk in and ti ssues. There is a strong relationship between nutrition and pressure ulcer development :'" The severity of pressure ulce ration is also correlated with seve rity of nutritional deficits, especiall y low protein illtake or low serum albumin levcls .......b ... 1 The nutritional assessment is key in determining the appropriate in terventions for the patient. A short nutritional assessment shou ld be performed on all patients determined at ri sk for presslire ul cer fOTlnation at routinc intervals. Malnutrition ca n be diagnosed if se rum albumin level s arc below 3.5 mg/dL, total lymphocyte count is less than
26 J
1.800 mm, I or bod y weight decreases by more than 15%'Exhibit 12- 7 provides an example ofa nutritional sc reening tool . Malnutrition impairs the immune system, and totallymphocyte co unts arc a reflection of immune competence. If the patient is diagnosed as malnourished, nutritional supplementation should be instituted to help achieve a positive ni trogen balance. Examples of oral supplements are assisted oral feedings. dietary suppl ement s. or tube feedings. Oral assisted feedings and dietary supplements are the first option for interventi on, and tube feedings should be tried after other methods have failed. The goal of care is to provide approximately 30 to 35 ca lories per kilogram of weight per day and 1.25 to 1.5 g of protein per kilogram of weight per day.' Patients should be encouraged to improve their own dietary habits. and education should focus on healthy nutrition with adequate ca loric and protein intake. It may be difficult for a pressure ulcer patient or an at-risk patient to ingest enough protein and calories necessary to maintain skin and ti ss ue health . Oral supplements can be very helpful in boosting caloric and protein intake. Liquid nutritional supplements are designed to be used as an adjunct to regular ora l fecdings. 69 Monitoring of nutritional indexes is essential to determine effectiveness of the care plan. Serum a lbumin, prote in markers, body weight, and nutritional assessment should be performed at least every 3 months to monitor for changes in nutriti ona l status. Hypoa lbuminemia (serum a lbumin levels below 3.5 mg! dL) may be associated with pressure ul ceration,.... ·.. 1 although so me have found no relationship and little prognostic value for pressure ulcer hea ling.1u 12 When protein intake is insuffici ent, the serum albumin decreases. Serum albumi n co ntributes to the amino acid poo l. and amino acids arc essential building blocks for new ti ssue deve lopment. Serum a lbumin also maintains oncotic pressures within the vascular nuid co mpartment . Colloidal oncotic pressure is th e total innuence of proteins on the osmotic activity of plasma. When a lbum in leve ls decrease. th ere is a decrease in the oncotic press ure (fewer proteins in th e plasma leading to increased osmotic activity from the vasc ular bed, as the blood vesse ls attempt to maintain homeostasis by al lowing osmosis of water out of the vesse ls and into surroundin g tissues), which leads to edema. further co mpromisi ng ti ss ue perfusion .24 Ensuring adequate protein intake is a critical e lement in nutritional interventi ons for press ure ulcer patie nt s and those at risk for press ure ulceration . Dehydration may innuence scrum albumin levels a nd ti ssue health. Nutritional assessment should include assessment arnuid intake as well as dietary intake. Vitamin and mineral defici encies may also be present in the patient a t risk for pressure ulcer development . Vitamin C and zi nc supplements may assist in wound healing when deficiencies exist. Use of a multi vilamin for those with deficiencies and supplemcntal
Ex hibit 12-7 Example of Nutritional Assessment Guide for Patients with Pressure Ulcers
Patient Name: _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ Date: _ _ _ _ _ _ Time: _ _ _ _ _ __ To be filled out for all patients at ri sk 011 initial evaluation and every 12 weeks thereafter, as indicated. Trends will document th e e ffica cy or nutritional support therapy.
Prot ein CO ml) :lrtm cnt s
Somatic: Current Weight (kg) Previous Weight (kg) Prccent Change in Weight
( _ _ dat e)
Il eight (cm) Il eiglll/Weight Current Body Mass Index (BMI) Prev ious 8M I Pcrcen t Change in 8M I
(wt(ht)' ] (_ _ date)
Visceral: Serum Albumin (Normal :::3.5 mg/dL) Total Lymphocyte Count (TLC) (White Olood Ce ll co unt x percent LymphocyteS/ IOO )
(optiona l)
Guide to TLC: • Immune competence • Immunit y partly impaired • Anergy
::: 1.800 mOl l < 1.800 but ~ 900 < 900 mm J
mOl J
S ta te of I" ydra ti o n 24·Hour Intake Notc:
mL
24-l lour Output _ _ _ mL
Thirst. ton gue dryness in non mOllth breathers. and tenting or ce rvical sk in may indicatc dehydration . JugulHr vein distcntion may indicate Qverhydration.
ES linUi1 cd
Estimated Nonprotcin Ca lories (N PC) Actua l NPC
_ _/kg _ _/kg
ulrilio na l RC(IUircm clIl
Estimated Protcin Actual Pro tein
- - (g/kg)
_ _ (g/kg)
It eco m m cnd a l io ns/ Pl a n
I.
2. 3. 4. Source: Reprinted from N. Bergstrom. M.A. Bennett. C.E. Cu rlson. et al.. Trealme,,' of Press un' U/een;. CliniclI l Practice Guideline No. 15. December. 1994. U.S. Department or lIealth and lIuman Services, Public lIealth Service. Agency for lIealth Care I)o liey and Research. AIICPR Publication No. 95-0652.
Pressure Ulcers: Pathophys;ology (lnd Pre\'ell1;on
vitamin C. z inc. and iron (if indicated by an emia ) can be supportive o f ski n and ti ssue hea lth as we ll as be nefi c ial for wound healing. Clearly. th e area of nutriti on inte rve nti on requires an interdi sciplinary approach. Invo lve me nt of th e dietit ian during th e ea rly assessment of th e pati ent is important to the overa ll success o f the plan.
Clinical Wisdom: When To Consult the Dietitian General parameters for con sultation with the dietitian for a thorough nutritional assessment are:
• Inadequate dietary intake, • Drop in body weight of 5% , or • Serum a lbumin level be low 3.5 mg/dL
Mo isture The preventi ve interve nti ons re lated to mo isture include ge neral skin care. acc urate diagnosis of inco ntin ence type. and appropriat e incont inence management.
General Skill Care Ge nera l skin ca re in vo lves rOllt ine skin assess ment. inco ntinence assessmelll and managemcnt , skin hyg iene interventi ons. and mCHsures to ma inta in skin hcalth . Routin e skin assessment invo lves obse rva ti on of th e pati ent 's skin with part icular attenti on to bony promin ences. Reddened areas should not be massaged. Massage can further impair the perfu sion to th e ti ssucs.,·l The skin should be evaluated for dryness and crack in g. Older adults arc at hi gher ri sk for dry skin , and dry skin may dec rease ti ssue tole ra nce to ex ternal forces. Lac k o f moisture in the a ir may contribut e to dry skin and ca n be co unt era cted by use o f a humidi f ier in the roo m.' 4 Att enti on should al so be focused on gentl e handlin g to prevent skin tea rs in o lder patient s. The epidermi s and dermi s j un cti on is lesse ned with age. makin g older pati elHs at hi gher ri sk for sk in tea rs. O ther factors to inc lude in a skin assessment inc lude tempcrature, se nso ry abilit y, turgor, and texture." Skin should norma ll y be warm to touch. The dorsal aspect o f the hand is more scnsiti ve to temperature changes than the palm of the hand ; thu s clinicians should use the dorsal aspect o f th e hand to judge skin temperature. Twopoim discrim ination is used to eva luate skin sensati on. Normally the pati ent should be abl e to di stin gui sh sharp, du ll , or pressure sensati ons aga inst the skin surface. Diminished sensation may be generalized or locali zed to a spec ific area such as th e lower extremi ties. Skin tone should be sl11 00th and clasti c. Edema cau ses th e skin to appcar taut and shiny, and dehydrati on is present if the skin is dry. wrin kled, and with-
263
c redo Observing the sk in surface for tex ture and mo isture may reveal signs of excessive moisture or dryness. Most factors in a skin assess mcnt ca n be reviewed thro ugh obse rvati on a nd palpation skill s. The in fo rmat ion ga the red th ro ugh the simpl e ac t o f inspecti on ca n form a bas is for genera l skin ca re interve nti ons a nd for pressure ulce r preve nti on interventions.
IJI (.'ontillell ce Assessment allfl Alall agemelll Spec ifica ll y re lated to moist ure, th e skin should be assessed for signs o f perineal derm atiti s. Eval uating perinea l dermatit is requires und erstand ing of the co nce pts of ti ss ue to lerance, pe rin ea l environm ent . and to ileting abi li ty. 76 O bj ec ti ve signs o f peri nea l dermatitis inc lude e rythema, s\\'ell ing. ves icul ation, oozing. cru sting, a nd scaling with subjecti ve symptoms o f tin gling. itching, burnin g. and pa in. 76 T he pe rineal region is broadl y de fi ned as the perin ellm (area between th e vul va or sc rotum and anu s), buttocks, peri ana l area, coccyx. and upper/ inne r th igh regions." The c linica l presentati on is va ri able and may be depe nde nt on the frequency of inco ntinence episode, rapidity a nd e ffi cacy o f postepisode hygiene. and du rati on o f inco nti ne nce. Acute and chro nic c linical manifestati ons o f sk in reactio ns in elde rly nursing home pati ent s have bee n described based on c linica l ex perie nce. 711 Sk in reactio ns ca n be d ivided into acut e reac ti ons and chro ni c changes. Pe rineal dermatiti s may prese nt with ac ute episode characte ri sti cs or with more long-standin g chro nic skin changes appa rent . In acute e pi sodes. the skin c haracteristi cs 1110st predomina nt are erythe ma, pap ul ovesic ular reacti on, frank e rosions a nd abras ions. and, in some cascs. ev idence of monili al in fec ti on du e to the moist wa rm e nvi ron ment. In ge nera l, a di ffuse bl anchabl e e ryth ema is present invo lving both buttocks. coccyx area. pe rin eum , peri ana l area. and upper/ inner thi ghs. The extent of the eryth ema varies a nd th e int ensi ty o f the reac ti on may be mut ed in immun oco mprom ised and so me e lderl y pati ents. A pa pu loves ic ul ar ras h is parti c ul arl y evide nt in th e gro in and perine um areas (upper/ inner thi gh. vul va/scrota l area). Secondary s kin c ha nges inc lude c ru stin g a nd sca ling a nd a re usua lly evidcnt at th e fringes of the rcae tio n. Eros ions and frank denudati on o f th e skin may be more co mm on with incontine nce assoc iated with feces. T hc di stributi on o f th e dermatitis differs in men and women, as might be ex pected . Typically. th e more seve re dam age in ma le pati e nt s occ urs on th e posteri or aspect o f the penil e sha ft a nd th e ante ri or as pec t o f the scrotum. More damage is see n in th e lower perinea l reg ions such as the in ner thi ghs and low buttocks tha n in th e higher perinea l reg ions suc h as the sac ra l/coccygeal area or g ro in. In wo men the skin damage usua lly invo lves th e vulva a nd gro in areas and spreads di sta ll y fro m those sites.
264
W OUND
CAR.
Chron ic skin changes in elderly patients wilh long-standing incontinence include a thickened appearance of skin where moi sture is allowed to maintain skin contact, and increased evidence of scaling and crustin g. The thickened appearance of the skin is similar to th e chan ges seen in peristomal skin of patients with urinary di ve rsions or il eostomi es who have pouches with
100
large an aperture , a ll o w~
ing the urine or fecal emuent to pool around the Sloma. This skin is Qvcrhydraled and easil y abraded with minimal fri ction .The reaction is notable at the coccyx, scrotum , and vul va. In a cognit ivcly impaired nursing home samplc 711 there was also ev idence of cxcoriation from patients' scratching at the afTected sites. This prov ides early clinical validatio n of the sy mptom o f itching in perin eal dermatit is.
In many cases partial-thickness ulcers are present over the sacral/coccygeal area and medial buttocks region, close to the gluteal fold . Although these lesions may present as typical pressure ulcers, the underl ying eti ology may be the effects of incontinence on the skin . There are some characteristics ofth esc partial -thickness ulcers that assist in differentiating them from true pressure-induced skin trauma. First. the lesions lend to be multiple in nature. The ul cers arc almost always partial-thickness or stage II les ions. The lesions mayor may not be directly over a bony prominence and finall y. the lesions are typically surrounded by other characteris ti cs of pe rin eal derm atiti s (eg, di ffu se bl anchab le erythema). When caring for patients who are incontinent of urine and feces, hea lth care providers are faced with the challenge of prevent ing perineal dermati tis and pressure ulceration as a result of the decreased tissue tolerance to trauma. True pressure ulcers result from compression of the soft tissue between the bony prominence and the ex tern al surface. Whellmoisture, urine, and feces have caused maceration and overhydration of the epidermis, the sk in and tissues are less to lerant of the pressure force. Stage II pressure ulcers and partial-thickness skin lesions such as abrasions are most commonl y allributcd to fri ction and shearing forces. It is likely that incontinence plays a critica l ro le in the development of stage II pressure ul cers. \/1 Manage ment of incontinence is a huge topic area, and volumcs have been written about vario us manage ment techniques. This discuss ion is meant to serve as a stepping stone to those resources ava ilable to clinicians onm3nage mcnt of thc incontincnt paticnt. The di scussion there fore by necessit y is noninclusive of all management stra teg ics and only brieny addresses several stra tcgies most pertinent to the patient at hi gh risk of developing a press ure ulcer and measures to pro tect the skin frolll we tness and irritants. Management of incont inence is dependent on assess ment and diagnosis of the probl em. III ('olltillenc:e Assessmellt. Assess ment parameters to be addressed include history, physical examination, cJ1vironmcJ1-
tal assessment, voiding/defecatio n dia ry, laboratory stud ies, and other diagnostic stud ies?:' The hi story is critica l to assessing the prob lem accurately. Hi story taking should elicit infonnation on patterns of urinary/fecal elimination and pastl current managemcnt program. patterns of incontinence, characteristics of the urinary stream/ feca l mass, sensation of bladder/rectal filling, and a foc used review of systems and medica l-surgica l history.1IO The physica l eX
pressure ulcer developement arc not ca ndidates for allmcthods of behavioral management. The 1110st successfu l behavioralmanagc ment stra tegies for the fra il cognitively impaired patient typica ll y at ri sk of pressure ulcer development include pro mpted vo iding and scheduled toileting prog rnms. Both stratcgies are caregiver dependent and require a motivatcd ca regiver to be sllccessful. Scheduled intake offluid is an important underl ying factor for both strategics. Schedul ed toileting or hab it tra ining is toi leting on a planned basis. The goal is to kcep the pcrson dry by ass isting him or her to void at regul Hf intervals. There can be attempts to match the interval to the individu nl patient 's natural voi ding schedule. There is no systcmatic eHo rt to 1110ti-
PresslIre Ulcers: Pathophysiology and Prel'elllioll
vate patients to delay voiding or to resi st the urge to void. Scheduled toileting may be based on the clock (toilet the patient every 2 hours) or based on activities (toilet the patient afler meals and before transferring to bed). Several studies have demonstrated improvement in continence status in some patients. !IO·!I~ Prompted vo iding has been shown to be effective in dependent and cognitivcly impaired nursing home incontinent patients.H'.'I-I Prompted voiding involves use of a toileting sc hedule (every 2 hours) similar to habit training or scheduled toil et ing. Prompted voiding supplements the routine with tea ch in g the incontinent patient to discriminate their continence status and to request toi leting assistance. The three major clemen ts in prompted voiding include monitoring the incontinent patient routinely. prompting the patient to use the toilet. and praising the patient for maintenance of continence. Prompted voiding result s in 40% to 50% reduction in frequency of daytime incontinence and between 25% and 33 0 0 of urinary incontinent patients in nursing homes respond to the therapy.!I\·1I4 Both of these behavioral management strategies have the added benefit of moving the patient at routine intervals. which should relieve pressure over bony prominences and reduce the risk of pressure ulcer development by allowing reperfusion of the ti ssues. Underpads and briefs may be used to protect the skin of patients who arc incontinent of urine or stool. These products are designed to absorb moisture , wick the wetness away from the sk in, and maintain <.I quick-drying interface wilh the skin. ~t> Studies with both infants and adults demonstrate that products designed to presen t a quick-drying surface to the sk in and to abso rb moisture do keep the skin drier and are associated with a lower incidence of dermatitis: 1I It is important to note that the critical feature is the ability to absorb moisture and present a quick-drying surface. not whether the product is disposable or reusoble. Regardl ess of the product chosen. containment stratcg ies impl y the need for a check and change sc hedule for the incontinent patient so wet linens and pads may be removed in a time ly manner. Undcrpads arc not as tight or constricting as briefs. Kcmp lH suggests a lternating the usc of under pads and briefs if the skin irritalion is thought to be related to thc occlusive nature of the bricf. Her recom me ndations echo the carly work of Willi s H~ on warm water iml11ersion sy ndrome, who found that the effects of water on the skin could be reversed and tempered by simpl y allowing Ihe sk in to dry out between wet periods. Use of briefs when the patient is up in a chair, ambulating, or visiting another department and use of und erpad s when the patient is in bed is one sugge stion for combining the strengths of both prodl1cts. l~ Ex ternal collec tion devices may bc morc cffective with male patients. External catheters or condom catheters are devices applied to the shaft of the peni s to direct the urine away frol11 the body to a collection device. Newer models of
265
external catheters arc sel f-adhesive and easy to apply. For patients with a retracted penis, a special pouching system, si milar to an ostomy pouch, is available- the retracted penis pouch." A key concern with use of external collection devices is routine remova l of the product and inspection and hygiene of the skin. There are special containment devices for fecal incol1linence as well. Feca l incontinence collectors consist ofa selfadhesive skin barrier attached to a drainable pouch. Application of the device is somewhat dependent on the skill of the clinician, and the patient should be put on a routine for changing the pouch prior to leakage to facilitate Sllccess. The skin barrier provides a physical obstacle on the skin to the stool and helps prevent dermatitis and associated ski n problems. In fact, skin barrier wafers without an attached pouch can be useful in protecting the sk in from feces or urine. The AHCPR panel on guidelines for the prevention and prediction of pressure ulcers in adults 26 recommends lise of moisturizers for dry skin and use of lubricants for reduction in friction injuries. The panel also discllsses lhe use ofmoisture barriers, to protect the sk in from the effects ofmoisturc. Although the recommendation is made to use products to provide a moi sture barrier, the readcr is cautioned that the recommendation is derived from usual practice and professional standards and it is nOI researc h based. The success of the particular product is linked to how it is formulated and the hydrophobic properties of th e product." Generally. pastes are thi c ker and 1110re repellent of moisture than ointment s. A quick evaluation is the case with which the product can be removed with water durin g rOlltine cleansing. I fthe product comcs off the skin with just routine cleansing, it probably is not an effective barrier to moisture. Use of mineral oi l for cleansing some of the heavier barrier products. such as z inc oxide paste, will ease removal from the skin. The role of incontinence as a ri sk factor in predicting pressure ulcer fonnation is so mewhat unclear. From a pathophysiologic perspecti ve. creating a sk in environment favomble to friction and abmsion makes incontinence a key risk ractor for those persons with additional ri sk for pressure ulcer development. When caring for the incontinent patient, health care providers mu st address prevention by assessment and treatment of tran sie nt causes of the condition. Systematic assessment is the key to defining manageme nt strategies. Assessment includes the parameters of patient history. physica l examination, environment. voiding/defecation diary. laboratory studies. and other diagnostic studies. Measure s to manage incontinence include caregiver-dependent behavioral management therapies of scheduled toileting and prompted vo iding. containment devices and products. and skin protection using barriers. Skill Hygiell e Jlllen 'ellliolls. kin hyg iene interventions involve daily sk in hygiene and sk in cleansing after fecal or
266
WOUND
CAR'o
urinary incontinent ep isodes. The older adults' sk in is less tolerant of the drying efreets of soap and hot water. Usc of warm water and a mild soap (ifany soap at all) can limit skin drying. Daily bathing is not necessa ry for skin health in most older adu lts. Usc ora schedule of twice weekly or every other day bathing or showering is sufficient for Illost older adults. Daily cleansing of the feet, axilla, and perineal areas is appropriate. but daily showers o r baths can be damaging to th e skin. Usc of solutions designed for incontinence care c leans-
ing can be protective of the skin and can dec rease the time and energy involved in postincontillcnt ep isode c leansing. These commercia ll y avai lab le cleansers include surfactants as ingred ients. The s urfactants make the removal of urine and stool residue easie r wi th less abrasiveness. Everyaitempi should be made to cleanse the perineal skin immediately after an incontinent episode to limit the amount of contact time between the urine and stool and the skin. Skill Mailllellllllce III/etTen/iolls. Skin maintenance interve nti ons involve actions to prevent skin breakdown and acli ons to promote hea lthy skin. Maintaining skin lubrica tion is an important skilllllaintenance interve nti on. Use ofl11oisturi zc rs on a fOUline basis can prevent sk in drying and crackin g. App li cat ion of moisturi ze rs immcdia te ly after bathing or showering helps to remoisturizc and lubrica te the skin . There arc three m
OUTCOME MEASURES The most app ropriate outcome measures to evaluate the effectiveness of prevention programs are incidence and preva-
lence rates. When a prevention program is successful , the organization's incidence of pressure ulcer development should decrease (ifappropriate) or remain at a low level. If a patient already has a pressure ulcer. a sllccessful outcome for pressure ulcer prevention is no further areas of sk in breakdown .
REFERRAL CR ITERIA Rcferral criteria for pressu re uleer prevention programs relate to the need for a interdisciplinary approach to prevention of pressure ulcers. Referrals assist with appropriate management for particular risk factors for developing pressure ulcers. Use referral in the followin g circumstances: • Nutritional consultation for patient s determined at ri sk for malnutrition or with nutritional concerns • Enterostomal therapy (ET) nurse (or c linical specialist in thi s area) consultation for patients with urinary or feca l incontinence • Phys ical therapy for assistance with correct positioni ng in seated individuals
SELF-CARE TEAClilNG GUIDELINES Patient's and caregiver's instruction in se lf-care must be individualized to spec ific pressure ulcer development risk factors. the individual patient's learning style and coping mechanisms. and the ability of the patien t/careg iver to perform procedures. These general self-care teaching guidelines mu st be individualized for each patient and caregiver. In teaching prevcnt ion guidelines to caregivers it is particularly important to use return demon stration by the caregiver as eva lu ation of learning. Observing the caregiver perform turning manuevers. repositioning. managing incontinence. and providing genera l sk in care ca n be enlightening and provides the context in which the clinician provi des s uppo rt and follow-up educatio n. Exhibit 12- 8 provides gcneral self-carc teaching guidelines.
Pressure Ulcers: Pathophysiology ami Pl'e\'tflllioll
267
Exhihit 12- 8 Self-Care Teachmg Guidchncs
I nst ru cti o ns G iven (D a te/ lnitials)
Self-Ca re G uide lines Sp ecific to I'res"ure Ulcer Pre\- enlion I
Demonstration or !levi e,\- of Mat erial (Da lo/l nitials)
RelUrn De m o nst r a t ion or S tat es Und erstandin g ( Dlil ell nilial s )
Idenllficatlon of speci rie risk factors for pressure ulcer de\ clopment
2. Inunobillty. macu\tty. and decreased sensory perception strategies
Demonstrates une-person turning
(2) Dcmonstrate., two-person turn ing (3)
I-reqllenc} of turning reposition ing
(4)
I·ull shins
(5)
A\oidance of 90 sidclying posit ion. demonstrates 30 i:"lIerally inclined pos ition
III
position \crsus small shifts in position
(I> ) Passive r..mge of motion exercises and frequency
b. Pdltl\\- britlgll1g
c
(I)
Usc of pillows In protect heels
m
lliUm\-·s bel\\een bony prommences
-
Pressure-reducing rclie\"lIlg support surface (I)
Management of SLIp port surface in use
m
De\ Ices Il)r s1U1I1!;
--(3)
Up
III
cha ir for
hour(s). _ _ time(s) pe r day
J. "iulntion strateglcs tI. Pn.)\ Ide adequate nutrition ( I)
Small frequent (si\. mcals a day) lugh-caloric highprotem meals
(2)
Nutntional "upplclllcnts pnw lded. Give - - olof supplemen t timcs per day.
-
b. 1>1'0\ ale adequate hydration (I)
bght 8-07 glasscs of noncallcillc thuds per day un less contI
c. J>rO\ Ide \ It
4. friction and shear strategies a. Use of turnlllg and dr.", sheets
b. Usc of cornstarch. lubrican ts. pad protectors. thin film
-
dressings. or hydrocolloid dressings ovcr friction risk sllcs c. General skin care ( I ) Skill cleansing (2) Skill mO lstu rl zmg (Use
prod uct areas
on
or skin.
times a day.) n"lfllll/es
268
Wm NI) C"-Itl
E ~h i bil
12-8 conllnued
Rerurn Instru ct io ns G h en (Dnt el1 niti a ls)
Se lf-Care G uidelin es Speci fi c 10 Press ure Ulce r Prft\ enlio n
5.
Demon st r ati on or Re\ ie" of Mat eria l (Olli e/ In itial s)
Demo nstra ti on or Sta tes Und erstanding (Dal e/ Initi a ls)
IIlColltmencc management strategies of ::Ibsorbcnt products (I) Pad \\ hen lying III bed
M()I~ture
a
U~e
Brief or panty pad when lip
(2)
III
chUlr or walklllg
b. Usc of ointments. creams. and skin barriers prophylactically 111 perineal and perianal arcas (Use product on perineal perianal areas of skin. _ _ limes a day.)
c. Use of behavioral management stlJtcgies for incontinence (I) Scheduled toiletmg: toilet every ___ hours Prompted vOldlllg
(2)
d. GCllcr::t1 skill care (I) Skill c1eanslIlg (n)
Cleanser'
(b)
Soap;
(e)
hequency:
(2) Skin moisturizing (Usc
product(s)
on an:as of skin. _ _ tIInes a day.)
(3) Skill IIlspection daily 6. Importance of follow-up with health care provider
N.
Bcrg ... trom N. Bcnnctt MA. (arl!.on (" L. CI al. Tretllme"l 01 PI'I!.~·· l kt'r\ Clinical Pmcllcc Guideline No. 15. AII CPR Publication f\<(l. 95-0652. Rm:k\ ilk. \10: Agcncy for IIcalth ('ure I'olicy ,Uld Rc!.carch. U.S. Public Ileallh Sen icc. U.S. Departmenl ofllci!llh and Iluman Sen ICC'>; December 199~ "',Ilion,,] Pre ...... urc Ulcer Ad\ lsory I)ancl. Pn'H/II\, l kl.."1".\ I/lCItIt'IKe', \1If'('
1:'("0/101111('\.
Ri\J. IHt·uIIJI.'/l/. ('onwlI\l/\ 1J1.·\·I.'!tJ/II1,('/Il (·onle'n'n(·I.'
We!.t Dundee. IL S·',J PublicaIIOll'>, Inc; 19H93 -4 1),1l11c! RI<.. Pnc ... t DL. Whe,Hley Dt i-.tlOloglc factor... III prc~!.lIrc "'~lfe .... an C"pcrilllcnt;1I model Inh Pltn \feci N(' haMI
10
Pari ... h, LC Witkuwskl JA. Cris ... ey JT Tilt' Ikwhilll\ York: Ma!.!.on Pubhshlllg; 19xJ
II
Sl;l1cr II PI"/..'.\.\lIrc: {'/n'n ill Ilu' Ehler/I" Plltsbuq;h. Pi\. Pubhcalion!.; I i)~5
12
\\alkcr PM Ischcnual rcpcrfu"'lon lIlJury
~
M Luology
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p;lIhnlog) of Ischcmic ulcer....JIl·" Phr\'
6 7.
Rculcr m. CIKllley 1'(1 Thc prc~!.urc ~orc pathophY:'iiology and pnnclplc... ulmanagcment 1/11/ 1"11.'/'11 Mt,cI 19X I ;94:661 Seiler WD_ Siahellll lIB. Recent f1l1d111g ... on dccubllu~ ulcer Pi!thnio!,!y Impl!catlun ... for care. (;,'ntunn 19X6;41 :47 6U \\.Ikl)\\ ~~I J.\, I'amh 1(" III ... top:lthology of Ihe decubulI" ulcer. .I 1m It'flcll>t'r",fllOl 19K2;6:IOI4 1021
S)'nap~e
!.kcJct;(1 rnu!.cle.
AIIII
I lcrT1ande,·~Ii1ldonUt.lo JJ, Teehan I:, I·mnco ('D, Duran WN, Ilob!.on R\\ SupcroxuJe ,IIl10n produellun b) lcukocYles e'<po!.cd 10 po... tIschemic .. kc!elal nlll ..cle. J Ca,.di(lI"f/\c· S/I"g 1992;3J:6t}5 699
14
Landi'" EM Mlcro·lnJccllon ,ludic" of capillary blood prc ... ,ure human ... l..ln. lit,,,,., 193CJ;15:2()t)
I;
I hl!.illIl 1\n c:o;, \\llh reference to the bcd\orc problem. J 1'1.111101 Bue/I.'rwl 195J;66:J47 J5S
16
Sakalo R. et al. 1I1 ... lopathology of decubltli!>; ulcer, .. , a re,uh of sequential prc ... !.ure "'e"'!.lon!. 111 a eomJlutcr·coTllfollcd funy rJt model. rll\· lIimm/ Ctlf"(' It)t)J;7(5):.JO
\It'd Re/wlld 19W;40:62 69
5
New
13
1.62( 10):492 ·WX
}\.(hla~
111
{'/("er.
Itl\(' Surg 1991 ;5(4):J99 402.
Sla/,''''c'lIl
19~
Lllldan O. Grecn\\ay RM, Pial/a J~1 I)re!.!.urc dl!.trihutor on the surface of the human body. It'd, Ph\·\ \Jed R,'/willl 1965;46:378 Scale!. JT Pre ...... urc on the p.lliCnI In Kenedi RN. (,o\\dcn JM. cd ... Bl't/wl\' Bi(l/Iu'l·htln;n Billtllllure: L:nl\cr... ,ty Park Ilrc~~; 1976.
III
Pressure Ulcers, PlIIhophy.\;olo?,y (1/1(/
Pre\'(~llIiOI/
269
17.
Ko:-.iilk ~I. Kubicek WG. Olsen M. DanL IN. Kottke Fl Evaluation of pres,urc ~h
40
Berg RW. \lilligan MC, Sarbaugh Fe Association of skill wetn..:" and pI I wnh diaper dermatllis Ihhalr l>ermalOl. 1994; I I 18 20
Ih'll Helw"d 1958;39:623.
41
IS.
Edbcrg I.L. Cerny K. Stauffer ES. Pre\ention and treatment of pressure son: .. P/II'\ Tha 1973;53:246 152
Zimmerer RI". Lawson KD. Callier! CJ The elTecb ofw":ilring diapers on skin Pedialr DermalOl 19X6;3:95 101
42 .
19.
Ilennell \1.\ Reran of the task force on thc Implications for darkly pigmentcd intact <;km in the prediction ilnd preventIOn of pressure ukcno.leI,' IJ(mmi Can'. 1995;8(6):34 -35,
::!()
(ira'e:-. OJ StJge I in ebony complexion Decuhitu.I. 1990;3(4)04 leller to the I'. dltor.
44
11
P
45 .
Buckingham KW, Berg RVv LilOlogic factors in diaper dermatitis the role of fcccs. Peelialr Dl!rnwrol 1986;3 : 107 112. Makiebusl J. Magnan MA, Risk faclor ... a ....oci .. tcd with h..ving a pressure ulcer: a .. econdary dala analysi:-.. Adl' II;JllIlrI ('I/I'e 1994;7(6):2541 Pincheo, .. ky-Dc\ in G. Kanunsky "'1\ Jr, CorrelatIon or pres!>urc sore!!. and lIulrillonal slJtuS, J A", Gl'I'illfr SOl" 19N6;34435-440 Bobel LM Nutritional implication, in the patlellt \\ itll pre .. sure sore". \'lIn ('fin \orlh ,1m. 19X7:21:379 390
n.
Mcehan M Multlslle 1990;3(4):14 17
"
Knight DIl, Scoll II. Contracture and pre!>sure nccon.is. OHm".\" lIinUff/ tfllllcl.IW 11)90;16(1):CIO 67,
->
14
pre~,ure
ulcer prc\alence suney. Dewhit'I\'
\Iaklebu .. t J, Sleggrccn \1 Pn'Hllre L"lea,', Gllidehllf'.\' jl/r Pre2nd ..:d. Springhouse. PA Spnnghou:-...:; 1996
46.
74775H. 47
1('I/riOll lim/VI/nil/X \I(Uwnem(,lIt
25_
Shea JO. Pr..: .. :-.ures ~ores: das:-'lflcatloll and management C/ill Orlhop 1')75;111:l('} 100
20
Pand for Ihe Pretliellon and Pre,enllon of Pre"ure Ulcers Pre;1/11'1' {'/t-a,\ III ,It/II/r, Prl'dicti(llllllld PH'I'l'lItloll CllIlical P... ctiec (iullJeline NO.3. AllePR Publication Nu. 92-0047. Rockville. MD Ag..:nC)-' for lI":illth Care Policy and Research. u.S. Public llealth Sef\'ice.l S DCP
Berg:-.trom N. Oraden B. A prospectl\C :-.Iudy of pres:-.ure ~ore ri:-.k
\'"n
49 .
Eaglc),tein \\'11 Wound healing ,lnd aglllg. Clill Gaiu/r 1989;5 183,
\/('11
50,
Versluy,en ~I Pressure liore~ III elderly patients: Ihe CpldCllllology related to hip operations. J 8011(' Jm,., SUf): 81' 19~5;67 : 10 13.
51
Shannon ML , Pressures sor..:". In 'Jorns CM, cd. COIICl'11i ('/IlriliCiailhcr.. hurg. MD A"'pcn Puhhlihcr<;. Inc : 19S2
('(ltiolllll\'lInm[:
M"klchu,1 J Prc"ure ulcer ..taglng ,y:-.tellw NPUAP Conference Prf)(..:cthng), MI' U;lI/tIIl Om'. 1995:XH):28-11 28-14
52
Anderson TP. Andbcrg \IM P,yehosociill factors
1K
Allman R~l Pre"urc ulcr.:r" among Ih..: elderly, \' Ellgi J \fed 19iW;.'2{J:850,
53
29
Br.ld..:n BJ. Ikrg:-.trom N A conceptual ,ehemn for the ;,Iudy of ctlology ufpn.:-,:-.ure :-.ore .. , He/willi \'/In. IQ87;12(1):K 12
Vidal J. Sarn
10
Ikrg,lrum N. Demuth PJ. Braden IlJ " clinicaltrilll of thc Bmden Scale for predlctmg pre,:-.ure .. or..: ri,k ,",WI Cltll Vorlll .tm 1987;22:4 1742K
11
I xlOn-Smlth -\N . ShefWlll R\V The prc\cnllon of pressure sores :-'lglllf";Lnce of "punl
3::!.
33,
.\4
Allman R~1. (ioode PS, Ilatriek "11\1. ct al Pressure ulcer ri ... k factor .. among hlhpllaliLcd pati..:nh \\ llh acti\ ity limitations, JIB/·I 1t)\}5;17:l:X65 X70 Curry K. CI\.tlly L. The reliltloll'.hip bctween eXlended periods of Illlmoblllty ,lIld del;ubllu, ulcer lormatlOn III the acutely splllal cord IIlJurcd 1/Idl\ ldual. J \"llnH("/ \'lIn 19 1)2;24: I X5 189 1I'lInmono \1('. Ilollacco VA. SlIen:-. SA. CI al Pressure ulcer ineidem:e on a 'ipmal cord IIlJury unn -Idl' II;J/md Care 1994;7(6) :57
54
55
3(1.
17
1R 39
I{eld,d S\1 ")hc.Jrlng force as a fHetor 111 decubllu!> ulcer.: 111 paraplegic)' .1.4\/1 1t}5~;166 :761763 Bennett I.. Ka\ ncr D. Icc BY. r ... inor FS, Skin stress and blood flow In slllmg paraplegIC patlenl' /1'('11 Plln ,Ht'd Rl'Il(lhil 19X4;65(4):IX6 190. DIIl:-.dak JM DccubllU\ uker" rotc or pr..::-.surc and friction in causallon, Ir,:11 /'lln Met/ HellII"d 1974;)5: 147 153 Kemp 1\-1(; Protecting the ,kill from mOl ... ture and associated irritanh, ./ Gawllo/ \///"\ 1994;:!0(tJ):X 14
n.. t..:,,-Jcn:-.en \\ltkow~kl
11 Inconllnence manugcmenl. In Parish Le. JA. Crissey JT. cd., TIlt' Oe"IfI1/fII~ l.ker m ('flr/Ie'al
Prat'lin' Berlin. Germany: \pringcr- Verlag; I t)97~ 189 199.
Norton D Calculating the ri .. k rell..:etlOl1'i un Ihe Norton Sc.:aie. 19X9;2(3):14 31
f)l'whitIH.
,'re,sure ,or..: rbk a~'ie,>,m..:nl. a (':"fltlqU":. I the (io'>n..:11 SCille O('('/I/)ill/\ 19S9;2(3):.J2 .J9
56
(jo~ncIlI)J
57.
{jo .. nelll)J.
ri .. k facto'" 5R 59
60
60.
35.
NOTton D. McLaren R. Lxton-Snllth NA III IIIH""nIlIWII til (h,,.IIdlllhurgh . Scotland: Churchdl I iVl1lgstone; 1962
Iltf'l{'\unilln Prohll'III\ illl-lrHpiwl,
61 62
63
Ilr..::-. ... ure ...ore fisk "s:-.c",ment .. cfltiqu..:. 11 an;ll),sl" of O"("Ilbll/I\. 1989:2(3)AO 4.l
Ilraden B. Bergstrom N Clinical utility of the Bmd..:n Scale for predicting pre:-.~ure ~ore ri:-.k f)t'(lIhi(/I\. 19Xt);:!(.'H4 51 Bergstrom N. Braden OJ. Bo)nton I~ Ilruch S l',,'g a rc,>c;trehba,cd as'e,:-.mcnt sC:lle III cl1mcal pr.:lctlce, \-I/n elm \'0/"(11 ·Im 1995 ;30539 Seiler WOo Allen S. Stahclin 1111 Influ..:nc..: of the 30 degr..:e, latcrJlly IIlcJlIl..:d position and the ",uper ,un" 3-pi..:c..: maitre,s 011 skill oxygen tension on arc'" of ma'l:illlulll rre..sure: linplic;lIions for prc .. sur..: ..or..: .. pr,,:\cl1tion (;('rolltollln,y 1986;32: 15X 166. Lowlluan PT. Praeucal nur:-'1I1g: turnll1g clock 'y .. tem 10 pr..:\cnt pres.. ure :-.orc~ \/11"' \Iirmr It)79;14X(21) :30 31 Smith AM. Malone JA Prc\cl1ung pr..:s,urc ulcer... III 1Il:-.lIIulmnall.fed cider.. : a,:-,c'islllg the err..:e,"" of :-.lllalL ul1,chedulcd ,Iult .. III body po~ItIOn, IR'cuhIllH I99(UH )::W 24 \leLcan J Pressure reduction or prc"ur..: relief maklllg the nght chOIce. J £1" 'V/ln 1993:20:211 215. Krouskop TA. Garber Sl. Cullen UIl , I'actur, to cOlhltkr 111 ..clCCI/Ilg a 'iUpport :-.urface, In : Kra;,ner D. cd Chmnic lIilllllil Cllre Kmg
270
WOUND
C WI
nll)ru""la. I'A Ile.llth Management Puhl,eiHlon .... Inc ; I'Nf)
7X
135 141
65.
(16
Garber SI . Krou,kop 'IA. Culten BB. The role ollechno!ogy 1Il pre"uI"C ulcer prc\entton. In Km,ncr D. cd ("/lIlll/;t· lIimml C/lI"I.'. KlIlgofPru~'la. J>. \. Ilcalth Managclllenl I)ublicatiom. Inc: 1990 Krou,kop IA . Garber SL. Interface prc ... ,ure confU\lon
D"("///l1I1I\
IlHW:2 :M.
()7
79
XO
Bryant RA. Shannon \IL. PlI:per B. ct al I)re"ure ulcer .... In : Bryant RA. ed kU(t· alld Chrollic II(Himl, \UI"';II.1: \!llIIlIxell/el/1. St I.olli<;. MO' Mu,by Year Book; IIN1. Inlcrnallollal A,,()cialion for l'nlero,tOlllal rher.lp~ (IAn). lk,.Slill/(hm!~ of ("art' In inc. CA IAII :
MI
69
\Vroble\\ .. k, JJ Nutnllonal,hpeets ofrres"ure ulcer COlfe. In: "-m .. ner D. ed Chroll;c 1fi:J//ml ("tlll.'_ King of J>rU""la. 1),\ Ilc,ll1h Management Publlcatlun". 1m:. 1990: I Xg 193
~2 .
70
BerluwLl/ D. W"klllg S_ Thc ... hort lerm outcome of prc,~ure ",-ue" .J 1m (;t:,./11I,. Sm- I 990;3X:74X -751.
71
11111 DI~ ('l'KlpCr D1I.1. Rob ...on (!..1( Serum albulllin 1...1 poorpmgnostlc factor for rre,,,urc ulcer healing in contfl,lIed c1iniealtri.11s
71.
Siolt, N NUlfillona! parJllletcrs at ho ... pilill adl1l"~I()n a ... predlclor.. of rre,,,ur~ ulcer de\ dopm~nl III dceli\e ,urgcr)'. .J Pal'cilia FIIII"I" \'u/I' 1'1X7; II :1i.)M )()l
6X
111111 if/milt!' Pn'HUrl' SOI"l." 19M7.
II(J/lnd\
7)
1994;6(5): 174 17M
191<9;2(4):)2
.n,
IranI RA. (j.udncr S_ ClIllit.:a! t.:oncerns: m;lIlagelllent of dry <;kin Cit'l'mlfol \'/In_ 199·L10(i.):15 IX. ~5
7;
(jo~nclIDJ
-\ ... ~es'lIlent ilnd e"liuation of prc"surc sorcs.
\01"111 .Im, 191<7;22399
71> 77
X/lI'\
("/in
~16
BrO\\n DS. Scm... \1 Per1l1ea! dermallu,; a t.:ollt.:Cptu
\!tJ/W.I!.t"
19t)3;W(7):20 25
Bflmn DS _ P\.'nne;lI dennallth can \\C \/1II1d.1:'· 19t»);)9(7):2X 31
~4
g5.
()I .. oll II The efTect-. of lIla,,,age for pre\entllln of pre\sure ulcer" /)('("//h/ll/\
74
!n
Illca~ure
11")
0.\/01111-
lIimlltl
Schnelle JI.\dalmon U. CrUl'c PA. ct ill S~ln disorder. and mll1<;lure III incontlllent nun.lIlg home re'alcnt..: InlencntiOn Imph calion,. (In Pn.:,,) Gray M ,h,c"'lllenl of paucnt~ wllh urinary lIlt.:tmtlllence . In Dnughty D. cd l'l'liW/T and h·t·lIl!nnU/lim'IIH':\"lInillg 111111 agwlt'I/I,5t Loui .... f!.IO Mo"by Year Book ; 1992:47 9~ Unnary Inconllllellce GUideline Panel l. ·,.tl/ar\' II/("Imii/lt'lln' III Idlii/\ Ollllnil Pllu'//n' (;/1111("/111("\ \IKllR I'ubhcallllll 1\0. 9:;!(X)J~_ Rochll1c, f!.1D_\gcncy f{lr Ilcillth Care Policy "nd Re ... c;lrch. U.S_ Public Health Sendee. L, S Department of Health .md Iluman Sen ICC"; f!.larch 1992. Kane RI .. ()u ... lander J(j. Abm .. , lB. cd,. InconlHlenee In : (wi, 0/ C/illiwl G("I'iarrin 2nd cd l\C\\ 'ork Mdiraw-lIlllinform,lIlOn Sen Ices Comrany. I ')X9: 1W I ')() Schnelle JF. '.jc\\man DR. h)garlY T \lan
F",·",
Inn·,1 th:rllllllOl.
1<6
1973;60: 1M 171
Jeter KI The usc of 1Ill,;OnlinCIlCC products In _Jeter "-I. laller ..... Norlon C. ed,,_ \llnlllX lor (·Ollfmt'IIc·t'. Plulatlclrh1<1 "11 Saundcr-. ('omrany; 1990:209 ,no
SlGGESTED RE.\OI\G Bryant RI\. cd .lulft' 111111 ("Imlll;" 11011111/\ Lou .... : MO ~Io,by Year Book; ! Q91
\lInilfg\ltlllll.1:t'lIIt'lIl St.
Jeter JI. laller N. Norton (.. cd ... , ,\lInlllX /01' ("ml/llll'lIn' Philadelphia \\<'.11 SJundcr.. Company. I'NO:12J 240 "-nhner D. "-ane D_. cd, Clmmit· IIt)/lml CUll'. 2nd cd I< IIlg of P:\ IIc;!lth Management Publu.:alll)!l,. Inc. 1996
Pru~sla.
CHAPTE R
13
Management of Pressure by Therapeutic Positioning Laurie M. Rapp/
osit ies. u. the major weigh t-bearing surfaces of the siltillgdependent person. It has also been estimated that 75% of the sitt ing-depe ndent popu lat ion wi ll experience the development of pressure ulcers. Of these, 75% will have a recurrence of that same breakdown.·1 S Recent literature reports failure rates for nap surgeries of76% to 91%. ·1 .-1 In addition, it is standard procedure for the plastic surgeon to plan for five more donor siles for naps on a patient before doing the first one! This confirms what is already known: treating the symptom docs not effect a cure. Therapeutic posit ioning using correctly chosen equipment plays a direct and criti cal role in reducing these staggering numbers. The human body requires support for proper balance both in the sitting position and in recumbent positions. Any person who depends on the sitting position for any part of the day or night should be evaluated to ensure that the optimal position is being attained. The more sitting dependent the person is, the more acute is the need for proper positioning interventions. However, although the full-time wheelchair lIser is often thought of as the only candidate for therapeutic positioning, the part-time lIser and the ab le-bodied who may on ly si t for re lati vely short periods of time each day are also candidates. Both full-tim e and part-time wheelchair users must be evaluated for approp riate support surfl1ces and positioning in recumbent postures.
INTRODUCTION
Therapeutic positioning is a dynamic and necessary part of the wound care management program orany person. Without properly positioning a person in bed or in a si tting posi-
tion. sk in management progra ms can be devastated by inappropriately high carrying loads on improper bony prominences. Persons who become sitting dependent more than ambulatory, and/or who use the lying down or the silting position for the majority of the day. arc al high risk of skin breakdown. And for the patient with an ex isting pressure ulcer. proper positioning in the most active and functional position possible both in sitting and in recumbent positions
will improve the healing (arc of the ulcer and help minimize the likelihood of recurrence. Advances in equipment to meet seating needs has, of necessity. elevated therapeutic positioning to a specialty within the therapist and technology supp lier ranks. The specialty is as complex as the numbers of people it services. and it is beyond the scope of this chapter to cover all seating/positioning topics thorou ghly. Information provided presents (1) an overview of the areas the clinician shou ld examine in order to determine the need for intervention, (2) the basics of thera peutic positioning, (3) how therapeutic positioning afTects body system impairments, and (4) some specifics in positioning the patient with an existing ulcer both sitting and lying down. Just as pressure ulcers cross all ages, from pediatrics to yo ung adults to middle age to older adults. so does the need for therapeutic positioning become appropriate for all age groups as well. Allhough incidence rates ofu1cers on specific bony prominences vary. it is conservative 10 estimate that 50% of all skin breakdown occurs on the sacrum and the ischial tuber-
T H E DI AGNOSTIC PROCESS A PPLI ED TO T HERA PEUTI C POS ITIO I NG
The diagnostic process outlined in Chapter I begins with the reason for referral. The clinician should obtain a history of the patient before examination in order to determine the systems to review. The review of systems will determine the 271
272
W OUND
CARL
evaluations needed and will dictate the examination strat-
Systems Review
egy. The clinician th en co llates the information gathered to
determine a functional diagnosis that will guide selection of the equipment and positioning interventions required.A prognosis and predicted ou tco me complete the process.
History The reason for referral will give the clinician the first clue to th e positioning needs. The rcason th e fami ly, th e ca regive r,
or the person seeks positioning assistance will usuall y translate into the main goal for positioning. a goa l that cannot be subordimltc to the clinician's. The goa l of the caregiver may be comfo rt in rcc umbclll positions for a nOl1co l11ll1l1l1i ca ti ve
patient. whereas the clinician may want to pursue a more aggressive program to reverse contrae tures. The cli nician's goal may be appropriate. but if the caregive r cannot devote the ti mc or thc financia l resources (Q an aggressive program, the clinician may have to consider less aggressive positioning goals. The medica l hi story is significant for any past surge ries or conditions that would limit the abil it y of the patiel1l to achieve the " idea l" position, or that may need accommodation to help the person maintai n that position. Note any conditions that arc progressive, such as multiple sclerosis, that would necessitate equipment that can be changed with the changing needs of the patient as the disease progresses and skills decrease. Conve rse ly, conditions Inay improve wi th therapelltic positioning interve ntion, such as a decrease in abnormal Illuscle tone and a corres ponding increase in posturalmuscle tone; thi s will also require modification to the seating intervention to match the patient's improvement. Orth opaedic intervent io ns that have been performed that affect normal joint movcment, or the normal funct ioning of the skeletal systcm, are of specia l note. For exa mple. spinal fi xation may lim it range of motion in the trunk and pelvis, and may necessitate equipment that docs not force the body to sit in level planes. but wi ll accoml11odate and support a tilted pelvis or cur ved back posture. The li vi ng situation and the person's leve l of independence will indicate the levc l ofin volvc mcnt the equipment can have. For example, a person in a solid. supporti ve home enviro nment wit h a limited number of consistent caregivers may be able to handle more involved equipment than someone in a group li ving situation with multiple caregivers. The number of hours spent in sitting or in lying down wi ll aJlude to the risk of breakdown; gc nerall y, increased time in sitting or lying down eq uates to higher risk of breakdown and more care in equipment selection and training.
Too orten the wound management program fails to encompass system impairments lead ing to pressure ulcers. instead focusing on the support surface on the bed and on the direct treatment of the wound throu gh dressings and modalities that arrec t n1icrocirculation . Impairments to be managed occur in the neuromuscular system. the musculoskeletal system, the cardiopulmonary and vasc ular systems, the integumentary system, and the psychosocia l/cogniti ve system. Many impairments in all or these systems can be managed by thera peutic positioning in the bed or the cha ir. Some orthese systcm impairments have been ca lled the "hazards or immobility" and are wcll knowll. Therapeutic positioning is a powerful modal ity to effect changes in treatment programs involving all systcms. Nelll"OlllUSCII/llr System
Impairment of the centra l or pcripheral nervous system will have proround efTects on the development of pressure ulcers. If sensation is diminished the bony prominences in the insensate areas of the body wiJl have an undue susceptibility to pressure ulceration. espec ially th ose that wi ll be weig ht bearing. Equip ment selection and positioning must protect and ul1\\'e ight the sk in over bony prominences in the impaired areas as much as possiblc. In silt ing. these arc the ischials, sacrum, and coccyx. It is well known that bed rest orten leads to breakdown on several bony prominences, including heels. malleoli (ankles). and trochanters (hips). The choice of support surface and instruction in proper recumbent positioning are crit ica l in protecting the insensate patient, especia ll y one with poor se lf-repositioning abi lities. If there is an insult to the central nervous system. such as a stroke, brain injury. or spi nal cord inj ury, or disease of the central nervo us system , there may be a lack of renex integrity or loss of motor control. A lack of reflex integrity wi ll ca use uncont rolled muscular movement patterns such as posturing or spasticit y. A high level of spasticity or a loss of motor control req uires equipment that otTers more su pport to the body, as the eq uipment will give the person the abili ty to mai ntai n a position . For example. excessive to ne in extension wi ll calise the hips to extend Ollt of the ideal 90 position, and the hips wi ll sli de forwa rd on the seal. Spasticit y. with its ullcomrolled, repetiti ve movements th rough specific ranges, causes sheari ng. a major ractor in skin breakdown. I f not inhibited with appropriate therapeutic positioning in the chair and the bed, spasticity ca n lead to the development of irreversible muscle and joi nt contractures. The equ ipment must support the body in renex-in hibiting postures (ne ut ra l Q
A1allagemel1l of Pressure hy Therapellfic Positioning
or fle,xion for extension tone. neutral or extension for flexion tone) in order to control involuntary movcmcnts and the devclopmcnt of contracturcs. With degenerative di seases of the ce ntral ncrvo us system such as multiple sclerosis. the clinician must select equipment that ca n be modified as the di sease progresses and thai can be altered to provide more support. l\1I1SCIl/oske/elll/ System
The musc uloskel etal system is responsib le for motor function strcngth , ergonomics. and acti vities of daily li ving. Impairmcnt of the mu sc uloske letal systcm such as fixed or ncx iblc contracturcs.limitations in range of motion andjoint integrity. and skclctal dcformities change strength and ability 10 perform acti vi ties of dail y living. A loss of motor function or mu sc lc strength, revealed in a manual mu scle te st and ergonomics or mobilit y assessment, will impair the pcrsons ability to self-posi ti on and to maintain correct postures. Incorrcc t posture s arc un safe for skin and wi ll lead to brcakdo\\ n and deformities unle ss accommodated for through positionin g. The equipment may again be required 10 be more supporti ve than for a perso n with more intact motor abilitics. Thc degree and location of mu scular weakness will also have an impact on the choicc of mobility base (wheelchair. scooter, recliner chair. ctc.), as powered bases may be requircd for higher nceds. or hcmiheight chairs may be required ror those who propel with their recl. A rirm support su rt~1ce that e nhan ces mobility may be necessary to assistthc perso n with mu sc ulo ske letal impairment in independent repositioning and thus cnhances the safety of the skin , The more activities of daily living that must be done sitting or lyi ng down. the morc positioning may be required to e n ~ urc proper body fun ction and sk in safety. For examp le. if the person ea ts in bed or in the mobility base. the positioning system must support sa fc swa llowing. Impairmcnts in ran gc of motion and joint intcgrity will directly affcct the ability of the body to maintain the ideal position and can re sult in thc body's carrying uneven prcss ures, resulting in skin breakdown. For example, the pcrso n who cannot reach 90° of hip nexion will sacral sit and cause excessive pressurcs on the coccyx and th c spinous processes. Equipment must accommodate for the limitations in range by supportin g the body at the angle available at the hip with a reclining back and a supportive cushion andlor an angled seal. The person who has had a cc rcbrovascular accident (eVA), with onc side or the bod y stronger than the other. will tend to sit unevenly. thu s ovenveighting one isc hium and putting skin in that location at high ri sk. When considering skcletal defo rmi ties, consider both those ind uced by trauma (accident) and those induced by surgery
273
(purposerul) and whcther they arc ri xc d or n cxiblc. Thc deformity 's effect on achieving the ideal posi tion is the overriding concern . A common example of a purpose ful ske let~ll deformity is a unilateral isc hi cClOlllY resulting in a flexible asy mmetric pelvis and scoliosis. The ischicctomy causes lhe pelvis 10 sit unevenly on a cushion that works by weighting the ischials and can lead to scoliosis or to skin breakdown on the sitting surface of the lower s ide. A c ushion that docs nO I depend on ischial wei ght bearing. but rath er 011 fcmoral weight bearing. will accommodate thi s patient bcttcr. as lhe cushion will not ca use the pelvi s to sit unevenly. despi te the surgical procedure. A flexib le deformity is an impairment that e311 be correctcd by thc proper equipmcnt, as desc ribcd abovc. A fixcd deformity. however, is a disabilit y that mu st be accommodatcd by the equipment. Rather than attempting to co rrcct a fixed deformit y thc equipmcnt mu st co nform to the deformi ty, and help hold it in th e position as close to propcr as poss iblc. Evaluation or reevaluation for seating needs must be done when significant weight loss is noted. Significant weight loss can make bony promincnces that were once fairly protccted much more vulnerable to the efTects of pressure and shear. ClIrllioplI/mollllry 1I11d VlIsclI/lIr Systems
Impairments in the cardiopulmonary and vascular systems directl y affect thc ability of the blood to ca rry oxygcn and nutri ents to the intcgumentary system. Medical diagnoses such as chronic obstructive pulmonary di sease (COPD), emphysema, cardiomyopathy, arteriosclcrotic vascular di sease, and hypertension indicHte impairment inthcse systcms and in their ability to deliver oxygen to the ti ssue s. inc rca sing ri sk of ischemia and press ure ulceration to areas subject to compression of ti ssues by bony prominences. The rapeutic positioning or those arcas or the body anectcd by thc above diagnoses is of paramount importance in he lping to avoid skin breakdown in th e patient with impairmcnts inlhcse system s. Inactivity and extended bed rc st have sevcral negative e rrects on these systems. Blood now will be red uccd throughout the body and therefore. to any wound sitcs. Dec rcascd tota l blood vo lume and dccrea sed hemoglobin concentration, increased resting heart rate, and decreased maxi mum oxygen consumption eVo2max) have also been documented. Immobility promotes fluid swsi s in the kidneys. which can lead to kidney stones and infectioll .6 Nutrition intakc can be be impaired, as the recumbent and inactive positions redu ce the appetite. Recumbency inhibits safe swallowing and facilitates aspiration of food, leading to pneumonia. Swallow-
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W OUNO CARE
ing occurs 24 hours per day, not just at mealtime. The COfrect head and neck positions conducive to safe swallowing should be identified and attained in the chair and the bed ; consultation with a speech/ language pathologist may be necessary for success in thi s area. Oxygenation of the blood may be impaired if the person ca rries any of the ca rdiopulmonary diagnoses. Proper upright positio ning allows greater diaphragmatic expans ion. improves breathing patterns and depth (thus improving oxygenation of the blood), and mobilizes pulmonary secretions.' Upright positioning in a functional and comfortable position will improve general ci rculation by placing the patient in a position that encourages activity and movement. Cardiac function is also improved in the upright posi tion . Upright positioning with pressure e lim inated on the bony promine nces will improve circu lation to the ulcer site by gravity, which pu lls blood down to th e ulcer si te.
Clinical Wisdom: Prone Positioning It has been suggested that, for the sitting-dependent person with breakdown on the sitting surfaces, the prone position with the wound uppermost actually inhibits circulation to the wound site by assisting blood to ftow as a liquid will, away from the highest point.
/Iltegllmellf(lry System
Skin is more susceptible to breakdown if it is dry, flaky, friabl e, aged, insensa te. prone to excessive swea ting , or subjected to incontinence, fri c tion , or shear. Positioning can affect the integume ntary system by protecting the skin over bony prominences on weight-bearing surfaces through correct usc of th e proper equipment to maintain safe postures and to unweight those bony prominences. For so me people, an equalization of pressure is s ufTicient to protect skin from breakdown. For others. complete removal of pressure may be needed for protection, as their combination of ri sk factors makes them highl y susccptible. For example, the skin over the coccyx is prone to breakdown because of the shape of the bone, lack of padding over the coccyx, and frequent use as a weight-bearing surface. Equipment that takes press ure ofT the coccyx in sitting, used correctly, can help avoid or Irem thi s breakdown. Persons who had pel vic irradiation prior to 1980 are at very hi g h risk for skin breakown over the sacrum. coccyx. and bUllocks arcas duc to thc skin changes that the irradiati o n used at that time incited .
Pl)'c/tosocioIlCogllilh'e System Often overlooked, but well -known. arc the hazards of immobility as related to the psychosocial/cognitive system . Extended bed rest or loss of mobility leads to cognitive dys· function . The recumbent position induces lethargy and inac· tivity. Onen, a patient who refu ses to follow prescribed treat· men IS, including extended bed rest. is labeled " noncompliant." In many cases, however. he or she may simply be issuing a cry for hclp in changing the wound management program becau se, for the si tting-dependent person, bed rest is a sentence akin 10 impri sonmenl. The patient with impaired cog nitive abili ties may be unsafe in self-mobility or in the ability to mailllain safe postures indepe ndentl y. The equipment for someone with cognitive impairmcnts will probably need to be more supportive than that for one with full abilities to reposi tion or to ask for assistance in maintainin g sa fe postures. Cognitive and psyc hologic impairments are definitely afTected by inactivity and poo r posit ioning. SU lIJlIJ ary
Wound management must be an interdisciplinary team efTort. The total wound management program is a combination of the therapi st 's eva luation of the prominences, the body position, and body movement, a long with evaluations by other clinicians with information on medications (eg, steroids), medical status, other health-related conditions (such as diabetes, cancer, and immunosuppressive di so rders), nutrition, blood levels of serum albumin and protein. habits that increase ri sk (such as smoking), choices of clothing that nega· tively afTect sk in, excessive sweat ing, bed mobili ty, and incontinence. FUNCTIONAL DIAGNOSTIC PROCESS The clinician rev iews the mcdical hi story and systems and then decides on the appropria te examination strategy for the patient. After the exami nations arc performed and the data coll ected, the in formation is reviewed and evaluated. The result of the evaluation is the functional diagnosis. The functional diagnosis will be based on the following: • The impairments found in th e examination that prevent the client from achiev ing the ideal position either sitting or lying down • Identification of the client's preferred posilion(s) • Identification of the client's alternative position(s) • Specific interventions in the form of equipmen t choices and proper use of that equipment Tables 13- 1 and 13- 2 list examples of medical and functional diagnoses relating to need for therapeutic posi tionin g,
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275
Table 13-1 Functional Diagnositic-Sitting Position Medical DiagnosisFunctional Diagnosis
Prognosis
Kyphosis-Patient cannot maintain 90° hip flexion and keep face vertical due to thoracic kyphosis.
Patient will sit upright with face vertical and as close to 90· hip flexion as possible.
Reclining backrest with stabilizing seat cushion. May need antitippers.
Patient able to sit stabilized as close to 90· back/seat angle as possible with face vertical.
Scoliosis (fixed)-Patient cannot sit with shoulders and hips level due to fixed asymmetric spine or pelvis.
Patient will maintain sitting position with shoulders and hips as level as possible.
Cushion with buildup under higher ischium to accommodate asymmetry; back support to assist in comfortable trunk positioning.
Patient able to maintain upright sitting with shoulders and hips as close to level as possible.
Scoliosis (flexible)-Patient does not but can sit with shoulders and hips level.
Patient will maintain sitting position with level shoulders and hips without strain.
Cushion with pressure elimination at ischials and full femur support or cushion with buildup
Patient able to maintain upright sitting with shoulders and hips level and spine straight.
Intervention
Outcome
under lower ischium to
raise that side of pelvis. <90· Hip flexion-Patient cannot sit at optimal 90° seat/back angle for maximal functional abilities and mobility.
Patient will maintain correct sitting position with hips on back of seat.
Positioning cushion to
<90 0 Knee flexion available-Patient unable to reach standard foot pedals for support.
Provide equipment that supports lower extremity at available range so that patient can maintain proper sitting position.
Elevating leg rest with full calf and foot support, set at full allowed knee flexion .
Patient will maintain upright sitting with hips on back of seat and LEs maintained at allowed knee flexion .
Foot propeller-Patient requires use of feet to mobilize chair; unable to reach floor to propel.
Provide equipment that allows efficient heelstrike on the floor.
Hemiheight chair with cushion or drop seat with cushion, so that total seat to floor height is 2 inches less than back of knee to floor measurement,
Patient will be self-mobile via foot propulsion while maintaining proper seating posture.
One-arm driver-Patient can use only one arm for self-mobility.
Provide equipment designed for propulsion with one arm.
One-arm-drive wheelchair.
Patient will be self-mobile using one arm while maintaining proper seating posture.
Above the knee (AK) amputee-Patient has limited femur length to support body weight; difficult to maintain posture in sitting; may lead to skin breakdown on ischia Is due to increased weight on ischials.
Provide firm flat support for femurs, and protection for ischials.
Stabilizing seat cushion; amputee adapters to move rear wheel axle backward from normal position; antitippers.
Patient will maintain upright sitting with full protection of ischials and ful l femur support.
stabilize pelvis, with reclining backrest to approximate trunk/lower extremity (LE) angle allowed by range of motion limitations at hip.
Patient will maintain upright sitting as close to 90· as is allowed by range limitations.
continues
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Table 13-1 continued
Medical OiagnosisFunctional Diagnosis
Prognosis
Intervention
Outcome
Skin breakdown on sitting surfaces (ischials, sacrum, or coccyx)Patient cannot sit without pressure eliminated at ulcer site.
Pressure elimination on ulcer wh ile maintaining correct postural alignment.
Cushion with selective pressure elimination.
Patient will maintain sitting schedule with pressure elimination provided at the site of breakdown .
Asymmetric tonic neck reflex (ATNR) influencePatient has difficulty controlling direction with side-mounted joystick when head moves.
Change placement of joystick to decrease influence of ATNR.
Position joystick in center of lap tray.
Patient will drive safely and in control despite movement of head.
Hip fracture-Patient cannot sit with full 90· hip flexion; may lead to skin breakdown due to coccyx weight bearing.
Provide seating arrangement that allows <90· hip flexion with skin protection.
Seat cushion that provides ischeal/coccyx pressure reduction or elimination with positioning and can be customized with unilateral sloping to accommodate the lack of hip flexion on the involved side; reclining backrest with sacral protection; solid seat beneath cushion-may require cutout in board.
Patient will maintain upright sitting with maximum allowed hip flexion and no pressure on coccyx.
Trunk/hip extensor tonePatient cannot maintain hips in proper position on seat due to uncontrolled hip extension; may lead to skin breakdown due to shearing .
Provide seating arrangement that decreases tone and helps maintain as close to 90° hip flexion as possible; antithrust seat assembly with preischial block.
Increase trunklLE angle past 90· ; firm contoured back support; 90· positioning belt.
Patient will maintain proper seated posture with hips on back of seat and trunk upright.
Source: Copyright C Laurie Rappl.
the prognosis. related interve nt io ns, and expected functional ou tco mcs for the silting-impaired and for the reclIlllbentimpai rcd c lient. Based on the functional diagnosis. the clinician wi ll establish a prognosi s and select interventions. with a targeted outcome for each inte rvention. Interventions include a naly. s is of th e most effective forms of eq uip men 1 required selec· lion of appropriate equipment to achieve co rrect therapeutic position. ana lysis of the patient using the selected equipment, and education of patient and caregivers in correct lise. Thera· pelitic exercise often is another important componellt of the tota l thera py plan of care.
RAT IONALE FO R INTE RVENTION IN H IE SIlT I G I'OS ITION
Sitti ng can be seen as either Ihe ca use of skin breakdown or as part of th e solut ion. In a proactive environment, with an educa ted clinician wit h access to the right equ ipmen t and armed wi th techniques in therapeutic positioning. sitting can and shou ld be a part of the healing of skin breakdown and
part of a prevention program thaI can improve the quality of li fe for the person; it can a lso decrease medical costs over the course of time.
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277
Table 13-2 Functional Diagnostic Process-Recumbent Position Functional Diagnosis
Prognosis
Intervention
Outcome
Cardiorespiratory or gastrointestinal compromise requiring elevation of the head of the bed .
Patient will assume Fowler's position with proper positioning and skin protection devices to protect heels and sacrum.
Hip aligned at gatch of bed ; sacrum protected by lifting under one hip with pillow or foam support; heel protection devices employed; frequent turning/ repositioning schedule. Do not substitute elevated head of bed for upright sitting in a supportive chair.
Patient will tolerate head of bed elevated while maintaining safe postures with support devices.
Less than full hip or knee extension allowed due to joint integrity impairment at the knees. Undue susceptibility to pressure ulcers due to potential exposure of heel and sacrum.
Patient will assume supine position with foam support devices in place to accommodate hip/ knee flexion requirements, and with protection of occiput, heels, and sacrum.
Foam positioning devices to protect occiput and heels, and to elevate lower extremities to accommodate flexion contractu res. One side of pelvis elevated slightly with towel roll or foam to protect sacrum.
Patient will maintain supine position with support devices correctly placed .
Influence of the asymmetric tonic neck reflex (ATNR) causes involuntary movements into trunk extension, and inability to maintain sidelying position.
Patient will be positioned with strong side down and trunk and upper limbs fully supported. Or patient will be positioned with strong side up, body fully supported along full trunk, and the bed situated so that patient is not required to turn the face up to view the room .
Position with stronger side down and trunk fully supported from shoulder to pelvis. Bed is placed so that need for cervical movement is minimized , ie, against far wall, facing door of the room.
30· Foam wedge fully supporting trunk, pelvis, shoulders, and uppermost arm and leg supported away from midline in abduction; head supported in midline in both frontal and sagittal planes.
Venous ulcers on lower extremity with edema.
Patient will maintain supine or sidelying positions with lower extremity elevated above midline to reduce swelling, and with ulcer pressure free .
Foam device to support leg above the level of the heart in supine position and in 30· sidelying position .
Patient will maintain safe postures with limb elevated and sacrum protected .
Source: Copynghl C Laurie Aappl.
When the sitting skeleton is viewed from th e side. it is apparent that the ischial tuberosi ties ( ITs) ex tend approximately 1.5 inches past the femurs, making the ITs th e major weight-bearing points on the sitting surface. These points are al so the 1110st vulnerable to skin breakdown because of their conicill shape and poor natural padding. As a person becomes more silting dependent , atrophy cau ses th e minimal natural padding to deteriorate, making that person even more vulnerable to skin breakdown . The ITs are the fulcrum point for th e pelvis. and when bearing we ight, cause the
pelvis to rock about a horizontal axis through the frontal plane that leads to anterior or posterior pelvic tilt. Most often, people tend to sit in a posterior tilt, or a slouched positi ol1. The act of moving into the slouch causes shearing forces on the ITs, and sacral sitting leads to the formati on of pressure ulcers on the sacrulll and coccyx as well. The goa l in sea tin g a client is to help maintain a positi on that is as close to ideal as possible. Orthopaedic or neurologic limitations may prevent achievement of the ideal positi on as a realistic goal. but it is the benchmark position.
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CARr
/deal is the position that the body should be in to be anatomically aligned ror muscle balance, to achieve proper alignment of the bones and joints according to their design, and to take advantage orthe most load-tolerant areas of the body
in handling pressure to keep the sk in safe from breakdown. In the ideal position, viewed rromthe side, the client should have a 90° angle at the hip, knee, and ankle. The ear should be in Iinc with the acromion process and the hip. and the root should be positioned under thc knce. The thigh should be paralle l to the ground so that the hip and knee arc in line with each other. The spine shou ld be supported in its natural curves in the cervical. thoracic. and lumbar regions. The face shou ld be vertica l (sec Figure 13- 1). Viewed rromthe rront, the tfunk and head should be comfortably upright wit h shou lders and hips (pelvic crests) level, the thighs in neutra l (not internally or externa ll y rotated), reet pointed straight ahead, a nd
a TITI S supported
so that the shou lders arc not elevated or
dep ressed when the elbows aTC resting on the armrests. Dignity issues c learly indicate the need for women to be positioned with their legs together rather than separated.
Sitting Posture Ex amination and Evaluation Kn owing the ideal position, the clinician then evaluates the patient to determine how closely the patient can come to ac hieving the ideal position comrortably, what prevents the patient from attaining that position, and what equipment interventions can assist the patient in maintaining a position as close to ideal as is possible or functional. Neuromuscular System Reflex I"tegrity Examillatioll. Noni ntegrated primitive reflexes in fluence seating when central nervous system disorders make them more appa rent than in the intact nervous system. One example of the influence of a primitive renex on function and positioning involves the asymmetric tonic neck reflex (ATNR). This reflex causes the person to extend on the face side when the head is rotated. This can cause the person driving a side-mounted joystick to have difficulty controlling the device. A center-l11o untedjoyst ick may solve this problem. The symmetrica l tonic neck reflex (STNR) is influenced by head position; the STNR must be accommodated ror by limiting the movement or the head so that voluntary control of the body is maintained . Extensor Ihrust is evident when the ba ll of the foot is sti mulated and causes extension throughout the body. Limiting contact with the ball orthe root on the root peda l will help to relax extensor tone and help maintain an upright position . Hypertonicity, spasticity, and athetoid movements all demand stabilization of the body so that extraneous or involuntary movements wi ll be minimized, and the person has some freedom to express voluntary movements. Sellsory EXllllliulifioll . The ab ility to detect both light and deep pressure must be assessed on all areas of the body that wi ll be weight bearing or th at may corne in contact with equipment. The inability to detect pain or pressure may lead to skin breakdown. If the person is insensate in the skin over the sitting surfaces. he or she wi ll not know when to shift weight to relieve undue pressure. For the insensate person, great care must be taken to search for and prescribe equipment that not on ly positions the body but also protects insensate skin (see the section on scat cushion categories).
ft111scIlIoskeletal Sy.'item
f igure 13- 1 Ideal silling position. side view. Courtesy or SpanAmerica Medical Systems. Greenville. SOllth Carolina.
Motor FUllctioll (IIItl Ergollomic.. Examillation. Note how dependent or independent the patient is in self-mobility and what means is easiest for him or her to usc. This will determine the mobility base (wheelcha ir. recliner chair, scootcr, etc.) that is prescribed. Irthc patient docs not have the physical, cognitive, or visua l perceptive abilities to be safely independently mobile, a Iota I support cha ir such as a recliner Geri-chair or recliner wheelchair may be nceded;
Mallagemellt oj Pressure hy Therapeutic Positioning
either one may require additional support devices, sllch as a commercially available seat and back. If the patient has the cognitive and perceptive skills. but not the physical skills. then H powered ba se. either a power wheelchair or a scooter style. is chosen. If the person can self-propel, the therapist h~ls a choice of a variety of manua l chairs. depending on Ihe body parts being used for mobi li ty. The patient who needs one or both feet to propel will require a hemiheight wheelchair. one with a lower-than-standard scal-to-floor height so tha t the person can contact the ground firmly with the foot without having to scoot the pelvis forward on th e chair. The mOSI efficient foot propulsion can be accomplished if the patient can achieve a heel-toe pattern in forward propulsion. Foot propulsion can cause shearing forces on the skin over the ischials as the person pulls the body forward with the leg. The patient who can propel with only one arm will need a one-arm-drive chair. The patient who will use both arms is a candidate for a siandard hcight wheelchair.
Shear tlIItl Fril·tiou EXlImiJltllioJl . While evaluat ing mobility capabilities. the clinician shou ld pay attention to the quality of those capabi lities. a nd assess them for the possibilities of friction and shear. These two causa tive factors in skin breakdown call become evident during propulsion or when postural changes happen whi le the patient is seated. Friction and shearing would be evidenced by irregular reddened areas on the weight-bearing surfaces. Proper equipment and positioning can limit trunk and pelvic movement 10 limit both friction and shearing. A"titlities ofDtlily Litling (ADL) Examinatioll . The more functional ac tivities done in the wheelchair, stich as dressing. bathing, eating, and toileting. th e more the equipment will have to accommodate beyond simple posi tioning. Waterproof materials will assist in toi leting. and non contoured sea ting may assist the caregivers in placing the person in many different positions to pull clothing on and off and to bathe the various body parts. Transfers, or the methods used to gct the person into and out of th e chair. are an important factor in determining seating equipment. Assess for the possibility of shear and friction during the transfer. Try to minimite the number of extra devices such as abductors and adductors. These tcnd to gct in the way of independent transfers and are cumbersome for the caregivers in dependent tran sfers.
Clinical Wisdom: Transfer Technique Poor transfer technique is a major contributor to skin
breakdown, because the skin is dragged across surfaces , or is subjected to sudden overload when the person is set down suddenly.
279
Rauge of /\101ion and Joint Integrity Examination. The spina l curves shou ld be in proper alignment; a fixed exaggerated thoracic kyphosis wi ll limit the person's ability to keep the face vertical. Ir hip flexion of 90° cannot be attained, the person cannot be accommodated in a chair with a 90° seatlback ang le: the back will have to be reclined, and the seat cushion should provide enough pelvic stability to keep the hips from sliding forward . A scat that tilt s up in the front may be helpful. Ifknee flexion is fixed at less than 90° from straight, or more th an 90 0 from straight, the legs will have a tendency to pull the body forward from the back of the seat and out of posi tion . Footrests that support the foot and allow the hip and knee to maintain as close to 90° as possi ble wi ll be helpful in positioning the lower body. Stabi lizing the pelvi s is critical to correct positioning. The pe lvis must be eva luated in all planes of movement. The antcrior/posterior rotation is assessed from thc side. The anterior superior iliac spines (AS IS) should be roughly level with the posterior superior iliac spines (PS IS). A posterior tilt where the PSIS arc lower than theAS IS will flatten the lumbar spine, decrease hip fl ex ion from 90°, and cause the body to attain a "slouched" position . An an terior tilt will th row the body forward, making it difTieult to attain upright sitting with arms free. A tilt to lefl or ri ght in the frontal plane is termed a "pelvic obliquity:'This obliquity mu st be defined as "fixed" or "fl exible:' To do this examination, place the person on a firm seat with knees at 90 0 and fect supported. Note whether one iliac crest is higher than the other, and note the presence ofa lateral curvature of the trunk both with and without upper extremity support. Place a support under the ischium on the lower side of the pe lvis to even the iliac cre sts. I f the trunk curvature remain s and th e person becomes more unstable when the arms are rai sed, th en the obliquity is fixed and should be accommodated for by building up the cushion under the opposi te ischium . Ir the trunk curvature decreases and the person is more stable. the obliquity is nexible and can be accommodated for in one of t\\'o ways: ( I ) by putting the person on a firm cushion with both ischials unsupported and both femurs fully supported and at the same height . inducing a leve l pel vis. or (2) by building up the cushion under the lower, supported ischium 10 even the iliac crests. Pelvic rotation, a twi st about a vertical axis. is noted if one iliac crest sits forward of the other. Limitations in ankle dorsiflexion or plal1larflexion or inversion/eversion will affect the support of the lowcrcxtremity on th e foot pedal. If th e ank le cannot be maintained in a neutral (right angle) position with 00 of inversion/ eversion, a foot pedal that can change angulation will be needed to accommodate the position of the foot as closely to idea l as possible. Limitations in the upper extremities arc also important 10 note. A flacc id upper extremity can affect mobility, as that arm wi ll not be useful for propu lsion. A flaccid, unsupported
280
WOUND CARE
a rm can also afTecl positioning, pote ntially causing the body to sag towa rd the flacc id side and inducing excessive pres-
sures on that side of the sitting surface. Reflex-inhibiting postures sllc h as suppo rt in elbow fl exion and shoulder pro-
traction to break up severe extensor tone wi ll help the client maintain a forw'ard upri ght post ure.
Skelellli Deformities Examillatioll. Note any limitat ions in th e range or motion that would affect the person's abi lity
to sit upright eas ily. As previously discussed regardi ng the pelvis. these problems shou ld be assigned a " fi xed," that is, immovable. or " fl exible," that is, movable or correctabl e,
designation; " fi xed" proble ms will need to be acco mmodated for as a disability. whereas "nexible" problems should be noted as places whe re the ri ght eq uipm ent or positioni ng can
hel p correct an impai rment. Integumentary Examination
The clinician must eva luate the status of all skin on the weight-bearing surfaces. The qualit y of the skin-dry, inelastic. friable. thin- must be noted. Use the bony prominences as anatomica l locations under skin to see signs of impairment, that is, change in color (red, blue, purple) from adjacent continuit y of sk in color. Also record the anatom ic locations of each area of breakdown. and include the size, date of occurrence, stage, history, and current plan of care of each. Note areas of previous breakdown and any previous surgeries to repair skin. as these areas are at high risk of reopening and must be protected at all costs. Even if they have not ex perienced breakdown, any bony prominences on weight-bearin g surfaces may be at risk, and palpation will reveal those at highest ri sk by showing which ones are most prominent, least protected and bearing the most we ight. Musc le atrophy or significant loss of body weight will make the ischium more prominent than usual, and may make protection from breakdown a primary need in the selecti on of seat cushions.
devices. The hand-held, single-cell monitors are more portable and less expensive, but the single cell has a tendency to move during the infl ation/denation cycle. It also gives the readi ng over one small area, when the peak pressure may be somewhere far removed from the placement of the cell. The multiple-cell device gives a better overall picture of the pressures on the whole seating surface simultaneously, and prints those pressures out in numeric or pictorial form on a computer screen. These larger, computerizcd mapping devices are much more expensive and less portable, but Ihey are valuable in that the who le si tting surface is read at the same time rather than just a single site. Single-cell meters operate in one of two ways: inflateplacemcnt-denate- read, or denate- placement- innate- read. Accurate readings depend heavily on proper placement of the cell under the bony prominence while the person is sitting upright and stablc. After tak ing the first reading, most clinicians wi ll then rcmovc the cell , replace it, and repeat the readi ng two times in order to get at least three readi ngs per bony prominence. Some manufacturers recommend tak ing three readings and averagi ng the results. Make sure that the ce ll is not wri nkled during use; that the sitting surface is up to manufacturer's directions ror inflation or suppOrt, placement on the chair, and support of extra pieces such as a solid base, a cover, or abductor/adductor/obliquit y wedges; and that the sitting surface is smooth and free of wrinkles and excessive layers of padding. The goa l of pressure rcading is to fi nd out the location and the va lue of peak pressures on a particular client on a particular cushion. High pressures on the most vu lnerable prominences (isch ial, coccyx . sites of previous or current breakdown) may indicate that that cushion and client arc not an appropriate match. It is preferred that the areas of highest risk (ie. ischials and coccyx) record lower pressures than those at lower ri sk. such as the femurs; the femurs arc load tolerant. can support the majorit y of the weight, nnd can therefore tolerate higher pressures than the vu lnerable ischials and coccyx.
Inter/ace p,.es.\·ure Examination
With the advent of sophisticated mapping devices that determine interface pressures, many facilities and clinicians arc using these measurements as the major factor in determining scat selection. Although pressure is one of the factors that cause breakdown, it is on ly one of several. The cli ni cian should co nsider shearing, fri cti on, heat/moisture buildup. and silting instability as equally important, even though they are more difficult to measure than interface pressu re. The clinician must use interface pressure measurcments carefully, and be sure to look at the total picture of the patient and the equipment. Pressure measurements can be taken with single-cell , handheld devices. or larger, 111llltiple-cell . cOinputerized mapping
In1ervention Us ing the Principles of Seating
Therapeutic positioning8 14 requ ires ski ll in evaluation and interpretation of the client's needs and in the matching of equ ipment to client. This has tradi ti onall y been considered the realm of physica l therapy and/or occupational therapy; indced, many physical therapi sts (PTs) and occupational therapists (QTs) are highly skilled in therapeutic positioning, and there are seating clinics staffed by therapists with a high level of specialization in positioning all ran ges of client involvement. Unfortunately, many clinicians and patients do not have ready access to the ski lled intervention of knowledgeable PTs and/or QTs. However, propcr seating and po-
A4allagemelll oj Pressure by Therapell{h: Positioning
sitioning must be attended {Q by all cli nicians or caregivers involved in health care, and the knowledge and applica tion of the basic principles of seating will benerit the majority of patients. These basic priniciples of proper positioning can be learned and applied in the home sett ing as well as the nursing home and rehabi litation facility by all know ledgeable and willing clinical stafT.
Clinical Wisdom: Basic Seating Principles
The basic seating principles include the following: • Level cushion and seat upholstery to keep thighs horizontal to the ground; knees and hips even. • Feet are supported so that the knees are even with
the hips. • Back is supported so that natural spinal curves are maintained; ideally the ear, shoulder, and hip should be in alignment. • When the pelvis is properly positioned on the seat,
the seat cushion ends 1y, inches from the back of the knee. The clinician or caregiver should also identify when the basic seating principles will not or cannot help the patient, when equipment will have to accommodate a position that varies from these basic prin ciples as
stated in the text, and when referral to a skilled outside source is necessary.
Peh'ic COlllrol
Pelvic control is th e cornerstone of seat ing. I f the pe lvis rolls out of position, the who le sitting posture will be difficult to control. Most seat products control the pelvis by putting some pressure on the most unstable aspect, the ischials, and attempt ing to contro l pelvic movement by padding all around the isch ials. Others eliminate this unstable point as the cOlllrol point and use the proximal femurs to com-rol the pelvis. Any chosen cllshion requires the assistance of a back support. The top of th e back of th e pelvis must be supported wi th the back support so that it canno t rock backward. The back support also fi lls in the lumbar curve for more supported and comfortable sitting and rel ieves stresses related to back pain by improving the sea tin g ergonomics. Thigh COlltrol Thighs should be parallel to the ground. The seat shou ld be nat, with the hips and knees horizontally aligned. If th e knees are lower than th e hips, tlte weigh t of the legs pulls the body forward and pulls th e pelvis into the posterior pe lvic tilt the clinician is trying so hard to avoid and the patient
281
slouches. Thi s is the position most commonly seen in settings where generic chai rs are used. and the footrests are lengthened as much as possible. or have been lost. Conversely, if th e knees are higher than the hips as in the usc ofa wedge cushion, the lumbar lordosis is lost, the proximal femur along wi th th e sacrum, coccyx, and ischials bear an inordinate amount of weight, and the patient is put at high ri sk of skin breakdown and back pain . These wedge type cllshions arc typically lIsed in an attempt to keep the person from sliding Ollt of the scat. Wedge cushions cause a number of problems, however, indicating that they should be prescribed wi th extreme caution, rather than as a genera l issue device. These problems can include skin breakdown on the sacrulll and sp ine due to excessive body weight being forced on those prominences, discomfort in a nexed lumbar spine, difficulties in transferring, and loss ofl11obility and ADL skill s. Sellf Depth
The scat depth should be about I y, to 2 inches shorter than the di stance from the seat back to the back of the knee. Scats with less depth than this do not take advan tage of the weight bearing or the support th at the posterior femur can give; greater depth than thi s and the sea t wi ll pul l the body forward on th e chair and out of position. Many people in neet or institution chai rs are silting on very short scat depths. and, therefore. have a tendency to slide about on their chairs and slide out of position . Large recliner-style cha irs have seal depths that are too deep. causing pressure on the lower legs and pulling the body forward on the seal. Footrest
The foOl rest should support th e leg so that the th igh is parallel to the ground. I f the footrest is too hi gh, tlt e we ight is unevenly distributed across the felllur; if it is too low, the weig ht of the leg pull s lhe body out of position. To keep th e thighs parallel to the grout1(~ simply adjust th e foo t support, or provide a footstool or other support under the fecl. Care should be taken to ensu re th at the individual wears the appropriate supportive footwcar to protect the feet frolll trauma. to evenly distribute pressures across the who le foot , and 10 assist in decreasing dependent fluid buildup in the fect.
Clinical Wisdom : Simple Tools A simple toolbox is a necessity and a relatively inexpensive investment when wo rking with seating
equipment. This should include a variety of screwdrivers, wrenches, and a lubrication agent. For example,
a simple wrench is usually all that is needed to change the height of a footrest so that the footrest plate is the proper height for full foot support.
282
W OLN"
I¥Jreeldl(lir
CAR'
Mea~lIl'e", ellt
rely stri ctl y on history or manufacturer's claims to determin e what products to use; predetermine wh at features the product should ha ve to fulfill the patient 's needs be fore assessing th e bene fit s of that product for the person.
Proper wheelchair seating requires th at th e scatlback angle
accommodate the person as close to upright 90° as the person's body will allow. Pro per measurements for a whee lchair include scal depth as described above. back height from scal cushion 10 th e point on th e back that gives needed sup-
Wheelchairs or Mobility Btlses Th e major piece of equipment ill seating. the one carryi ng th e hi ghest price tag and actin g as the basis for the rest o f th e seatin g system, is the chair. somctimes referred to as the mobility base. Figure 13- 3 is an algorithm to guide the c linici an throu gh th e decision-making process to determin e mobilit y needs. Th e appro priate mobil ity base must be determined along with th e sea ting system. It is onen impossible to make any seating system, even th e appropriate one for the patient, work on an inappropriate sea tin g base. For example, many peoplc mobili ze th eir c ha ir by prope lling with the ir feet. Ifthe wheelchair sea t is too high to allow th e foot to reach th e ground, all sea t cushions will put the person even higher and further
port w ithout hinderin g function. w idth fro m hip 10 hip and
shoulder to should er kept as close as is comfortabl e so that the overall chair is as small as possible, a nd foot support placed so th at th e knec is eve n with th e hip. This foot support will be the floor-la-seat height in hemi-stylc chairs. or footres t selec ti on and selling in a manual or power-propelled chair. M easurements Illu st include the cushion when measuring the backres t height. seat to fl oor. and footrest length (see Figure 13 2). To choose equipment. match the needs of the cl ient with th e features of a product. Th e client's needs will be assessed in the evaluati on; th e fea tures of th e product arc assessed with clinical skills, analytical skill s, and common sensc. Don't
i
c
1
B
r ,, ,
A
o Figure 13- 2 M easuring for a wheelchair. A = Scat to foo t support height B = seat to top of sac rul11 for place ment of lumbar support : C height o f bac krest needed for back suppor!: D = scat wichh: E = scat depth. measured from backres t to popl iteal fossa less 1.5 inches.
A1allageme11l of Pressure by Therapeutic Positioning
283
Candidate for independent mobility? (Consider physical. cognitive, visual perceptive abilities)
No
Can patient self-propel using arms and/or legs?
Total support chair
No
Does patient fatigue quickly when pushing a manual chair?
Yes _ _ _ _ _ __
Powered mobility with hand or head switches, scooters
---'J
No
Manual chair
I Propulsion by one or both feet or one arm/one foot
Hemiheight wheelchair (consider drop seat with 24-inch wheels)
I Propulsion by one arm
One-arm-drive wheelchair
Figure 13- 3 Algoriliull: determining mobility base needs. SOl/ree:
reduce the mobilit y of the patient. "Qui ck fixes:' such as a drop scat. arc oft ell onl y fair com promises at best. In the sa me way. using a scaling system on a base it is not designed for will compromise th e effect of th e system. Reclining geriatric or Gcri -c hairs ofTer little to no support and are not designed lO accept most seatin g syste ms. However, so metimes these cha irs arc th e onl y ava ilabl e alternative 10 bed rest; therefore, attempt to adapt thi s chair to fit the indi vidual's needs by utili zing Ihe appropriate back cushi ons, head suppo rt s, lateral trunk or hip guides, scat cushi ons, a nd lower ex tremit y support. The stand ard wheelchair, a fo lding frame style with adjustable or fixed arm rests, a seat 18 inches wide by 16 inches deep. and eleva ting or adjustabl e footrests, is more for temporary transportation than for all-day eve ryday mobility and posi tioning usage. The vast majorit y of uscrs require more support than th ese chairs ca n give. There are a multitude of va ri ati ons on the stand ard theme:
Propulsion by two arms only
Standard height wheelchair
opyriglll tt', L aurie Rappl.
• Hemiheight- The axle for the back wheel is fixed hi gher on the frame than standard, thereby lowering the hei ght of th e seat and allowing the use r who foot propels to reac h th e noor with a hee l-toe pattern , whi c h is more functi onal and efTi cient . • Sport or lig htweight- These chairs a rc for th e very active user who needs the light est frame possible for transportin g, and for max imum mobi lit y. They ca n also assist th e frail elde rly to co nserve energy, and ca n have a signifi ca nt impact on overall endurance for acti vities of daily li ving. • Rigid- Thi s is a non folding frame style for the very acti ve use r; it is less prone to breaking and loose nin g. • Pediatri c~s i zed-These chairs a rc for th e chi ld or the child-sized adult . • Recli nin g back chairs- These arc adjusted by manual releases, hydrauli c releases, ratche t-style fixation , or power. The seat to back angle ca n be cha nged to aceom-
284
W OUND CARE
modate the persoll who cannot attain upright silting or who needs to recline for some time during the day, but Ilot necessarily oul of th e chair. Similarly, upholstered recliners such as Gcri-chairs or living room reclining chairs allow the body to relax from upright. However, these chairs calise many posi tioning problems.
• Power chairs- These arc available in wheelchair style or as scooters. Sellt Cushions Scat cushions arc commonly considered to be the primary intervention in positioning the client.' ~ 17 Products should be evaluated 011 how they control several physical and physiologic factors that cause skin and sea ting problem s. These factors are pressure. shear, heat and moisture buildup, and postural control and stability. Pre,\'!mre. Pressure causes ischcmia or loss of circulation to the cells under pressure. Pressure is considered the major
Clinical Wi sdom: Seat Cushions Are Not Mattresses in Miniature
Understand that the seat cushion is not a mattress in miniature! Consider that a mattress has the advan-
tage of the entire weight-bearing surface of the body over which to spread the load. There is more tissue in
contact with the bed, so the goal of a mattress can be tissue support, that is, equalizing pressure across the bony prominences and plateaus such that pressures
are not high enough to cause breakdown on anyone point. Compare thi s with the seat cushion, which must bear 75% of the body weight on a small area, average size 18 x 16 inches. In seating, that body weight is concentrated on two prominences, the ischials. which are the lowermost skeletal points on the sitting sur-
face . The ischials are small, pointed , and unprotected , and therefore less load tolerant than the large, flat, padded femurs. With this disparity in load tolerance in mind, it is imperative that the seat cushion be exam-
ined for the skeletal support it can provide to protect the skin over these at-risk areas, and shift the support to the load-tolerant areas. This is not equalization but load distribution consistent with tolerances. Equalizing the pressure over the sitting surface causes
low-tolerance/high-risk prominences (the ischials) to bear the same weight as the high-tolerance/low-risk areas (the femurs). Skin management dictates that the ischia Is should bear less weight than the femurs, and should not bear any weight in the presence of skin breakdown or for those individuals who are identified
as being at high risk for skin breakdown.
causarive factor of skin breakdown on the silting surfaces and has the great est effect on bony prominences. where high forces are generated on small areas. Large. flat surfaces sllch as the posterior femurs seldom break down because they distribute forces over a larger area. It is generally acknowledged that the ischials can sa fel y tolerate only one third to one half the amOllnt of pressure thai the femurs can. Also. beware that musc le tissue is affected by pressure before sk in is. This is why pressure ulcers often show deep tissue destruction well before indications on th e skin surface appear. "A little bit of breakdown" can be the tip of the iceberg. Sltellr. Shear is the distortion force applied to the skin when bone movement pull s the sk in one way. and the surface pulls the skin the opposite way. The resu lt is a weakening or tearing of the skin and capillaries. Not only docs shearing magnify the effects of pressure and cause sk in damage, but it also makes it even more difficult to keep dressings on ulcers in place. To address shear. the sca t cushion cither mllst eliminatc one of the two opposing forces at work on th e skin (ie. the force coming from th e surface onto the prcssurcsensitive prominences) or must provide inherent movemcnt with significant amplitude in individual cells that can shift with th e body and dccrease drag on th e skin. fiell' a ll d A-'Ioisfll re. On cushions that depcnd on immersion to equalize pressure, sweat and heat are contained around the ischia Is. This buildup causes macerati on of the skin. which pUIS the sk in at even more ri sk of breaking down. In addition, sweat and heat loosen th e adherents that keep dressings in place. Cotton or air-exchange covers help. but cannot combat total contact around th e ischium. A cllshion shou ld provi de ventilation of th e ischial area. Posfll ru l Contro l a mI S/llbilily. No product will help the patient fully ifit docs not address sitting stability and comfOri. The patient must be supported in as close to an upright and aligned posture as poss ibl e. This will keep pressures 011 bony surfaces that can tolerate it (femurs) and off surfaces Ihat cannot (ischials. coccyx, sacrum. spinous processcs). As has been stared throughout thi s chapter. it also makes the person as fun ctional as possible and helps prevent further complications sllch as contractures and internal organ compression. It is commonly held that the pelvis is the cornerstone of positioning; stabili zing the pelvis is the foundation for stabilizing th e entire body. However, the bases of thi s cornerstone, the ischial s. are also the most vulnerable areas for skin breakdown and the pivot points for pelvic rotation . Most cushions. in equalizing pressure across the sitting surface, maintain pressure on the ischia Is and address pelvic stability by padding all around th e ischia ls.An alternative way to keep the pel vis in place is to stop the fulcrum action of the ischials by eliminating pressure on them. TIte pelvis can be stabilized
Mallagemellt of Pressure h)' Thempelllic Positiuuiug
by stab iliza tion of the femurs. because they are intimately connected to the pelvis and prov ide a larger surface area for the cushion to contro l. The cushi onl11ust match the posterior surface oflhe fe mu rs with fi rm, nat support , especially the prox imal fe mur closest to the pelvis. Stabilizi ng here contro ls rotation of the enti re fe mur. and holds lhe pelvis on the back of the seat. Movement oflh e ischials and pelvis is contained wi thin the elimination area (Figure 13- 5). Cushions can be di vided into gro ups accord ing to their features and abilit ies to meet va ri ous levels of pati ent need fo r both positioning and for skin breakdown risk or treatment. Here. cushio ns have been di vided into fo ur groups: sim ple pressure redu ction, ge nerica ll y contoured, selecti ve pressure elimination, and full y customi zed contourin g. Si mple pressure-reduction cLishions decrease pressure on the ischials and coccyx (compared with no cushion at all ) and attempt to equalize Ihal pressure across the entire sitting surface. They usuall y do lill ie to address shearin g forces, and may address heat/moisture via cover materials only. These cllshions arc for th ose aI low risk for sk in breakdown. Use rs may spend ve ry little time sitling because they are partiall y ambul atory or may have sensation and the ab ilit y to shin weight, and have adequate nutrition and skin integrit y. There are many cushions in many price leve ls that satisfy these basic requi re ments. Most of these cushio ns arc in the lowe r price levels under S I00. Some are pri ced ve ry high, but sti ll give onIy basic protection.The cl inician Illust assess the pressure-rel iev ing capabilities of the cushion without regard to price, and balance the capabilities of the product with the cost and the ac uity of the patient 's needs. Ge nericall y contoured cushions are shaped with a depression area under the isc hial s to assist wi th pelvic placement, and tro ughing under the femurs to assist in neutra l alignment or optimal lower ex tremity posit ioning. These cushio ns are more sophi sticated than the simple cushions because they have some means of act ively molding to the body to equa lize pressure across the ischials and the femurs (air cells. gel or viscous fluid s. viscoe lastic foam. etc.) while offering contouring for body support. These products are for th ose who are at moderate risk for sk in breakdown andlor for those who req uire more assis tance with posi ti onin g th an a noncontoured cushion can provide. Understand that the generic conto ur base is shaped to a musc led bottom, not to the atrophied bOlloms of the silling dependent , and so oft en do not hold the pelvis as securely as cushions more specificall y contoured to fit individual bone structure. Many manufactu rers have added the fi ex ibility of prov iding optional components such as abductors, adductors, or hip guides that can customi ze the cushion to furth er control lower extremity posit ioning. The third category, selecti ve pressure elimination. is identifi ed by an area that eliminates pressure on the ischials via a
285
pocket that is sized to the user's ischi al span- the measurement from the center point of one ischium to the center poi nt of the other. It also olTers nat Sll ppOrt tO the flllliength and width of the posteri or femurs. thereby support ing the body on the fe murs, 110t in the elimination area. This not only protects the skin over the ischials, but also pro tects the femu rs by pressure di stribution. Although app ropriate for the l110denlle-risk patient as well. these products are oft en lIsed for the highest-needs patients, who may be characterized by some of tile fo llowing: sitting dependent. minimall y ambu latory if at all , insensate. may have limited abil ities to reposition themselves to relieve press ure. have existing or recurrent breakdown on the bony pro minences of th e sitlin g surfaces (ischials, sacrum , or coccyx). are in the granulat ion or remodeling phases of wound hea ling, or have a history of skin breakdown on those sitting surfaces. Se lective pressure elimination at the ischial s, shearin g elimination, and max imum ve ntilation puts the skin over the ischia ls in the health iest poss ibl e environment. Th ese requ ireme nt s mirror and foll ow basic medi cal prot oco l fo r press ure ul ce r treatment. S.IM 22 The benefits of this cllshion design have been well documentcd.8.,4.'7 . B !9 Th is time-tested, fitt ed cushion des ign should never be conrused with the donut design, whic h is spec ifically recommended aga inst by the Age ncy for Ilcalth Care Policy and Research (A HCPR ) guide lines. Unlike a true selecti ve presure eliminati on cllshion, whic h involves a full seating surface with a small relie f area fitted to the user's bone structu re. a donu t cushion is simpl y a closed ring of material that cuts off circ ulat io n by ind uci ng the to urn iqLlet effect. In add ition, the rin g forces wieght bearin g on the area around the ischia Is. rather than on the fe murs, the anatomicall y load-tolerant areas. For these reasons, the do nut cushion should never be used, es pec iall y by persons at high risk for. or with ex isting. breakd own. As with any sitting-dependent person, especially th ose with skin breakdown. maintenance of the proper seated pos ition is essential in order to enhance fun ction and endurance and to protect the skin under other areas of the silt ing surface from breaking down . The pressure el iminat ion cushion positi ons th e pe lvis in two ways. First, th e isc hi a ls a re unweighted and cannot act as pi vot poi nts fo r pelvic rotation . Second the body is cont ro lled by full y supporting the femurs (both length and width ) in a nonrotated position. and such that they are even with each other in the hori zo ntal plane. Thi s keeps the pel vis and the trun k level (ra ther than obliquely inclined), keeps the pelvis towa rd the back of the seal, and prevents the pelvis fro m falling into the cutout area. Third, the walls of the elimination area confine movement of the pelvis to a defin ed area and keep the ischials fro m sliding fo rward with 3n effective pre-ischial block. As with any cushion. the lOp of the bac k of the pelvis must also be supported with a bac k support so that it cannot roek baek-
286
WOUNI) CARl
wa rd. The back support also fi lls in the lumbar curve for
maintenance, easy to usc co rrect ly. cosmesis. durability. and
morc suppo rt ed and comfortable sitting. The fourth ca tego ry. fully custom ized co nto urin g. refe rs to o nc-of-a-kind c ushi o ns fa shi o ned spec ifica lly for the in-
sli p resista nce. The algorithm in Figure 13-4 may help th e cl inician ca t-
dividual client. These arc usually prescribed for users with severe structural deformities that cannot be accommodated for by off-the-shelf products, or for those wi th excessive trunk and lower extremily tone that pu ll s them uct s.
Ollt
of oth er prod-
Other featu res to consider when eva luating cushions include urine-proof surface, stabili ty of the sitt ing surface, clcanubility, IVcight for portabili ty, leakproof surface. 10lV
egorize seal cushion choices. A pictorial comparison or cushions that equali ze press ure ve rsus Ihose that elim inate ischia l pressure is shown in Figure 13- 5. Back Supports
A seat cush ion is a key part, but on ly a part, or the sealing system. To support a body adequately, the proper back support mllst also be prescribed. Most wheelchairs have a malerial back that allows the chair to raid . Unrortunately, this
Existing skin breakdown on ischium/sacrum/coccyx? Moderate/high risk for breakdown? History of breakdown? Pelvic irradiation pre-1980?
Yes Low risk for pressure ulcer on sacrum/ischium/coccyx?
Pressure elimination
Yes Simple pressurereduction protection
Maintains moderate risk for breakdown sitting position without extra support?
~I
Yes
What prevents optimal sitting position ?
Generic contour to facilitate optimal position
Structural deformities
Pain
CNS disorder (eg, CVA, CH t, CPo etc.)
See Tables for suggestions
1. Determine source 2. Trial products and therapies 3. Medications or pain management techniques 4. Alternate sitting time with rest time
See Tables for suggestions
Excessive trunk or hip extensor tone
Devices that stabilize pelvis , increase hip flexion to break up tone (Consider antithrust seat assembly, firm back support, 90" hip belt.)
Hypotonic
Maximal pelvic pOSitioning and UE and LE support; may need customizing.
Figure 13-4 Algorithm: determining si lling surrace . The surrace must work with the mobility base to achieve op timal sitting height. CNS
= Central nervous system: e ll I "" closed head injury; CP = cerebral palsy: UE = upper ex tremity; LE = lower ex tremity. Source: Copyright l ')
Lauric Rapp!.
Management of Pressure by Therapeutic Positioning
287
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Figure 13- 5 Pressure cquali7ing versus pressure eliminating. A, Side view of pressure cqualil.ing cushion: loads the ischium which allows
pelvic lilL B. Side view of pressure eliminating cushion. Note pre-ischial bar limiting forward ischial movement. C. eliminating cushion.
RC;'lr
view of pressure
ote press ure distribution across full width of femur to support the load of the body. Courtesy of Span-America
Medical Systems. Greenville. Soulh Carolina.
material bows in the opposite direction that the back requires. Therefore, almost every patient sitting in a standard folding wheelchair will require some accessory back support as a means of accommoda ting the lumbar and thoracic curves.
The complexilYand expense oflhe back support depends on the needs of the clicnt and the number of roles the back suppOrtmuSI fill. The algorilhm shown in Figure 13- 6 may help
and Ihe back 10 be supporled al Ihe appropriale degree of recline to facilitate safe swallowing, maximum mobility, and maximum function for the patient. Those patients who have little inherent trunk support abiliti es will benefit from back supports thai have the nexibility of lateral supports to help maintain the trunk in an uprighl
posilion. Back supports can also be fully cuslomized 10 fil
the clinician categorize equipment when choosing a back support for a paticnt.
the unique contours of an individual. These would be indicated for the patienl with fixed trunk deformities or severe
Skin breakdown on Ihe sacrum will be one deciding fac-
Irunk weakness. Flexible Ihoracic or lumbar kyphosis or scoliosis can be handled by correcling Ihe posilion of Ihe pelvis and possibly using lateral supports on Ihe Irunk.
tor in selecting a back support. kin breakdown will requ ire that the back support remove pressure from and ventilate the area. Postural support in an upright sitting position may requirc support on natural spinal curves, accommoda tion for fixed deformities, or correction of flexible deformities. None of these needs can be overlooked when positioning a patient with sacral skin breakdown in sitting. Look for a commer-
Accessories
cially avai lable device Ihal is designed 10 meel all of Ihese goals for Ihe palient.
ing.
The patient who can maintain th e upright ideal position with little or no assistance may require only minimal back support, perhaps a firm contoured back that can be slid into
Ihe chair wilh allachment 10 Ihe upholstery. If the lumbar spine is flattened and hip range of motion is compromised so that it is less than 90°, a chair fixed at a 90° seat/back angle is inappropriatc. This combination ofphysi-
cal faclors. often found in Ihe older adull populalion, can be accommodated by a reclining backrest with adjustments to
Ihe degree of recline. This allows Ihe palienllo be posilioned wilh Ihe hips all oflhe way back on Ihe seal for full sup porI,
The seal, back , and mobililY base are Ihe Ihree key elements in a seating system. Many patients require the ex-
Ira assislance of accessory producls Ihal include Ihe follow-
lIeatl Supports. Head supports come in a varie ty ofmod-
cis, depending on Ihe amOUI\I ofsuppon needed and Ihe abi lily of Ihe backrest 10 support Ihe headresl. Models include flat (attach to the seat back uprights of manually reclining chairs), molded around the neck and occipital regions. ad-
justable in heighl and angle, and fixed. Seat Cushion, Seat cushions have already been discussed, When cushions are placed on sagged seat upholstery. 111any of the positioning effects are negated. The scat support can
be slifTened by adding a solid scat or board 10 Ihe chair or
Sacral or coccyx pressure ulcer or at nsk of sacral breakdown?
Yes
Pressure elimination
Full range of motion and posture maintenance abilities?
Yes Firm contoured back Insert
Flat lumbar spine and decreased hip range of motion?
Yes
Reclming back
No Trunk muscle weakness?
Yes
Reclining back with lateral trunk support
I
No Extensor tone?
No
Yes
Firm back angled properly with seat
Fixed thoracic or lumbar kyphosIs or scoliosis?
Yes
Customized support
Flexible thoracic or lumbar kyphosis or scoliosis?
Yes
Correct with pelvic and trunk stabilizers
Figure 13-6 AlgOrithm: determmmg back SUppOrl needs. Copyright
adding a drop scat that drops the seat pan beneath the level of the scat rails and lowe rs th e patient c loser to the floor. Co nsider adding a cutout scatboard under the seat cushion both to eliminate the slin g of the upholstery and to distribute
interface pressure away from the ischial tuberosities. Be aware that when a solid scat is added. this may increase the interface pressure over the ischial tuberosities if the cushion is inadequate III pressure distribution over time: in other words. if the cushion bottoms out. the ischial tuberosities will be pres~ing into a solid unforgi\ing surface that could then contribute to the formation ofa pressure ulcer.
(.~
Laurie Rappl.
Armre.\/.\', Armrests generally come in two styles: tubular w ith padding or standard with flat mctal skirt guards. Either can be attached to the chair in a fixcd position or can swing away or be removed for ease of transfers. Standard armrests come in full length. shortened dcsk Icngth (allows the chair to be pulled up closer to a table or desk). and height adjustable to accommodate the needs of a \\ ide range ofpalIent heights. Foo/reM.\, Footrests arc critical piecc~ in the seating system . As a general rule. the footrests arc adjusted so that the
MOllogemelll of Press lire hy Tlterapelllic Positioning
knee is eve n with th e hip. Most footrests are adjustabl e in height. and some allow adjustment in the sagittal plane to chan ge the ang le of the ankle. The pedal or platform of the footrest ean be orde red in various sizes to support as much of the foot as possible. Elevating heig ht footrests. although thought usefu l for edema. o llen act to pull th e body out of position and extend the turning radius of the chair. thu s limit ing mobility. The e leva ti on has little effect on edema. as the extrem ity must be positioned above th e level of the hea rt for passive cdcma con trol.
H{/ck "'''eels. The back wheels o f whee lchai rs arc usua lly 24 or 26 inches in diameter a nd come in a va ri ety of wid ths. The major choice to make is whether to order soli d or inflated tires, and treaded or nontreaded tires. For eve ryday, ge nera l use. Illost people usc an inflawble tire with moderate tread. There arc now solid tires made with treads for th ose who do not wa nt to deal wi th the possibili ty o f tl at tires. For mainly indoor usc. co nsider a minimal tread. Ilint : The height of the sca t from th e fl oo r a criti cal factor in the pati ent's mobil ity--can be affec ted by cha nging th e di ameter of the back wheel. Fro,,' JYI, eel.\·. The front wheels of the wheelc hair (casters) come in almost as many varieties as the back wheelssolid or intlatable, a nd variolls widths and diameters. The sta ndard caster is 8 inches in diame te r. solid rubber, and minimally treaded ifat all. Sport-type chai rs are o llen seen with caste rs as small as ro ller blade wheels for increa sed turning abilities. Outdoor chairs have more substa ntial casters with larger diameters and wid ths, and often treads.
Allcillary De_';ces. Ancillary devices incl ud e the fo llowIIlg: • Lap belts- usuall y placed at a 45° angle to the seat! back angle, but ofte n more effec tive when secured to the scat siderail a few inches in front of th e seat/back junction and crossi ng the proximal femur at a 90 0 ang le just below the trun k/leg crease. • La p trays full or pa rtial. clear or so lid, padded or !lonpadd ed, ass ist with upper ex tre mity support. These should not be used as a restraint. but as an ass ist to daily li ving sk ills, including communi cati on, for support to a Oaccid arm or to he lp provide a point of stability for hypertonic ex tremities. Lap trays ca n also provide trunk support for those who may fatigue ove r time. • Antitippers- small wheels that auach to the back of the wheelc hair to keep it from tipping ove r backward, usua ll y used as a safety factor. In everyday life, tipping backward is a necessary abilit y 10 lift the front of the wheelcha ir over small bumps and curbs, and antitippers may limit mob ility whil e provi din g safety for the patient.
289
• Amput ee adapters allow the rear wheels to be moved posterior to the scat back upright to keep the user safe from tipping ove r backward. • Residual lim b support- holds th e residual limb of th e be low-the-k nee amputee. • Chest st raps- provide anterior support for th e c hest and upper trunk . 'Vork;IIK w;t" Suppliers
The suppli er is an important resource on the wo und ca re tea m. A good supplier will help th e clinician mat ch equipment to indi vidual needs. The suppli er also should hel p the clinician keep abreast of new tec hnology and new items on the market. Do not work wi th a su pplie r who limits access to equipment by offering onl y one or two lines of chairs and sea tin g eq uipm eili. Look for suppli crs who carry multiplc lines a nd arc proact ive in ass isting with thi s critical part o f patient ca re equipment select ion. Ultimate accountability for th e decision making resides with the clini cian working with th e patient.
Self-Cure Treatment Guidelilles The patien t and hi s or her caregivers must be taught as much as possible about the eq uipm ent that has been presc ribed including why eac h piece was chosen, how to usc it properly. where it was orde red from for warranty repair. and ho w to ca re for it. The pat ie nt may ne ed to follow a wea nin g-on sched ul e because new eq uipm cnt may sit th c patient differently o r put loads o n th e sk in in patterns different from those of the old equipment. A sa mpl e of a weaning-on sc hedul e is as follows: Day I:
I hour in mornin g and afte rnoon; assess skin response after each session. Day 2: 1.5 hours in morning and afternoon: assess skin response a ft e r eac h session. Day 3: 2.0 hours in morning and afternoon; assess skin respo nse afte r each session. Increase the s itting time grad uall y until a full day ofsi lling is achieved. Posit ion in g in th e sea led posit ion requires co nstant learn ing. creati vity, a nd patience. It is up to the res ponsible clinician to begin and co ntinue the lea rning process by evaluating ne w tec hn ology as it is develo ped, dete rm inin g th e client needs, assessing the features of new products. and mat chin g needs with features to benefit clients optimally. Since seati ng is a dynamic process. a rea ssess me nt date shou ld be se t so that the therapi st ca n monitor the fit and functioning of the eq uipme nt and modify it to match the patient's needs.
290
WOllM)
C ,.,
RATIONALE FOR I TERVE:'>TlO'\ 1'1 TilE RECUI\IBENT POSITlO'l The average person spends abollt one third of life in bed. The client who cannot maintain standing or sitting for norma) hours spends increasing amounts oftimc recumbent. Just as with sitting. chooslIlg the proper support surface and cor-
rectly positioning the person on the surface are necessary parts of humane treatment. The human body requires support for proper alignment in the recllmbent positions. Technically. any person who depends on the recumbent position for any part orthe day or night should be e"aluated to ensure that the optimal positions arc being attained. The morc time spent in bed the morc need there is for positioning intervention. Certainly the person who has a musculoskeletal or neurologic insult Ihal limits se lf-mobility. limits sensation to detect the need fllr po~ition change. and 'or makes the bony prominences more prominent and therefore at higher risk of breakdown is an uncontested candidate for therapeutic positioning. \11 '-I Bcd rest puts many bony promll1ences of the body al risk of skin breakdm'>'n OCCIPUt. shoulders. elbows. Irochantcrs. sacrum. heels. and malleoli hence the proliferation of "support surfaces" to protect the body in this relatively dangerous but needed em ironment. Statistics show that the S"lcnll11 and Ihe heels arc the 1110stlikely areas to break down. with references reportlllg IIlcidence rates of up to 48 0 0 and 14 0 0. 1 respecti\-cly. Bcd rest causes slowed circulation throughout the body and reduces the functioning of the respiration and elimination systems as well. Proper utili/arion of sup POri surfaces. both through proper chOice and correct and cOl1sbtellt posilIoning on the surface. C,111 minimi/e contractures. mininlize the effecls ofpml1I1i,"e reflexes relcased during central nervous system insult. affect the integrity of the skin. provide restful sleep, and maXH11I/e a person's Indepcndence in sci r-mobil ity. Mattresses either cquHli/c pressure by maXllllum distribution of pressure or Hltcrnately remove it from areas at cvcn intervals" The c1inicinn chooses the appropriate surface. determines the therapeutic positions for the patient. chooses the equipment to alll1ln those positions. and instructs caregivers on usc of the .;qulpment. Effects of Lying Donn on Pressure Ulcer Formation
No maLter how conformll1g the surface of the bed, when Ihe many contours or,he body arc placed on a rel,,"vely nal bed bony prominences me likely to endure high pressures and end up with skin breakdo\\ n. Thcse prominences the occiput. shoulder. elbow. laleral trochanter. sacrum 'coccyx. ribular head. malleoli. a"d heels must be prolecled when
they arc on the ,\eight-bearlng surface of th.,; client. Supporting body parts so that the major Jomh arc in positions of least strcss and highest relaxation wi II decrease muscle stimulation, and therefore reduce spasticity and the formatIOn of joint contracturcs.As with seatlllg. the goal 111 positIOning In the recumbent positions IS to help maintHin a position that is as close to ideal for tissue load management and muscle relaxation as IS possible for the indi\-idual client. In supinc. the head and neck should be centered and the cen ical and lumbar curves supported. The trunk should be aligncd and ~traight. Anatomically. the resting ro~ition for the hips and knccs is not fully ext.;nded or straight. but bent or flexed 25 to 30' .~' Maintaining this slight flexion can put increased pressure on th.,; sacrum and the heels. Therefore. thcse prominences IllUSt be watched carefully and pro,ided with extra protcction if the surface itself i... not adequate. This protection may take the rorm ofhftlllg one SIde orthe pclvis so that thc sacrum is not directly weight bl.!aring. The hecls may be protected by placing a pilhm under the calves, or by using heel protection dentes on thl.! feet to ul1wcIght the heels (Figures 13 7 A and 13 713). The a"kles should be maintained close to 90 en right angk)
A'/lIl1l1gemel1l of Pressure hy Therapeutic Positioning
S, .... ·i\I ().
291
· ',',. ,.:,".... ,.
E-,:;::''::;:-:1:'" Figure 13- 7 A. Limb eleva tor. Courtesy of Span-America Medical Systems. Greenville. SOUlh Carolina.
Figure 13- 7 B. Footdrop stop . Co urt esy Medical Systems. Green\ ille. Soulh Caro lina.
or S pall - Arneric
Figure 13- 8 30° Wedge of body alignment in side lying.
comfortably so that it docs not fall forward across the body, or fall backward, pulling the trunk into a twisted position . The prone position requires full range of motion of the cervical , thoracic. and lumbar spine. and is not well tolerated by most patients. This position requires full extension at the hip and knee, and full external rotation of the shoulders. The trunk should be centrally aligned with the head turned to the side. The hips should be in neutral rotation and slight abduction. and the ankles plantarflexed. The bony prominences at risk are the cars, patellas. and the dorsum of the feet. Not only does the prone position put the shoulder into its most stressful position of full external rotation with abduction, bUi it can also encourage foot drop due to the ank le position. Exami nation and Evaluation As with seating. the clinician mllst have an understanding of what the optimal or ideal positions are. During the examination. the clinician determines what preven ts the patient
from attaining ideal. rccogni Lcs what may be improved with therapy or other interve ntions. and accOlnmodates for those factors that cannot be improved upon . NeurOmU!!ClIllir System Reflex Illtegrity Examill{J(ioll . Nonintegrated. primitive reflexes, re leased after neurologic insult, greatly afTect recumben t mobility and posi tioning. A dominant ATNR wi ll make maintaining a sidclying position very difTicult. The strengthening of the face side will cause the client to rotate backward and extend the uppermost leg and arm. The trunk and uppermost side will need to be firmly supported in flex ion in order to overcome the extension tendencies.A pproaching the client so that he or she does not have to turn the face over the uppermost shoulder will also help combat this extension tendency. A dominant tonic labyrinthine reflex (TLR) will cause activation of flexion in prone nnd extension in supine. The prone position will cause breathing difTiculties, and would be contraindicated without extreme caution to head
292
W OUND CARl
tlnd neck position . In supine. the TLR and extension tone in ge nera l may increase the risk of breakdown on the occiput and Ihe heel s. and should be broken up with head/cervical support. and fl ex ion of the hips and lower extremities. In sidc lying. the TLR causes extension on the weight-bearing side and flexion in the uppermost side: therefore. this is the prererred position ror the elient domina ted by theTLR. Break up reflex postures as much as possible with support devices desig ned ror controlling the body position. Usually. pillolVs afC not stnblc enough to do this; an investment may have to
be made in roam positioning aids specirically designed ror certain positions and body parts. These may, on first glance. appear morc expensive than pillows. but their effectiveness wi ll outweigh cost (see Figures 13 7 and 13 8). Sensory EXllIllilllltio ll . Neurologic insults often ca use a lack of sensation in some part orthe body_ Those areas with loss of sensat ion are obviously at the highest risk or breakdown and will require the greatest care in positioning, support. and protection. Assess ror the ability to detect both light and deep pressure and pain throughout the body. especially over the bony promincnces. Those patients having a complete scnsory. proprioceptive, and visual loss on one side of the body need attention to protect the involved limbs and to pos ition for maximum environmental interacti on. For example. position the individual so that he or she c,m visuali ze the entrance to the room with eHse. Thi s si mple act will eliminate mllch fear and agita tion. Caregivers should be instructed to approach from the nonil1\'olved side first. and then move to the invoh-ed side as the patient learns to visua lly track to and beyond midline.
J\1I1!tJ'culo.'ikeJetaJ System A1nfor Funclion and Ergonomics EX(fmiIlClliol/, Assess for level of skill or assistance required to acco mplish rolling right or left from supine, moving from sit to supine, supi ne to sit. sit to stand (ex it from bed), stand to si t (enter into bed), move body toward head or bed, move body toward root or bed shili body side to side. Firmer. stable sllrraces that do not move under thc patient make bcd mobilit y much easier to aecomplish ror all patients. Assess ror the ability 10 perrorln transfe rs independently. dependent ly. or assisted in many combinations: bed to chair, chair to bed commode to bed bed to commode. sit to stand . The choice of support surface must directly and positive ly affect functional mobilit y to be considered a patient benefit and for eligibility for rcimbursement ofserviccs and supp lies. For the patient with sk in breakdown. functionall11obility occasionally may be compromised ill favor ofa less stab le surface for improved tissue load management. Once the pressure ulcer is closcd, a morc stable support surface can bc evaluated for both the fUllctionalmo-
bi lity of the patient on the surface and its efficiency in managing tissue loads.
Acti vities of Daily L;"illC ExalllilllltioIJ . All ADLs done in bed such as eating, bat hing, and dressing. shou ld be taken into account when determining the support surface and the recommended positions. Eating. especia lly. requires correct head elevation and cervica l support for safe swa llowing. The speech therapist should be eonsulted to determine the best head and neck positions for swallowing. This position may include aligning the ear over the acromioc lavicular joint and the face in a vertical plane wi th the chest. Occupational therapy may be indicated to determinc the upper extremity adaptations that can be utili zed by the individual. Note that there arc serious skin concerns ill elevating the head of the bed for extcnded periods of time without protecting the sacrum or the heels. Thi s posi tion should not be used as a substitute for sitting in a chair properly positioned. Rauge of A'lotioll Examiuation. Note any surgeries that limit mobility, or that limit placing the client in the ideal posture in a given position .These wou ld include orthopaedic surgeries that immobilize part of the body and therefore limit overall mobility. ote limitations in range of motion in the cervical. thoracic. and lumbar spines. hip extension. hip rotation, knee extension, ankle rotation. and plantar/dorsiflexion . Whether limitations arc fi xed or flexible. the limitations must be firmly supported as close to anatomically correct as poss ible to minimize progression of deformities, It is most important to note where limitations affect positioning. For example. a progression in spinal kyphosis wi ll make the supine position dangerous to the ski n over thoracic spinous processes and the sacrum/coccyx. One possible solution to thi s problcm is to elevate the head of the bed just enough to accomlnodate ror the kyphosis and to support the head and neck with or without the use of pillows. Gravity can then assist in at least maintaining the current degree of kyphosis without facilitating increased kyphosis. Consider managing tissllc loads over the bony prominences with the effecti ve use of support surfaces. Another example of accolllmodation 10 limi tations in range of motion dea ls with hip extension. Limitations in hip extension will necess itate support under the full lower extremity in supine to maintain the degree of hip extension allowed. This can be most easi ly accomplished wi th foam devices designed to position the leg (Figure 13 7A). Jntegumenttu:)1System Exalllillllti()l1 Pay special attention to surgeries and resulting incision or rcpair sitcs involving skin breakdown . Any area that has previollsly broken down or areas that havc sca r tissue are risk areas that require protection in the recumbent posit ions, All
J\4allagemellt of Pressure by Therapeutic Positioning
disciplines should note condit ion of the sk in on weight-bearing surfaces- turgor. elasticity, hyd ratio n. edema) and th innesslbrittleness. Note any sites wit h a past hi story of breakdown. Sites wi th curren t brcakdown are obvious areas of primary concern in choosi ng surfaces and usi ng thera peut ic positioning. Where moist wound hea ling is be ing employed the potent ial for low-air-Ioss or air-fluid ized beds to dry out the wo und should be cons idered. The patient shou ld be positioncd so that there is no weight beari ng on areas of brokcn skin or on areas of scar tissue that are most vul nera bl e. If feca l or urinary incontinence is present. it is nccessary to clca nsc thc sk in with an appropriate acid-based (4.5 to 5.5 pH scale) ski n cleanser, hydra ted and to protect the sk in with a sea lant. Be awa re that every laye r of incont inent liner that is lIsed incrcases the interface pressure over that part orthe body and inhi bits the effect ivcncss of thc support surface both in bed and ill the chair. Interface pressure measurements taken wit h ei ther a singlecell moni tor or a bed-sized computeri zed model may be hel pfu l in determi ni ng areas at risk, and effecti ve ness of the chosen dev iccs or positions. The proccd urc for performing interface pressure measure mcnts is outlined in the seat ing section of this chapter. Record measurements at the bony pro minences on the wcig ht-bearing surfaees with body positioncrs in place in all of the positio ns that the patie nt will utili ze. In sidelying. th is includes the car, shoulder. ili ae crest. rib cage, trochanter, fibu lar head. la teral malleolus. fi ft h metatarsal. and firs t metatarsa l of the up permost fool. In supinc. these include the occiput , scapulae, spinous processes. posteri or il iac crest. ri b cage, sacru m, coccyx. isch ial tuberosi ties. and postcri or hee ls. Assess pressures wit h the head both elevalcd and flat. Cartiioflill mOIJ aryl Gmitroi" l esti IIlll S)'Sl emS
Involvcme nt of the card iopulmonary or gastroi ntestinal systems may require frequent posit ion changes or may require elevation of the head of the bed. No te the reasons why the head of the bcd must be elevated to what degree. and for how long each day. Ti me in thi s pos it io n should be minimized; peo ple tend to sl ide toward the foo t of the bed when the head of the bed is elevated. Thi s causes shearing forccs on the skin, especially over the sacrum and the coceyx. Whenever the patie nt is in this posi tion. linc up the hi p with the ga tch angle of the bcd to minim ize slidi ng of the patient towa rd the foot of the bed. If this pos it ion is necessary for more than a half hour at a time. place a pillow or f08m support under one fe mu r. hip. and shou lder to till the pat ient slig ht ly off the sacrum. Altern ate the supported side at freque nt and even time segments. Prov ide support under thc plantar surface or the fce t so that slipping down is minimized.
293
Assess for respi ra tory move ments, leve l ofbrcat hing. and any oral secretions coming from the lu ngs. Take vital signs in the full y recumbent posi ti on and in the head-e levated position. Review the medical history for gas tri c rcn ux associated with hiatal hern ias that requ ire elevating the head of the bcd. A patient taking oxygen pro bab ly cannot lie fl at; extra ca re with positioning must be ta ken with these patients beca use of breath ing difficult ies and to ensure transport of oxygen to tisslles. C hoosing [(Iuipmcnt Many factors go into choosing bed support surfaces. Each of the categories detai ling va ri ous surfaces of the skin have positive and negat ive feat ures fo r mai ntaining position and max imizi ng mobility. OllerlllY.~. Whether powered altcrn ating surfaces. or contourcd foam. all overlays raise the leve l of the bed surface. Sitting to standing is easier and sa fer to accomplish when the height of the surface of the bed is eq ual to the distance fro m popliteal fossa to the bottom of the foot. OverJ ays tend to raise thi s level, making ingress and egress more dangerOli S. However. overlays are inex pensive, and foa m overlays with contoured, cross-cut cell s (eg, Geo- Matt ' ) are extremely elTective pressure dist.ributors. If the level of the height of the bed can be changed, or if ingress or egress is not an issue, an overl ay may be a cost-effective and appropriate choice.
ft111ttress Repillcemellts. Most cl inicians prefer a mattress replacc ment with a stable bolster edge for patient safcty when silt ing on the cdge of the bed. A trapeze SC I - UP will help the patient lift his or her body to move rather than sliding across the surface. Th is helps to li mit shearing fo rces. Stlltic M llttress Replllcemellls. These come in a varicty of mediums: all foa m. foam/air, foam/wa ter. and foa m/ge l. These surfaces replace standard matt resses and offer bettcr distribu tion of pressures than the standard mattress. They eliminate the extra height that an overlay entail s and arc often purchased as permancnt equ ipment fo r the patient, ra ther than a rental item. However. they are more expensive than an overl ay. Static surfaces gencrally offer a morc stable surface to accompl ish bed mobility and ingress or egress than alternating pressure or low-air-Ioss mattrcsses. Powe"ed Dy,uuIlic ft.tJllttress Repillcemellts. These cntail some means of moving ai r th ro ugh the ma ttress to noat the
body. as in a low-air-loss mattress, or movi ng air th ro ugh chambers in the mattress to alternately put pressure on and take pressure ofT of each area of the body at regul ar interva ls. The air movement is acco mplished by electricall y powered motors. Although some clinicians fee l that these sur-
faces are sa fer for the skin than stati c mattresses due lO the constant changes in pressure on anyone body part. the movement in the surface makes maintaining or changing a posilion more of a challenge th an on a slati c surface. Surfaces that alternate under the patient may make transfers more dangerous as the bed surface is constantly shifting beneath the patient.
NOllpowet ed D)'lIillll il: A,r autess Replacemellf!i . A new breed of maLLress (eg. PresslIreGlIard ' eFT) ofTers the stabilit y of the stati c mattress rep lacement for maintaining or changing position . along wi th th e skin protection of a dynamic mattress. Dynamic air movement for self-adj ustm ent to bony prominences is accomplished by elasticized reservoi rs that accept air from and rel ease air into the support lUbes.
and prot ection of bony prominences. Pillows are an inexpensive support . but only minimally effective. They are puffy rec13ngles that do not naturally conform to body contours, have a tenden cy to slide on the surface when body pressure is applied, and arc oft en not readi ly ava ilable for positioni ng if th ey have been confiscated for other purpo ses. Foam posi ti oners arc available that arc shaped for supporting specif ic body contours, wi ll not shift on the surface when pressure is applied, and will be less likely to be confisca ted for other purposes. These devices arc often inexpen sive to purchase and more than pay for th emselves in th e qual it y of alignment, positioning. and protection th ey afford the patient. Table 13- 3 describes the use and expected outcomes for commonly used and available positioning supplies.
A ir Fillitli:.ed. A lthough felt to be the best surfaces for equalizing pressures acrosS th e whole body. air-fluidized surfaces are ex tremely difficult to maintain therapeut ic positi ons on. and independent ingress or egress is nearl y impossible; maximal assist is usually required. Positionin g Supplies
All patients will require th e usc of posit ioning devices to help maintain therapeutic and anatomica l body alignment.
Clinical Wisdom: Photographs The use of photographs of the patient in position with the devices. displayed in a place easily seen by caregivers. is the most helpful way to describe positions and use of devices to all caregivers so that devices are used consistently and appropriately.
Table 13-3 Positioning Supplies Device
Abduction pillow
30· Incline wedge (See Figure 13-8)
Cradle Boot or Heel Protector
Function
Ac tion/Outcome
Maintains lower extremities in slight abduction, neutral rotation , and knee extension.
Supine-maintains lower extremities in neutral positions.
Sidelying-maintains separation of LEs to protect medial knee and malleolus of upper leg.
Supports trunk and pel vis in 30· sidelying position.
Sidelying-protects lower greater
Keeps heel elevated off surface while
Supine-Protects heel from breakdown by suspending off surface. Should also protect malleoli. fifth metatarsal heads, and Achilles tendon. Sidelying-suspends lower malleoli and fifth metarsal head.
maintaining right angle or neutral ankle dorsiflexion .
trochanter by maintaining 30° incline position.
continues
i\lol1agemelll of Pressure hy TIlerapelllic Pos itioning
295
Table 13-3 continued Device
Function
Limb elevator (See Figure 13-7A)
Action/Outcome
Uses wedge with leg trough to put lower extremity in slight hip/ knee
Supine-maintains neutral hip position
with slight hip/ knee flexion and
flexion with ankle elevated above
foot elevation.
Sidelying-is used with trough side down to cup the lower leg and maintain leg separation for skin protection.
knee.
Flexion/abduction pillOW
Maintains slight knee flexion with separation of medial knee surfaces.
Supine-maintains hip/ knee flexion while breaking up adduction tone.
Cervical pillow
Is shaped to support cervical curve while cradling occiput.
Maintains cervical curve in supine or sidelying.
Occipital pillOW, head-neck cushion, Occi-Dish
Cradles posterior surface of skull to reduce or eliminate pressure on occiput.
Supine-protects occiput by pressure removal, supports cervical curve,
inhibits tonic lab reflex. Sidelying-protects lower ear and supports cervical curve.
Source: Copyright C Laurie Aappl.
Case Study: Therapeutic Positioning for Pressure Ulcer Healing History The patient is a longtime resident in a nursing facility.
Past medical history includes surgical removal of a benign brain tumor 10 years prior to therapy intervention .
She has paralysis of the lower extremities and significant cognitive deficits (see Figures 13-9A and 13-98). Reasons for Referral
Musculoskeletal Motor Exam . Trunk strength is poor, upper extremity strength is fair. The patient has no volitional movement in lower extremities.
Joint Mobility Exam . All jOint ranges of motion are within functional limits with the exception of knee flexion
• Right ischial tuberosity pressure ulcer, stage III , increasing in length, width, and depth
con tractu res, which measure 20' bilaterally. There is a flexible right pelvic obliquity, 2 inches lower on the right than on the left.
• Abnormal extensor tone in trunk and hip musculature with mild flexion contractures in knees • Sitting in wheelchair for 6 hours, two times per day,
Postural Exam. The patient prefers full fetal positions with flexion of all major joints in sidelying when recum-
for a total of 12 hours daily • Dependence in position changes in bed and sitting • Dependence in all transfers , requiring a two-person
lift • Dependence in all ADL (feeding, wheelchair propulsion, personal hygiene, dressing) Examinations
Neuromuscular Reflex exam shows severe trunk and hip extensor tone present in recumbent and sitting positions.
bent; in supine recumbent pOSition , head and neck are
hyperextended into the pillow and extensor tone dominates all other major joints. In sitting, she demonstrates trunk, hip, and knee extension with pelvis sliding forward on the seat and into posterior tilt, and the cervical spine is in hyperextension .
ADL. The patient is unable to move or change positions volitionally in the bed or wheelchair. She is dependent in all transfers, requiring total assistance of two persons to transfer, and in feeding, personal hygiene, wheel-
chair propulsion , and dressing. continues
296
WOUND
C \01
Case Study continued
A
B
Figure 13- 9 \ , br.:rorc. Note ccnlcal and trunk hypcn.!\tcnpelvis 'chest restraint. right pelvic obliquity. hips forward
Figure 13-9 B, aft!.!f. \jule Ihal head and ned arc in a ,>afe and functional posll10n. ilnd lo\\cr C\ln:mItICs arc Slipportl!d. Courlesy of D\;bby Ilagkr. ClU':YCIlIlC ","·luullla1ll Rdlahilitalloll.
Sion.
on scat, h1\\cr C\lrCl11ltlcs unsupported. Courtesy of Debby I lagier. Cheyenne.: \10UIlIIlIIl RehabIlitation.
Sensory The patient is unable to detect deep or surface pressure on sitting surfaces and lower extremities. Integumentary
The patient has a Braden Scale risk assessment score of 12. She presents with Stage III pressure ulcer on the right ischial tuberOSity, measuring 3 cm x 3 cm x 1 cm deep. The pressure ulcer is 50% yellow slough and 50% granulation tissue. The surrounding skin is pale and the perimeter is macerated. Drainage is serosanguineous. No undermining or tunneling is present. Interface pressures over the sacrum, trochanter. heels, and shoulders in the
supine and side lYing pOSitions In bed were considered unsafe, as they ranged from 70 to greater than 100 mm Hg. Interface pressures over the right ischial tuberOSity and the coccyx in the sitting pOSition In the wheelchair were also considered unsafe, as they were greater than 100 mm Hg. Evaluation The patient has impairment of sensory, neuromuscular, and musculoskeletal systems, causing improper positioning and susceptibility to skin breakdown. There are impairments in musculoskeletal and neurologic systems that, in turn, affect the cardiopulmonary and circulatory
continues
Atlallagelllelll (~r Press/lre hy Therapeutic POSiliollillg
297
Case Study: continued system function to transport oxygenated blood to the wound site. Functional Diagnosi s • There is functional impairment of volitional movement. • There is functional impairment of reflex muscle tone
resulting in dysfunctional body positions (postures) in sitting and in recumbent postures, • The impairments of volitional movement and reflex
muscle tone and dysfunctional body positions produce undue susceptibility to unsafe interface pressures on intolerant bony prominences: coccyx, ischial tuberosities, sacrum, heels, trochanter, and
shoulders. • The patient has risk factors of immobility, lack of sensation, joint integrity impairment of the knees , and abnormal extensor tone, which contribute to undue
susceptibility to pressure ulceration. Need for Physical Therapist Services The patient needs intervention by a physical therapist to achieve the following goals: 1. Heal pressure ulcer 2. Correct impaired postural alignment 3.
Position for redistribution of interface pressures
from bony prominences to tolerant areas 4. Reduce risk of additional ulcerations Prognosis
1. The ulcer will heal. 2. The risk of further pressure ulceration will be reduced by intervention with support surface and positioning equipment.
sure readings on all bony prominences in all positions.
6. Staff will demonstrate correct use of all equipmen t supplied and in therapeutically positioning this patient at all times, whether in bed or in the wheelchair.
Intervention: Therapeutic Positioning • Analysis of patient for selection of adaptive seating
equipment requirements. The following are recommeneded : 1. Side-to-side 5- to 3-inch, side-to-side, wedged seat assembly with full pressure-relief pocket at ischials and coccyx, sized to distribute pressure
fully over posterior trochanter and thighs. 2. Firm back support to maintain 85· seaVback angle to inhibit extensor tone.
3. A 90· positioning hip belt to facilitate 90· hip angle and keep pelviS in appropriate posilion. 4. Padded lap tray to provide upper extremity and trunk support. 5. Footrests, calf support, and protective footwear to protect and support lower extremities and to facilitate appropriate positioning . 6. Hip abduction wedge to inhibit adductor and extensor tone and to facilitate positioning and pressure distribution on the seat assembly. • Analysis of patient using adaptive equipment for ap-
propriateness and safety • Analysis of patient for recumbent positioning and pressure- relief devices. The following are recom -
mended: 1. A self-adjusting, dynamic air/ foam mattress replacement to encourage mobility and allow skin protection
2. Positioning in 30· sidelying to distribute interface pressure away from the trochanter and shoulder
3. Utilization of wedges and a pillow between the
3. The patient will sit in a functional upright position
in wheelchair with a 90· hip/ back angle with a sideto-side wedged, pressure-eliminating seat cushion and a firm back cushion, wi th lower extremities
supported and protected. 4. The sitting schedule will be 2 hours, three times per day for a total sitting time of 6 hours; the time up in the wheelchair will be coordinated with the meal schedule 10 facilitate safe swallowing and im-
4.
knees to maintain the sidelying position In supine, utilization of a leg- positioning cushion to inhibit hip extensor tone , to accommodate for the knee flexion contractures, and to position
heels off the bed 5. Utilization of a head-positioning cushion to provide occipital and cervical spine support and to inhibit cervical extensor tone in supine
6. Utilization of an over-the-bed trapeze and side
tions in supine and 30° sidelying on a prescribed
rails to assist patient in self-mobili ty • Analysis of patient using recumbent positioning and pressure-relief devices for safety and proper pressure relief • Staff instruction: In stru ction in appropriate usage of
support surface in bed, with safe interface pres-
all seating and bed-positioning supplies and equip-
proved nutritional intake. Sitting time will be in-
creased gradually according to a prescribed si tting schedule. 5. The patient will be positioned in functional posi-
continues
298
WoP,!> C\RI
Case Study continued ment and in safe and effective position changes, transfers, and positioning in the bed and the wheelchair for two shifts of nursing personnel because of prolected silting schedule of 2 hours, three times per day, coordinated with the meal schedule. Increased sitting time according to a prescribed schedule as the patient's strength, endurance for sitting, and tolerance improve over time, • Follow-up assessment of staff for appropriate and safe use of devices and components of the devices
3, Posture is corrected: The extensor tone in the neck, trunk, and hips is inhibited, and the abdominal musculature and cervical flexors are facilitated and strengthened, facilitating wheelchair self-propulsion, and self-feeding. 4, The patient is positioned In a safe and functional position in bed on a non powered dynamic air/foam mattress replacement with safe Interface pressure on all bony prominences In all positions; In sldelYlng, using a wedge cushion behind the back, a wedge cushion under the bottom leg, and a pillow between the knees, and In supine, using a leg-positioning cushion and a head-positioning cushion, 5. The patient is able to assist in repositioning self from side to side, using the trapeze and the side ralls. No additional ulcers have developed, providing a reduced pressure risk score, 6. The pressure ulcer on the Ischial tuberosity is healed.
Functional Outcomes 1. The patient IS able to Sit In a functional and safe position for a total of 9 hours per 24-hour period (3 hours, three times per day). 2, Interface pressure is eliminated on the ischial tuberosities and coccyx, and the flexible right pelvic obliqUity IS corrected.
Note: Case study and pictures provided by Debby Hagler, Cheyenne Mountain Rehabihtatlon,
RESOUIKES The following is a rcprescnt3ti\-c listing of manufacturing sources for the categories ofsc discussed in Ihe text Some manufacturers hmc products in multiple categories.
Customil.ed Contour Freedom Designs Im·acare
Ot\(-(jlrlllllllll B Prc.,'ur..: ukcr pn:\ah:l1I:c, 1Il(.'IUCIKC ,lIld ""'IWIall.'d ri,\'" f"!.:Ior .. illlhc I.:tllllIllUI11ty f)nIl/Jlf/l\ 199.1,6(5):2-1 l:!.
Simple Pressure J{eduction AhMed Ken McRight Supplies; Bye-bye Decubiti Maddak Skll-Care Span-America Medical: Gco-Matt
Ma\"'ldm ... t 1. Slcgg.n:cn 1\1 "j'/II;rJ/ltllld
/'/('\\/11.('
t "In'/"I Ci/lltlclllln IflI" 1'1"," S·' Puhllca-
\lInill.1! \hlllll.I!I'I1I"1II \\.":\1 Dundee, II
lilln .. ; 1991 .1
4
Dt'><1 J,
(arlron
1. (iuldhcrg .... I meac) of Opcr..III\C care
III
pre .. -
.,ure ..ore
PilllCllh /'/ml
(:\;111'. (i,
cl al Surgical cnrrCClltll1 of prc ..... urc uln'r, 111 an urh;m
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center; i .. 11 dTICaCIOU.,·.' Itll" fliJIIIltI('tI/"l' 199-1.7(1)40 ~(l
Generic
('urllll I W(HmO m;lI1agcll1cllt ' (;;trc and en ..\ an (I\cn le\\ tllll/lI~(' 191\4,15(21:22 .
('OUI"OUl'
Cascade Dcsigns: Varilitc Crm'vll Therapeutics; Roho family Flofit Medical; rle"eat Invacarc~ PlnDol
Jay Medical; .lay' family Span-America \I1cdical~ (jeo-Matt Contour Supracor
"
Rm,.., J. Dean I Inh.:gr.lllIlg ph) .. mltlllit.:ill pnm:lpl..·., 1I110lhc e(1I11I'''n
prChClhl\i! 1ll,IIliIgcmcni of t:,"irlIIUpulllwllary dy .. ful1t:11U11 1111'1" 19X9;(}I):255 :!59
7
(jcrharl I\.. WCII/cnkamp I). Charhfuc S I he uld gct nldcr· change .. \Ur\1\llr,. Report Ih)1ll Rehat'llhta,
u\cr thret.! yt.!ap, 10 agll1g SCI
lIun Re ..Cilreh and Tr.uning ('enter lIn \gmg \\Ith an S<-1. (-rJlg Ih"'pllal. \"('u· \lahilll! June 1996;IX :!I R
~Iuoncy \: el al CompanMlIl nf pre .... urc dl .. tntHlIIon qUilhlle .. 10 ..cal (.'u,11Ion,. HIIIII'lm"'t" RI'I. 1t)7I,IO(l"i)1:!t) I ..n
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Lnplrom Il St'ut;ng 10,. hlllt'PI'l/dl'I/( '(' Waukc .. ha, \\1 I T\(' lS.\, IIJIJJ
Selective Pressure Elimination Span-America Medical: IS('II-DISII
\'Inl'
\lIlIIIW/oll"·;III;p/n
lHwwgement of Pressure hy Therllpelllic Positioning
10.
Krellv I). Se,Llmg, and positLonmg ror the newly LLlJured, Rellflh
23 .
Ferguson-Pell M\o\. CI al. Pressure sore prevcnlion for the wheel· chair-bound spinal injury pUlicnt . PClnJp/egia . 19HO: 18:42 51.
24 .
Key AG, Manl~y MT Pressure redi:i!ibution in wheclchnLr cu~hion for paruplegics: ils application anti c\'lllu:ltion. Paraplegia , 197X
M'll1Il~l'_
II 12.
13.
14 . IS . 16.
191)3;6:67 75. Manser S, Uoeker C SCUling considcnllions: silinul cord Injury. PT Magfl:llle. December 1993;-17 51 , (lrc-sperln J. Postural considerations for scating the person with spinul cord LlLJllry. In: Procecdmg:; from RESNA SC!ltmg Conference: JUIlc6 11,11)92: Vancouver, Be WlIlpin LA . Postun.:: the proc;;.'ss of body usc: principles and deterIllLnants. In : (iI.:lb II. cd. Nell' COII('l!J1I,\ 11/ Cllrllio/l/llIUlihu/(l1' (/lui Chrolli!' Pui" }\/(If/(lgl.!lIIl'lII SI. Louis. MO : Mosby - Year Book: I<)\)'-l 13 76. lacharkov.. D Whce!dwi"l'o _"(/lre (l1/(1 Prp.'-.w/"I! SOI"l! $. Springfield IL Charles C Thomas: 19H4 Rappl L. A conservative treatment for pressure uiccrs. O'UmIU Huund IItJ/WK(' 1993:39(6):46 48. 50 55 . Garber S. Wheelchair cushions for spum1 cord injured indi\'idua1s .
In9; 16:.03-412. 25 .
IX .
19.
20 .
21.
22.
Pcrkash I. CI a1. Dcvelopment and c\aluatLon of iI uni\l!l"sal contoured cushion. Parap/e),{i(l. 1984:22 :35R 365 .
26 .
Peterson M. Adkins II. ~'tcasurc!l1cn( and flxll.stribution of Ctcc,",sive prcsSlires during wheelchair silting. P/~r~ /1/(,,,. 19R2;62:990 994 .
27 .
Rcswick JB. Rog\!rs JE . Expo:ricncc- at Rancho Los Amigos Ilo~p]1;11 \\ L1h devices and techniques 10 prevcnt prc~sure sores , In : KenedL RM. Cowden JM. Scales JT. cds. Bedsore mOIllt"c/wII;n B"ltllnorc ' Uni\ersilY Par].. PreSS: 1976:30 I 3 IO.
2M .
Am.l ()r-CIiP 1111' /: IIJK5;J9:722725 .
17.
299
Rogers J, Wilson L Prc\cntll1g rccurrcnt tissue breakdO\\ ns :lftcr "pressure sore" closures. PI(HI Re('(JIIlrr Sllrg. 1975;56:419422.
Fcrguson-Pcll M_ Scat cushion sekclion J Nehahi/ Re, De" 1990 ; (~uppl 2)..\9 73 . KllIght A . Melli!::;!1 man:lgl!nll!L1l of prl!sslirc ~ores . J Fum Pmci.
29 .
19X5;17:95 100,
30.
Melder D. Harr J. Positioning your patienl pmpcrly. Alii .IVlln. 1996;96:3337.
31 .
Plautz R. Positioning can mukc thl' lIifferencc. .'1111,.1' Term C,,/'e Mml(lge. 1992:41 :3034 .
National Pressurc Ulccr Ad\ Isory Panel, Prcssur~ ulcl!rs : prcvalence. co~t, and risk a'isessll1ent ~ consensus de\elopment confcn:nce slatcmi.'nl. Dewhilll,\ _ 19X9:2(2):2..\ 2X. Noble PC The prc\'cllIion of prCSSLlrl! sore~ in flcrsons with !'ipinal corll injuries. In : IIIWmaritJIIIl/ Exchallge of /nfi".,,/Olioll ill RcllIIhi/1I01illll New York: World Rchllbilu:nion Fund Inc : 1981. Slotts N. The physiology of wound healing. In; SWlIs N. Cuzzell J. cds. Pmc l!cdillg.\' fro/ll lite ,-IACeN Vulimllll Ti!ClChillg IlIsrilllle. Kan1>us City, MO: Marion Laboralories: 198.S v
Rappl L. SCc]Iing for skin uml wound l1lanag.... rncnt In: P/'(I('('l '(/Pittsburgh, PA. January 23 25. 1997.
illgs limJl 71,i,.,e('1I11J III(e/"lwrifllm/ Seliling Sl'IlIposillm
32.
1/0111(',\
Long
Cantin JE . Proper positioning eliminatcs pallelll injury. 'T()dm<.. ON Nurse. 1989:11 : 18 21 .
33.
Kozlcr B, et at. FlIlltimll(!IIW/S of NlInillg : CO/lcepts. pIYJ{'en tl/u/ Pmclie/!. 4th cd. Redwood City. CA: Adllison-Wcsky Publishing
Co: 1991. 34.
Magee D. OrtJwfJedit: Plt.,·sic(d Saunders Company; 1992
A ,\ ,\·('S.H1/l'1I1
Phillldclphia: W.B.
C H APTE R
14
Diagnosis and Management of Vascular Ulcers Car/os E. Donayre
TRODUCTION
The main role of arteries and veins is to provide a pulsa tile now of oxygen-rich blood to the foot and to return Ihe oxygen-depicted blood back to the heart for re storation . The aorta, the largest blood vessel in the body, divides into twO large branches, the right and left common iliac arteries at the level of the umbilicus (see Figure 14- 1). Each of these branches divides again into an external and internal iliac artery. The internal iliac artery, also known as hypogastri c artery, supplies the pelvis via a variety of branches. The external iliac artery trave ls distally and becomcs thc co rnman femoral artery when it crosses the inguinal ligament. This vessel again divides and gives rise 10 the superficial femoral and deep femoral arteries. The deep femoral artery, or profunda femoris , supplies the muscles of the thigh and is truly the workhorse of the leg. This vessel becomes a major collateral pathway to the lower extremity in Ihe event that the superficial femoral artery becomes occluded due 10 [IIherosclerotic disease. The superficial femoral artery becomes the popliteal artery when it crosses the adductor canal. which is formed by the tendon of the adductor magnus muscle. This is the most common site of atherosclerotic disease in the lower extremity, and may be related to local vessel trauma caused by the constant pulsation of the superficial femoral artery against thi s hard tendinou s structure. The popliteal artery co ur ses mediall y and divides below the knee to give ri se to its first branch. the anterior tibial artery and the tibioperoneal trunk. This trunk di vi des into the peroneal and the posterior tibial arteries (see Figlire 14 2). The peroneal artery terminates at the ankle, and only the anterior and posterior tibial arteries travel into the fool. The anterior tibial artery continues in the foot as the dorsa li s pedis anery, but it is absent or terminates early in 2% of individuals. When thi s occurs the perforating branch of the peroneal artery ca n become the dorsalis pedis artery.
When one takes into consideration what feet routinely accomplish, il is nOI hard 10 see why Ihey develop so many problems. A man of average weighl (160 to 170 Ibs) walks 7.5 miles OIl an average day. This requires that each foot carry morc than 500 IOns a day! Women's lighter bodies place fewer
demands on the feet lhan the usually heavier men's bodies, but fashionable footwear nullifies thi s weight advantage. High-heeled shoes put 75% more pressure on the ball s of the fecI than does going barefoot. The constant wear and tcar thm fect are submitted to daily takes its toll , and the older one gets the more likely one is to develop fool prob-
lems. At one time or another 85% orall Americans have fOOl problems se riolls enough to require professional allention. In nursing home patients thi s figure rises to nearly 100%,1 Most people amicted with foot ailments fail to seck professional help promptly and rely on their self-diagnosis for treatment. The causes of foot problems are rarely obviolls. and delays in correcting them give the underlying disorder more time to develop and worsen. Furthermore, when a seri· ous disease is misdiagnosed as a minor foot malady, results are often drastic and costly. Dry skin, brittle nails. numb· ness, discoloration, and coolness are usually minor signs and sy mptoms of foot ailments, but they can also be the first indication of vascular insufficiency or diabetes.
VASCULAR A ATOMY OF' H I E LOWER EXTREM ITIES In order to have a clear understanding of the effects of altered circulation to the fOOl, a basic knowledge of vasc ular anatomy is needed. Neither the vascular system of the lower extremities nor the task it performs is terribly complicated. 301
302
Wm '" e\.,
Figure 14- 1 Normal artenal anatomy 111 the pel\ic region. An angiogram dClllon..,tralcs the usunl cour... c of the right Iliac vessels: common ibac (e/), external iliac (E). and II1tcrnal iliac (/) arteries. The external Iliac artery bccolllcs the cOl11mon femoral nrtery (CF) when il crosses the IIlgumal ligament. and gives ri'ic to the profunda femoris afll:ry (P) and the superficial femoral artery (SF).
Figure 14-2 \lonna I arterial anatomy 1I111le: hl\\cr c.\tn:I1lIlY. An angiogram orthe len lower cxln:lI1l1}' demonstrates Ihe usual course of the vessels. The superficial femoral artery tra\crscs the adductor magl1l1s canal to become the popiltt!al artery (lJ), \\hich blfurcales inlo the anterior tibial .ulery (,-In and ;lllhlOpcronc:1i trunk The tibiopcroneallrunk also btfllrc,lIcs 10 gp.:e risc 10 Ihe posterior tibial (pn and peroneal (Pt') arterlcs. The peroneal artery tCflllI· nates at the ankle. anu only the antenor and pu~tcrior I1hial arteries travel into the foot. The anterior tibial .mery cnnllllUCS III thc foOl as the dorsalis peuls .ulery. and Ihe pnsh::nor tlhlal ,utery hi fur· cales 1Il10 the meuwl anu lillcral planlilr artcncs
Diagnosis and Alauagemell'
In up to 5~o ofindi\ iduals the posterior tibial artery is either absent or terminates early. In this situation, the communicating branch of the peroneal artery gives rise to the plantar arches. ' The plantar arch is rorrned by the lateral plantar artery. rrom the posterior tibia l artery, and the deep plantar arch rrom the dorsalis pedis artery. The predominant blood sllpply to the plantar arch originates from the dorsa lis pedis artery. In mo't individua ls the dorsalis pedis artery and the deep plantar arch give rise to the dorsal and plantar metatarsa l arteries. which go on to supp ly the toes. The venous system to the lower extremity is in a se nse more complex to describe because of the numerous vessels involved and the great number of anatomic variants. A short description will ,umce to pro' ide an adequate background to the discllssion of chronic venous insufficiency that follows later. The veins of the lower extremity arc divided into superricial. deep, and perrorating vcins (see Figure 14 3). The superficial veins are located in the subclitaneolis tissues, superricial to the rascial emelope orthe thigh and calr muscles. The deep veins accompany the above-mentioned arteries and lie deep to the raseiae a nd muscles. The perrorating veins penetrate the deep fascial envelope to connect the superficial and deep venous systems. Venous flow is norma ll y rrom the superrieial to th e deep veins and is directed by a system of one-way bicuspid va lves. which are present in all three venous groups. These valves are more numerous in the deep \enous systcm and in the distal veins. 1 One comment about \ enous nomenclaturc needs to be made about the superficial femoral vein. which begins at the adductor hiatus as a continuation of the popliteal vein. It is joined by the deep remora I vein just below the inguinalligament to form the common femoral vein. which receives the venous drainage from the longest \ein of the body, the greater saphenous vein. The superficial femoral vein is not a superficial vein at all. and any evidence of thrombosis or reflux in this vessel must not be ignored.
OCCL US IVE I' ERII'II ERAL VASCULA R DI SEASES IG SA D S YMI'TOMS Inlc rmiucnl C la udi culi on Ailments of the lower extremity can usually be diagnosed accurately by obtallllllg a careful history and performing a detailed physical examination . Intermittent claudication is the most common presenting complaint in patients with chronic arterial occlusion of the lower extremities. The first case of intermittent claudication in man was described by Charcot in 1858. The word claudicatioll comes from the Latin word clUlidiCalio. which means to limp. but the patient with claudication does not limp: he or she stops to rest. The pain due to intermittent claudication is characterized by a cramp-
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Figure 1"- 3 Normal \cnOliS anatomy. A schcmallc diagram dcmonstrates thc VClll5 of the lower cxtrcnllty. which are dIvided into superfiCial. deep, and perforating \·clns.
ing or aching sensation. most often in the ca lf. that is associated with walki ng and is re lieved by stopping witho ut the need to sit down. Intermittent claudication 1110st commonl y oecurs as pain in the calf area, but higher vascular obstruction. such as aortic or iliac occ lusion, will cause pain in the buttocks and in the upper thigh, and is rrcquently accompanied by impotence in men. This is known as Leric hc syndrome or aortoiliac occlu ive disease. The symptoms of intermittent claudication depend on the degree of ischemia that the muscles in the legs are submitted to . The distance a person can walk wi ll vary rrom patien t to patient. and intermittent claudication can occur after a short distance if a person is walking up a hill. is on a hard surface. or is walking fasLThe distance a person walks wil l be longer if he or she wa lks more slowly and avoids inclines or hills. People with progressive intermittent c laudication note that
304
WOl "D ('·\RI
ovcr timc they are only able to walk shorter and shorter distances before discomrort develops. Examination orthe patient with intermittent claudication involving the cal f muscle may reveal both a remoral and a pedal pulse hut no popliteal pulse. In these patients aner a brisk walk. the foot will become pate and pulseless because the blood Ilow bypasses the skin of the foot and tends to now to the skclctalmusclcs orthe calr instead. Intermittent cl;.ludic~lIion usually results rrom a single arterial blockage. which can be predicted accurately by a carefully performed pulse examination. Ira femoral pulse is present but a popliteal pulse is diminished or absent. a stenosis or occlusion call be expected in the superficial femoral artery at the adductor canal. Intact pedal pulses ill the presence ora popliteHi pulse imply disease of the inrrapopl itea I vessels or Iri rurcation diSease. Physical findings slich as lack of hair growth on the dorsum or the root, thickening of toenails. and delayed capillary filling should also be looked for because they point to chronic arterial insufficiency. Another part or the physical examination that should be routinely performed on palients with suspected vascular il1sufTiciency is the resting ankle-brachial pressure measurement or indc'c With the patient placed in a supine po~itioll. bilateral brachial and cll1klc (posterior tibial and dorsalis pedis Hrteries) pressures are measured by obliterating blood flow with a standard adult-size sphygmomanometer (blood pressure) cufr. The exact pressure at which there is cessation or arterial blood flow as determined by the use of a continuous-wave Doppler instrument placed over lhe area of maximum audible flow is recorded. Because systemic blood pressllre m~ly vary in patients, the absolute ankle pressure is USlIally normalitcd by expressing it as a ratio of the highest obtainable brachial pressure. or ankle-brachial index (ABI ).' In the normal patient. the ankle pressure is usually greater th
E\hibil 1-'-1 Noninvasive haluation or Aflt!fiallnsufTicicney: Ankle-13rachlal Index
Indc\
-"1. 1 (), Q 1.1 0.5 0.8
<"0.)
Clinic~tl
Dcscril}tion
Calcified. nOllcompresslblc \cssds must bi.": suspected
Normal vesscls InICnnillcllI claudicallon Rest pain; ulccraL10n and IIssue loss
Nocltlrnal pain is a rorm or ischemic neuritis that usually precedes rest pain. It occurs at night because during. sleep the circulation is essentially of the core variety. with little perrusion to the lower extremity. The pain is classically described as occurring in the toes, across the base orthe metatarsals. and in the plantar arches. The ischemic neuritis produced becomes intense at night and disrupts sleep. The patient gains rciiefby standing up. dangling the feet O\er the edge of the bed or on occasion walking a few steps. This increases the cardiac output, lcnds to improved perfusion of the 100ver extremities, and resuits in relief of the ischemic neuritis. Thus, in patients with rest pain a chronically edematous. erythcmatous foot and anklc mHy rl":nect a reliance on dependence for relief of symptoms. Rest pain usually indicates the prcl-icncc or al leasl t\VO hemodynamically significant arterial blocks. The ABI is reduced by 0.6 with two arterial blockages. and thcse paticnts usually have an ABI of less than 0.5. I f the lesions that produce nocturnal and rest pain are not corrected by vascular surgery. tissue necrosis and gangrene almost always develop, necessitating amputation. Ulceration and Gangrene Ulceralion and gangrene of thc lowcr extrcm ity represent the most advanced complications of arteri
Diagllosis CllldHuIIOg('IIU!1If O(/llsC'lllar L'ln'rs
)05
Another risk factor of Importancc ts Sl1l0klllg. (,11I11cal experience strongly confirms that patients \'Vho smoke and have chronic occlusive arterial disease allccting the extremt· ties do not do \....ell.~ Among patients under the age of 50 yc;ars who quit smoking ailer they developed intermittent claudication. nonc progressed to rest pain. as opposed to those \\ ho continued to smoke. Smoking causes a decrea!)ed blood now to the extremities and a decreasc in the skin temperature of the digits. A single cigarette can cause spasms orlhe artCTlCS and reduction of blood now that may last as long a.., I hour or more. The mechanism by which smoklllg is atherogenic is unknown but may be rclatcd to intimal IIlJury causcd by incrcased Ic\"els of carboxyhemoglobin, or it may be caused by an efTect on platclet function and an IIlcreascd tendency toward thrombus formation. " Another ctTecl of sIllok111g IS the innucnce it c'\crts on prostacyclin. an important prostaglandin produced by the endothelium of blood vessels that prevents platelct aggregation and promotes \asodiiaullion Recent work has sho",n that cigarcttc smoking IIlhlbll!-i prostacyclin formation. Ilypcrtension is another cxtremcly lI11portant Tlsk factor in the development of penpheral "ascular dISease. In the Framingham Study hypcrtension imposcd a threcfold increased risk of dcveloping intcnnittent claudication dUTlng a follow-up period of26 years.' The frequency ofhypercholesterolell1ia and hypcrtriglyeeridemia has also been found to be significant in most clinical diseascs of the pcripht.!n:tl vascular system. It has been suggcsted that a high level of high-density lipoprotein (IIDL) cholesterol docs not protect the patient If the 10\\-denSity "poprote"t (LDL) IS "bo 1Il0rdinately high. It is probably the ratio of IIDL to LDL that determines the risk factor rather than the ahsolulC level of each. Patients presenting with signs and symptoms of arterial Insufficiency shou ld be counseled and educated about Tlsk factor modification if diseasc progression is to be a"olded
Fi~tlre
14-4 An angiogram rc\eals occlusion of len common Iliac artery (C/). reclln:'tlnullnn of the common femoral (( F) and pro·
fund'l femoris (1') arteries, HI cllllilter.1I p..llhways. and occlusion of the supcrflcl'll fcmor,lI artery. Multllcvel atherosclerotic dis· case IS consistent \\ IIh ';lIlure of tl ..Slll:: healmg and ;1 decreased \HI (Sec Color Pllit/.· .J9 for photos of the ulcer on this samc pallent.)
I11CIlI will vary widd) from p.lIicnt 10 patient. Genetic fae· lors are c'\trcl11ely Important nsk factors. \\ Ith premature atherosclerosis frequently seen in fmnily groups with an age of onset of 40 years or older. lIowcvcr. it is not rarc to find significant peripheral \'ascular disc;ase before thc age of 40 in the diabctic patient.
DIABETES AND FOOT ULCERATlO"l Ulceration and other complicalions of the fOOl associated with diabctes are incrcasing problems of signtfic~lI1t epidemiologic proportions. Ncarly half of the major ~ll1lputations performcd cach year are for patients sutTering from diabc;tcs. '" Only 8°'0 of the Q\'crall population 111 the United States. however, has diabetes at the present IIIne. Fach year 35.000 to 40.000 di;lbctic paucnts undergo major 11mb amputallon at a cost of 1.2 billion dollars. In This figure docs not includc the costs of rehabilitation. prostheses. loss ofti111c frol11 \\:ork. loss of jobs. and "elfare payments. Thc amputation ratc 111 peoplc with diabetcs is 15 times that of the nondiabetic population. The initial lesion in 1110s1 of these cascs is painless trauma occurring 111 a ncuropathic.
306
W ()U~I)
CM'
insensate foot. It is the presence ofpcriphcral vascular di s-
ease, however, that prevents these lesions from healing. impaired ci rculation is a major contributor to infection because
the delivery of leukocytes and antibiotic agents is compromi sed by the lack of sufTicient blood fl ow. The decreased delivery of oxygen to infected ti sslies further promotes the growth of highly destructive anaerobes. tudies have demonstrated that oxygen is necessa ry for ma crophage mobilit y
in wound debridement and the ingrowth of gra nulation tisslie during wound healing,ll The function of some tisslIe growth factors is oxygen dependent. Furthermore, so me antibiotics. principally the
ami noglycosidcs. depend on oxygen for their function. The triopathy of neuropathy, vascu lar insufficiency. and an altered res ponse to infection makes the diabeti c patient uniquely susceptible to pedal complications. Not surprisingly. foot probl ems remain the most common indication for hospitalization in patients with diabetes mellitus.
3105 years required a contra latera l amputation (greater than 10% per yearlY Diabetes poses a special risk because diabetic individual s tend to have severely di ffu sed vascu lar di sease: therefore, the diabetic patient must pay particular attention to foot care to ward off ulceration and infection, which mandatc an increase in blood flow that their vascular system cannot provide. A major risk factor that has ah,vays been considered important in the developmcnt of diabctic vascular disease is the co ntrol of blood sugar.1.I The Diabetes Control and Complications Trial Researc h Group in 1993 published a study of 1,444 patients followed for 6.5 yea rs to assess the pro-
diabetic patients have evidence of peripheral vascu lar dis-
gress ion of retinopathy, ncphropathy, and ncuropathy. Clinical neuropathy was defined as nbnormal neurologic examination findings consistent with peripheral neuropathy. plus either an abnormal nerve conduction test result in al least two peripheral nerves or uncqui vocal autonomic ncr ve testing. In this multicenter study patients were randomly assigned to standard insulin control or to an intensive therapy administered by either external insu lin pump or by three or more
ease (PVD) at th e time of diagnosis. The incidence of PVD
daily injections of insulin, guided by frequent blood sugar
rapidly increases with age and duration of diabetes. early 45% of patients wi th diabetes over 20-year duration have evidence ofJ>VD. and this percentage is much higher in those patient s who smoke. Vascular di sease affecting the lower ex tremity in diabetic patients has many si milarities to that found in the nondiabetic patient. The changes in the vessel wall , in both the media and the intima (consisting of depos-
monitoring. The developments ofncuropathy and nephropathy were each significantly reduced by the strict monitoring of insulin levels. In patients assigned to an intensive management group, the incidcncc of retinopathy was reduced by 76% compared wit h that in patients receiving the usua l twice-daily insulin inject ions. Equally impressive, a 69% reduction in the onset of neuropathy was reported. The findings represent the 3% incidence of neuropathy in those with intensive insulin management versus 10% developmcnt in those with the usual insulin management during this 5-year
Approxilllately 8% of non- insulin -depe ndent (type II)
its of platelets. sillooth Illuscle cells, lipids. cholesterol, and
ca lcium), arc qualitatively the same in both groups. although these changes are quantitati vely greater in those with diabetes. There are, however, some important differences. The atherosclerotic process is more commonly seen in diabetic patients than in nondiabetic patients. occurs at an earlier age. advances more rapidly, and is almost as common in women as in men . Differences also exist wi th regard to the vessels that are in volved and the extent of the involvement. The femoral , iliac. and aortic vessels appear to have a similar degrce of atherosc lerotic changes in diabeti c and nondiabetic patie nts. The profunda femoris artery is affected wi th greater frequency and extent in diabetics, but the vessels most frequently involved in diabetes are those below the knee- the tibial and peroneal artcries and their smallcr branches. In a diabctic patient l11uiti scgmcnt occlusions can bc secn with diffused mural changes proximally and distally. whereas in the nondiabetic subject the occlusions most often involve a single scgment with a normal adjacent arterial trce. Once the process begins in the diabetic patient, both lowerextremities are usuall y invol ved: in thc nondiabctic patient the lesions are more likely to be unilateral. A summary of 485 patients in fi ve studies showed that following the initial limb amputation. 42% of diabetics in the first 3 yea rs and 56% in
study. The results wou ld support the theory that more strin-
gent insulin managemcnt will reduce the onset and progressio n of neuropathy. The study did 110te. however, that there
was a two- to threefold increase in severe hypoglycemic reactions, which required management in the strict control group. No fatalities and no serious complications were reported despite this complication. Thi s and other studies support the need for optimum insulin cont rol in diabetic patients . A therapy regimen designed to achieve blood glucose values as close to the normal range as possible would seem to prevcnt the onset and progression of diabetic cOl11plica· tions. Thus, such monitoring should be part of optimum diabetic foot care. In summary, the risk for developing peripheral vascular di sease in the diabetic patient stems from a combination of factors. Heredit y. age. and the duration of diabetes are factors that cannot be controlled. Nevertheless, the blood sugar level should be we ll controlled but balanced against the risk of hypoglycemia . Although each ri sk factor may have a vari-
able degree of importance by itself. a combination of these factors can becomc very significant .Thcrcfore, it is extrcmely
Diagllosis and A-Iallagemelll o/Vascular Ulcers
important to co ntrol hypertension and reducc cho lesterol and tri glyceride levc ls. Needless to say. one of the strongest ri sk factors di sc ussed above is smoking. It is critically important that diabeti c patients and certainly all patients who have peripheral vascular di sease do not smoke. A co mmon complaint ofpaticnts with peripheral vascular insufficiency is cold feet. It is the discomfort of cold feet that prompts the diabetic patient to reso rt to the use of hot water bottlcs. heating pads. or hot watcr soa ks. This practice ca n result in seve re burns to a foot that has beco me insensiti ve to heat beca use of a peripheral neuropathy. At an ambient foot tcmperature of approximately 70°F the patient requires I mL of blood now per lOa g of tissue per minute. A paticnt with even moderatc peripheral vascular di sease can manage thi s. Soaking the foot in hot water can quick ly rai se the skin temperature to 104°F. This requires an increase of 10 tim es th e flmv of blood . A patient with peripheral vasclllar disease ca nnot achieve this. This result s in bliste ri ng. ulcerat io n. infection. and gangrene, which not infrequently may lead to an amputat ion. Another symptom that diabetics complain of is rest pain . In the diabetic patient . re st and nocturnal pain may be absent despite seve rc isc hemia because neuropathy has destroyed se nso ry perception, stress ing the need for a careful examination of the se patients for vascu lar sufficicncyat every c linic visit. All of the modern advances in medic ine. including sophisti cation of mi crobiologic analyses. new and more potent antibiotics with improved antimicrobial activity, advances in radiologic imaging of th e foot and leg, and better educati on and understanding on the part of health care profess ionals and patients about the etiology and the therapy of the diabetic foot infections. should have redu ced the major amputation rate in diabeti c patients. Unfortunately. the major amputation rate for diabetic patients has not bee n significantly reduced. The triopathy of neuropathy, vasc ular insufficiency. and an altered response to infection makes the diabetic patient unique ly susce ptible to foot problems. Diabetics li\'c quite normally with all of thc se complications until minor trauma results in cu taneou s ulceration and the development of an acute infection that may lead to hospitalization and limb loss. Neuropathy probabl y represent s the greatest risk for ul ce r development. Diminished or absent proprioception and se nsa ti on quite often delay early recognition and treatment of a seemin gly benign problem . Autonomic nervc dysfunction characterized by dry skin , absent sweating, and increased capillary refill secondary to arteriovenous shuntin g leads to fissure, c rac king. and a fa lse se nse of sec urity about th e c irculation . Motor ne uropathy leads to denerva tion of the intrinsic and skeletal muscles of the foot and leg, resulting in abnormal bone-related problems due to a compromised foot architecture that is susceptible to traumati c IIlJ ury.
307
Ischemia may complicate up to one ha lf of the diabetic foot ulcers; 40% of diabeti c patie nt s presenting with gangrene or seve re limb threat infections will have palpable popliteal pulses. Aggress ive vascular evaluation and treatment are essential for healing ischemic ulceration and IllUst be considered for chronic ulcers that fai l to respond to treatIllent. Diabetic patients tolerate infection poorl y. Defects in the ho st defen se include altered leukocyte function and wound repair. Most important is the fact that systemic signs and symptoms of a septic process often occur late, making unexplained and uncontrollabl e hyperglycemia the only reliable sign of a potentially serious limb and/or Ii fe- threatening infection. Less than one third of patie nts with pedal osteomyelitis have elevated tcmperature or white blood cell count. The lack of blood now reduces oxygen to the amicted tissue and contributes to the development of foot sepsis. Studies have demon strated that oxygen is necessary for mac rophage mobility in wound debridement and the ingrowth of granu lation ti ss ue during wound hea ling. Restoration of blood now with increased oxygen levels to ischcmic ti ssue is of the utmost importance if limb salvage is going to be achieved. I" The extent and seve rity of the infected diabetic foot ulcer determines the course of treatment. To determine the severity one must do a carerul initial in ~ spection of the wound, which because of neuropathy can usua ll y be done at bedside. Sterile forceps, a probe, sc isso rs, and a good li ght arc all that are needed . The seve rity of ti ssue destruction and se psis may not be totally apparent from just looking at the ulcer or infected callus. especially in those patients who co ntinue to bear weight on a painlcss area or who do not have the visual acuity to recogniLc a problem. One mllst unroof all encrusted areas and. using a probe, inspect the wound to determine deep ti ss ue destruction and possible bone or joint involvement. A determination can be made whether the ulcer is superficia l so that treatment ca n be done at home. or whether there is any limb-threatening potcntial that require s immediate hospital admission. Patients with supe rficial ulce ration and minimal (less than 2 cm) cellulitis may be treated on the outside initially if there is no evidence of systemic toxicit y and the patient is compliant and re liable and has an adequate suppo rt system at home. TreatmeJ1l requires that the patient be non- weight bearing to provide complete and total rest. Co ntact casting and other imlllobilizati on endeavors do not replace non- weight bearing and are used only in se lec ted instances. The wound specimen is cultured at initial debrideme nt and broad-spectrum oral antibiotics are beg un. with changes made based on sensitivity reports and the response of the wound. Simple dressings appear to work best. with wet-to-dry dressings of cit her saline or dilut ed antiseptic solutions app lied one or three times per day depending on the s ize and th e area being treated. Dry, sca ly sk in is best treated with lubricated creams, and
308
WOl"" CARl
cracks and fissures arc best managed with antibiotic ointment. Patients must be examined every 24 to 48 hours: if there is no improvement. hospitalization is recommended. Once healing is ensured weight bearing is progressed in modified footwear to protect the high-risk areas. Simply allowing the patient to return to full activity or weight bearing may result in acute Charcot's foot or recurrent breakdown. Shoe modification and periodic follow-up are essential to all patients at risk. Patients with limb-threatening infections
arc managed with hospitalization. Again, inspection is essential because one cannot rely on systemic signs and symptoms to ascertain severity. Indications for hospllalization arc deep ulcers with bone or Joint invol\"cment, cellulitis greater than 2 cm, lymphangitis. and systemic toxicity. Initial management includes immediate hospitalization. medical stabilization. control of blood sugar. and complete bed rest. There is probably no greater controversy right no\\ in the treatment of diabetic infection than the proper diagnosis and treatmcnt of osteomyelitis. One thing is knov'on for certain: inadequate diagnosis and treatment of osteomyelitis increase the risk for major amputation. Methods to diagnose osteomyelitis Include plain radiographs. bone scans. leukocyte scans, computed tomography scans. magnetic resonance imaging. and clinical e\'aluation. Proponents of each radiologiC test quote acceptable scnsltivity and specificity but largcly without confirmation by microbIOlogic or histopathologic proof. Whatever test one uses. it should not delay urgent or cmcrgent surgical IIlterventlOIl . Cost IS no\\ also an important consideration. with fixed reimbursement the norm. These tcsts are costly; thus the lISC of a sterile probc to examlnC the \\:ound IS very cost effective. If a sterile probe taps the bone or a jom!. there IS excellent scnsili\'ity and specificity that thc area is il1\'ohed with osteomyelitis. A plain radiograph should be obtalllccl wllh or without magnification views. Lo look for gas. foreign bodies. associated fractures. or other bony abnormalitic~. Antibiotics arc adjunctive 10 good surgical debridement and managemcnt. At the tUlle of debridement deep culture specimens arc obtainecl and bone or biopsy of deep tissue is sent whenever possible 10 ensure n reliable specimen. The majority of cultures from patients with limb-threatening diseasc grow gram-positi\'c bacteria and S()Oo grO\\ gram-negative enteric bacteria. and 5011./0 to 70°0 of these patients also gro\\ anaerobes. Therefore. anllbiotlc selection must takc this into account, and brand-spectrum intravenous antibiotics or combination therapy to ensure maximum dcllvery to the infected site are recommended . AntibiotiC changes arc made only on the basis of the sensitivity reports and the response of the wound. Except in rare Clrculllstances antibiotics do not cure ostcomyelitis. Studies supporting the usc of antibiotics alone for curing osteomyelitis III gcncntl lack histopathologic or microbiologic proof and accept a major amputation rate of
almosl 30~/O after treatment. l~ Opponcnts also note that bacteremia, open wounds after treatment. gangrenc. and ischen1l3 are associated with poor outcome. Courses of antibiotics of 6 weeks or longer arc also quite costly. even \\lhen delivered on an outpatient basis. Infected limb-threatening ulcers are a surgical emergency. Surgical debridement and drainage of the infection should be carried out as expeditiously as possible. Diabetics do not tolerate undrained sepsis. and patients with systemic toxicity will not impro\'c until this is done. A good monitor of accuracy of debridement IS to fol1o11 the blood sugar levels and management. which should improvc dramatically as infection is controlled. Incisions are carefully placed ensuring adequatc debridemcnt and conservlllg as mllch healthy tissue as possible. such as small skin naps that may later be lIsed in reconstruction. Any \·iablc area should bc Icft and protected even if this mcans multiple tTlPS to the operating room for infection control. Most of Iht! debridement can be done with little or no anesthesia because of the presence of neuropathy. The location of the ulcer. the c\tent of thc infection and its control, and the adequacy of circulation will determine what the final result will be. It is Important to rcmember that the morc ischemic the lo\\'er extremity is. the more important it is to close an 111\'01\ ed area pri1l1~lrily. A neuropathic foot with excellent circulatIOn IS managed dIfferently than the same infection 111 an ischemic foot. Once sepsis is controlled. evaluation and treatmcnt of the ischemia are the next most important options. The merwhelml1lg success of surgical revasculari/ation even to the pedal vessels !)Upports an aggressive approach. Once clrculatlolllS reestablished revisions or morc definitive local surgical procedures can be performed. It is imp0l1ant to try to sa\'c as mllch of the \vcightbearing pan of the foot as possible. espcciHlly the first toe and its metatarsal head. Only \\ IIh an aggrcssl\e control of diabetic sepsis and restoration of foot pulses by revascularilallon can the amputation ratc be rcduced in this challenging group of patients. VENOUS STASIS LLCERS
Despite decades of clinical and laboratory rcsenrch. the exact mechanisms by \\ hich patients de\elop venous stasis ulceration remains Ullcertalll. There is little doubt that SllStained venous hypertension remains the underlying etiologic factor COllllllon to nil pHtlents wllh \'enous stasIs ulcers. Venous hypertension can occur primarily In the deep venous system or may be isolated to the surerficial saphenous veins. These entities may also occur in combination. This has been associated with congcnital or acquln:d valvular dysfunction within the deep veins. or With val\ ular 111compctcnce locatcd at the saphenofcmoral junction or \ ia IIH.:ompCLellt perlbra-
Diagllosis and Afallagemem oIVascll/a,. Ulcers
tors below the knee. Clearly, the underlying pathologic process must be determined in each individual patient prior to embarking on a specific treatment plan. The S\\ollen Leg One of the first complaints ofpaticilts with venOliS insufficiency is swelling of the legs. which on occasion is accol11panied by di scomfort and a heavy feeling in the lower extremities. As opposed to similar complaints in patients with
arterial insufTiciency. thi s comp laint is readil y relieved by leg elcvalion in the person arnieted by venous di sease. A
basic understanding of the function and structure of the venous system is needed in order to comprehend the pathophysiologic derangements that are responsible for the development of lower extremity edema. The main and foremost task of' the venOli S system is to return blood from thc periphery to the hearl. In addition it serves as a storage nctwork intimately involved in blood volumc regulation . It also nlcilitatcs the exchange of substances between tissue and blood in the capi llary region . In order to carry out these functi ons and to maintain a vigorous flow of blood in a low-pressure system, the venous vessels have to rely on the clastic components of their walls (sec Color Plale 50). The walls of veins consist of an intact endothelium that coats a thin basal mcmbrane. An adjoining layer of fibrous connective tissue with strands of collagcnolls and muscle fibers helps to stabilize the walls of the vei ns and in conjuction with a delicate system of valves is responsible for the return of venous blood to the heart . The slightly helica l structure of muscle fibers and collagenous strands enables healthy veins to return to their original position after undergoing distention of length and girth from increased blood volumes. Failure of this collagenous and muscular infra structure results in veins that becomc widcr, longer, and convolute(L giving rise to the formation of tortuous varices. Progressive venous dilatation can lead to va lvular incompetence by interfering with the de licatc apposition of venous val,e leaOcts. which is required for transport of blood up the leg and into the central circulation. Thus. the failure of proper veno us valve closure may be the result and not the primary cause of blood vessel widening. Venous congestion can also alter the delicate balance that ex ists between arterioles. vcnules. and the capillaries. About 20 L of Ouid are fihered inlo the interstitial space by this complex system each day, with 18 L (90 0 0) being reabsorbed by the venous branches of the capillary system. The rcmaining 2 L (10%) return to the circulalory system through lymph drainage. Il ydrostatic and colloida l-osmotic forces work toge ther in capillary filtration and reabsorption. Intraeapi llary pressure drops from 35 ml11 Hg in the arterial branches to 15 111111 IIg in the venous branches. Higher pressure in the artc-
309
rial side leads to outward filtration. which is counteracted on the venous side by a continuous reabsorption driven by coll oidal and osmotic forces. A delicate balance is maintained as long as the amoul1lS of filtered and reabsorbed Ouid remain equal. Altered venous return due to increased ve nous dilatation and valvular deficiency rcsults in perceptible increases in capillary hydrostatic pressure and permeability of the capillary endothelium. These two factors lead to an enhanced filtration of nuid into the interstitial space and the classic appearance of the signs and symptoms ofperiphera l cdema. As can be gleaned from the above discussion. the lymphatic system can also be involved in chronic venous insufficiency. Both the lymphatic and venous systems share 3n early embryologic development and an intimate anatomic relationship. The lymphatic channels course along the pathway of the lesser and greater saphcnolls ve ins to drain into the superficial inguinal lymph nodes. The deep lymphatic vessels of the lower extremity likewise accomp~lI1y the deep vessels of the leg 10 the popliteal lymph nodes and then continue along the femoral vessels to reach the deep inguinal lymph nodes. Congenital or acquired insuffic iency of the lymp hatic transport results in lymph stasis and the acclllllulati on of protein-rich illterstitial fluid . Chronic lymphedema , however, develops only if the collateral lymphatic circulation is inadequate or ti ssue macrophagcs (which aid in the removal of macromolecules from the interstitial space) are overwhelmed. Impaired lymphatic drainage results in significant structural changes in the lymphatic vesse ls themselves and the subcutaneous tissues they serve. This leads to fibroblast proliferation, sclerosis of the subcutaneous tissues, and increased vascularity. changes that are usually associated with chron ic innaI1111latiol1 . 16 Secondary changes in lymph vessels due to lymph stasis include fibrosis of the wall with loss of permeability and lymph-concentrating ability. Furthermore, lymphatic valves, just as in the venous system, may also fibrose or become incompetent as a rcsult of proximal lymp hatic obstruction and distal vessel dilatation. The lymph vessel wall loses its intrinsic contractility, and the muscle pump is rendered ineffective. Lymph stasis favo rs the development of obstructive lymphangiti s with further destruction of the main and collatera l lymphatic channels. Chronic venous insufficiency can lead to recurrent attacks of sk in cellulitis. which may result in incrcased destruction of cutaneous lymphatic channels and subsequent obstructi ve lymphatic patterns. 17 Thi s is strongly suggested by Iymphoscintigraphy. a noninvasive imaging mod31ity lIsed to interpret the morphologic and functional altera tio ns occurring in the lymphatic system. Lymphosc intigraphy has been used to show that the lymphatic system is often impaired in patients with chronic venous insuITiciency. This
310
WOlIND
C A"'
impairment is renected by the de\elopment of anatomic changes in lymphatic vessels as well as the presence of a delayed lymphatic now. These changes ultimately may interfere with the absorption of interstitial fluid in the extremities of patients amictcd with chronic \cnous insufficiency and thu s contribute to the increased clinical swelli ng that is
seen in them .
temic or local problem that comp licates the healing 0 wounds. which are inevitably traumatic in origin. Once-mi· nor trauma leads to a chronic. rccalcitrant wound which is 1 cha llenge to heal. Those ulcerations that arc not venous. bu may mimic or bc confused with venous ulcers. are to be dif ferentiatcd on the basis of a different historical evolution the prcsence of other system ic or local disease proccsses and often subtle but important difTerent physical finding' (sec Exhib it 14- 2).
I)ulhophysiology of Venous Ulceration There arc sc\'cral mechanisms described in the literature that outline the pathophysiologic events leading to skin ulceration. The concep l of fibrin cutTs de\'eloping at the capi l-
lary Ie, el \Va, initially described by Browse and Burnand in 1982.111 Thc~c authors suggested that sustained venous hypertension is transmitted to the superficial \cins in the subcutaneous tissue and the o\crlying skin. This in turn causes
widening orthe capillary pores. thus allowing the escape of large macromolecules (including fibrinogen) into the interstitial space. Owing to associated defects in the fibrinolyti c process. fibrin accumulates around these capillaries. thus formi ng a mechanic~11 barrier to thc transfer of oxygen and other nutrients. Ultimately. this leads to ce llular dysfunction, which in turn leads to ce ll death and skin ulceration. Unfortunate ly. there is no published evidence that fibrin provides a burrier to oxygcn diffusion . In morc recent years. additional physiologic changes hm e been noted in the microcirculation of patients with chronic ,cnous hypertension. Specifically. this relates to an altered inflammatory mechanism in thcse paticnts. These changes have been linked to the accumulation of "hite blood celi> at the capillary Ie, el. "hich has been termed the" hite blood cell tntpping hypothcsi s"'1_:l1 Transient clcvations in \enous pressures ha,e been shown 10 decrease capillary blood flo w. resulting in trapping of white blood ce lls at the capi llary level. This occurs to a much greater degree in patients with long-sta nding venous hypertension and liposclerotic ski n. These marginated \\ hitc blood cell s in turn plug capi llary loops. rcsulting in area!o! of local ilcd ischem ia. These cells may also become ac tivated at this level. which in turn causes rcle,lse of ,",uious proteolytic enlymes as well as supcrox ide free radicals and chcmotactic subMunces. Thcse substances ultimntely lead to direct tisslie damagc. thus leading to ulceratiOl1. ~' Differential Diagnosis of Venous Sta sis Ulce rs
All that ulcerates is not \enOliS in origin. The coml11on feature of all ulcerations of the Icgs is an underlying sys-
Medical Treatment of Venous Stasis Ulcers
Definitive treatment of \cnOliS stasis lIlcer~ is depend en on the operative repair of the underlying reason for venou: incompetcnce ofthc affected c\trelllity. This is seldom pos sible. howc\cr. and long-term ~uccess is rarely achie\ed Excision and grafting of the ulcerated area and surroundint scar tissue. even when accompanied by local and region; subfascialligation ofpcrforating \ es!otels. docs not uniforml~ result in returning long-standing skin integrity. Therefore there remain a grcat many patients \\hose \cnous st ~lsis ul cers hmc to bc managed nonopcrath I!ly:l~ Before attcmp t ing a mcdicall11anagcll1ent ofa \enOliS stasis ulccr. the diag nos is mu st bc assured. Noninvasive measurements mus elim inatc a significant ischemic com ponen t to that ct iology TI1C AS I must be at least greater than 0.5 and prcferabl~ greater than 0.75 . If transcutaneous oxygen l1lea s urel1lent~ arc performed, the foot dorsal pressures shou ld exceed 3( Illlll Ifg. I fcmoglobin electrophoresis shou ld eliminate sickh ccll disease and if suspected :I biopsy should eliminatc \ ":lS culitis as thc caliSC of the ulcer. To allow the ulcer to heal by sceond
Diagnosis allc/\/cmag('IIIC!1lf (?f lel,\'(',,/ar L kC!r\
Ischemic \rt~T1allnsullicleI1CY
Eliolog) l",ual IOCIIliuli
1)1"lal to lllt.!dlilll1l~lIleolus~ dorsum or 1(101 or loes
Venous Stasis
]\eurollathic
ChrOniC \-cnQUS mSlltliclcncy
Dlabett.!s
Pro\lmal to meJialll1allcollls;
A long. prt.!sslIn.,: POlllh; planlar aspCCI or Ilh!t<1tarsal hl!
lateral lower leg
JII
filih) Pain
Sc\cre; noclurn;11. rt.!ile . . ed by dc.:pcndcnc)
Mild: relic\ed by dc\:tlJon
None
Bh~t.'ding
Little or nonc
Venous ooze
May be brisl..
Lc-;ion ch:lnICIt.'rj'ilic'i
Irregular edge; poor granula. lion tissue
Shallow. irregular shapc~ granlilallllg bast.! "llh roundcd edgcs
PUllchc.:d·out; c~illous edges \\ Ilh deep s1I1us
Trophu:: "kill changt.!s (dry skill. bnttlc nalb. alopeCia): absc.:l1t pulst.!')
Stasis dermalltis; hypt.!rpigmcn. la1l011; palpable pulses
Neuropathy; warm skill: pulses Illay be present or
\SliociUICd
findillg~
absent
SII/mc: \lOOII' ..:J from Rutherford Ril The " .... cular cOIhuilation In Rutherford RB. ed liH('fI/uI'S/fI'],!(,rI 4th cd_ Philadclphi.l \\Il. S
Istration prcscntly consldcrs compression therapy to be the standard of carc for \cnous st:.lsis ulcers. C%r Plare 51 shO\'.;s a patient \\ ith \CIlOUS stasis ulceralion_ Color P/alt! 52 shows an ulcer and associated sIgns ufchronlc n:nous Insufficiency. Recently. a \'ariety of grm\th factors ha\c been introduced for the tremment of\enous stasis ulcers. The trial with transforming growth factor (TGF)·bela in a collagen sponge delivery system has givcn the most encouraging data of those trials that hmc been completed. '4 Interestingly. rhe topical antimicrobial siher sulfadiazine (Sil\'adenc) has also shown beneficial results. It is thought Ihat the base of this compound has properlu,:s that sttmulate \\ound epitheliali/ation. Contrary to pn.!\'IOUS expencl1l:c. many patients who have healed during carefully controlled clinicaltrial\ hme rcmained healed as long as they comply \\ ith compression therapy. Since the underlyIIlg cllology of the ulccr IS not treated with medical therapy, such treatmcnt call only be considered palliativc. Ilowc\'cr. as morc IS learned about modulating the wound healing proccss. palliation may bc c\tenuell for the life of the patient. In order to e\,aluatc properly the many therapeutic modali· ties that arc being apphed III the treatment of chroniC venous disease the Ad Iloc Commillec on Rcporting Standards III Venous Disease of the Society of Vascular Surgery and the NOflh American Chapter of the International Society for Car-
dlO\,ascular Surgery have recommended the usc of a classd"ication designed to allO\\ such compartsons.~< Limbs With chronic \enous disease should thus be classified accordlllg to climcal signs (C). etiology (E). ana tontlC dIStribution (A). and pathophysiologic condllion (P) (sec ExhIbIt )-1 3). Any limb with possible chronic venous disease i:-. first placed into one of seven clinical classes (Cn 0) according to objectt\'e clinical signs. and is further characteri/ed as being asymptomatic (ell fo.,d or symptomatic (en ",s). Since therapy may al· ter the clinical category of chroniC venous disease . limbs should be reclassified after any form of medical or surgica l treatment. The venous dysfunction encountered is thc.!n 10 be classified accordlllg to olle of threc mutually cxcluslve categorics: congenllal (E.). primary (E,,). or secondary (t,). Next. the anatomic site or sites affected \\!th venous disease arc to be descnbed as IIlvolvlIlg the superfic,"1 (A,). deep (All), or perforating (Ap) veins. Finally. the pathophYSIologIc rcason for the de\'c lopment of signs and symptoms of chronic \'cnous dIsease arc to be determined as belllg the result of reflux (P II.>. obstruction (Po). or both (P It ,II). Observance ol'thls classification in the clinical arena will lead to an improve· ment JI1 co:nmul11CallOllS 111 the field of venous disorders and help in the cva luation and proper application of therapeutic regimens.
E~hibit
14-3 ChronLc Lower J·xtremity Venous DLsease
CLI'IICAL CLASSIFICATION Clnss
o I
2 3 4
5 6
Clinical Description No visible signs of venous diseasc Telangiectasias. reticular \ems. malleolar flare Varicose veins l.dema without skin changes Skin chl.lngcs ascribed to venous dlsensc (eg. plgmclll3l1oll. \cnous eX/em3. IlpodcrmalOsclcrosis) Skin chnngc!'. as defined abO\c wllh healcd ulceration Skill changes as defined nbo\'e wllh aClivc ulceration
ETIOLOGIC CLASSIFICAl ION Eliolog~
Congenital PrilHllr~
S('condar~
DC!lcriplion
Cau!'.c of chronic venous dl:-,c
"cill~
Imohcd
SUI)crficial Dccp Pcrforatinj!
CLASSIFICATION
Dc~criplion
Telangiectasias rcticular veins and greatcr saphenou" \ellls: lesst.:r sapht.:nous \cms and nonsaphcnolls \CIIlS Inferior \·clla cava. Iliac. peh is. gonadal. femond. poplneal. tibml. and Illusculnr \ems Thigh and calf
PATIIOPIIYSIOLOGIC CLASSIFICATION ". ~ IlC
Dc'\crilHioll
I{
Refll" Ob ... ,ructlon Reflux and obstruction
o R,O
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In
Diagnosis
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19
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11
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23
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15
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CHAPTER
15
Management of the Neuropathic Foot Nancy Eljimiln
INTRODUCTION
The multidisciplinary cllmc rC{lulrcs speCial tralnlllg 111 treatment of chronic disabilities. Although the lIutl\ Idual training programs of profe!)sionals include 110rmal fOOl anatomy and biomechanics. few describe the neuropathic foot and associated complications. leading to inadequate medical ad\icc or treatment:' In the clinical settlllg no initial prob w lem is too small to addres!'i. The clinical team IS important and must treat minor trauma 1I11111ediately to prc\ ellt deterioration of thc condition. There is a destruct I\"e chain oftraullla surrounding the neuropathiC foot. as follows:
Medical research has pTm'idcd ad,'tUlCements in medication and technology that now extend the lives of patients with previously raral diseases: the prognosis has changed from fatality to chronic complications. I The chronic disease complication addressed in this chapter is neuropathy. The objective ofmanagclllcllt or the problem is to control progression and reduce amputations conservatively. The patient with neuropathy onen has dysvascular components that must be addressed by a medical team rather than onc specialty (sec Chapler 14. Diagnosis and Management of Vascular Ulcers). With the tcam approach the limb can be evaluated treated and monitored through follo\\-up to prm ide continucd alllbul~tion for the paticnt.': The team goal is the prevention or delay of Hmputation andior limb salvage of lower extremities. In the form3tion of clinical teams there has been a trend to include practitioners of several disciplines. including wound carc nurse. advanced practicc nurse. or cllIerostomalthcrapy (ET) nurse. diabctologisl endocrinologist. \'aseular surgeon. physical therapist. orthoIIstpcdorthist. orthopaedic surgeon podiatrist. and dermatologist. The multidisciplinary approach to treating foot problems is an optimum intervenllon for pre\'cnlloll of amputations. The dlsciplmes playing the 1110st nnporl
Trauma Innallllllation Ulceration Infection S. Absorption 6. Deformity 7. Disability
I. 2. 3. 4.
ThIS chain can be broken with proper obJcctlve Illl:asurcments. treatmcnt. and patient education. The patient with neuropathy requires a consistent follO\\'wup schedule relating to le\el ofin!)ensitivlty. history ofcompli w cations. and general physical condition. A patH.':nt with loss of protective sensation ( 109 of forcc) and no history of ulceration will require less frequent follow-up than the p~llient with a chronic breakdown history. Records shuuld rellect as Illany objective meaSUrl:IllCllts as possible and a method of classification of p~llient types. Management of the neuropathic and dys\ascular limb is a process of cont inuing c'v'aluallan. The process of his lory, c,amlnation. and chartlllg details cannot be o\'erempha~i/ed. All clinical findings should be charted and relayed to the patient\ primary care pro\- ider.
315
316
WOlNDLAKI
Although neuropathy exists in many disease processes, there afC concerns aboullhc growing number requiring management. When breakdown occurs in one neuropathic limb. the contralateral limb is commonly involved within 18 to 36
months. so prophylactic measures arc especially important. Many considerations must be addressed by the Icam treating the neuropathic and dysvascular limb before a treatment plan is developed . Once the plan is in place it is imperative 10 educate and involve the patient in the plan . PAT II OGENES IS
The neuropathic process is poorly understood and there arc man y theories regarding its etiology. When evaluating the neuropathic patient . the Illcdicallcam encounters the following ob!'ltaclcs:
• Lack or clear derinition or diabetic neuropathy • Absence or single repeatable tests or neuropathy that arc not dependent on either expensive technology or subjective clinical judgment • Varied manifestations of neuropathy: distal symmetric, l1lononcuropathics. autonomic neuropathies
• Separation of diabetes from other potential etiologies or neuropathy The neuropathic fOOl is alTceted by a trineuropathy, which con~isls oflhrcc phases that occur si multaneously: manifes-
tations of two of these phases arc shown in Figure 15 I. I . Sensory ncuroparhy - loss ofsens3tion.lc3ving patient
incapable of sensing pain and pressure. The patient has no sense of identit y with the feel. 2. MOlor neuropathy the loss of intrinsic muscles. resulting in clawed toes (Figure 15 2) and eventual foot drop. The ankle jerk renex is absent.' 3. Autonomic neuropathy the loss of autonomic systcm function. resulting in thc abscncc of sweat and oil production and Icaving skin dry and nonclastie. Until recently, all rorms or neuropathy were lumped together. It is now c lear that there arc different types, which develop dirrerently. Peripheral neuropathy can be broken down into two majo r groups: I. Gradual onset, those that develop gradually and arc usually pailllcs~. The exact cause is unkn own. but may be related to duration or diabetes and level or blood :,ugar control. Symptoms may include numbness. tingling. burning. and a pins-and-nccdlcs sensation . 2. Sudden onset and disappearance. those that develop suddenly (or acutely) and are almost always painrul . thcn the pain disappears leaving sensory loss.
Figure 15- 1 Fect orn pnttent with sensory. motor. nnd autonomic ncuropatlllcs . Maillfcsiallons of motor neuropathy (ddormJly. cI'l\\cd toes. loe ampulallon. rool lI11balnnce needmg 1111llledlate IIltencntlon) and autonomiC neuropathy (dry. crad,cd Sh.IIl) are c\ ident. Note the difference 111 trophIC change ... bemccn Ihe feet. Sour('('. Reprinted \\ Ith pcnnlsslOll from I I finmn. ClInIcal Management of thc Ncurop.uhlc Lltllb . ./0111'1/(/1 01 Pm\/Iu'lin ali(I 0,.,11011(-.\. Vol -l. No. I. pp. II:.!. Copynght l Amcnciln Academy ofOrthOlislS nnd Proslhcll"l"
Many belie\e that neuropathy is caused by hyperglycemia high le\ cis or glucose in the blood. Tight eontrol11lay be the best prevention of severe ncuropathy. MEIlICAL IIISTORY
The medical history is a useful \\ay to identify poteJ1lial neuropathy that Illay be present III many diseasc processes. The neuropathy may be isolated (ncne damage or cntrapmcnt). but for most chronic dlscasc processes the effcct is pcripheral. The mOSot common disease processes resulting in peripheral neuropathy arc the rollo\\ IIlg: • Diabetes • Spina birida • Ilanscn's disease
HlIl1agemell' olllt(' I\/('umpalhic FoOl
Figure 15- 2 Cla\\cd
10CS
Note the corn on the rourth toe caused
by rubbll1g lOp of shoe
• Systelllic erythematosus lupus • Acquired immunodeficiency syndrome (A I DS). human Immunodeficiency \ IrliS III fection. A IDS-related COI11-
pie, • • • • • •
Cancer Vital11l1l B deficH.!Ilcy Multiple sclerosis Uremia Vascular disease Charcot-Marie-Tooth muscle disease
TOXinS and to\IC syndromes can also calise insensitivitY in the limbs. IIlclliding those related to overuse of or e.xposllre to alcohol. arsenic. le'lll steroids. gollt and isoniazid. Many other chroniC complications may result in neuropathy. but the abo\"e list indicates why all patients mllst be c"alumcd for ncuropathy regardless of reported history. Congenital sensory loss. as in spina bifida. IS importanlto the examiner because the patient has never experienced normal sensation and cannotl!\aluate his or her own sensory status. ~ III Diabelic Neuropalh) Thl! most common discase process seen 111 neuropathy is diabetes. \\-hieh results in true pcripheral neuropathy. Statistics on diabetes are growing. and the medical cost related to diabetes," Ihe United Stales" currenlly S 14 billion per year. Included in this COst arc 54.000 lower extremity amputations
317
per year. of which 50% to 70°0 could hm c been prc\cllIcd by team management. It is cstlJnatcd lhut 50 u; 0 to M4°" of the lower extremity amputations wcrc preceded by a 1'001 ulcer. More than 14 million Americans have diabetes (halfare undiagnosed). with 700.000 cases diagnosed per year. In Ihe general population. t in 20 has diabetes. Many diabetics arc diagnosed when they present a nonheallng foot ulcer." If, Of major concern is the mortality mte after amputation. \\ hich is 50°0 within 3 to 5 years. The rate of contra lateral amputation IS 50°,'0 within 4 years. 1 Although there are sevcral different divisions of diahctl!s. the two main categorics arc insulin-dependent diabetes mellitus (100M). orlype I. and non insulin-dependent d",betes mellitus (NIDOM). or Iype II. In 100M the insulin defi· ciency is due to pancreas islet cell loss. II occurs at any age but is COlTunon in youth. NIDDM is IllOn.: frequellt in <.tdults bUI occurs al any age. The majorily ofpatien!> "lth NIDOM arc o\"cn. . ·cighL 'M The dys\"ascular patient may 31so be dtabellc. which leads to impaired healing ora limb that cannot dcli\"er anl1biollCS sufficiently to combat e ... tremity infection (sec ChHptcr 14). One limb may be severely insensitive. while the other IS mildly affected (sec figure 15 I). The loss of vasculanty caused by calcified arteries or 3 disease process is first referred to the vascular surgeon fbr pOSSIble correctton or Improvement. The four types of stress that lead to ulceration and destruCtion oftlssuc tn the nl!urnpathlc 11mb ~Ire as flllhms. I. Ischemic necrosis is usually sc,;en llnlhe lateral side of thc fifth metatarsal head and is due tn \\-caring a shoe thai i~ 100 narrO\\ . Thl! ischemia is caused by a \·cry low Ic\"cl of pressure (2 to 3 psi) mcr a long period of tllne. causing death of the lIssue 2. Mechanical disrupllon occurs \\hen a direct II1Jury caused by high prcssurl! (600 + psi) inflicts imll1c,;dlate damagc 10 tissue. This can also be caused hy heat or chemicals that damage the skill. Such JIljuries COIllmonly occur by stepping on a foreign object. 3. Inflammatory destructIon occurs \\ Ith repetit i\ c moderate pressures (40 to 60 psi). Inllal11l11atlon dc\clops and \\eakens the tisslle. Il!adtng 10 callus formation and ulceration from Iholls3mts of repetitions per day. 4. Osteomyelitis (and other sepsis) destruction is the result of a moderate force in the presencc infection. Infection is spread i.lS forces an: applll:d by Intl!rl11l1tent prl!ssure. 1~
or
Thc highest incidence of ulceration occurs at sites of previous ulceration. The history should bl! rc\ ie\\l!d carl!fully for previous ulcers or infcction. ~u A l1e\\ Iy healed ulcer IS covered by thlJ1 skllllhallS likely 10 tear. )11 completely healed ulcer areas. SC~lr tissue may adhere to ulUiI!rlYll1g structures.
The healed arcas arc composed of tissues of ddTcrent density and therefore compress uniquely, causing shear between
Neuromuscular System
oppo!'oing ljS~lIC duromclcrs. ! 1
A foot with neuropathy is dry, with small fissures, has toes that are clawed, and is incapable of sensing trauma. The rigid anesthetic foot is more likely to break down than a nexible anesthetic foot. lO The insensitive foot should be evaluated carefull y and bilaterally. Any form of peripheral neuropathy can produce the discomfort of paresthesia: prickling, burning. and jabbing sensations."·n The length of this period of discomfort is unknown; it varies among patients. Neuromuscular system examinations to assess for neurologic changes are the focus of the foot screening process and are described in detail later.
The progression of breakdown continues at the metatarsal heads due to migration of fat pads. lem'ing bone and skin (0 absorb shock. The neuropathiC limb has lost heat and cold sensation and reflex response. The incidence of ulceration is 71 ~'o on the forefoot. with the third metatarsal head Il'lQst commonly afTected followed by the great toe and first and finh metatarsal heads. Once breakdown has begun on the foot . 53°() of the cOl1lralatcrallimbs follo\\ the progression of brcakdov.. n \\ Ithin 4 years. Nc'Wly healed \vounds need time to mature and become strong. yet there \vill always be a potential for breakdown ill a previous area of ulceration. Scar compresses at a different rate titan other tissue. and the area of adherence \v'ill be prone to shear stresses/-1 Of all amputations. 86°0 could hme been prevented by pallent educallon and appropriate foot\\;ear. The aglllg process ,llone \\ III produce changes 10 appearance and alterations in senslti\ity.joint motion. and muscle-force production. 3ny of which can lead to dysfunctlon.: J Improper nutrition can also delay heallng.- · The majority of amputations are due 10 gangrcnc ('lO'.). followed by infection (71"0) and nonheallllg ulcers (65°;,) ..'/' The dry. dark ulcers of gangrene are usually found on toes or bony parts of Ihe foot. Neurop~lthic ulcers arc usually lnolSt and draining. Diabetic ncuropalhic ulcers occur III a fOOl with se\'ere sensory impi.urmcnl. yet they typically 11[I\e adequate blood supply for healing."" There arc 1\\0 types of gangrene: wet and dry. Dry gangrene is due to loss of nourishment to a part. followed by mummification. The area is dry. black. and shri\clcd and results In a well-defined Ime of demarcation with specific locali7Cltion and self-amputation (autoalllputation: Figure 15 3A). Wet gangrene is the necrosis of tissue followed by destruction caused by exceSSI\ C ll"lOlsture. Bacterial gases aCCUllllll<1le in the tissue. The Iine of demarcation is ill-defined and the limb is palllful. purple. and swollen. v.,.'et gangrene is coml11on when lIlf'ection e:\lsts . ~ ~" Figure 15 -38 shows wet gan,gn::ne of the fifth toe:. f)o 1101 debride. The patient needs immediate referral to a surgeon .
S\SI EMS RE\' IE\\ \r-.O E:\M11,\\TIO'\
A multisystems re\ic\\ and examination for the patient \\llh neuropathy IS reqUIred to determIne the cOlmpairments that will afTect \\ound healing and require management. Four systems 10 rc\icw for this patient population are the ncuromuscular system. the vascular system. the musculoskeleta l system. and the integumentary system.
Research Wisdom: Interventions for Paresthesia Paresthesia may be helped by use of a transcutaneous electronic nerve stimulator (TENS) unit, which generates small pulses of electriCity similar to an electric massage. Another method of controlling the discomfort is with topical creams.3.),,34
Vascular System Peripheral vascular disease (PVD) is a scnous complication afTecting millions of Americans. Of the 500,000 vascular-related ulcerations, 10%, arc arterial and 70 0 0 are venous ulcerations; some individuals have both venous and arterial diseases. Many patients with neuropathy also have PVO. Therefore. it is critical to review the vascular history bcfore planning any intervention to identify strategies that arc being used to manage vascular problems that will affect the prognosis and outcome for the patient. Some of the related circulatory systems diseases that usually accompany neuropathy and management recommendations are described here. Chapter 14 describes the pathogenesis and management of vascular problems in more detail. Atherosclerosis is also known as hardcning of the arteries. The interior wa ll of arteries is usually smooth, but with atherosclerosis platelels, calcium. and connecth"c tissue de· posit on the walls. In early stages the patient may experience intermittent claudication or cramping in the lower limb. which goes away \vith rest. As the disease progresses. symptoms appear when the patient is not wa lkin g (rest pain).' ~ Arterial compromise can be noted by Ihe loss of hair growth. shiny skin. atrophy. and cool skin over the toes. H Atherosclerosis leads to impaired circulation in the legs and is one of the most important causes of gangrene. leading to amputation. 16 Arterial ulcers are located on tips or between toes. heel,
A1anagemel/t a/the Neuropathic FOOl
319
Figure 15-JA Dry gangrene. uch a lesion needs immediate re-
Figure 15-38 Wet gangrene. Such a lesion needs immediate re-
ferral
ferral to a surgeon. There is probable infection.
10
a surgeon. II should
nOI
be debrided .
metatarsal heads, side or sole of foot. and above the lateral malleoli . The ulcer will look punched-out, with wc ll-demarcated edges, and be nonbleeding (sec Color Plate 48). The ulcer base may be deep and pale or black and necrotic. Treatment involves vascular reconstruction, bed rest. and immobililation. Arterialllicers have a poor prognosis. Misdiagnosis of an arterial ulcer as a venous ulcer can lead to serious compl icalians. The venous slasis ulceration has a better prognosis for healing than the arterial ischemic ulceration. Veins are less c lastic than arteries. The valves within veins no longer function to return blood to the heart against gravity. leaving blood to pool in the lower limb. The pooling does not allow new oxygenated blood into the area, and th e cell walls of the veins begin to break down . The waste blood products begin to weep through the lower limb. Venous stasis ulcerations arc commonl y located in the anteromedial malleolus area and pretibial area. The ulcerations are irregular in shape, surrounded by bluish. brown skin. These ulcers are exudative and show evidence of bleeding. Treatmen t of venous stasis ulcerations begins with leg clevation. 17 The limb mu st be treated with compression bandages or an Unna bool. The Unna boot is a semirigid dress-
ing of gelatin and z inc oxide. Its application protects vul nerable skin from the weeping exudate. especially below thc ulcer site. The Unna boot is applied weI. When it dries it forms a nonelastic. nonexpandable. non shrinkable. porous mold that sticks to the skin . This treatment has been used on venous stasis for 100 years. It is a means of controll ing edema when it is app lied across a joint. The motion of the joint generates a pumping action. I The chronic venOliS stasis lower limb without an open ulceration will show signs of edema that must be controlled. The presence of small water blisters or weeping wi ll be a sign that compression should begin (see Color Plates 53 lIml 54). This limb should be treated with pressure-gradiated stockings as daily prevention ; an Unna boot with Ace bandage wrap is required for severe edema or pcriods of breakdown. Press ure-gradiated stockings have a graduated pressure to facilitate pumping action and assist the venous system in removing nuid s from the lower limb. Anticmbolism stockings are not de signed for the ambulatory patient and do not supply the pumping action required. All ti embolism compression is for the recumbent hospitali zed patient. Compression can be ordered to begin at the metatarsal heads and decrease pressure in th e calfas a further assist to
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the venous system. Most patients do well with compression in the range of 30 to 40 mm Hg at the foot and ankle. When using these stockings for the neuropathic ldysvascular patient remember to avoid seams around bony prominences, and never place a zipper over the malleoli.
When venous stasis ulceration occurs on one limb. begin compression therapy on the contralateral side. The appearance of small water blisters or weeping is a sign that compression should beglO. Chapter 9 describes procedures for management of cdema. Musculoskeletal System Examination The musculoskeletal system examination includes examination of joint integrity, range of motion. skeletal deformity. and muscle strength. Motor neuropathy will distort skeletal alignment and Charcot jOlOt will lea,e a foot deformed as shown in Figure 15· 14. An analysis of abnormal gait should also be included. Beginning with the joint range of motion review. it is important that the foot has a dorsifleXion range of at least 10' to allow ambulation without harm to the great toc. 111 The forces on the plantar surface can peak to 275°-0 of body weight when running and 80°/'0 when walking. '
prominence is due to the constant high forces and must be provided an area of pressure relierbefore ulceration occurs. A sinus tract formation will result when previous areas of ulceration heal over a pocket of bacteria instead of healing from internal to external tissues. The small pocket ofbacteria will be moved anteriorly through the tissues, causing infection to spread. A common complication of the neuropathic patient IS se'ere foot deformity followmg neuropath,c fractures or Charcot arthropathy including joint subluxation or dislocation (Figure 15 14). The presence of severe foot deformity has been shown to be predictive of prolonged healing time for patients treated with total-contact casting. Sinacore et al. 4J found that fixed foot deformity prolonged healing of ulcers with total-contact castll1g when located in the midfoot and rcarfoot. Ulcers located in 'he mid foot healed in 73 ± 29 days, rearfool ulcers 90 ± 19 days. Individuals without fixed deformities with chronic diabetes mellitus and those with forefoot ulcers healed in 41 days. Therefore, early detection during the musculoskeletal examination of a fixed foot deformity in a patient with an ulcer located III the mid root or rearfoot can be used to determine a prognosIs that healmg time \vill be significantly longer when it total-contact cast is used as the trcatment IIltervention . Motor ncuropathy produces cOlllmon abnormal gall characteristics 111 the neuropathiC population . The shoes arc \I,.·orn on the lateral side of the sole because of a varlls deformllY (sec Figure 15 ·-4A). ThiS \\cakness often callses ankle InJuries. A ncr further deterionllion. footdrop can occur. The sti ffness III the complex jomt structures leads to abnormal 1110tion In thc foot's functioll.
Clinical Wisdom: Mod/ficalion of a Standard-Depth Shoe To compensate for varus galt abnormalities, shoes need to be modified. The modifications reqUired are (1) a full, lateral-flare sale as shown in Figure 15-48, (2) a strong counter to support the heel, and (3) a high top to support the ankle. A standard-depth shoe can be modified by an orthotist, or a shoe repairperson may be able to do the job if gUided. While not all orthotlsts will agree to modify an existing shoe, others will. ThIS will save the patient money.
Integumenlar) S)Slem
E\~lInination
Integumentary system cxamination of the foot Includes the toenails. Toenail derormllies arc commonly seen in the neuropathic foot. Jlypertrophic nails arc causcd by fungus and are common III the diabctic population. The nails tear
.HlIlIlIgeme11l ollhe .\t!w-opllIhic' rim/
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Figu re I5-4A Shoe 1'\ worn on the lateral side dut.! to a varus dcfonmty. SOllrn'-" Rt.!pnntcd \\ ith permission rrom R.B. Chambers and N. 1-.1 flman. Orthotic Management orthc Neuropathic and Dysvascular Patient. 111 AlIas (lOrl/wse,\ (JIu/.-I'oi.'if/I'(' Del'ices, 3rd. edition, B. Goldberg .lI1d J.D llsu. cds .. p. 443. ( 1997. MoshyYear Book. Inc
shoe lining and create areas of rough surface to abrade the
toes (sec Figure 15 5). Nail care for onychomycosis (fungus). ingrown toenails. and trimming must be performed by trained medical pl!rsonnel to ensure injury is not inniclcd. Soft corns are hyperkeratotic lesions found between toes
(usually between the fourth and fifih toes) due to pressure of an opposing toe in
it
region lhm is
moist. ~"
Figure Is-4B Standard-depth shoe with sole 1ll0dd·ll:alJon. The shoe has a full-narc so le. a strong counter, and.) high Hlp 10 slabll/c the varus abnormality. Source: Repf1nlcd \\ Ilh panllssion from R.B. Chambers and N, E1ftman. Orthotic Managemcnt urthe Ncuropathic and Oys\a'tcular Pattent. 111 Iflw 0/ O,.,hon'.\' (Wt/. IHiHiw! De\'ices, 3rd. editIOn. B. Goldberg and J.D. 11su. cds .. p. 443. (
1997. Mosby-Year Book. Inc.
Injury and mac-
eration of the toes IS commonly controlled by the use of lamb's \\"001 between the toes or tube foam to space toes and pre-
vent friction (Figures 15 6A and B). Buildup of callus is indicative of high pressures and stress of an isolated area that must be relieved, The thickening of the skin in the area ofa callus is preceded by abnormal pressure or friction. NoW Areas of excess pressure require pressure redistribution
in the clinic setting rather than scheduling additional appointments. Dryness of the skin is the result of autonomic neuropathy in which the sweat and oil production is decreased and moisture must be replaced. Loss of hair growth may be indicative of vascular Impairment. Ulcerations that are necrotic are debrided to allow heallIlg to progress from internal to external tissues for optimum closure of the ulcer site,
Another common occurrence is burns, duc 10 either heat or chemicals such as o\er-the-counter remedies. Soaking the foot in hot water is a specific cause of burns, A coml11on wisdom is that neuropathic pallents should 1IC.'I 'C.'I'WJlIh their feet. The insensitive foot cannot produce the warning signals necessary to prevent severe burns (see Chapter 4). Dermatologic conditions can afTect treatment programs until they are resolved. Necrobiosis can be confused with venous stasis disease but docs not rl!quirc or rl!spolld to extensive tremlnent. The round firm plaques ofrcddbh brown to yellow are seen three times more oficnll1 \\-0111CI1. I < "hThese ulcerations are C0111111011 along the tibia and requirc only protective dreSSings.
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Figure 15-5 This foot has sofi corns between locs.thickened tocand onychomycosIs (fungal) infection.
nail~.
Figure IS- 6,\ Lamb\ \\001 plcec:-. an: plal.:l.'d hcml.'cn I.'..lch IO!.' to pn.:\Cnlm:lCCratltlll. They shnultl he rcplaccd ,I ncr bathing. SOl/rH"
RcprinlcLi \\ IIh pcrnliSSIOI1 frulll R.ll Chambers ancJ N. Uftman. Orthotic Management of the Ncuropathu.: ..lIlcJ I)) s\Jsl:ular PatH!'n!. III ..It/d.\ of Or,lw.\n (IIul.h.\I\II\"(.' OtT/cn ..~n1. edition. Il (jold~rg and J.D. Iisu. cds .. Jl . ..t..tl. t 1997. ~hlshy-\~ar llooJ...lnc. Clinical Wisdom: Tube Foam and Lamb's Wool for QUIck Relief of Pressure on Toes
Claw toes. hammer toes. calluses, corns, and small ulcerations can be reheved of pressure by inserts and shoe modificalions and spaced with tube foam or lamb's wool separators to allow air flow. Separators prevent maceration and skin breakdown; they should be removed before and replaced after bathing. In addition, the custom tube foam separator serves as a toe separator, reduces shear from the shoe, cushions metatarsal heads, and can be used as a positioner for overlappIng toes. Figure 15-6A shows lamb's wool pIeces placed between toes. Figure 15-68 shows a tube foam toe separator in place. Figure 15-6C and Exhibit 15-1 Illustrate and describe the diagram of steps to create a tube foam separator. The tube foam is available from podiatric supply companies.
Fi~ur(> 15-68 1\ CU'itom tuhe foam tue 'ieparalor. SOIIIH': Reprinted \\-lIh PCrIlliSSUUl fmlll R.B thamhers and N. I· Inman. Orthollc f\.lani.1gement of the Neuropatillc ;.lnd Dys\<'lscular PallCnt. III III", of Orthow.\ (//u/l \\/\11\'(' /)n"/(-('\ .."\rd edition. B. (iuld~rg and J.D. II .. u. cds .. p...n I. (" 1997. Mushy- Year BuoJ.... Inc.
Maltagem em
(~l (lI e
Nellroparhic rem(
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Ex h ibit 15-1 In st ructions To Make a Foam Toe Scp.ualor
Make a cus tom foam toe separator (Figures 15 6B and
15 6Ci by the fo llowing steps: 1. Select
Figure I5-6C Diagram of construct ion o f a tube foam se paralor.
11 size of tube foam with a diameter that will not const ri ct the toe. 2. Cut a 21/2- to 3-inc h piece of lhe foum . 3. To make the toe cuff: 3. Measure back Yl to 0/4 inch from one end of the lube foam and mark . b. Cut across the diame ter of the tube three fourths of the way th rough. c. S lit up the tube to the markin g on the side that is cut to the diameter cut (sec diagram) d . The foam w ill flattcn o ut (sec diagram) . c. The tu be will s lip o\er the toc and the flat section will be located on thc plantar s urface of the fool.
Keratoderma plantaris, characteri zed by keratin cracks and ulcerations. is caused by the loss of sweat and oi l clasticity in the sk in (autonomic neuropathy). As keratin builds up it creates small fissures that allow entrance of bacteria, and infect ion begins. The entire sole around the margin of the heel will undergo difTuse thickening and develop painful fissures if the fOOl is sensate or go undetected ifinscnsate (see Figure 15 7). Prevention inc ludes reduction of keratin buildup and retention of skin moisture.2Q There arc many forms of rashes and dermatological conditions that must bc eva luated and trcatcd in thc ncuropathic limb. These are usually di scovered by inspection rather than patient di scomfort. Typical skin cond itions in the diabetic population include shin spots and diabetic bullae (with less frequency than necrobiosi s):'~
Infections arc com mon ly seen in the neuropathic foot. including Pseudomonas infection, which is bacterial growth that occurs wi thin a moist environment. Signs and symptoms of infection are lIsually absent in the neuropathic foot even th ough thc infection is present and virulent due to impaired circulation and immunosuppress ion. Both arc other common coimpairmcnts of neuropathy. The problems of infcction are idcntifi ed durin g the integumentary system review. Sec Chapter 8. Management of Exudate and Infection, for strategies to assess and treat infection. Dry gang rene is another findin g that may be discovered during the integumentary system review. When dry gangrene is present. there is a line of demarcation at which the body will autoamputate the affected area. This proce ss of au toamputation could take weeks to l11onths;42 it is nature 's way of protecting the body from infection and should not be disturbed. Figure 15- 3A (Wagner grade 5) is a photograph of a foot with dry gangre ne. A patient with dry ga ngrene nceds immediate refe rral to the surgeo n.
Figure 15-7 Typical neuropathi c foot \\ ith keratoderma plantaris. Note the dry. c rackcd skin. di rt imbeddcd in the s kin . ope n wounds. and the absence o f drcss ing due 10 lack of
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FURTlIER VISUAL AND PHYSICAL ASSESSMENTS
Wound Assessment
LX:JJ11IO:Jtlon ofthc ncuropathlc limb IIlcludcs further VIsual and phy~ical examination to m'oid future complications. The patient is nc\er asked for his or hcr O\,n foot evaluation. The shoes arc remm.-ed to allow the practitioner to examine the foot. The neuropathic patient ,!,.'ill not limp. even with a root ulceration (see Figures 15 7 and 15 8). Inspection should be both weight bearing and non weight bearing. FOOf\\ear Assessment
The footwear must be examined for wear of orthosis and sock patterns indicating excessive pressure. The ends of the toes should be examined for injury caused by a short shoe. Figure 158 shows a toe wound caused by a short shoe. Notice the toe is to the end of the shoe insole. Figure 15 18 shows the alignment required when fitting a shoe for proper weight distribution and length measurement. The interventions section of this chapter describcs orthotics and adaptive equipment and includes in~tructions in footwear interventions. Shoes should show a normal wear paltern on the lateral heel of the sole as contrasted with the pattern in Figure 15 4A . Shoes should be resoled on a regular basis to keep sides from wearing down. Inserts arc replaced as required when n.:liefmodifications arc no longer sulTicient and shock absorpllon IS decreased.
The Wagner scale~7 for grading neuropathic ulccrs classines ulcer severity in six grades based on the depth or the ulcer and the presence of inrection or necrosis. Ulcer grading is useful for prognosis and for selecti on of treatment intervention. In addition, the Wagner ulcer grading system is a uniform system that is used by health care practitioners or different disciplines to describe ulcers in neuropathic limbs. Ulcers with low grades are managed by conservative measures, whereas ulcers with higher grades are a direct threat to limb loss and require surgical managcmcnt. The neuropathic limb often suffers rrom dysvascularity as well; thererore, the system is oflen used ror both populations. The Wagner ulcer classification system dilTcrs from other grading systems by including a grade or O. which describes preulcerative skin. healed ulcers, and the presence ora bony deformity where the skin is intact. Preulcerative areas include calluses located under the metatarsal heads or areas or weight bearing."'M For continuity of documentation and communication the team must understand the Wagner scale of ulcer grading and usc it consistently. Exhibit 15 2 shows the six Wagner ulcer grades. The preferred conservative mcthod or treatment is guided by the Wagner grade. Exhibit 15 3 shows how the dilTerent grades dictate different treatment strategies.
Sensation Testing When evaluated ror insensitivity. most patients who had hypoesthesia could sense pinprick and cotton wisp applications. Patients wi th foot ulcers were observed to have less
Exhibit 15-2 Wagner Scale
Grade
Description
Grade 0 Grade I Grade 2
Skin iniaci (Figure 15 9A) Superficial ulcer (Figure 15 9B) Deeper ulcer to tendon or bone
Grade 3
Grade 4 Grade 5 Fi~ur(' 15 8 Short . . ho~_ The toe extends 10 the end of the Insole. Sown'" Reprinted \\llh permis . . lon from N. IJflmnn. Clinical Managemenl of Iht: Neuropalhic Limb. Journal Pmsfhefics alll/
or
Vol. 4. No. I. pp " I 12. Copyrighl ( American Academy of Orlhll"IS and Proslhell . . ls.
OI"lJw(/C'i.
(Figure 15 9C) Ulcer has abscess or osteomycillis (Figure 15 9D) Gangrene on forefool (Figure 15 9F) Gangrene over major porllon of foot (Figure 15 9F)
SOlln"i' Reprinlcd wilh permission rrom ~ ~ W Wagner. The Dysvascular FOOl: A SYSICIll ror DiagnOSIs and TrcatmcllI. FoOl amll"kle, 2:64·122. ~ 1981. Wilham~ & Wilkllls"
AllIl1agemelll qf the Neuropathic Fool
Figure IS- 9H Superficiaiulcer. Wagner grade I.
Figure 15-9A Sk in in tact. Wagner grade O.
Fi gure 15-9C Deeper ulcer to tcndon or bone. Wagner grade 2.
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Figure IS- 9E Gangrene on forcroot. Wagner grndc 4.
F il! ure 15- 91> Ul cer ha s ab scess or osteomyeli tis. Wagner grade 3.
Figure 15- 91' Gangrene Q\cr major portion of fool. Wagner grade 5.
\lolJugemel1l
pressure .\'el/.wlioll than those without foot ulcers. ~j In 1898
von Frey attempted to slandardile the stimuli for testing the subjccti\c sense of light touch by lIsing a series of horse hairs of varying thicknesses and stiffness. Wienstcin used nylon 1110nofilamcIlts mounted on Lucile rods as substitutes for the hairs. ~1 The Semmcs-Wienstein monofilaments can be obtained commerCially 111 elaborate sets for precise measurcment. but research at Carvi lie Ilansen's Disease Center, Carville. LouisIana. has consolidatcd the testing to three si:7es of monori laments for grading the IIlscnsitive foot. The 4. 17 monofilamcnt supplics 1 g of force and is indicative of normal sensation. If the patient cannot feel the next monofilament (5.07). he or she docs not have the protective sensation leycl of 10 g and cannot sense trauma to the fOOl to cease weight bearing. Failure to sense the 10-g monofilamcnt is used as the dctcrl11l1ling nlctor for usc of protect he footwear and accommouau\'e orthotics. No patient with protcctive sensation can ambulate on an ulcerated fool. /\ large percentage of patients do not feci the largest monofilament (6.10). "hich indicales a loss of sensa lion at 75 g. Thi> largest-diamcter monofilament indicates <.In insensate foot th<.lt must be accommodated and followed closely. Usc of thc monofilament is not to bc confused with the testing for sharp dull !;cnsatlon. The sharp:'dull test stImulates multiplc nerves as opposed to a single-point perception tcst. The monofilament is a single-point perception test and requires the e.xamlllcr to place the monofilament on the skin. press until the monofilament bends (diameter of monofilament controls point of bend), and removc from the skin sur-
or/he Vl.'tII1Jlwl/Ji(' Nml
327
face. The monorilamcnts arc tc!)tcd and detennllled LO be reliable at the 95% confidence Ic\-c l. ~· The patient is to respond when he or she feels thc pressure sensation. To avoid errors in tcsting, the monofilament IS nc\cr used 111 arcas of scarring. calluses. or necrotic tis~ue . The bilateral testing for sensation is especially important fOrlhe ullIlatcral and bilateral amputee to determine areas ofinsensiti\, ity ;lIld progrcssion of the neuropathy. Figure 15 10 sho\\ s proper mcthod for monofilament testing procedure , Note the bend of the monofilamellt. This must occur to measurc correct pressure sensatioll. Birke. ~' at Ilansen \ Disease Center. developed a risk classification system based on the loss of protcctlve sensation. Loss of protecti\c sensation. history of prior ulceration. and reduced circulatory perfusion are important factors in developnlent of foot ulcers. A risk classification system based on these factors is uscfuilll identifying patients who would benefit from different levels of intervention (Lxhlbll 15 3). Risk is classified by fOllr grades: O. no Joss of protective sensation: I, loss of protective sensation (no deformity or history of plantar ulceration); 2, loss of prate clIve sensation and deformilY or abnormal blood no" \\ ilhOlll hlSlory of planlar ulcer; and 3, hislOry orplanlar ulcer. Three IIllerVCntions have proven effective in reducing risk of ulceration : protective footwear. patient education. and frequent clinic follow-up. For example. when a patient's ulcer is grade 0, preulceration. and the patient can sense the IO-g monofilament (has protective sensation), he or she will sense pam before damage occurs to the feet. Patienh In this category
Figure 15-- 10 Monorilamcnt tt!~tll1g. Source: Reprinted with permIssion from R.B. Chambers and N Ullman . Orthullc ~hni.lgement of thc NeuropathiC and Dysvascular Patlcnt. In Atlm (~l Orthoses and Assislit'e /)nices. Jrd. edItion. 13 Goldberg .lIld J I> Iisu. cds .. p, 433.
(' I()l)7. Mosby-Year Book. Inc.
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io.:).hibil 15-J ConSCnall\C Management by W
"lrgner Ulcer Gndc and Recornrncndcd Treall1lelll Grade 0 may be trt.::awd With cxtra·dcpth shoc and Insert Crade I cast or PIJsla/()IC hcailllg shoe. reducing \\eight to ulccr;lIiun; anllbic.1IIC inlcncntlon as required"" Gn,de 2 debridement and cast; antibiotic IIllcncntion as n:qulrcd41
reman:: IIlfi:ctcd tisslie and c.p\l; antlhlotlc inter·
Gnulc 3
\-clllUm 'IS rcquircd~~ .\'OIllH' 1) .. 1..
Ir()Tn M Cilugla and G, Mulder.lhe DlaNtlc 1-001.
H('(linl/ \lmw}.:('IIICfl/ II/ Foot (,'/c-cr\ 11/ ("lmmit' U(I/IIIt! (tm' . 1 ('l/lIinll Smlrn' firm/.. lor 1It'lIllhum: Pm!t'_\\/(m/ll~, D, Kra .. ncr. 10
cd. pr· 22~ 2.'\9, ,-.. 19911, Mo..,by IIca1111 Manascmclll PuhllCilllOll". Inc. and "-.\ Wagner. -, CIt,,\\'lkatiOlI tlllel 1i-('UlIII{'1If PmKI~I'"
/(11- /)Iuhel/{
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In the eyaluation process. PhYSical sIgns of upper extremity involvcment include chaeroarthropathy (motor neuropathy in upper cxtremity). when the patienl cannot touch his palms together in the prayer posItion. Another phys ical sign is atrophy of the \\:cb space between the thumb and first finger. This is the first sign of motor neuropathy in the hand. ConSIderation orthe hand deficit musl be ta"en inlo accoulll for donning. don'ing. and choice of closures for orthotics and footwear."" Little attention has been paid to the diabetic hand syndrome. or Iimited joint mobil lIy (LJM). III which the joints of the fingers and wrists become Illnited. This condition occurs 111 Joo'il to 50 no of people who hm·e had type I diabetes for more than J 5 years. One test for LJ~1 IS pl:Tformed by hm·ing thc patient place the hands flat on a table Patients wJlh seyere LJt\.1 ,. .·!l1 not be abk to nallen the fingers onto the table. The sk in \\ ill a lso be thic" and can be tented on the bac" of the metacmpophalangeal (MCP)joint (sec Figure 15 II).
19X.l
Body Temperature Testing usually do \vell with a standard shoe of correct sizing and a Simple shoc~-absorb,"g pad. The patient without protecttvc sensation will not cease ambulatlllg \\ hen damage begins to tisslies. Patients with feet such as those in Figure 15 ·7 who walk into the climc are insensate. They require extra-depth shoes with a total-contact accommodati\c insert to distribute prcssure and reduce forces on 4lTeas of potential breakdown. The insert may be molded to the patil.!nt or fabricated on a cast. The cast docs not have correcti\·e forces added only accomll1odation. The accommodative insert docs nOI apply correction; it rills only the spaces between the nat shoe and the root contours. Any rorce added will receive rull weight bearing and breakdown will occur. Ir the addition or metatarsal head (MTII) pads orscaphoid pads is requested these pads must be ora soli durometer. Rigid pad additions will cause excess pressure and ulcerations. The MTII pads are placed proximal to the metatarsal heads to rcdistributc the \'v·eight from the heads to the metatarsal shans. Testlllg for \ibratory st.!nsmion may be accomplished by using the bioesthesiometcr, This instrumcnt is essentially an electric~lI tuning fork that uses repetitive mechanical indenunion of skin delivcred at a prescribed frequcncy and amplitudc. '" Thc slmplc graduated tuning fork is a rapid means of sensory testing ,~~I>The purpose of all sensory tcsting equipmcnt IS to idcJ1Iify thosc at risk.~· Upper and lo\\"cr extremity peripheral neuropathy is prcsent when sensatIon tc~tll1g rc\cals that the le\el of sensation Joss is symmctric and equidistant from the SplllC in both arms and legs. The hands or these patients should be considered
Since Hippocrates. phYSIcians ha\"\." "nO\\n that body tcmperature variations otTer important clues for diagnosing disease. Diagnoslic tools COJ1yeTl infrared radiation and display il on monitors \\ilh the lise ofthcrmography, There arc many
Fi~ure 15- 11 Neuropathic hand Mtllor llellrop.Hhy tesllIlg rc\cals tClltlng on the had. of thc MCr .101111. cla\\ lilt! (If the lingers. and atrophy of the \\eh 'pace het\\\.'cn the thumh i..lIu..lthc first ftn ger
\/lI11agemellf o/Ihl' V('umpulhic Foot
329
ObJecl1\es and Procedure for Taklllg Temperature
r
>bJCCIIVCS for taJ..lI1g temper.Hure:
• To e\alualc baseline lemperature al sites of high incidence of ulceration • To dl'lcrmme;: pre;:..,e;:l1cl;! of II1I1::JJllmallOn • To e;:\aluate sites of b~ISc11111;! ek\aled te;:l11pcraturc for de· crease in tcmperature;: aBer IIlten enllon to relieve pres· sure Proceliure for taJ..lIlg and recording temperatures.
l"pose the bare sJ..m ofthe foot to the room temperature for 5 J() mlilutes before rccordlng any temperature. 1 r'lJ..e temperalure ,II J() local ions on the so le of foOl and toes (shO\\ n by circles 011 foot evaluation form I,hlbll 15 1). 1 I'ollm\ ... teps lor me,ISUnl1g temperature. ~ Recon.l re;:adlllgs III t..legrces at l;!<.Jch iocmion on fOOl cvalu· allon form and date 5. Record rC<Jdlllgs al each location on successivc cV<.Jlua· tlons belO\\ the Iilillal readmg and date
Figure 15-12A Infrared scanner temperature display.
methods of acquiring surface temperatures. Thermistors or thermocouples arc accurate recording dc\ ICCS that, when touched to the skin for 10 seconds. give a Ilumeric display of tell1perature. ~'1 The infrared unit allows accurate immediate spot temperature readll1g and allows the feature of scanning the foot quickly. The use of temperaturc is \"aillable as an objecli\c measurement of tissue damage and inflammation produced by repeated mechanical (pressure) trauma /"· When evaluating the limb. the most distal aspects of extremities arc cool. Muscular areas with good blood supply arc wanner than bony regions. Arches arc several degrees warmer than heels or toCS. ~" ExceSSive heat in an area of the foot is a vascular respo nse to trauma. The trauma may be due to external
Prm:edure lor Usc of an Infrare;:d Scanner Thermometer Follo\\ these stel'~ in me:lsuring temperature nith an infrared scanner thermometer:
Tcmperature testmg may be done \\ IIh or without con· lacl of skill 1. Read the first number seen 3 Avoid pressure against the sJ..1I\ Ihat causes ischemia. ("Ilurlc.,y of Mca ... urcmcnb 1m: NC\1; Orlean .... LOUisiana (Sec
Hgurc ... 15 12A and 15 t20)
Figure IS-J28 PlaCing the infrared scanner for Icmperatun!
reading.
forces. infection. Charcot JOint, or other mternal complications. The examiner can feci the increased hC~1I manually ~lIld determine where complications may reside. but without instrumentation to record actual numbers. there will not be objective documentation for follow-up and comparison. Using a surface-sensing temperature device (thennocouple or infrared). temperature!'! arc recorded in predetermined nreas, usually those related to common arcns ofbrcakdO\\ll. When there is one definite area \\· ho~e temperature is J I higher
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'"I
than that ofauJacent areas, It can be assumed an area of high pressure or stress. If there is no current breakdown, this area mllst be relieved of pressure and the pressure distributed over
the remaining weight-bearing surfaces. Upon follow-up of this same palienl the temperature difTerentiation should decrease as healing of tissue progresses. In a comparison of
unrestricted data collection." Progress is also bemg made to produce live scanning of the foot in order to produce a positive mold for orthotics as well as custom shoes. tll Using computed three-dimensional digitizing computer graphics, a plastic sock may be molded to the patient and converted to a shoe cast. M
contralateral limbs. vascular impainnent should be suspected when one limb is significantly colder. or distal portions of
the fool show an extreme drop in temperature. A chronic hot spot points to the fact that there is a chronic stress or an underlying bone or joint problem. Increased temperature tells that there is a problem and where it is not what it is! :!1
."rcssurr Tcstin~ A rubber mat was developed by R.l.llarris that would print light foot pressures in large light sqtlftres (formed by tall grid ridges) and heavier pressures in darker smaller squares (deep ridges).'The Iiams mat will give a gridded analysis ofpressure distribution at a relatively 10\, cost per patient. The Ilarris mat can be used ror static and dynamic assessment and provide permanent records. Figure 15- 13 shows an imprint on a Ilarris mat. The darker arcas arc areas of high pressure. Force plates ha\-e gi\'en us \'aluable information regarding peak pressures during ambulation. but represent a single step upon the plate. Attempts to place sensors in the shoe, have been unreliable because of the sensor structure and attachment within the shoe .... 1 The new age of computer-aided documentation pro\'idcs color replicas of three-dimensional pressure recordings and illustrations that can be lIsed for static or dynamic documentation ,A lthough costs of the computeraided devices arc high. technology IS advancing to provide
Charcot Joi nl Exa mi nalion
Charcot joint (Charcot arthropathy) is a relatJ\ely painless. progressive. and degenerative arthropathy of single or multiple joints caused by underlying neuropathy. The neuropathy may be periosteal and not cutaneous. There arc several theories behind the causes of Charcot joint, as follows: • Multiple microtraumas to the jOints cause microfractures. These fractures lead to relaxation of the ligaments and joint destruction. 6 \ • There is increased blood flow (osteolysis) and bone reabsorption. Patients with Charcot joints have bounding pllises. • Changes in the spinal cord lead to trophic changes in bones and joints. • Osteoporosis is accompanied by an abnormal brittleness of the bones. leading to spontaneous fracturc ,M In clinical observations, the limb is usually painless. swollen. and red. Unhealed painless fractures arc ollen radiographically present. In advanced Charcot disease. there are multiple fractures accompanied by extensive bone dcmincrnlization and reabsorption. Later stages reveal architectural distortion of the foot with shortening and widening of the joint:lll The foot joints 1110st commonly affected are the following:
• • • •
Figure 15- 13 Ilarns rnal pre:ssl1rc Ie:"tlng. record Darker areas represent lugher pressure:.
tarsometatarsal (30%) metatarsophalangeal (30%) tarsus (24%) interphalangeal (4%)
Charcot joint is frequently misdiagnosed and mistreated. leaving the patient with deformities that require further medical intervention and/or expensive footwear (see Figure 15 14). The acute stage will show a foot that is 5° to 10° hotter than the contralateral limb in the same area. The red, hot, swollen foot will usually not ha,e a .kin opening or ulceration. Laboratory tests. including radiographs. may not
M allagemellf o{ fh e Nelllv plIfhic FoOl
331
show changes in the acute stage to differentiate Charcot disea se from other diagnoses. The duration of the cata strophic destruction, dissociation, and eventual recalcificati on fOllnd with Charcot joint will vary with the individual , but the average hea ling timc in a ca st for the hindfoot is 12 months; for the mid foot. 9 months; and for the forefoot , 6 months. By evaluating with comparative temperature measurcmcnts of the contralatcral foot, the stages can usually be verified by radiograph . As the involved fOOl temperature increases, thc destruction and dissociation are taking place. The temperature gradually decreases as recalcification is in progress. A radiograph shows that recal cification is complete when tempcratures bilaterall y arc within
3°F.
Figure 15-14 Classic Charcot rocker bottom root derormity. Note ulceration over bony deformity surrounded by callus formation .
The treatment plan for acute Charcot joint is the IOta lcontact cast. The ca st must be changed in I week to accolllmodate volume change s. Following the period of volullle changes. the cast should be changed every 2 to 3 weeks. When the tcmpcrature is equal to that of the other limb. the patient may be weaned gradua lly from the ca st to a splint and then 10 shoes. Follow-up should continue to ensure that there is no recurrence of an episode of Charcot joint.
Case Study: Charcot Arthropathy The patient was a 44-year-Old woman with a 15-year history of non-insulin-dependent diabetes mellitus (NIDDM). She had neuropathic extremities to mid-calf bilaterally. loss of sensation and motor function demonstrated by bilateral drop foot. She had a right foot Charcot arthropathy post 4 years. The extremity was treated with a series of total-contact casts for 11 months and gradually weaned to ankle-foot orthotics with shoes. Contralateral side used ankle-foot orthosis to control drop foot. The patient came to the clinic for an emergency checkup due to weekend traumatic injury to the left foot. She recalls twisting the left ankle and slight discomfort. Within an hour, there was swelling so she went to a local emergency department. The patient was told that she had possibly torn a ligament and was put in a precautionary plaster cast with a rubber walking pad . When the patient came to the clinic two days later, she was in a great deal of discomfort and the plaster cast seemed to have absorbed exudate. The toes were left exposed in the cast and had swollen beyond the con-
fines of the distal cast edge. When the cast was removed, it was observed that the walking pad had been forced through the plaster on the plantar surface and traumatized the entire plantar midfoot. The patient had Charcot arthropathy of the mid foot that was further destroyed by the nonreinforced walking pad . The edges of the plaster caused open abrasions to the exposed toes. leading to infection . The patient was treated for abrasions and put into a
total-contact cast. After 16 months, the Charcot episode was over but the foot was left with deformities that could not be accommodated in a standard shoe. A custom shoe was ordered for the left foot deformity. Key Points
1. Immediate total -contact casting could have reduced the deformities and length of treatment. 2. A total-contact cast differs from a standard short leg cast and should be applied by a skilled technician.
332
WOl
Nil (",.,
Ostcol1l~cliti~ E\.amin~,tion
The chllleal observat ions for Charcot jOint ::Ind osteomy-
INTERVENTlO,,/S Orthotics and Adaptive Equipment
elitis arc vcry similar. and the patient should be monitored close ly to verify the diagnosis. Laboratory tests will also be si milar. The only exec pilon would be the presence oran opening in the skill 10 allO\\ an entrance for bacteria to in fect the bone (sec rl gurc 15 lSA). 13kc the temperature over the best surrounding skill. Refer for IIlllllcdwtc medical management. The rccalcifiC\llion would not occur rad iographica lly as III ('harco! disease (rigure 15 158.) Verificat ion may be made for osteomyelitis \\ ilh a three-phase bone scan or biopsy.'" Diabetic patients \""th foot ulcers that expose bone should be treated for osteomyelitis. evcn if th ere IS no c\ldence of inflammation ,,7
Treatment of the neuropathic foot requires accommodation. relief of pressure /shear forces. and shock absorption. Regardless of materials used for accommodative inserts. the combinat ion of materials must be compressible by one half of original thickness to accommodate for pressure relief through the gait cyc le. z1 It is important to evaluate the materials you wi ll be utilizing in the manufacture of inserts. Cellular polyethylene foams such as Alip last lM • Plastuotc nl • and Pclitc™ arc composed of a mass of bubbles in a plastic and gas phase. The bubb les are cells Wllh li nes of mtersection called ribs o r strands and the \!';alls are ca ll ed wlIldows. In closed-cell materials the gases do not pass free ly: opcn-
Note puncture wound 0\ cr Ihe ri nh mc::laUlrsal hcad. Ihe SltC or the o:-.Icomychlls. SOllrn'. Rcprinted with perl111s:-'lon frol11 R.B. Ch,1I11bcrs and N. Uliman. OrthOI1C Management oflhc:: Nc::uropalillc ,111<1 Dys\ascular Paliel11. mlt/lI\" o/Orr/w\('s tim/ I\\/,tl\"(' lkl"l("("·. 3rd. edItion. U. Goldberg and J.D. Ii su. cds., p. ~W. t' 1997. Mnshy-)car Book. Inc
Figure IS- IS8 Radiograph of same fOOl ;:IS 111 FIgure 15 15A sh()\\s calCIfication change ... at the hcad of the fIfth metatarsal. SOllrce: Rcpnnted \\ IIh permISsion from RH. Chamber ... and N. 1·11"11110111. Onhol il,; Managemenl orlhe NClirupalhic Clnd DY"''''!sl,;ular Pattent.1Il lIlli, a/Or/I/O.H'.,· tlllcl.I\\H/iI"c J)C\·ICt'.\, 3rd c::dllion. B. Cioldhcrg and J.D. Ibl1. cd:-. .. p. ·n9, ( 1997, Mosby)Car Book.. 1111,;.
Figure 15--15/\
O:-'h!ol11yc::liti~.
Hal/agen/em Olllll! Neuropathic FoOl
cell material has no '\mdow~. lem ing many cells interconnected so that ga~ may pass between cells. Cell wa lls are not total ly impermeable to the flow of gases. Under a sUMained load (especially the hcavy patientl gases arc squeezed out; whcn the load i~ rcmoved gases are drawn back into the cells. M These materials \\ iII bottom out from compaction of the matcria ls as cells fracture under repetitive stress. The advantages are low-temperature molding. nontoxicity. water resistance. and washability \\ ithout absorbency of fluid. ltO) Plastazote has a limtled effecltve period of about 2 days; Paron (PPT) remains effective for 6 {Q 9 months. The two materials can be combined for their attributes and perform well as a single unit. ,n,'1 There are different types of inserts, as follows: • Soft: cushioninglaccommodation. improves shock absorption • Semirigid: some cushion./accoml11odation; affords pressure relief • Rigid : hard single layer of plastic: it controls abnormal foot and leg motion ': The AllplaslfPlasta/olC insert is an immediate preparation and can be pro"ided within a clinic setting. but it has a relatively shoTt life of compressibility (6 to 8 months). Plastazote is a closed-cell polyethylene foam that can be heated to 280' F and molded dlTectly onto the patient's fool. " Care must be taken never to mold the toes or create ridges
333
that the toes will ride ovcr as the patient ambulates. By combining materials over a cast model of the foot. the compOSlh! type of insert can achicve all goals of the accommodative insert and provide a life of I year nllnJmum An insert with a Plastazote surface in contact \vlth the fOOl can be used as an excellent diagnostic tool for future followup. The self-molding properties or PlaSlalote reveal deep sock prints in areas of high prcssure. These high-pressure areas should be noted and relieved In future I11scrt deSign for the patient. By using temperature as a tool for cvaluation, the areas of high trauma will be noted as increased temperature locations. After the paticl1t has ,\"'orn accoml11odative inserts. the temperature differentiation will decrease if the proper accommodation has been achlevcd. If thc tcmpcnl· lUre has not decreased in the area. the rcllcr may reqUIre enhancement. or there may be other underl yi ng complications to be investigated. All relief areas arc applied on the underlying surface in contact with the shoe. never in contact with the fool. The surface in contact \\ ith the foot IS ah\.'ays a so lid, uninterrupted surface that will 110t apply edges for the foot to receive shear forces. Figure 15 16 diagrams the fabrication of se,·eral different layer:s into an accommodative insert. Shoes for the IIlsonsitive foot should be orson leather that will conform to abnormalities on the dorsal surl~lce and allow for the depth of an accommodative IIlsert. Figure 15 17 shows modifications of the depth shoe appropnate for the insensitive foot.
SHOCK ABSORBING MATERIAl. AOOI11ONS - - "
J
INNERFACE MATERIAl. .~==~--------~~~====------------
~'ND ~>KX
C
~-:-----~
Figure 15- 16 DiagrJlll of accommodauvc Insef! fabricallol1. Source: Repnlllcd wllh permiSSion from R,B. Chamhl.:r.-. and N, Llftman. Orthotic Management of the Ncuropalhic and Dysvascular I)atient. in Allw olOrtJlOse.\' amI I.nis/il'e D('dn',\, J rd . t.!d lIiOIl , Il. Goldberg and J.D. Iisu. ed~., p, 444. l 1997. Mosby-Year Oook, Inc .
334
WOLIN!)
C'RI
High Top
Pillow Back
Lateral Flare
BLUCHER STYLE
DEPTH SHOE
Rocker Figure 15- 17 Depth shoe modifications, Source: Reprinted with permission from R.B. Chambers and N. I:-.lftman. Orthotic Manag~l11el1t orthc Neuropathic and Dysvaseular Patient. in A fh,s oiOrrhoses wICIAssistil 'e D(!\'ic('s. 3rd . edition. B. Goldberg and J.~ . I bu. cds .. p. 443, c 1997. Mosby-Year Book. Inc .
Clinical Wisdom: Choose Crepe Sole Shoes for Pressure Relief Crepe sales, which are full of air cells, provide pressure relief to the plantar surface, whereas air or water "pillows," which are enclosed in an inflexible compartment, create pressure,
Lealher gradually ada piS 10 the slope oflhe fool and will retain shape between wearings. The leather will breathe and absorb perspiration. I,,! The patient should not depend upon the "feel" of a shoe for correct size. The shoe must be full width and girth and allow lh- to %-inch space beyond the longest toe to prevent distal shoe contact through the gait cycle. Standard modi fications of ext.ra-depth shoes for the neuropalhic palienl include siretching orlhe softloe box for clawed toes. nared lateral soles to discourage varus instability, nnd shank/rocker bottom for a partial fool, hallux rigid us, or decreased motion at the metatarsal heads. A rocker bot-
10m should be added to Ihe shoe when metatarsophalangeal extension is to be avoided.:!:' When properly fit, the instep Icather should not be taut. There arc thrce tests 10 determine the proper fit of shoes (sec Figure 15~ 1 S, how to mensure for proper shoe rit) :
I. Length: Allow \12 to % inch of space in front of longest toe. 2_ Ball ,,-;d,": With Ihe palient weighl bearing, grasp Ihe vamp of the shoe and pinch the upper mnterial, if leather cannot be pinched. it is too mllTOw. The ball should be in the widest pan ofthc shoc.n 3. /-led to hal/lenglli : Measure the distance from the palienl-s heel 10 Ihe firsl and fifth metalarsal heads_ Bend the shoe to determine toe break. and repeat measurements on the shoe. They should be close to the same measuremcnts. ~4
The simple addition of shoes instead of barefoot may correct many defor111ities .;~ Laced shoes will give the best control. but Lhey must be broken in slowly. beginning with
\fclllag(,II1f'I/I l?fthe Ncuropathic riwl
....
--
v~,'
Natural Elongation of the foot lIeel-off stage
Full weight bearing Partial weight bearing
Figure I~ IH lIow to measure for proper shoe fit. SOl/ree: Rc· prITlIcd \\-lIh Jlcrl1liS~IOn from R.B. Chambers and N, Elftman, Orthollc Management of the Neuropathic and Oys\3scular Patient. IIllrlm ofO,.,hows ""dAs\;_~'/iI'e f)el'il'('.\, 3nl cdulon. B. Goldberg and J.D. IIsli. cds .. p. 442. c 1997. Mosby-Year Book, Inc.
2 hOUr> per day and slO\I Iy adding ume." Caution should be taken with cutout sandals for the possibility of irritation along
the borders of the sandal and straps.7hTo evaluate pressures
within a shoe. there is a pressure-sensitive sock that is coated I"th dye-filled lIax capsules. The capsules fracture when a certain pressure threshold is exceeded leaving dye stains in areas of high pressure, to., To protect a healing area in which dressings will be applied. a healing shoe lined with Plastazotc will :1110\\' greater circumference and volume adjustability. Socks for Ihe neuropalillc limb should have no mended arcas or scams over bony promincnces.A cotton/acryli c blend willnssist in the wicking of perspiration away from the fool. ~" The soc~ should be fully cushIOned and have a nonreSlric-
]35
tive top. The partial foot rcquires ~l sod.. that \\ill confllTl1lto the shape without distal prominl!nt S\!HmS or c\cess I11Hlerial at the distal end. For thc actl\"c patient. socks can bi: obtained with silicone over high-stress areas to prevent . . hear for full or parlial feel. The partial foot may require a bloc~ within the shoe lor the area of amputation. The purposc or a block IS to r\!uuce migration of the partial foot und medial luteral shear for the toe amputation. No block or "prosthctic lOC" IS to be used for a central digit amputation. The 10'W pressures applied by a block to central digits calise ischemic ulcerations on opposing surfaces. Medial or lateral amputmions (first and finh lOes) may require a block 10 hold Ihe fOOl in Ihe correci posilion Within Ihe shoe. The lorcfool bloc~ holds Ihe shoe leather away fromlhe distal cnd of the foot and discourages distal migration of the fool. All forms of blocks mllst hnve space from the amputation slle and be an integral part of the insert. not added to an existing orthotic. Forefoot bloc~s require a rigid rocker sole to pn!\'cl1t ulcl:ration to distal end. By utilizing state-of-the-art foams and room tcmpcTilture vulcani7cd (RTV) siliconc elastomers. shear can be reduced in areas of skin grafts, chronic ulcerations, and cnlcancctomies within more rigid orthotics. The viscoelastomer gel is a two-pari gellhat can be adjuSied for durol11cler demed. The mixture can be used for shock absorption and shear reduction. Scar-adherent areas can benefit from a medium duromele r mixture. The disadvantage is weight. so it should be used in small areas. Low-density foams can be designed into orthotics. such as toe breaks and forefoot blocks and rehefs. Reliefs for heel pain can be deSIgned into the insert OT shoe sale as a Sach heel. Snch heels use soft and medium duromcter soling to simulate plantar flexion .md provide shock absorplion al heel s((ike.
Total-Contact Casting The tOlal-conlacl ca.llng (Tee) melhod prOlldcs decreased plantar pressures by increasing weight bearing over the entire Imver Icg. It has been sliccessful as a treatment for plantar ulcerations but requires careful application. close follow-up. and patient compli ance \\ith scheduled appointments to minimize complications.' Brand introduced the 10lal-conlacl casl to Ihe Uniled Siaies III Ihe 1950s 10 redIStribute walking pressures. prevent direct tnwma to the wound redu ce edema. and provide immobili7ation to Joinh and son ti ssuc. The average healing time for ulcerations treated with the healing cast was 6 weeks. 71> This method has been used for patients with and without evidence of severe peripheral vascu lar disease. ~" The cast spreads weight evenly over the lower limb so that no part of the foot takes mOTe than 5 pSI . There is never a \Vindo\'. cut III thc cast OT there may be 10-
336
WOl iJ'\1> C\RI
call/cd swelling. shear stresses, and cventually a secondary \,;ound (sec rigure 15 - 19). Application methods of the total-contact healing cast vary Vr'ith different IIlstlllitions. The healing cast was originally designed \\
1. The ulcer is covered with a thin layer of gallic.
1. Cotton is placed between the toes to prevent maccralion. '. A stock1l1el\c IS applied. ..j. . I\. I(/ol-inch piece or felt is placed over the malleoli and anterior tibia. 5. 1:0am padding is placed around toes. 6. A total-cont~lct plaster shell is molded. 3
7. The shell is relnrorced with plaster splints. 8. A walking heel is attached. 9. A riberglass roll is applied around the plaster. The patient is instructed to ambulate only 33% of usual activity. The cast is rem oved in 5 to 7 days and reapplied. New casts are applied every 2 to 3 weeks. 7HTo allow thorough drying, the patient shou ld not stand or walk on the cast for 24 hours. 76 There have also been attempts to heal ulcers by using a healing cast shoe molded or plaster. This healing cast shoe must be changed in 3 days and then reapplied every 10 days. Results have reported hea ling of plantar ulcers in 39 days.!\fJ Contraindications for the use of a healing cast shoe include inrection (redness. swe lling, warmth, rever) and hypotrophic skin {thin. shiny appearance. marked dependent edema).71'1
Clinical Wisdom: Bathing Whife Wearing a TCC Is Simplified by Wearing a Seal Tight' Cast and Bandage Protector
This heavyweight plastic vinyl bag slips over the cast and forms a seal that is watertight. The product is convenient to use, durable, and has a sueded sale to minimize Slippage in the shower.
Orthotic Dynamic System Splint
FiJ.!ure 15- 19 Total-conlact cast
The orthotic dynamic system (ODS) splint was dC\eloped to take advantage of th e cast ing method of a Iota I-contact cast with the inclusion of a custom-mo lded insert that could be removed and reliers modiried. With all or the advantages of the total-contact cast, the advantages that were added with the ODS spli nt included the possibilities ror daily inspection, regular clean1l1g/dressings/debridement, and adjustments to areas of excessive pressure and/or friction (see Figure 1520). The PlastazoteiAliplast insert is rirst molded to the patient's fOOl and trimmed to follow th e plantar surface, with 1/4-inch length added beyond toe s. A stock inette is placed on the leg, the insert is positioned, and another stockinette is applied to hold the insert in place. A padded total-contact cast is applied using riberglass only. The cast is bivalved straps are added edges are finished and the insert is removed relieved and replaced to deweight the area or ulceration. Aller 1I1sert modification, it is replaced within the sp lint. and the patient may ambulate with a rocker bottom cast shoe under the splint. The patient is instructed on volume control with sock thickness.
Managemellt o/tlle Neuropathic Foot
337
Stockinette
:,---t- Webril
Fiberglass Cast Bi -Va lved
Plastazote / Aliplast Insert Figure 15-20 Diagram of the ODS ~pli nL Source: Reprinted with permission from R.B. Chambers and . Elftma n. Orthotic Management of the Neuropathic and Dysvascular Patient. in ArIas oj Orthoses and A!isisri l'€ Devices. 3rd. edi tion. B. Go ldberg and J.~. Iisli. cds., p. 441. '.C 1997. Mosby-Yc4lr Book. Inc.
The di sadvantage wi ll lie with compliancy of the patie nt. The splint design allows donning und doffing by the pat ient , therefore allowing him or her to remove the cast. The total contact ora healing cast cannot be com pared in its superi ority, but th e clinical experience of the a uthor ha s found the dail y inspection and reliefadjustability to be a great asset in
cot di sease, and chronic ulcerati o ns. The o rth os is is easily
donned and dotTed and fabricated ofa co polymer plastic with
the treatmen t protocol.
a closed-cell lining. The removable insert may be adjusted to re assign weight-bearing areas o n the plantar surface. The insert may also be formed over chronic breakdown areas such as the malleoli, poste rior heel, and bunions to reduce pressure. The rocker sale allows for easy ambulation, but the
Neuro path ic Walker
contralateral shoe must be adjusted for height. When casting for lhe neuropathi c walker, the patient's limb is wrapped and placed on a soft foam bl ock until the plaster
orthosis (AFO) and a boot that is custom designed to be to-
is set. The plantar s urface will be acco mm odati ve without excessive press ures o n bony prominences. Modifi ca tion s of the positive model include smoo thing the plantar s urface but
tal cont act for weight di stribution. The ankle is locked to reduce force th rough the Lisfranc joint and/or a nkl e. The
durin g modificat io n will be an a rea of excess press ure in th e
The neuropathic wa lker is a combi nat ion of an a nkl e-foo t
design is indicated for the patient with changes of Charcot joint in the tarsa l and ankl e joints. chronic recurrence of Char-
never removing plaster. Any area that has had plaster removed finished orthosis. The distal end is built up at the media l and lateral metatarsal areas and the length extended %-i nch to
338
W OUND CARl'
allow room for the toes and decrease (he chances of maceration. Fabrication is completed on the modified positive cast. The insert is rirst rabricated, rinished, and placed in position. The posterior Plastazo tc lining is pulled over the insert , rollowed by the copolymer (plastic) vacuum-rormed shell. The entire posterior secti o n is finished and trimmed . The anterior Plastazote is positioned and the copolymer shell is applied over the entire posterior. There should be a '12- to linch overlap or copolymer on the rini shed orthosis. The Ve lcro straps and rocker bottom arc attached (apex of rocker proximal to MTH ; Figure 15- 21). The patient Illust be instructed to check sk in for redness and poss ible breakdown . The patient should be ro ll owed and temperatures of the plantar surface recorded for possible
adjustment orinsert pressures. Sock management wil l be very important to continlle a snug fit of the orthosis and volume control.
Total-Contact Ankle-Foot Orthosis Similar to the neuro pathic walker, the total-contact AFO is utili zed for Lhc patient who has an area of trauma in the mid- or hindroot. The orthosis includes a custom removable insert and is lined with Plastazote. This orthosis mu st be fit within a shoe. which may be difficult in standard shoes. The casting procedure is the same as that for the neuropathic wa lk er. The toes are open. and the anterior shell terminates at mid fool.
Copolymer Shell
Removable Plastazote Aliplast Inset
Rocker Sole Figure 15- 21 Diagram of the neuropathic walker. SOllrce: Reprinted with permission from R.1l Chambe rs and N. Elftman. Orthotic M
Mallagemem o/Ihe Neuropar/tic Foot
339
O lher nevices Shonleg \\alkers and onhopaedic walkers have been used by some clinics. but they compromise the total-contact realure. They arc Iradilionally used for acule ligamenl/muscle
and fracture illll11obililation . Patellar tendon bearing (axial resist) designs arc intended
to decrease forces 011 the plantar weight-bearing surface of the foot. With this design as a casting procedure, there have
Toe amputation
been attempts at its usc in place of plaster cast immobilizations.81 The design lransmillcd considerable axial forces from the knee region onto the cast. but it did not offer rotary sta-
Transmetatarsal
bility. The results olTered very little effectiveness in reducing the load ofTthc lower Icg,II1 Thc patellar tendon- bearing designAFO has been used successfully fOrlhe calcaneclomy,
planrar skin graft. and heel ulceration. This orthosis is contraindicated in the patient with vascular impairment because of the excess restriction in the popliteal area of arterial flow. The prosthosis has been the orthotic replacement when the amputation case is complicated and the patient is not a candidate for prosthetic management. The prosthesis becomes a useful device for transfers and limb protection. This is always a creative design. with 110 two the same, unique to the individual and his or her needs.
Lisfranc
Chopa n
Sy mes
Surgica l Ma nage ment The most conservative treatment of foot infections will be utili.lcd to rehabilitatc, but antibiotic therapy alone is not always sufficient to trem aggressive virulent foot infections.8J Surgical intervention may be in the best interest of the patielll if conservative therapy is not an option or has proven inefTeclive. Oplions should be discussed wilh Ihe paliel1l and Ihe family. and Ihey should be involved in Ihe final oulcome when possible. Surgical debridemcnl of all oSleomyelilis and
nonviable tissue must be completed./U The surgeon wil l preserve as much length and width as possible to ba lance the motor function .'I The goal of amputalion is ambu lation and reconstruction. Typica l locat ions of partial foo t amputations are shown in Figure 15 22. Metatarsal osteotomies can eliminate the intrinsic stresses caused by elongated or plantarnexcd metatarsal joints in neuropathic limbs and decrease number of amputations. lls Toe resections are the most distal amputation choices available. Expected outcomes of each toe resection are as follows: • First toe
Interphalangeal disarticulation for an infected
di slal phalanx gives good balance. When possible a
wafer of the proxima l phalanx should be left to maintain the position of the sesamoids beneath the first metalarsal head .
f igure 15- 22 Typical locations of partial foot amputations. Source: Reprinted with permission from R.B. Chambers and N. Elt1rnan. Orthotic Management of the europathic and Dysvascular Patient, in Arias of Orrhoses mul Assisrh'e Devices. 3rd. edition, B. Goldberg and J.~. Hsu. eds .. p. 432. 1997. Mosby- Year Book. Inc.
• Second toe- Disarticulalion rcsu lts in loss of lateral support of the fi rst toe. A second ray resectio n is usua ll y belter
10
avoid seco ndary ha ll ux va lg us.
• Third or fourth toes- The rcmaining toes wi ll tend to shif! lo c lose 'he gap. • All five loes- A long fo re foo l lever is lef! wi lh good
weight-bearing properties. 9 The advantages of the partial foot amputation are the fo llowing:
• • • •
It preserves end weight-bearing function . It preserves proprioception. II provides for limiled disruplion of body image. It requires shoe modification/orthosis or limited pros-
thesis.
340
W OUN D CAKF
Limitati ons of th e partial foot amputation are the loss of
no rmal foot functio n rel ated to loss o f forefoot lever length and associated muscles, and the challenges presented in selecting appro priate adapti ve equipment. The Chopart amputation is selected when a patient retains sensa ti on in the heel pad. Metatarsa ls and tarsa ls arc removed, leaving a ve ry short limb. It is diffi cult to suspend a shoe
without the aid o f an AFO or prosthesis.
The transmetatarsalfLisfranc amputation is preferred for the resultant length of foot: amputation is through the metatarsa ls. The longest partial foot amputation is the distal metatarsal amputation in which th e IOCS are amputated. Thi s leve l will require a short shoe or forefoot bloc k to prevent forwa rd motion. In all partial feet
it is important to watch fo r an equinus
deformity. The toes arc no longer present, and visual inspecti on is more difTicult without their reference. Wh ether from trauma or chronic infecti on, the partial removal ofth c calcaneus is a follow-up challenge for the orth oti st. Removing weight bearin g from th e heel is di ffi cult, and the patient who has had a ca lcanec tomy must be foll owed carefull y. The most successful meth ods o f co ntrolling future breakdown have invo lved th e patellar tendon- bearing (axial resist) orth osis or th e neuro pathic walker. A soft RTV foam has been used to fill a void between the orthosis and the heel area. The sam e orth oti c treatm ent is useful for chron ic heel ulcers and plantar skin grafts that require reducti on in weightbearing and shear forces.
DOCUMENTAT ION Documentarian continuity is essential for all patients and requires a stand ard form to be used for assessment and future follow-up (Ex hibit 15- 3). Tracing the ulcerati on on transpare nt film will allow for accuracy o f detailed healing progression. Providing the patient with a duplicate tracing can improve compliance as th e pati ent can follow his or her own progress. Photographs of ul cerati on sites are important for noting improvement in depth and granulati on of ulceration. M ethods for making traci ngs and takin g photos are described in C hapter 4.
SELF-CA RE TEAC HI NG GU ID ELI NES
Foot In spectio n Th e patient is the most important member of a clinical team approach to the treatment of his or her neuropathi c limb. There is no complication too small to be addressed. and the patient must bring abnormalities to the team's attent ion. Self-
care begins with dai ly inspecti ons of th e feet with the help of mirrors, magnifying glasses, and family members when necessary. Examinati on includes footwear and orthoti cs for wear and foreign obj ects. The diabeti c paticnt must understand th at thi s examinati on may be complica ted by oth er disease processes, including retinopathy, autonomic neuropathy (loss o f smell and se nsory signals), and dec reased mobi lity of j oints. These patients are handi ca pped by th e lack of pain as a warning signal and requi re systematic instructi on to educate th em in the proper skills requ ired for daily inspec ti on and detecti on of impending trauma.
Precautions a nd Ri sk Redu cti on Me th ods There are several precautions fo r the pati ent with a neuropathic limb. The skin is very susceptible to damage and infecti on and Illust be treated carefull y. It is advised th at th e patient not soak the fee t in wa ter because the chance ofbuTIls is always present and the soaking will leave the skin moist and suscept ible to funga l infecti on. Prolonged soak ing can remove the natural protective barrie r frolll the skin and lead to othe r infecti ons. Fee t should be washed with a nondry ing soap a nd lOwe I dried. A n er th e foot wash, petro leum jelly can be applied to retain natural moisture and covered with socks. Care should be taken not to lise creams with perfumes (a lcohol) as th ey will furth er dehydrate th e skin. Dehydrated skin is es pecially susceptible to traum a. Adhesives of any form should never be applied directl y to the skin of a neuropathi c limb. Upon re moval of th e adhesive, there is a ri sk of loss of th e outer layer of skin , leaving an area open to infecti on. The adhesives could be in th e form of tape, a Band-A id, or over-the-counter self-adhesive pads. When th e pati ent selects footwea r he or she should choose not only th e correct size and width. but also shoes wi th no stitch ing over the forefoot. The stitched areas will never mold 10 th e foot, but instead will cau se breakdown of the sk in. especially over bony areas. Keep current on recalled products. For exa mple, olle hair re moval system published a product alert on its device because of problems occurring with diabetic patients. Small areas were bleeding aft er hair was removed, leaving an entrance for bacteri a and possible infec tion! Ove r 50% of the over-th e-counter foot care products should never be lIsed by a patient with a neuropathi c limb or diabetes. Th ere are occasionally warnings, but in very fin e print. Care must be taken with exercise program s. Whell we wa lk, each step ca rri es one and a halftimes our body we ight; jogging increases the force to three times th e body weigh!." The patient with a neuropathic limb would be advised 10 choose an exercise program that includes aerobics, swimming, cycling, dance. or chair exercises. Even walking should include slow, short steps only: no joggi ng."7
A1anagemelll oj lite Nelllvpalitic Fool
341
Exhibit 15-3 Foot b a lu all o n Fo rm
PATIENT _ _ _ _ __ _ _ _ _ __
DIAGNOSIS _ _ _ _ _ _ _ _ _ __
ORTHOTIST _ _ _ _ _ _ _ _ _ _ __
CODE _ __
DATE _ _ _ _ __
INSENSITIVE FEET WITHOUT ULCERATION CATEGORY
MONOFILIMENT RESPONSE
A
B C
o E
+5.07 5.07 5.07 5.07
( 10 g ) ( 10 g ) ( 10 g ) ( 10 g)
6. 10
(75 g)
ULCER GRADE o Inlacl Skin I Superficial 2 Tendon or Bone 3 Abscess or Osceo 4 Forefoot Gangrene 5 Fool Gangrene
ULCE R
DEFORMITY
No No No Yes Yes/ No
Yes/ No No Yes Yes/No Yes/ No
CHARCOT ARTHROPATHY O Aclive O Hx UR _ Phalanges
Forefooc Midfooc Hindfool Ocher
FOLLOWUI'
INSERT
12 Mo 6 Mo 4 Mo 3 Mo 2 Mo
Cushion Molded Molded Molded Molded
FOOT DEFORMITY Pes Cavos _ Pes Planus Valgus - Varus
o
TOE DEFORMITY Claw Toe Mild Severe Rigid
=
Hallux Valgus - liigidus - Extension
o
COMPLICATIONS Proximal Neuropathy Calf Knee Thigh
o o o
Uppe r Ex!. Neuropalhy
o o o o o o o o o o
Fingers Hands Forearm
Dialysis Vascular Impaimlem Venous Slasis RetinopaOly
DORSAL
Proprioception O('rnHllologic Br('a kdO\\ II
FWlgal Nail Edema Concrol Full FOOl Ocher
o o
SO lllt:e : Reprlntcd In
\10
RIGHT
o
o
LEFT
Ith pCrlllIssion rrom R.B. Chambers and N. Elflman , Orthotic Managemcnt o f the Neuropalhi c and Dy~ \a !;c ul ur l)atlcllI , Il. Goldberg and J.D. I1 su, cds .. p. 441. c 1997, Mo:,by- Year Bool. . Inc.
AI/as 0/ Or,hw,(') a"d A.Hixli l'(-' DCI'ice) , J rd. edition,
342
WOl 'I' C ,.,
[ ~hibit
I S-t
Sdf-(;.lr!.~
Guidcllllcs for the ')aticnl \\ilh I\curopalhic Fool
Relll,." Demollsflli lioll
I"'HmC/iolls
Self-('an: Gflic!e/il/('sf(w Paliell/II-illl ,\-""1'01'(1/11;(" Fuol
Gil'e" (Date/llI;tials)
or Ret'iew Material
or
(I)Uf('i/llifiais)
DemoIHfm/ioli
or SWles Um/en'lIJlldi"g (Olllf!,IIIII;O/'\)
I. Foo l In\I)CClioll 1\l clhods iJ.
U!o,c mirror to chcd fect
b. U!o,c lIlugnifymg g l a~s to ched.. fec t <. I r blind famdy member pcrlhrl1l:S 1'001 inspection 2. Foo l In'\pccfion It e m a Toe mill s: check for broken. cracked. or sharp nails b. Broken skin: chcd between toes. along sides of fect. tops and ends of toes, soh: of foot c. son to\! corns: check between toes d. Callus: check for cracks
c Drainage: check for any drnll101gc from a sore
r.
Odor' ehcck for odor from any source 011 the foot
3. 1),Hienl Und ers tand s a. Siglllfieancc of findll1g~ of foot inspection: break in nails. ~"II1. or callus b. When to nOlify 11I..:allh care prm-Ider If there IS break in nails, .. kill . or callus c. To nOllfy health care prm Ider Il1lmediately if there is any Injury to the Ice t
4. Fool Ca re Ro utin e
"h. c
\VilSh kct with nOlldrying soap and lowel dry Apply coatlllg of petroleum Jelly 10 all ~kin surfaces of ket Cover coaled fec t \\ lIh clean" hlle socks
5. Foot Ca re Preca ution s a. Ne\cr watk barefool b Nc\cr lise adhesm.! tnpe products on the skin c. Never put feet III hOI w~lIcr or appl) a healmg pad or hot pack d. Nevcr soak feet c. Nevcr apply over-the-counter foot care products to remove curns or callus. or to trent na ds 6. S hoe \Veur O r th otic Ins pecti o n a. CllOOSI! shocs that arc correct S\.lC and width b. Ma!..c sllre there is no stllchlllg over the forefoo t of shoc c. Chcck for wear: heels. soles. lOpS. Inside. bottom. edges. counter d . Ah\ays check shoe~. socks. and orthotics for fore ign obJecl~; remO\c obJecb beforl! donning 7.
E\crci ~c
Precaution s Never jog b. \\ialk \\llh short sl()\\ steps
J
C()"tllllle.~
MOllogemelll oJthe Neuropathic Foot
34 3
Exhibi t 15-4 contin ued
Rew,."
Self-Care
Gl/idelill e,~I(H'
Patie'" with NelllVpatltic Foot
Instructions GiI'ell (Dflte, Initials)
DemOllSfratiof/ or Review of Material (Date/Initials)
Demoll.\'tratioll or Stfltes Ul/{Ier~/(I I/{lillg
(Date/lnifials)
8. Preferred Exercises a, Aerob ic: low impact b. Swi mmi ng (wear soti ba th ing shoes in wa ter to protect fee t, dry fcct thoroughly fo ll owing) c. Cycling: protect fcct and ankles from trauma d. Da ncing c. Chai r and mat exe rcises 9. Imp orlance or Fo ll o\\ -U I) "ilh I-I eall h Care Prov id er
The pati ent with a ncuropath ic limb should never wa lk barefoot. Even in the pool or on the beach. water shoes should be wo rn . Il ot sand can cause burns, and undetected obj ects in the sand can ca use inj ury. Burns can be caused by th e fl oorboard of an automobile, as well as any wa rmth -producing equipment. Th e interi or of th e shoe must be examined be fore every donning. Small objects can easily drop into a shoc.
Co mpliance Iss ues The practiti oner must understand compliance prob lems of patients with neuropathic limbs, and cspec ially diabetic pa ti ents. They do not willfully neglect se lf-care ac ti vit ies but simply arc not aware of th e possibl e dangers and are not taught adequately or moti va ted sufTi ciently.' Diabetic patients may have other complications that th e pract itioner does not consider in the compliance of th eir activities. Many cannot see (retin opathy). feel (sensory neuropathy), or smell (a utonomic neuropathy) when there is an infecti on or a potenti al problem.Those wi th vision impairments will need help from a fa mily member or caregiver to perform se lf-care guidelines. Pati ents with neuropathi c and dysvascular limbs requi re knowledge and skills to admi nister self-examinati on and scifcare. The medica l communi ty must educa te the pati ents as wcll as the medical tcam to treat conserva tive ly and accommodate the chro nic compli ca tions th at ex isl in a growing porti on o f the popU lat ion. Ex hibit 15--4 is a chec kli st of in-
slructi onal items with documentation to ve ri fy learn ing and understanding for th e pati ent with neuropathic foot.
RESO UIKES Sea l T ight' cast a nd ba nda ge protec to r Brown M edica l Industri es 48 1 South 8th Ave. East Hartley, IA 51346 800-843-4395
Thermometer- Infra-red M easurements, Inc. 2946 Ponce de Leon New Orl ea ns, LA 70 11 9 504-949- 1 192. Fax 504-943-3489
Monofilament North Coast Medi ca l 187 StoufTe r Bl vd . San Jose, CA 95 125- 1042 800-82 1-93 19. Fax 408-277-6824 Harris Ma t, Prcmade Foo t Orthosis and Mat erials Thcradynamics Division of Nati onal Pedorthi c Services, Inc. 7283 W. Appleton Ave. Mil wa uk ee, WI 532 16 800-803-78 13. Fax 4 14-438- 105 1
344
Wm Nil C.\01
(';ulllet R. rimt IIIItI AI/Alt' lSI II
J)/tInt'tl,'
Nm, Baliullnfl!: \\ill·
2.
SllIplcy 11 Clinical e\a[uallon and cOIn: Mlhe m"cn .. lli,,: foot PII\"\ l1/t'r 1'171.);51}: n 22
.1
Vc-.c,A. BoulionA Commentary J)wh('!t,\ 1.\7.
4
UO\\kr.:r
S.
Urcnncr M M;.ul;lgcmcnl May 19XX54 5K
6.
SP~'t'/n/'"
It)IJ2;5:.H6
Pllliadelphlil : I.A I)::I\IS: 19!U'
10
Jah.,s \1 Shoes ami .. hoc modlric.IIIOn .. In : ·llltH 0/ Ortlwtin St Loul". \10: (" \ Mo.,by; IIlX5:267 279.
11
TS'lITh P DII"!crcnllal dlagno ..... \ltlllll.l{"flU'1II 0/
or peripheral
i'aiplll'mi \,·lTt· Plt/hlt'1II1
neuropathIC., In Rancho Lll~'\mlgll"';
19XO: 712725 .
:n,
Thoma., I) Climcal I"cature ... ;md dlncrentml dtagno ... l.. In ' Palph· aal \"('lIro/WIIt.. Philadclplll;l W B Saunders Comp.IIlY: 19X4 ;2: 1161) IIX5 .
!'utlilllr;c' Pmdlll'H
.ll
WakcJec· Lynch J Rcltc\-lIlJ,; paUl with pCjlper" Oiahl,It" f(II"l'w\l . Junc 1992:.1S H.
Ulcnhcrg M Di .. bcli, ncuropalhu: ukcr J lIt Smu; IltHp
1..
Dadey (i I 11\:(;1 of tn'-;Llment 1\ IIh e
J Commentary /)wht'fl'\ ,\p.-drum 1119:::5::\35.
ur the t!tabetlc h)ol
196X;35:SKS 594 7
(ircen
X
Bowker J Neurological a .. pcct .. 01 prll ... thcti, llrthotu: prm;ticc. J Pm\lh,,( Orl/IOI 1993:5(2):52 54
t)
BO'Nkcr J 1\lrllill fOOl and Symc amputatIon:>.: an PI"II\III('IOr/I/OI. 19)17;12:111 '1
10
PiUfI.
I). Waldhau ... 1 W A forum
()Jl
neuropathy Oillffl:fl'\. 19XX: 10
ll\Cr\
ie\\. ellll
LeiI'. M The orthotic ... of mydomening.ol.;dc In .-lIlt/I o/Or/IIO/· in St loUiS. MO, (' V \Io .. by; lI}1t"UOf) 106 .~jll'("/lWI/
15
Oillh('lt'\ \/dlllll\,
\ltUltl.t:l·ml'''' lI"d ("ompht'flllOl/l
Nc\\ York
Churchill l.illl1!! ... tone : 191<5:214 21S. 277 29.1.360 161 ..16
Apclq\ ist J. Castcnli.lr.. J. lar....on J Pmglw ... tie ,alut: of sy ...lOlic anklt.' and toe hlootl pre .... ure le\d" III outcilmt.' uf lliabetic fOOl ulcer /)ill"('/{'.I Ca/1-'. 19X9; 12:37J UK
.'1
Cherry (j, RYitn T. Camcron J Blueprint for the tre,lIment of Icg ulcer ... and Ihe prc\-entlUI1 orrecurrt.'nee. Uillmt/\ . 1992;3:1 15 Perry J. Normal and p.uhoillgical gall In: Illal 0/ On/w/in St loUl". 1\10: C V ~llI.,by: 19X5:1<3 96
II
\\"clIl!!arten M Commcntary. Dwht'/n
IIN2;5:3"2 141.
3X
12 .
Pccoraro R. Reiber G. Burges .. I Palll\,ay ... to tI ..lbclil; lunb ampu· latlun ba .. i... for pre'clltlCln. lJillht'/t'l Cfln·. 1(1)();,",.5]] 521.
11}
n
I"yillng (" ConL"iu ... ion ..
14
Bamberger D. SIOITk " Sc\crc tll'lbclic fool problem ... : aV(.lI(ling OImpU1;1l1Un H"w~ {)t'('il 191<7:10Q:21 14 ()Im J Pcnphcml arlerial di ...ca ...c. f)illhl'/t'l f(m·("(I1/. Octoher 1992 7X XI
4()
Il;erh~r I Slrength and r.LIIge·of-l1lllllOn c'>.amlllallon ~kills fi.lr the chme,\! orthol1'.t J Pml/"I'1 ()"llwl. 19t}):5(2)..J9 51
41
Thol11;1"
..... Cl\ man B \ dla!x:le ... Cilmp for 'at Ill! AmenCan adult .. {);tl"('/t'~
42
Oakley \\ . Cattcmll R, M'lrlin M ACllology ;lIld management of Ic.,ions of Ihe reel III lli.lbetes fJr l/ed.1 11}~(d6:4999 5003
43
Sillacore OR, 1.lsncr R, Rubcllll\\ C IIt'l1ll1/g Ralt'., 0/ /);ahdi{' Fool l "In'l"\ III SlIh,I'I"/1 111111 Flu'd ("/ltlfnll /)('/orlllll\·. Platrorm Prescntation, 11hy ... ieillThempy 1997 APIA Sdentlflc Meetlllg and I '>.po. "Hllln; S'1Il Diego. CA: M.I) 10 June 4. 1997
44
Tiberio D Il alholl1cchal1lCs M structUr.lIIi.l(lt dctonnltlc .... P"n Tlla 19KX:68:IX40 IX49
IS. 16
SPI'dl"/lll/
17
I "Irkm· ..... I . I.",ery L. Dlabete .. fi.lOl care: a team approach. Dill"!'.
n/(· SIII/·.
.~t/cH
R. LlIUlnedl:IIlICHlf thc foot. In
/lfllIlltr
I 1)92;S: DC, In
Robhln" D. omec guide to dlaglltl ... l...
~Iann
o/O,.,/wlln SI Lou ... ,
1\10: CV \1osby; Ii}X5 :112 125.
11)92:5:151< lS9.
199J;6: 166 202.
1,·\ SPI"("/I"IIIII
IX
/)it/belt'l .~jlCd/'lll1l.
Ma)"Junc 19X1:1 4
I~ I·liasson S. DlahctlC ILcuTllpalhy. In: Pltt·riphl'rlll .\(,I1"· PllIladelphla \VB . SaunJe .... Company: 191(4:2:1773 IXOI
19
Brand I) Neuropalhlc uker,Jlion.
20
A.. hhur)" 1("11.)\ care in patient-. \\nh dlabch: ... mellitus f);abt'/t'l Can· 1991.14("uppl 2):11< 19.
21
Ik.lIld Pin: If/lt·lI.luln- /-(:('1 j Jlml"linllllullllolIl 0" riml Pmhh'lI11 III Lt'/IIYI.\r Lllmlon, I'ngland lhe Lepru .. y \1I"slon; 1977
22.
Br.ln(] I) Management or sensory los .. 111 the e,lrcmllle .. : mil1lilgcmcnt 01 pcTlphcral !lcn e prublem ... J Rt'lwh. I L}NO;!.:62 1<72,
47.
\\";t!!ncr IT \\ Thc dy ... " ....cular lil(lt a ... y .. lem furdlagm)sl-. ;lnd trcal ment FeNI! ·I,,/.;h· 19XL2 :M 122
23
Myer..un M. 1\lpa J, I'aton K lhe total contact casl for managcment of ncuwpathic plantar ulcerallon or tIll' fOOl Dwhl'/1I1 .S/1I'£"· Imm. 191,125:]52 353.
4X
24
I :dcl~telll J "oot carc for the aging. Plin
(ilugl" M. Mulder (i. The f...Ii'lhcIIC t~"II.)I. In Kr.... ncr D. cd. l/edlwl lIUI1UJ.:('IIICIII III f-jW! L ken III ('/I11I11;e lIil/llUl ('are . j (·lilli{."tll SOIll"('I' 800/'; 101" I/lIlJllhom' Pm/t'\\;/IIwk St Ioui'>. MO Mosby-' lIe.lIlh M,lIlagemelll l)uhllcaIIOl.... Inc; 1990:221 2.19
25,
Ulley R. NutTiliunal faclors associated \\uh wound hcaling in the elderly: the role nf<.pcclfic Ilulricnh mlhe healing procc ...... /);0"('· ft,., Sp~'l"Irum. 11j1J2;5:3S4 .155
49
Wagner 1 A cI.L ... ~irication ;lIld trenlmcnt program for dlahctlc. neu· ropathlc and dys\ ....cular fOllt pmblellls. 1-"001 Il1kh'. 19X1:1 .... 7
50
2(1.
KllIghton D. Ficgel V. Doucelle M lre;JlIll!:! dlabellc 1'001 lIlce!'> /)/(/III.:/{'.1 .\jJI'(·!rum. 19IJO:3 :51 5<J
So ..enko J, Kato M, Solo R. Comparison of 4u.mtltatlle "cn~ory Ilm:sholtl measure .. for Ihelr as"'OCHItlOli \\ IIh loot ulcerallon in diabetic paticnts. /)Wht'fl'~ Can'. 1l)t)(}.13 : IOS7 1062.
27
1'lIcnbcrg M Don', be rooled by peTipheral neuropathy. I-ill"('(l/I/. J,Lnuary ·l·ebruary 19X1
/);O}'('/('I
5I
Omer G. Sen ... lbillty tesllllg. In \ltJllfIgcml't11 01 Paipheml J\-t'n't' Pmhh'lI/~ Philadelphia: \\ B Saunder.. ; 19!o1(J:3 14
21<
Yale J. )ill('\ /Jod;mrit · \kdit·;IIt'. lrd cd Uallllllurc: Willimn., & Wilkm ... ; IIJX()
~.,
TIler.
4~
\\II.,on J. Foster Silundc~
4(1.
I) "f('.\lhoo/.;
II/ FIII/II("f"IIIOlflKI' Philadelphia
\\oJ}
('omp
Olehky J, Sherman R. Diabetes In: IIll1/dollloll f(101 Probi.·1111
11/
j Pmt"llntl Londun. Lngland The Lep-
111\('1/\;1/1'1' {-('t'l
I .• ·W"(I\I·
rosy MISSion: 1977
11)};1<:6X: II
Lllrke J, SlIlh D. 1)lant|
1.1'1,r Rt'lie/
Management oJthe Nelllvpathic Foot
345
53.
Dirkc J. ManagcIllc111 of thc diabetic foot . II'OII//(I Care Mmwge . 1995 .
69.
Lcv in M. O'Neal L. The Diabetic FOOl. S1. Louis. MO: C.Y. Mosby:
54.
Ashbury A. Diabetic neuropathy. Diabetes ('are.
1991:1~(suppl
70.
rral1 D. Mcdium term comp:lrison of shock al1cnuating insolcs using a spectral ana lysis technique. J Biomed Ellg. 1988; I 0 :426-428.
55.
Thi'
7 1.
National Aeronautics and Space Admin istration. Mission accolllplished (thermography aids in the detection of neuromuscular problems). NASA Tech Brief January 1993:92.
72. 73.
l'lack M. Filling shoes. Diabe/es Foreem.t. January 1989.
1988.
2):63 68.
56.
57.
58. 59.
Apelq"ist J, Larsson J. Agardh C, The inn uencc of external precipitati ng fa ctors and pcripheml neuropathy on the dc'
Bergtholdt II . Temperature a:-.se:>sllIcnt of the inscns
rratt D. Long term comparison of shock attenuati ng insoles. Plt)s/lte/ Ol'lhol lilt. 1990; 14:59 62.
Lockard M. FOOl orthosis. Pltys Titer. 1988:68: 1866 1873 .
74.
McPoil T. Footwear. Pltys Ther. 1988:68 :1857 1865.
75.
Mcroil T, Adrian M. Pidcoc P. ElTects of foot orthoses on ccnterof-pressure patterns in women. Phys Ther. 1989:69:66 -71.
76.
Coleman W, Brosseau D. Methods of treating plantar ulcers. Phys Ther. 1991:71: 11 6 122.
77.
Dwyer G. Rust M. Shoe business. Dial)('te.\' Forecast. Ju ne 1988:60
63.
1979:59: 18 22 .
78.
60.
Chan A. MacFa rlane t. Bowsher D. Contact thermolllography of paInful neuropathic foot . Diahe/l's Carl'. 1991: 14:918 922.
Mueller M. Diamond J. Sinacorc D. Total contact casting in treatment of dialx'tic plantar ulcers. Diahetes CatT!. 1989; 12:384-388.
79.
61.
Zhu II. Maalej ,Webster J. An umbilical data aquisition system for Illea:-. uring pressures between foo t and ~ h oe. IEEE Trmu Biomed Eng. 1990:37 :908 911.
Sinacore D. Muellcr M, Diamond J. Diabetic plantllr ulccrs trcated by tot:ll contact casting. Pity.\' Titer. 1987:67: 1543 1549.
80.
Diamond J. Sinacore D. Mueller M. Molded double-rocker pIaster shoe for healing a diabetic plantar ul cer. Phys TIter .
62.
Wensch J. Wcb:-.ter J. Tomp\"ins W. A portable insole pl anta r Illca.,urcmelll system. J Rehahil Res Del: 1992;29: 13 18.
81.
Birke J. Nawoczenski D. Orthopedic walkers: effect on plantar pressures. elin Prosthet Or/ltol. 1988:12 :74- 80.
63.
Lord M. Clln ieallrial of .. computer-aided !lystem for orthopaedic :-.hoc upper design. Prmth(,t OrthO/I",. 1991;15 :11 17.
82.
64.
McAlli ster D. Cancr D. De\araj:lll R. An interactive compute r graphic:-. sY!ltem for the design of mo lded lind orthopedic shoe lasts. .J Helwhil Re,<j Del'. 1991 :28:39--46.
Lauridsen K, Sorensen C. Chri st iansen I ~ Measurements of pressure on the sole of the foo t in plaster of paris casts on the lower leg. J Int Soc Prosthet Orthot. 1989: 13:42-45.
83.
Mc Intyre K. Control of infection in the diabetic foot : the role of microbiology, immunopat hology. antibiotics. and guillotine amputation. J Hue SIII'g. 1987:5:787 802.
84.
Lai C. Lin S. Yang C. Limb sal"agc of infected diabetic foot ulcers with microsurgical free-musclc transfer. Diabetic Spec/ruIII.
19R7:67: 1550 1552.
65 .
Sims D. Ca\anagh P. Ulbn:cht J. Risk fac tors in the diabetic foot: recogniuon and management. PIli,' 77,er. 1988:68: 1887 1916.
66.
Delong R. Thl' Nellmlogic E.wmillatiOlI. Ncw York: Harper & Row:
67.
Newman L. Pale,tro C, Schwartz M. Un:>uspccted osteomye litis in diabetic foo t ulcers: diagnosis and monitoring by leukocytc scanning with Indium in oxyquinolinc. Dillhett!.\' 5iJectl'llm. 1992:5 :346-
85.
TillowT, lIabrshaw G. Chr.£all J. Rcview of metatarsa l osteotomies for the treatment of neuropathic ulcerations. Diabetes Spectl'Jllll.
347.
86.
KUllcir E. Wir!a R. Golbmnson F. Load-bearing characterist ics of polyethylene foam: ::tn examination of strllctuml and com pression properties. .J Htdlllhil Re.\· Del'. 1990:27:229 238.
Furmlln A. Give your feet :1 sporting ch:lIlce. Diabetes Forecasl. April 1989: 17- 22.
87.
Grah:ull C. Neuropathy made you stop. Diabetes Foreclut. Decem-
1992;5:356- 357.
1969:742 743.
68.
1992;5:357-358.
ber 1992:47-49 .
P A RT
IV
Management of Wound Healing with Physical Therapy Technologies Carrie Sussman
INTRODUCT ION
Interventions inc lude th e purposeful and ski lled interaction of the skilled professional and th e patient to produce changes in the patient 's condition consistent with the diagnostic process. The diagnostic process described in Chapter I guid es the phys ical therapist to se lect interve nt io ns that will promote the healing response. This process begins with th e reaso n for referral , th e hi story of the patient, and th e wound. Interve ntions have three recogni zed components: direct intervcntion; paticnt-related instruction; and coordi nation, communi cation , and documcntation. Thc physical therapy educat ion curriculum includes instructi on in th e selecti on, protocols, and application of physica l agents and elcctrotherapcutic modalities. Licensing exa mination includes testing of knowledge in appropriate, sa fe usc: protocols; and interpretation of the results. Liability iss ues also suggest that phys ical therapi sts should be the hea lth ca re professional responsible for treatment or instruction in th e use of these interventions. Therefore. the phys ical th erapist is the legally licensed and the most qualified practitioner to refer to for th ese interventions. Nurses are usually the init ial treatment providcr and onen initiate refe rral to the physica l therapist. as we ll as se rvi ng as case managers and medical reviewers. Therefore, it is ve ry important that nurses und erstand the ca ndidacy. re ferral criteria, and clinical outcomes expected from the therapy. The chapters in Part IV have technical informat io n that may be beyo nd the interest of most nurses, but there are also clinica l deci sion-making sections that will g uid e th e nurse through the rationale for treatment selecti o n used by the phys icallherapist. Collaborative practice requires mutual understanding of the treatment recomlllended and the ex pected results. In addition, nurses, patients, or ca regive rs may be the ind ividuals who deliver the direct treatment establi shcd by the phys ica l therapist. Those modalities suited to self-
The management of\\ound healing with physical therapy technolog ies, including physical agents and elcctroth cra -
peuti c modalit ies common ly used by phys ical therapi sts, is presented in Part I V,
Ph ys i c~ll
agents and c!ectrothcrapcuti c
modalities arc phys ica l th erapy techn ologies with long histories of clin ica l app licati on and cfTccli ve ness. They arc defi ned by th e American Physical Therapy Associat ion in the following way: " Phys ical agen ts use hea t. so und. or light energy to increase the connective tissue extensibility, modulate pain. reduce or eliminate son tissue inflammation and swelling caused by musculoskeletal injury or circulatory dysfunction. increase the healing rate of open wounds and soft tissue. remodel scar tissue or treat skin conditions."!tPNb l These modalities include deep th ermal modalities (eg, th ermal ultrasound pulsed short wave diathermy). nonthermal modaliti es. (eg. pubed ultrasound, pulscd radi o frequ ency energy), hydrotherapy (eg. whirlpool. pulsati le irrigation with sucti on). "Electrotherape uti c modalities include ... physical agents that use electricity to mod ul ate or decrease pain , reduce or e liminate so ft tiss ue inflammation caused by musc ul oske letal ... peri phera l vascu lar or integ um entary injury. disease •... or surgery ... or increase the rate of healing in open wounds.''I(rr701 t> ~oI~I These modalities include alternating, direct, and pulsed current (eg. hi gh-voltage pulsed current. low-voltage pulsed current. and transcutaneous electrical nerve stim ulation [TE S]). Chapters 16 to 20 describe the rationale. device. applicati on of. and case studies fo r six modalities: electrical stimulation. pulsatilc lavage with suction. pu lsed short wave diathermy, pulsed radi o frequency stimulation, ultrasound, and whirlpool.
347
348
W OUND
C A.,
care or ca re by a prov ider olher th an a physical therap ist arc ex plained in each chapter's sectio n on self-care treatment guidelines.
CAN I) ID ACY FO R T HE INTE RVENTION Ca nd idacy for appli ca tion of physic al agent s a nd clcclrolhcrapclIl ic interve nt ions fo llows a th orough di agnostic process described in Chapter 1 to determine those condi tions that wo uld benefit from or preve nt lise of the interve ntion and to determ ine that the body systcms lack the abil ity to pcrrOfmlh c necessa ry process of repair wi th out inte rvention. The clinical decision-mak ing process used for selecting each of the modalities is related to the system impairments it aOccts, as we ll as pract ica l conside ration. Candidates for physica llhcrapy technologies incl ude patients wi th obscrvn blc ac ule inflammation of the tissues. includi ng pain , chro nici ty of or absence of any phase of repair, circulatory comp ro mise and edema. as wc ll as impai rmcnts ofd ifTercnt body orga n systems such as the cardi opulmonary, musculoskeletal. ncuromuscular. and integumentary systcms. Thc mode of interve nt io n best suited to the patient, the treatment selling. and the wo und wi ll be determined by the physical therapist. As a guide, the paticnts should be referred to the physical th e ra pis t for int erve nti on with a ph ysica l age nt or elcctro thcrapeut ic modality whcn the additional followi ng candidacy cri teria are met: • Medica l comorbi di tics ex ist that predict that a wound needs ex tra help to heal (eg, insensitivit y associated with spinal cord injury, diabetes). • Ilealing will be speeded by the thera py. • The wo und has been reca lcitrant to other methods. • There is an acute wo und in a patient wi th a coimpairmcnt such as chro nic obstructive pulmonary disease or imp::t ircd ci rculation, ind icating a high proba bility of nonconforming hea ling. • The ac ute trau matic wo und(s) is associated wi th neuromuscul ar or musculoskeletal prob lems that may require illlmobi lizat ion. • The wo un ds ex tend into subcutaneous tissuc and deeper underl ying structu res and interfere with functional acti vities: eg. the patient is unable to sit up in a wheelchai r beca use of the wo unds over thc ischial tuberosities or coccyx. • The patient s functional status is im pa ired by slow wound healing; eg. gait will be helped if the wound is healed more ra pidly. or patie nt may be ab le to return to wo rk. I~ easo n s
fo r Referra l
The patient referred to the physical therapi st for wo und hea ling is usuall y an indi vidual who has not shown signs of
normal wound repair. Often other treatment interventions are being used or have been tried with lim ited or no success. Actuall y the ve ry best time for intervening with physica l agents or electrotherapeutic modalities is during the first 72 hours immediately aft er injury. Several recent stud ies show that intervention by a physical therapist soon after onset of the problem (eg, stroke,u ac ute musculoskeletal painU) reduces cost. Appropriate early intervention by the physica l therapist has a prove n track record of signi ficantly reducing the development of costly chronic health prob lems. A review of the research literature eiled in the chapters on electrical stimulation, pulsed radi o frequ ency. pulsed short wave diathermy, and ult raso und all cite research that demonstrates optimal effecti ve ness when the treatment interve ntion is applied earl y. However, since in rea lity more chronic wo unds than acute wounds are referred to the physica l therapist, other research cited in the chapters dcmonstrates efficacy of thesc technologies for hca ling of chronic wounds or to alter factors related to chronic wound healing such as circulation, oxygen uptake by cells, and edema. Ex pected outcomes should be based on the reason for the referral, the efTi cacy of the treatment interve ntion selected, and the chro nicity of the wound. Patients, caregivers. and physicians seek carc for a wo und for many reasons. Although it seems as if thc obvious goal of treatment is healing, healing is not the highest priorit y for everyone with a wound, and that assumption should not be madc. It is ve ry important to ask the patient, famil y, physician, and payer the reason for the referral and base the interve ntion selected and ex pected outcomes on meeting those objectives. Most of the time the patient and fa mil y arc looking for a simple fun ctional outcome. For example, the patiellt with a foot ulcer secondary to pressure and insensi ti vity is fearful of amputation and loss of the ability to walk . The patient wa nts to kn ow if the limb can be saved.The family of a debilitated nursing home patient wants thcir loved one with a pressure ulccr to bc comfon able. They may rcalize that closure is not an option. Fea r is a concern and creates a reluctance to come to therapy. All of these issues need to be addressed. The physical therapist's first intervent io n will be to learn as much about the patient and his or her goa ls and then begin education about the treatment options, effects of the treatment. and the ex pected outcomes. Di agnosis The diagnosis is the synthesis of the information gathered. Physical therapists use a fun ctional diagnosis to describe an impairmcnt, disabilit y, or handicap of an associated body fun ction. For examp le, the patient wi th a neuropathy as a consequence of alcoholism, dia betes, or spinal cord injury or the il11mobile or il11l11obil izcd patient could all have
Par/IV
a functional diagnosis of impaired sensa ti on with undue susceptibility to ischemia. ti ssue anoxia. infection. and pressure ulcera tion. The impairmen t is decreased immunity. ti ssue anox ia. infecti on, and cell death , The disability is desellsit ized skin and ri sk for skin breakdown. The handi ca p is inability to maintain normal activit y and mobilit y. Patients with chronic wounds have an abse nce ofprogression through th e phases of repair. that is, a functional impairment to wound hea lin g at th e cellular leve l or the ti ssue level. Ahsence of il!/iammatiull alld il/abilily 10 progress 10 proliferatiou is a functional di agnos is about functional impairment of the process at the cellular leve l or ti ss ue leve l. This could be applied cqually 10 a funclional impairmelll of the prolife rati on phase: abse nce of proliferation or wound contraction with inab ilit y to progress to closure. Chroni c wound edges do not produce functional epidermal cell s to mi gra te across the wound to c lose it. Ahsence oJepitheliali:atioll due 10 impail1l1elll (?f epidermal cell activity is a functional diagnosis ro r abse nce of wound progressio n to closure. A poorly healed wound or a minim ally healed wound has a functional diagnos is of absence of remodelillg due to il1leglll1l e111111)' .~ystem impairmem. Although traditionally patients with non-healin g wounds are referred for physieallherapy. palienls wilh mu sc uloskeletal injuries and so n tissue trauma should also be viewed as patients with a closed wound. Patients with wounds such as ligamentous tears. muscle stra ins, sprains, sk in tears, hematoma s. stage I pressure ulcers. stage 0 vascu lar ulcers. and abrasions that interfere with one's ability to wnlk, work. or co mpete in a sport should be viewed as cand idates for inte rventi on with physical agents and e lec trotherape utic modalities including elec tri ca l stimulati on, pul sed radio freque ncy stimulation. pulscd short wave diathermy, ultraso und and whirlpool. In patients with metabo lic di seases (eg. lupus or diabetes) who sufTe r wounding. acute wounds can. and onen do. become chronic. Also. mi crotrauma resulting from excessive forces and repetition ca n also lead to closed wounds such as tendinitis and nerve e ntrapmcnts. In these patients, the imp3inncnt is also a closed ti ssue wound. The di sability is pain and usua lly limitation in ran ge of moti on. A handi ca p would result from prolonged di sability and the resulting inabilit y to work or pa rticipate in normal ac ti vities of daily living or recrea tion . Ea rl y and e fTecti ve interve ntion to accelerate repair with the listed interven ti ons should be co nsidered. In summ ary. a patient who has a functional diagnosis of impairment or a body system at the cellular. tissue , or organ level (or a combination) related to ti ss ue repair shou ld be co nsidered a candidate for interve ntion with e lectrica l stimulation, pulsed radio frequency stimul at ion, pulsed short wave diathermy. or ultra so und. In addition, patient s with mu sc uloske letal injuries in need o f acce lerated repair should also
349
be co nsidered candidates for the sa me intervcntions used for closed wound healing.
Prognosis The functional diagnosis is predicti ve of the need for the interventi o n . Inter ve ntion with ph ys ica l a ge nt s and electrotherapeutic modalities must have a predicted outcome, or prognosis. that the intervention wi ll reduce the impai rment or alter the consequences oflhe di sease assoc iated with the fun ctional diagnosis. A wound diagnosis of absence of the illJ1ammllfioll phase, for exa mple, is predictive that the wound needs an inflammation phase fo llowed by progression Ihrough Ihe phases of healing 10 reach closure. The prognosis is ;1I;I;al;OI1 oj inflammation fhl/oll'ed by progression oftlte wOllnd through the phases oj healing. Part of a prognosis is th e ex pec ted due date. There is enough information in th e literature to evaluate the expected length of tim e to reac h an outcome. The individual chapters in Part IV provide this informati on. Electrical stimulation . pu lsed radio frequcncy stimulati on, pul sed short wave diathe rmy, ultrasound whirlpool, and pulsalile lavage wilh suclion are all ex pected to re initiate an inflammation phase followed by progressionlhrough Ihe phases of healing. AnOlher example of functional di ag nosis is impairment a/sensation witlt 1II1 due s usceptibility 10 pre.5SI11l1 ulceration. Reflexive neurona l mechanisllls are impaired. and other methods Illust be used to stimulate circulatory responses; the prognosis ror thi s functional diagnosis would beadeqllare circullllOlT peljilsiollJor deli\lelJ' 0/mygell ami nUlrielllS to tisslles tu pmgress thlVugh phases ofl'epail: Multiple fun ctional diagnoses may be made that lead to l11ultipl e interventions, all of which will afTec t the outcome with the phys ical agent or electrotherapeutic modalit y interventi on chosen for th e wound. For instance, the patient with an impairment of se nsation with undue susceptibilit y to pressure ulceration mu st be assessed for pressure ri sk. An interve ntion of press ure relief or elimination the n must be included in the trea tment plan so that the enhanced circulalory perfusion broughl abo ul by Ihe se leeled interventi on can reach the ti ss ues. The phys ical therapist would apply Ihis melhodol ogy 10 predici an ouleome. The progno sis for repa ir of a c losed ti ss ue injury would be acceler(l!ed ah.mrption a/hematoma. acceler(l!ed deposition 0/collagen. aud reslOratioll ofl1ormal range.\' 0/ motiol1. tiss lle extensibility. fiSSile s freng fh forfi mCfiollal activifie,\' (eg, self-ca re, work. leisure, or play). Clinical resea rch studies are very useful to guide the cli nician in predicted outcomes and can function as a guide for a target due date. C lini cal research studics should identify whether the wound s treated are acute or chronic. Because clinical resea rch studies are usually carried out in ideal settings under optimal co nditions, th ey should be considered
350
W OUND CARl
onl y as guidelines that need to be tested in the individual clini ca l settin g to determin e th e outco mes for th e spec ific
program . For example. the literature describes wound healing by closure or improvement. Imp l'Ol'emell l is less cl earl y
defined and usuall y is described by reduction in depth of tissue loss or size and is listed as incompletely hea led. Depth of ti ssue involve ment (severity) will alter the ex pected length oftimc to closure. Parti al-thickn ess wounds heal fas ler than full-thickness and deeper wo unds.' Normal wound healing takes 3 to 4 weeks,' while the defin ition of chronicity is hea ling that has not occurred in the normal tim e fra me. The con-
and exudate that leads to an outcome of wo und hea ling. There are also practica l considerati ons in choosing an intervent ion. These include th e treatm ent setting, th e treatment provider, th e trea tm ent payer. th e tre atm ent avai labilit y, medica l contraind icati ons. and adj uncti ve tre atm ents (dressings,
multiple technologies). Ifthe treatment provider is to be other than a physical therapist or physica l th erapi st assis tant, the
treatment must be safely app lied by a person not trained in physical therapy. This would prec lude use of pu lsed short wave diathermy or ult raso und, for example. The treatment paye r must be agreeable to payi ng for the physical thera py
cept of using physica l age nts and electrotherapeutic modali-
intervcntion selected. For cxamplc. Medicare contractors
tie s is to initiate or acce lerate th e ra te of repair of acute or chro nic wounds. For example, Dyson andYoung8 found th at
have an exc lusion poli cy for payment of ultraviolet light to
appli cati on of low-intensity ultrasound duri ng the earl y inflammatory phase accelerated the inflammatory ph ase of repalT.
Choosing between In tervent ions A frequentl y as ked questi on is, How do I know which intervention to choose? There is no si ngle answer to thi s question. The mechan isms of acti on on th e biologic system are different. but the expected trea tment outcomes of progression through the pha ses of hea ling are sim ilar for each of the deviccs prese nted in Part I V. Somc have optimal tim es fo r application, however. For instance. ult rasound is best deli vered in th e inflammatory pha se--early proli fe rationSor to restart th e inflammatory phasc, but it is not effec ti ve fo r improvement of tensile strength if used in the later proli fe rali ve or epitheli alizati on pha se. 9 Figure I V- I is an algori thm
showing the phases of wound hea ling with a key to highlight whi ch arc the putati ve effec ts on the phase or factor of healing of th e six physical therapy technologies descri bed in Part IV. If one or more of the technologies affects the same biologic aspect of the phase, oth er criteria will be used to choose the modality. For instance, most dev ices desc ribed have th e
ability to increase tissue perfusion. What diffe rs is the degree of tissue perfusion. The th erm al modaliti es heat and increa se circul ati on more vigorously than the nontherm al modal ities. Thi s effect may be suitable for some pati ents who necd a vigorous attcmpt to enhance blood fl ow to reac h ischemic ti ssues. Th e nonthermal dev ices affcct the microcirculation but may not have a vigorous enough effec t on circulation for all patients. Research is highly va lued as the basis for sc lcc ti on of an intervent ion, and conscquently the intcrvention with th e most support ing research may bc given th e nod over less testcd deviccs; however, cli nical ex peri ence still must be valued. For example, whirlpool and pul satil e lavage with sucti on havc no controllcd c lin ical tri als for cfTi cacy of wo und hea ling, yet clinica l experi ence demonstrates that both have the abi lity to clean wounds of debris
treat wo unds. Treatm ent ava ilabi lity is as practical a reality as anything. I f th e preferred intervention is not available and cannot be obtained, th en it is inacccssible and another choice will have to be made. M edical cOJ1traindications ex ist for all of th e different technologies. but the medical contraindication that rul es Ollt the use of one will not necessari Iy rul e out oth ers. For exampl e. a semicomatose pati cnt should not be
seen in the whirlpool. but wound cleansing with pulsatile lavage with sucti on at bedside would be an appropriate al-
ternati ve. The following Casc Study illustrates where thoughtfu l evaluation of the history and systems review narrowed down th e choice of treatment intervention to one appro priate technology aft er considering all th e factors.
Trcatmcnt Outcomcs Ma nage mcnt Clinical managers havc an obl igation to revicw trea tment outcomes systemi cally for wo und patients referred 10 physical therapy. Most oft en the patient population refcrred are those individuals with comp lex wo unds and comorbidities and many arc also vcry debi litated. areful screening and monitoring proced ures arc necessary to utili ze trcatment ef-
fecti vely. Sussman Physical Therapy, Inc. (S PT) is used to illustrate how a clinical program lIsed a wound databa se to do progra m evaluati on and quality improvemcnt, and eva luate program outcomes. SPT trea tcd a popu lation of complex
and debili ta ted nursi ng home patients. SPT developed and conform ed to a se lf-i mposed standard of 50% reducti on in wo und size within a 4-to-6 week peri od using Sussman's noninvasive. surgery-altcrnative trcatm cnt approac h with
physical therapy technologies and debridement. The first requirement was identificati on. fo r the pati ent 'S medi cal manager, wound stability, and the candidacy for surgical and oth er more costly interventi ons. SPT used paper-and-pencil instrum ents to record wo und data information. The information was th en transfcrred to bubble sheets and scanned into a computer databa se. tatisti ca l analysis of the SPT wo und database was performed by Swanson and Co., Inc.lO Findings were th at SPT had cxcellent success wi th chronic
Pari I V
35 1
Injury
I
r
Inflammation Phase l'
Epithelialization Phase
l'
Proliferation Phase
Pain 6....JOX=
6 l'
Immobility 6 0 0 = X
+
l'
Impaired 6 0 0 = X Circulation
Infection Control 6 XX= l'
Edema 6 0 = l'
Oxygenation Nutrition 60=XO
~
Macrophage 600
~ Granulocyte 6
Fibroblast 600 Formation
~
Angiogenesis 600
+
Wound Contraction 60
Hypoxia l'
Necrosis 60 () X
l'
Collagen Lysis
!
• Remodeling Phase .. I 6~
Collagen Synthesis 6 0
j
l'
Wound Recovery
KEY :
6.
Electrical stimulation Ultrasound Pulsed radio frequency stimulation
,~
X )<
Pulsed short wave diathermy Whirlpool Pulsatile lavage with suction
Figure I V- I Putative Treatment Effects of Phys ical Therapy Technologies 011 Phases of Wound Hea ling. Source: Adapted with pcnnission from Sussman CA. The role of physical therapy in wound ca re . In: Krasner 0 (cd), Chronic Wou"d Care: A Clillical Source Book/or Heal,II Care ProfesssiOlwJs. Wayne, PA: lIealth Management Publications, Inc .. 1990, pp 327- 367. Copyriglll 1990, Heahh Management Pub-
lications, Inc., King of Pruss ia. PA .
352
WOUND CARI-
Case Study: Choosing the Appropriate Treatment Intervention
A case example where multiple factors had to be considered when making a choice of intervention was
required for E.F. E.F. An elderly lady, E.F. lived in a nursing home because of incompetence related to Alzheimer's disease. She had venous disease and a
history of recurrent venous ulcers of the lower leg. A new episode of ulceration occurred and the patient was referred to the physical therapist. The patient had a pacemaker, would not stay in bed or in a wheelchair for 5 minutes, and would not tolerate dressings or compression devices. The venous disease diagnosis ruled out whirlpool. The pacemaker ruled out any form of diathermy. The low tolerance for compression ruled out compression devices. The inability to tolerate staying in one place more than 5 minutes and intolerance
for dressings ruled out electrical stimulation. Pulsatile lavage with suction was not available and would not have been tolerated by the patient. The only choice remaining was ultrasound because she could be kept still and amused for the 5 minutes required for a periwound ultrasound treatment. This was also an appropriate choice because ultrasound is particularly effective during the acute inflammatory phase and effects absorption of hemorrhagic materials. This patient is included as one of the case histories in Chapter 19, Ultrasound. The results are viewed in Color Plates 65 to 67.
leg ulcers with its treatment approach. Patients were referred to SPT when other methods failed. The program eva luation demonstrated that morc than two thirds of the chronic leg
ulcers treated by the SPT method healed. This information was of va lue to the contract faci lity administrator. to the managed care contract payer, to the total qua lity assurancc committee of Ihe facility, and to the health department survey team. Furthermore, the information derived from the data analysis determined that the average length of stay for the patients in Ihe healed group was 49 days. This information was then applied to do cost outcomcs analysis as described
below. I I
Functi o nal Wound Cost O ut comes Ma na ge me nt In 1992. the cost for treatment of pressure ulcers in all settings in the United States was $ 1.3 billion. 'l The average cost of treatment of a pressure ulcer in the United States.
based on 1990 data, is $2,000 to $30, 000. The typical cosl for a medical approach to treatment of pressure ulcers by surgical debridement is at least $4,000-" How do costs for treatment with physical therapy technologies for wound healing compare? Based on data from Swanson ,14 Maver,1.S and Birke,16 physica l therapy technologies are competi tive for certain wounds. Swanson l4 compared the costs of a course of wound care with hydrotherapy (whirlpool) with a highvoltage pulsed-current (HVPC) type of electrical stimulation and found that the course of3 months (90 days) of care with hydrotherapy treatment (whi rlpool) for necrotic wounds with an unknown outcome was $4,500 compared 10 52, 100 for a 7.5-week (52 days average) course of care with outcome of wound closure fo llowing treatment with high-voltage pulsed current electrical stimu lation. Mavcr ' ~ compared the cost of conventional treatment for stage I I I pressure ulcers that did not heal during a course of care with a mean time 004.62 weeks at a cost of$7,946.33, with 8.5 weeks course of care to healed status with Diapulse, pulsed radio frequency stimulation, 17 combined with conventional care cost of$2,929.62. The reported savings per ulcer in this study was $4,484. Birke 'fl reported on numerous studies using total-contact casting (TCC) to heal plantar ulcers in patients wi th neuropathy. The average time to closure was 42 days. The average cost for a closed wound was $1.250. These cost savings do not include savings derived from reduced mortality, morbidity, and reduction in ampUlation s. Comparative lengths of care and expected outcome for hydrotherapy. HVPC, and TCC are illustrated in Figure I V- 2. Cost comparison allows for a profile of wound cost outcomes and competitive analysis of the result s of a course of care. Physical therapy is cost competitive for certain wounds (Figure IV- 3). Physical therapi st managers and program directors need to understand the information required to predict and manage cost for proper utilization management of services. The necessary information to predict cost and outcome are available from several sources: clinical trial s. program eva luation reports, the facility's clinical database. the Agency for Health Care Policy and Research (AHCPR) standards, and payer data-based reports. Does your clin ic know your cost ou tcomes? Cost outcomes are differentiated from the technical outcome for th e wound (eg, closure). Cost outcomes are what it costs to provide a course of care compared with the bi lied charges . Thai determines the cost to the provider as differentiated frol11 the charges to the payer. The cost outcome is based on all the related costs for providing the service: labor cost, supply cost, and equipment cost. To determine the cost oflrcating a wound the cl inicalmanager needs to predict the number of expected vi sits to achieve a predicted outcome. For example. if an
Parr / 1'
• Hycro: Necrot ic > Unknown • HVPC: Necroti c > Closed o TCC: Neuro/O pen > Closed
Course of Care in Days
Figu re 1\1- 2 Le ngth of stay dependent on wound Iype and procedure .
5,000
$4,500
4,000 3,000
• • • o
2,000
Surg.Debr: Necrotic> Open Hydro: Necrotic> Unknown HVpe: Necrotic> Oosed Tee: NeuralOpen > Oosed
1,000 0
$ Figu re IV- 3 Cost companson for different wound interve ntions and out comes. Physica ilh crapy is co mpeti tive for ccrw in wound s.
35 3
354
WOUN D C ARl
outcome of closure is expected in 84 visits a cost analysis can be done as fol lows: Labor cost at $30/visit x 84 Supply cost at 56.25/visi t x 84 Equipmcnt cost at 0.50 x 84 Total cost Billed charges at S60/ visit x 84 Net profit
52.520 $ 525 = S 42 $3.087 S5.040 $1.953
of healing when wounds were treated with physical therapy technologies. For example. reduction in wound depth is a finding of acute proliferation phase. Reduction in size is a measure of wound contraction and of epithe li a li zat ion. If these benchmarks of healing are not occurring in an orderly manner, thi s may be due to a poor response to treatment or changes in medical status and should trigger a change in the treatment approach. The following are some examp les of situations that trigger a change:
The cost for a different Olilcomc to co nvert the wound to clean and stable may take half the time to closure. Cost to the payer would be reduced by half to 52.520. The case manager for the payer may be morc willing to authorize an interim step for a known cost than an unknown outcome at
unmanaged cost. Utili zat io n a nd Cost Management Utilization and cost Olltcomes management !TIcan that con-
tinued ongoing evaluation of the patient candidacy be reviewed. Candidacy determined ar the initial evaluation may change as the patient experiences a course of care (Figure IV-4). This would initiate a reevaluation (0 assess appropriateness for furthcr treatment. The Sussman Wound Healing Tool. described in Chaptcr 5. was deve loped as a diagnostic (001 to evaluatc progression through the phases
• Failure to progress: If the wound(s) are not progressing through the biologic sequence of repair aner 2 weeks of treatment with high-voltage pulsed current (HVpe). for examp le. the enti re wound management plan needs to be reviewed to determine whet her it is the treatment wi th the HVpe or other factors th at are respons ibl e for failure to progress. Since all wounds have multiple associated interventions, including wound cleansing, topical treatments, dressings, and debridement. along with the HVpe. each intervention should be reviewed to determine whether continuation is appropriate or if there needs to be cha nge in these intcrventions o r with the HVpe protocol. It is standard wisdom that wounds shou ld be progress ing in the rcpair process during a 2-week interval or the treatment should be revised. I;!: • ~"o ull d regressioll: If th e wound has golten larger or deeper and is invading named structures or areas or has
Still Treating: pen- Candidate? Total $ Spent
Discharged: Closed ~--------n ischarged:
Stable & Open Start of Care
Course of Care and Outcome
Fig ure IV....4 Monitor candidacy and outcome throughout course of care.
Par' IV
•
•
•
•
•
bccome infcctc(L indicating that another management strategy is nceded (eg. surgcry for incision and drainage or antibiotics). thi s is referred to as wound regression. Although the physical therapist. phys ical therapist assistant, or nurse would not make the decision for the subscq uent therapy. he or she should be able to recogni ze the signs and sy mptoms of di sease and has responsibi lity to make a referral to the appropriate practitioner. ft!lel/icill illslllbili~v: Ifthe paticnt has bccome medically unstable (eg, pneumonia. sepsis, renal failure), the body's ability to heal is impaired. and the si tuation requires a change in ll1ediea lmanagemcn t bcfore continuing wi th physical therapy. The phys ical therapist may determine that the physica l therapy interve ntion may need to be put on hold ulltil the medical conditioll is stabili zed. Other IIIllltllgemellt rel/uired: If the wound has progressed to a clean and stable wound in the proliferat ion phase. it may indica te that the wound is ready for grafting. It may be the best prognosis for the wound and/or for the patient and may have been the reason for referral. the objecti ve of the palicnt, the family. the therapi st, and the physicin n. Uv tllld lIeells less skilled ClIre: The wound is now at a phasc of repair that dcmonstrates that the healing response is slistHined and the wound is clean and stable. Now thc patient/caregiver or nurse can provide standard wound care procedures to keep the wound clean and if body systems support the process of healing, take it to closure. GOlll.~' m et: Sometimes. thc patient and family have reached their goa ls and do not wish to continue or become noncompliant with trcatment. In other cases, the wound has hea led to closure. Closure (111(1 beyond: Wound closure may be the intent of the trcallne llt. but closlIrc does not include rcmode ling. Wounds that arc minimally c losed are at very high ri sk for recurren ce, especially when located over areas of fri ction . shear, and pressure. such as on the seating surfacc or plantar surface o f the foot. Wounds in those areas of hi gh risk would benefit from further stimulali on o f collagen synthesis by electrical stimulation until the minimall y healed scar is acccptably healed. III Acceptable healing is achicved when thcre is a thickening of the sca r formati on and the color of the scar blanches from bright red or pink 10 light pink or white.
Plan of Carer rre:Hment Part IV focuses primaril y on the usc of exte rnally app lied treatments for wound repair and does not address specific
355
dressings and deb ridement, nor does it olltline the specifics of an exercise program. It must be reinforced, however. that all of the described techno logies are supplemental to the traditional wound managemcnt program ofdebridcmcnt. dressings. and medications. In addition to physical therapy technologies. every patient who is able to participate in exerc ise must be instructed in an appropriate exercise program. For so me. traditional strengthening and condition ing exe rc ises would be appropriate (eg, wa lking, running. stationary bike). In others it may be active range of motion of the extremities or isometric exercises. Every physical therapist mu st address the issues of immobilizalion and prevention of demincral ization. atrophy, and contractures. In some cases, so ft ti ss ue mobili za tion techniques could be used arollnd the wound. In all cases. the patients and caregivers must also be educated about hydration, nutrition , and a balanced lifestyle that addresses stress reduction and positive health. The physica l therapist is lIsually the only team member who can manage the electrical stimulation program, the therapelltic exercises, and appropriate soft ti sslle mobili za tion procedures along with the wound care.
CONCLUS ION The rules for selection oftreall11ent interventions includes consideration of the medical tatu s of the patient, th e status of the wound healing phasc, and all treatments lIsed to achieve th e expected outcome. Wounds all rece ivc multiple intervention s. Treatment efTects arc additive. Therefore. all treatment interventions mu st be compatible with the patient, one another, and the wound. They will change during the progressio n ofhcaling. The most universa ltreatll1ent intervention is the wound dressing. Modern wound dressings have specific efTects and times for reapplication. Because wounds need to be cleansed periodically, the wound c leanscr is another common intervention. Topical agents from cnzymes to a ntimicrobia ls are often added to the wound intervention regimen. Depending on the phase of wound healing, one or more of these interventions will be needed , The addition ofa physical agent or an e lec trotherapeutic modality must be co mpatible with the other trea tmcnt interventions. This will require collaboration of the te3mmcl11bers-nurse, physician, pharmacist, and physical therapi st- to select interventions that are compatible and efficacious for wound healing. Ex hibit IV- I li sts three rules of treatment selection. an example of how each is used, and a formu la for selection of treatments to achieve a desire outcome in a prescribed period. The letters "A," " 8," and "C," in the formula represent three treatment interventions. The number of treatmcnts usually give n is often three, but is not limited to three. Each chapter in Part IV will address the issue of treatment interactions and compatibility with other interventions.
356
WOI ' "
Elhibit 1"- 1
I.
C·,.,
Rulc~
~lcdjCltl
REF ERE.\ CES
ofTrcatmcnt Selection
HsseSSl11cn' ilTtd
li~sue :ls~cssmcnl
determines
the ticlcclion of treatment.
Ew"'p/L': Client has a vcnous stasis ulcer in inflammatory phase and has a cardiac pacemaker implant_ \Vhirlpool. li Vre. PRfS and PSWD arc contramdicated. Ultrasound would be a good choice
American PhY"lcal Thcmp,\ ....ociallon A g.ulde to phY"lcal thempi .. 1 praclicc. \"011 a llcscriplion ofpal1cnl m:lOagemcnt Ph,'( Ther 1995;75 :707 · 764
ror local (lpplicallon.
2.
(icncnll Accountlllg Olllce. L, S t"ongres ... reported III PT Ilullelin. American PhysicalTherap), :\ ....OCUlIH.\Il. \'01 12. No. 10. \Iareh 7. 1997.
J
lIa)e .. S. Carroll S. Larl)' IIltencllllOll care III the acule Mrokc patlcnI . lrd/ Plln' \kd He/whit 19H(';i.7:31(j 321
4
LIIHon S. Ilett~lIlg t\. Andcr.. ~on D. A controlled !!Iully of the ct"of carly IIltenentlon on acute museuloskdetal pam problcm .. /1l1ill 199.t54(3):353 3~9
fecl~
2. Treatment changes during the progression of healing
so 115 to affect the
recOHr~
process.
~.
Amcrkan Ph) .. ical Therapy As.. uciatloll. 01111"01111' f:.llt'(·ln·('lIl·n of Phnicul 711l"~IJJ\ III Inl/(JUlln' B;h1/(jW~/p/II' A1cxandria. \"A ·\PTA. 11}<)3
(,
Ferrell BA. (hleNcii D. ("hri~lelhlln t> A r.lIldmni,..ell trial of 10\\' bed .. t(lr treatment of pn,:s .. urc ulcer.. J.Hf.I 199L?M 494 497.
EWl1Iple. Chell! has a necrotic Illp ulcer \\ tlh eschar. Treatment ... tarts \\ ilh \\ hlrlpool. cll.Iymcs, ::lnd oCelllSI\C
air-Io~ ..
drc:-:;s1Ilg. Necrollc IIsslie IS removed, Treatment changes.
3. Each selected trc
7.
Ilardll1g I\. Wound cure putllng theory 11110 cllIlical prilellcc . In I\.msncr I). ed C/Iroll/(' 1I{"md ('lm ' l Cillll("lll .)ollrn· lor 1I""flll ('''n' Pm/t·.I\;I"'I" .. t\.lIlg of Pru .. ,,;). P.·\ Ilcallh "-tallagcmcnt Publications Inc. 19I}O:\9 ."\()
X
I);r ..on M. Young S. !\cccler'.lllnn uf lI ..sue n.:pa1r hy Im\ IIltelNt~ ultra .. ound applied dunng thc Inll 1:\ ( P r..\ JOInt Congre ...... Ahslr'.lCI No. R-I Xfl. prc .. t·ntcd 101" \"eg.ls. ",c\.lda, June 199~
<)
IIMI J. The clrcel of therapeullc ultra'UlIlld on damal repair 1\ Ith cmpha .. i... on flbrobl .... t.. acll\lt). rhl) Ihes1 .. , london L:nl\'CNt;r of London, 1'193
10
Swan ..on (; SII\\/1/wll'hninI1711l"n/l'l' ICJCJI lIiwlIIl nt/labOlt' Rt·· IHIrI. l.ong Beach. ( \ S\\;lIhOIl .lIlll Co.
II
SUSSlllilll C I ullclmnal \\ouml 1.:110,;1 oulctlmcs. Pre~entcd at the Amcrican Ph)"lcal Ther.lp~ 1\ ....(H;lalwn ("omI:JlIlcd Sectilln .. Mectin!!. Ichruar,. 1l)96, :\tlallu. ( iA
12.
Berg .. trom '. Bennctt M .\. (.Irhnn ("I • ct al 7i"'tllml"lIi1l/ Prn\lire l kt'''\ C1LllIe'll Pracllcc CiUltlcllllc \,10 15. AII("PR Publica· tion 1\0. 9~-HM2 . Roct...\llk. \11) \gency fllr Health (Me I'olic~ .lIld Re,earch. G.S. Public 11c.. lth Sen ICC, L S ()epanment 01 I Icillth illlll 1I1IIllan Scn ICC .. ; l)el.:elllOcr 1994
13
\Velhe J. Sharp llebridelllellt uf\\ollmt.. In .. trucIlOllalcouf',c Wound ("arc \tatlil!!CmCIll ('tllll"crent·c October IIN3.
14
S\\;ln~On (i Lo,;c of I.:lht llalil, prmillcr e'penencc. and clLnlcal guidelineo,; in the 1r.II1 .. ilion 10 nUllilgeuc.lrl·.J II" l/t'd 1(1)1;23( I) 7{) 74
I~ .
Ma\cr R\\· An .Ictuanal rC("lI.m nn thc t:u .. t ellcl.·tl\cne .... of a mcllicill tcchnolugy. ./ /1/\ lied 1991 :2]( 2): 120 12-'
16
Blrkc J. Managemenl of thc dlaheuc I(l(ll In .. lrucllOn31 C(lur,c Wtl\1I\d ("arc \t.lIla!,!cmellt Conference. \/o\cmbcr 1995
17.
!toh "-t. el ill Aceelemtell l\lluntl healing ofprc .... ure ukcn. by pul ..ed high peat... powcr c1eclnllll.lgnetlc energy (Dlapuhe). /)"("/lbllll.1 t99Io4
IX
I ;1/;ln... (;. cl .. 1 DefinitIOn .. ilnd gUlllelinc .. for ;... o,;c .... mcnl of \\uuml .. and e\illuallOn of heallllg In 'II J)l',.",ulol 11}94; I ]0: 4~N 493
E.mll/ph-: Client has a clean rarlJal-lIl1dness wound III
thl.! 'Iclite prolifcration phase. PrognosIs i~ \\Olllld closure. Trcallnelll sclcclctl: clean \\ nh normal sallnc. usc hytlrogel Imprcgn:Hetl g.llI/C dreSSing. apply IIvpe Ihrough drcsslIlg. and cO\cr ,\-jlh second
Formula To Select I rcatment
\\ound \\ound
IIc :llin~
Phase ofThOiiue + Treatment A + Treatment B + Treatment (' =
lIe:llin~
Pha se
ofTi.!t~ur
in X Prriod ofTirnr
CIIAI'TER ORGAI\IZA 1'10'1 Each chapter in Part IV cO\crs the following information abollt each modality: • • • • • • • • • •
Rrclated definitions and terminology The theory and science or the therapy Clinical trials when 3\aiJabJc Indic"ltions. contraindic
Jl'~\\
C H A PTE R
16
Electrical Stimulation for Wound Healing Carrie Sussman and Nall cy By !
INTROD UCTION
Ca paciti ve Cou pling
Elec trical stimu lation (ES) for wound healin g has ac hieved acknowledgment by th e medical community. resulting in morc referra ls. All ES procedures a re not alike. crea ting con-
Capaciti ve ly coupl ed ES invol ves the tran sfer o f e lectri c Clirrent through an appl ied surface e lectrod e pad th at is in wet (e lectro lytic) conta ct (ca pac iti vely co upl ed) with the exte rna l skin surface and/o r wound bed . Wh en ca paciti ve ly coupl ed ES is used, at least two e lectrodes are required to compl ete the e lectri c circuit. Electrodes a re usua lly placed over wet co nducti ve medium : ( I) in th e wound bed or on th e skin a di stance away from the wound- monopolar tec hnique, or (2) straddling the wound- bipolar techn ique.
fusion about which one to use for wo und healing. This chapter tri es to stra ight en out so me of th e co nfusio n. It begins
wi th defi nitions and terminology used to discuss and distinguish e lectrica l stim ul atio n para meters. The seco nd sec ti on de tails the scie nce and theory oCtile th era py a nd re lates bac k to the parameters. Clinica l decision making applies the science and theory by considering the indications for the therapy,
reasons [or re ferra l. medica l history. and systems rev iews that are pa rt of th e diag nos ti c process. Thi s secti on is followed by description o flh e equipm ent and accessori es used, the ra tiona le fo r se lecti on of pro tocols. th e ex pected out comes, and the pati ent sc t-up. Since ES is a treatm ent inte rvc nti on th at can be taught to pati e nt s or other caregive rs, se lf-ca re teaching guidel incs arc included. Case studi es applying the fun cti ona l out come report (FO R) to document the ra tiona le for selecti on of e lectri cal stimul ati on as the inte rvc nt ion fo ll owed by a di sc ussio n revea ling th e c linical decision-makin g process and th e actu al outco mes conc lude the chapter.' Chapter 2 describes th e FO R.
DEFINITIONS AND TERM INOLOGY Electrica l stimul ation for wound hea ling is defined as the use of a ca pac itive co upl ed e lectri cal c urren t to tra nsfer energy to a wo und . The type o f e lectri ci ty th at is transferred to the target tissue is co nt ro lled by the e lectrica l source. 2
Am plitude a nd Voltage Amplitude re fers to e ither th e vo ltage or th e curre nt intensity o f an e lectri c current. Voltage is a measure of the force of the fl ow o f electrons and amperage is the measure o f the rat e of fl ow of th e current. Whe n vo ltage is turned up , the curre nt will also go up, a nd vice ve rsa. Some stimulators prov ide a readout o f vo ltage and so me a readout of current. The rel atio nship between vo ltage a nd curre nt is ex pressed as Ohm 's law. The formul a for th is is current times resistance equal s vo ltagc [V = IR, where V is voltage, I is current, and R is res istance]. In gene ra l, low-voltage devices produce vo ltages o f ditTerent ran ges from 60 to 100 V. Hi ghvo ltage devices range from 100 to 500 V. Thcse arc pcak ranges. Amp erage The unit o f current is th e ampere (A), whic h is de fin ed as the rate at whi ch e lectrons move past a certain po int. A mil-
357
358
W OUND CARl
liampcre (mA) is onc thousandth oran ampere. and a microampere (~IA) is onc millionth of an ampere. Microampcragc current is lIsuall y between 5 and 20 ~A of current (less than 1.0 mAl.
•••
C harge Time
Electrical charge is the excess or deficiency of electrons o r ions. An electrically neutral s ubstance that loses electrons becomes positively charged, and if it ga ins electrons it becomes negativel y charged. The unit of mcasurc for charge is th e coulomb. In bio logic system s th e charges are small and ex pressed in microcoulombs (fl )] A typical hi g h-vo lta ge stimulator. for example, has a maximulll pulse charge of only 10 to 15 ~I C. which is very safc."'(pli5I Th e charge densit y is the electrical c harge per cross-sectional area of the electrodes. The large r the size of the electrode the smaller the c harge densi ty, and conversely.
DIRECT CURRENT
Figure 16- 1 Graphic represen tati on of the unidirectional now of charged part icles. Source: Reprinted wi th permission from ElecllVlherapelllic Terminology ill Physical Thempy, p. II. C' 1990. Section on Clini ca l Elect rophysio logy and the American I)hysical Therapy Association.
Pulse (phase)
Interphase Interval
~
I'olari ty Polarit y refers to the propcrt y of having two poles that are oppositely charged . The positive po le is ca lied the anode and the negati ve pole the cathode. The positi ve pole lacks electrons and attmcts electrons from the nega tive pole , o r ca thode. Polarity ca n be chose n or emphasized for biologic efIcc ts.
I
I
•
•
Cvcle Time
• I--
r--
•
MONOPHAStC PULSED CUR RENT WAVEFORM
Note: tn a monophasic waveform, phase and pulse are identical.
\ \'avcfo rm s Different types o f current have diITerent characteristic waveforms. Waveforms are th e g raphi c represe ntations of a c urrent on a current/ time or vo lta ge/time pIOL ) Wavefo rm s arc classified by the direction of current flow. Current flow is e ithe r unidirectional o r bidirectional. Figures \6- \ lO \6- 6 show exa mples of direct current. mo nophasic square wave pul sed c urrenl, twin peaked pulsed monopha sic current, alternating current, and balanced biphasic and asymmctri c biphasic waveforms. Each wavefo rm and related characteri stic s a rc descri bed.
Direc t C ur re nt _ nidirecti o nal cu rre nt is also ca lled ga lvani c or direct currelll (Figure 16- 1). Direct current ( DC) is co ntinuous, unint errupted, unidirec ti o na l current. Directio n of the flow is determin ed by the polarity selected . Direct current wavefo rm s may be subdi vided into pulsatile curre nt s (PC).
Figure 16--2 Graphi c rcprescnlJtion of monophasic pulses. Source: Reprint cd with permission from Elecllvtherap(!wic Terminology i" PhYSical Therapy. p. 13. 1990, Scction on Clinical Elcc trophysiology and the Americal I)bysical Therapy Assoc iation.
Mo noph as ic Pulsed C ur re nt Pu lsed current is phasic. Mo nophasic pulsed current is defined as pu lsed direct c urrent (PC) that deviates from baseli ne and relUrns to baseli ne after a designated timc peri od. The monophasic pul sed current waveform may be either a square wave or the traditional twin peaked pulsed wave of the hi g h- vo ltage pulsed current. Mo nophasic pulses and phases arc identical (Figure 16 2). Monophas ic waves are such that at one electrode the polarity is positive a nd th e other is negative. This stays constant throu ghou t the treatment unless changed by th e clini cia n. Pola rity appears to have s pecific eITects on biologic responses.
Electrical Stimlliatioll for WOlllld /-Iealillg
Fre'lu ency or Pulse Rate A pu lse rate or frequency is the number of pulses dcl iv·
cred per unit of time. TIle rate of the ofT and on cycle is defined as pu lses per second (pps). The mnge of pulses per second is usua lly from 0. 1 l iz to 999 Hz.A pulse of 0. 1 Hz is on for 10 seconds and a pu lse of999 Hz is on fo r I mill isecond. The time between pu lses when no electrica l activity occurs is the interpulse in terva l (Figure 16- 3). Pulsed electrica l sti mu lation (PES) has a trai n of pulses that are repeated at regu lar intervals and arc termed th e pulse ratc or pul se frequency. Pulsed current can be ei ther unid irectional or bid irect ional. Pulse Duration The on time duri"-£ whic h cu rren t is fl owing is th e pulse duration. Pulse dura tion arTccls biologic respo nses. For examp le. direct Clirrent has a continuous du rati on and has th e ab ility (0 raise tissue temperat ure and change the pH und er the electrode. However. a short pulse duration, typ ical of hi ghvoltage pulsed current, produces insigni fica nt changes in both tiss ue pH and tisslie temperat ure:' 6 Such a current is therefore ve ry safe but raises questions about th e effect of
359
polarit y when th e pul se duratio n is so short. Fo r purposes of muscle stimulation, the stimulati on must be prov ided at an intensit y and a durati on that will stimulate a muscle contracti on. If the goal is to keep the sti mul ati on tolerable, the amplitude may be kept as low as possible, forc ing the du ra ti on of th e st imulus to be longer. Muscle is most se nsit ive to a stimulus from a negati ve electrode. When providi ng electrical stimulati on to denervated muscle, some reco mmend that th e st imulus beon for onl y I and 50 mi lli seconds. 7•K Beca use high-voltage pul sed monophas ic current has a short er pul se durati on it cann ot be used to stimul ate de nerva ted muscle. Fo r pain manage men t and wo und hea ling, the pulse durati on and th e amplitude of the current are variable. Some clin icians and researchers suggest th at thi s current must be on for al least 1 second 10 produce strong polarit y efTects of th e tissue under the electrodes. Duty Cycle Thc on/otTrati o is th e rat io of th e timc th e cur rent is on to the timc the current is off. A du ty cycle is th e ratio of 011 time to the IOwl cycle time inc lud ing both th e on and off time (Figure 16- 2). A rat io is used 10 ex press th e relative propo rtion of the on and off time and can be expressed as a percentage. For instance, if th e total cycle is 60 microseconds, the on time is 20 microseconds, and th e off time is 40 microseconds, there is a 1: 2 on/otT rat io and th e du ty cyc le is a 1:3 ratio, or a 33% dut y cycle. Uigh-Voltage Pulsed C urrent
PUlS( CHAliCE
-1': ._ L _._
~ 'oooo~
..c
I
~
Figure 16-3 Typical pulse characteristics of a high-voltage sti mu lato r. Source: Rep rinted with permiss ion fr0111 A Ion G, Dc Domenico G. I-ligh ~vltage Stimlliatio,, : All Integrated Approach to Clil/ical Electrotherapy. 1st cd .. p. 62. 1987. Hixton. TN: The Chattanooga Group.
Hig h-vo lt age pul sed curren t (HVPC) typ ica ll y has a twin peaked monop hasic wavefo rm (Fig ure 16- 3). HVPC is a misnomer if ga lva nic is used with it. Th is current was named incorrectl y by th e manu fact ure rs. The acronym HVPC does not have galva nic in the acronym. The pul se rate 1110st frequ ently used for wo und hea li ng is 50 to 120 pps (0.83 to 1.25 mill iseco nds). Each peak or spi kc has an effecti ve 5- to 20-microsecond phase duration. Vo ltage can be se lected with in tensit y betwee n 100 and 500 V. The ampl itude selected fo r wound healing is usually between 80 and 200 V, and the polarity and pulse rate are vari ed. There is a long int crpul se interva l between pulses that makes a low ave rage current. The hig h-voltage st imulat ion has a high peak current that means greater penetration into tiss ue, allowing fo r sti mu lati on of deep Illotor points:'II'P59 71) On th e skin surface, alkaline/ac idity changes under th e electrodes have not been measured.s.6 Since HVpe is not galva nic, th is ex plains why there is no alkali ne/aci dity effects. Absence of chemica l changes under th e electrodes has led to questi ons abo ut how polarit y efTects can be th e fac tor that stimulates ce llular res ponses
360
W OUND CA"'
when the duration of the IIVP pulse is so short. However, multiple studi es demonstrate different effects under th e anode and cathode using I-IVP . Table 16- 1 lists errects reported by v~lri ous rcse. u c hcrs using H V pe th at nrc polarity depcndent. For instan ce, one stud y showed that fibroblasts were attracted to th e cathode of an HVPC stimul ator, sugges ting th at th ere may be some cellular polarity effects under th e electrode." Althoug h multiple studi es show cellular crrects and respo nses to HVPC, each study shows something different: the re fore. corroborating research is needed to support th e findin gs of th ese single studies. Microcurrcnt Electrical Stimulation A pul sed monophasic stimulu s is referred to as monopha-
sic low-voltage microcurrcnt electrical stimulation (MENS). Thi s refers to a pul sed curre nt at an intensity less th an I mA
( I to 999 ~IA) and the voltagc is less than 100 V. MENS is deli ve red at amplitudes that have minimal detectable sensati on and are inca pable of motor nerve stimulation . ME S typically has a si ngle modi fied monophasic square waveform . The pu lse durati on o f these devices ranges from 0. 1 to 999 liz, cq uiva lent to on timc of 10 seconds to I microsecond. The pulse durati on is inverse ly related to th e frequency. Microcurrent stimulation has a prolonged pulse duration at the lower frequencies. which will have a different tiss ue polarit y effectthall a short er-dura tion pulse most typically used in hi gh-voltage stimulation. For example. a low-vo ltage pul sed stimulus at 0.1 H/ is 0 11 for 10 seconds, whereas the hig h-vo ltage monophasic simulators arc used at 80 to 120 pps and arc on for o nl y 0.83 to 1.25 millisecond s_ Thus. pu lsed low-voltage current of at least I pps can mai ntain the polarity effect deli ve red to the ti ssues under th e electrode. The peak ampli 