Oxford Handbook of Critical Care, 2nd Edition

Editors: Singer, Mervyn; Webb,

Andrew R.

Title: Oxford Handbook of

Critical Care, 2nd Edition

Copyright ©1997,2005 M. Singer and A. R. Webb

Ovid: Oxford Handbook of Critical Care

file:///C:/Documents%20and%20Settings/MVP/Application%20Data/Mozilla/Firefox/Profiles/2...

Ovid: Oxford Handbook of Critical Care

Ed itors:

Si nge r, M ervyn; We bb, An dre w R.

Ti tle : O xf ord Ha ndbook of Cr itic al Car e, 2nd Ed ition Cop yri ght © 1997,2005 M. Si nge r and A. R. W ebb , 1997, 2005. Publ i shed i n the Uni te d Stat es by Oxford Uni ve rsi ty Press Inc > Tab le of Co n te n ts > Resp ir a tor y T h e r ap y T ech n iq u e s

Respiratory Therapy Techniques Oxygen therapy Al l cri t i call y i l l pat i ents shoul d re cei ve add i ti onal i ns pi red oxy gen on a ‘ more not l es s i s b est ’ p hi l os ophy.

Principles Hi g h fl ow , hi gh conce ntrati on oxy gen shoul d b e g i ve n t o any acut el y dy spnoei c or hypoxaem i c pat i e nt unt i l acc urate ti trati on c an be performed usi ng arteri al bl ood gas anal ysi s. In general, mai ntain SaO 2 > 90%, t hough pre ferabl y >95%. Compromi ses may ne ed to be made duri ng acut e on chroni c hyp oxae mi c re spi ratory fai l ure , or p rol ong ed sev ere AR DS, when l owe r v al ues may suffi ce provi d ed ti s sue oxy gen del i v ery i s maint ai ned. Al l p ati ent s p l ac ed on mec hani cal v ent i l a ti on s houl d i ni ti al l y rec ei v e a hi g h FIO 2 unti l ac curat e t i trati on i s pe rforme d usi ng arteri al bl ood gas anal ysi s. Apart from p ati ent s rec ei v i ng hy perbari c O 2 therapy (e.g . for carbon monox i de poi soni ng, di v i ng ac ci d ent s), there i s no nee d t o maint ai n s upranormal l eve l s of PaO 2 .

Cautions A s mal l p rop orti on of pati ent s i n c hroni c Ty pe II (hy poxaemi c, hyp erc apni c ) re spi ratory fai l ure wi l l dev el op apnoea i f the i r ce ntral hyp oxi c d ri v e i s removed by suppl emental ox yge n. How ever, t hi s i s s el d om (i f eve r) abrupt and a pe ri od of det eri orati on and i nc re asi ng drowsi nes s w i l l al ert me di cal and nurs i ng st aff to consi der ei the r (i ) FIO 2 red uct i on i f ove ral l c ond i t i on al l ow s, (i i ) non-i nvasi ve or i nvasi ve m echani cal ve nti l a ti on i f fati gui ng or (i i i ) use of re spi rat ory sti mul ants suc h as d oxep ram. T he corol l ary i s t hat cl ose supervi s i on and m oni tori ng i s nece ssary i n al l cri t i call y i l l pat i ents . A norm al pul se oxi met ry readi ng m ay obs cure d ete ri orat i ng g as exchang e and progre ssi ve hyp erc apni a. Oxy gen toxi c i ty i s de sc ri b ed i n ani mal model s. Normal vol untee rs wi l l b ecome sym ptomat i c aft er sev eral hours of bre athi ng pure oxy gen. Furt hermore, was hout of ni trogen may l ead to mi croate l ec tas i s . Howev er, the rel e vance and rel at i ve i m portance of oxyg en toxi ci ty com pared to other forms of v ent i l a tor t rauma i n c ri ti c al l y i l l pati ent s i s s ti l l far from c l ear. Effort s s houl d nev ert hel ess be made to mi ni mi se FIO 2 whene ver pos si bl e . D ebate conti nues as to whe the r FIO 2 or othe r v ent i l ator s ett i ng s (e.g . PEEP, V T , i nsp i ratory p res sures ) s houl d be red uce d fi rs t. The authors' prese nt vi e w i s t o m i ni mi s e t he ri sks of venti l at or trauma.

Monitoring An oxy gen anal y ser i n the i nsp i ratory l i m b of the v ent i l ator or CPAP/Bi PAP ci rcui t confi rms the p ati ent i s re cei vi ng a known FIO 2 . Mos t m ode rn vent i l ators hav e a bui l t -i n calib rati on d evi ce. Ade quacy and chang es i n art eri al oxy gen saturati on can be conti nuousl y m oni tored by pul se oxi met ry and i nt ermi t tent or c ont i nuous i nvas i ve bl ood gas anal ysi s. P.3

Oxygen masks Huds on-typ e m ask s or nasal ‘ spe ctacl e s’ gi ve an i mpreci se FIO 2 and s houl d onl y b e used when hypoxae mi a i s not a major conce rn. Hudson-t ype mas ks do al l ow del i ve ry of humi di fi e d g as (e.g . v i a an ‘Aq uap ak’ ). Val ves fi tte d t o the Aq uapak s yst em do not del i v er an acc urate FIO 2 unl es s g as fl ow i s at t he rec omm ende d l eve l . Mask s fi tt ed wi t h a Ve nturi val ve del i v er a reasonab l y acc urate FIO 2 (0.24, 0.28, 0. 35, 0. 40, 0. 60) ex cep t i n pati ents wi t h v ery hi gh i ns pi ratory fl ow rate s. The se mas ks do not al l ow del i ve ry of hum i di fi e d g as but are pre ferabl e i n t he s hort term for dys pnoe i c pat i e nts as they e nab l e more p rec i s e moni t ori ng of PaO 2 /F IO 2 rati os. A t i ght-fi tt i ng anaes the ti c mask and re servoi r b ag al l ows 100% oxyg en to be del i ve red .

See also: Venti l at ory support— ind i c ati ons , p 4; Conti nuous pos i ti ve ai rway press ure , p 26; Bas i c res usc i t ati on, p270; Re spi ratory fai l ure, p282 P.4

Ventilatory support—indications Acute ventilatory insufficiency

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Defi ne d b y an ac ut e ri se i n PaC O 2 and a si g ni fi c ant re spi rat ory ac i d osi s. PaCO 2 i s di re ctl y p rop ort i onal to the body' s CO 2 producti on and i nversel y p rop orti onal to al veol ar venti l at i on (m i nute venti l ati on mi nus dead s pac e v ent i l a ti on). Causes i ncl ude: Resp i ratory centre de pre ssi on, e. g. dep res sant d rug s or i ntrac rani al pathol og y Peri pheral neuromuscul ar di sease, e. g. Gui l l ai n–Barré sy ndrome , m yas the ni a gravi s or s pi nal cord pat hol ogy Therape uti c mus cl e paral ysi s, e.g . as p art of balanced anaest hes i a , for m anagem ent of tet anus or s tat us epi l ep ti c us Los s of chest wall i nteg ri t y, e.g . c hes t t rauma, di aphrag m rupt ure Hi g h CO 2 p roduc ti on, e.g . b urns, sep si s or se vere agi t ati on Reduced al veol ar ve nti l at i on, e .g. ai rway obst ruc ti on (ast hma, acut e b ronchi ti s, forei g n b ody), atel ect asi s, pneumoni a, pul monary oede ma (ARD S, cardi ac fai l ure), pl eural pat hol ogy , fi broti c l ung di se ase , ob esi ty Pul monary vas cul ar di sease (pul monary em bol us, cardi ac fai l ure, AR DS)

Oxygenation failure Hyp oxaemi a i s d efi ned by PaO 2 < 11k Pa on F IO 2 ≥0. 4. May be due to: Venti l ati on–perfus i on mi sm atc hi ng (red uce d ve nti l a ti on i n, or pre ferent i al pe rfusi on of, som e l ung areas ), e.g. pneumoni a, pul monary oede ma, pul monary vascul ar di se ase, ex tre mel y hi gh cardi ac out put Shunt (normal pe rfusi on but abs ent ve nti l a ti on i n s ome l ung zones), e. g. pne umoni a , p ul m onary oede ma Di ffus i on l i mi t ati on (re duc ed al v eol ar surfac e area wi th normal ve nti l at i on), e.g . e mphysem a; red uce d i nsp i red oxyg en tensi on, e.g . alti tud e, suffoc ati on Acute vent i l atory i ns uffi ci ency (as above)

To reduce intracranial pressure Red uct i on of PaCO 2 to ap proxi m ate l y 4kPa cause s c ere bral v asoconstri c ti on and the refore re duc es i nt rac rani a l pre ss ure aft er brai n i njury. Rec ent st udi es sug ges t t hi s effec t i s t ransi ent and may i mpair an al read y c ri ti c al cerebral bl ood fl ow.

To reduce work of breathing As si s ted ve nti l at i on ± sed ati on and muscl e rel a xat i on re duc es res pi rat ory muscl e acti vi t y and thus t he work of bre athi ng. In c ardi a c fai l ure or non-c ard i og eni c p ul m onary oed ema the re sul ti ng red uct i on i n my ocardi al oxy gen dem and i s more eas i l y matched to t he sup pl y of ox yge n. P.5

Indications for ventilatory support Venti l at ory support (i nvas i ve or non-i nvas i v e) s houl d be consi d ered i f: Resp i ratory rat e >30/m i n Vi t al cap aci ty <10–15ml /mi n PaO 2 <11kPa on FIO 2 ≥0. 4 PaCO 2 hi g h wi th si gni fi c ant resp i ratory aci d osi s (e.g . p H < 7.2) Vd/V T >60% Qs/Qt >15–20% Exhaust i on Confusi on Seve re shock Seve re LVF Rai s ed ICP

See also: Dys pnoea, p278; Ai rway ob st ruc ti on, p280; R esp i ratory fai l ure, p282; Atel ect asi s and pul monary col l aps e, p 284; Chroni c airfl ow l i mi tat i on, p 286; Ac ut e chest i nfec ti on (1), p288; Acute che st i nfec ti on (2), p290; Acut e res pi ratory di s tress sy ndrome (1), p 292; Acut e resp i ratory di s tre ss syndrome (2), p294; Ast hma—ge neral manage ment , p 296; As thm a—ve nti l a tory m anag eme nt, p298; Inhal ati on i nj ury , p 306; Pul monary e mbol us , p 308; He art fai l ure— ass ess ment, p324; Heart fail ure —manag ement, p326; Acute l i ver fai l ure, p360; Acut e we akness , p 368; Agi tati on/c onfusi on, p370; Generalis ed sei zures , p 372; Int rac rani a l haemorrhag e, p 376; Subarachnoi d haem orrhag e, p378; Stroke , p 380; Rais ed i nt rac rani al pres sure, p382; Gui l l ai n–Barr é s ynd rom e, p384; My ast heni a gravi s , p 386; ICU ne uromus cul ar di s orders, p388; Te tanus, p390; Botul i s m, p 392; Poi soni ng—gene ral p ri nci p l e s, p452; Sed ati ve

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poi soni ng, p 458; T ri c ycl i c anti d epress ant poi soni ng, p460; Coc ai ne, p464; Inhal e d p oi s ons , p 466; Organophosp hat e poi soni ng, p 472; Syst emi c i nfl amm ati on/mul ti -org an fai l ure, p484; Mul t i pl e t rauma (1), p500; Mul ti pl e trauma (2), p502; Head i njury (1), p504; He ad i nj ury (2), p 506; Spi nal cord i nj ury, p 508; Burns—fl ui d m anagem ent , p510; Burns —ge neral managem ent , p 512; N ear-drowni ng , p526; Post-ope rat i ve i ntensi v e c are , p 534 P.6

IPPV—description of ventilators Classification of mechanical ventilators The se may be cl ass i fi ed by the met hod of cy cl i ng from i nsp i rati on to expi rati on. Thi s m ay be w hen a pre set ti me has el a pse d (ti m e-c ycl ed), a preset pres sure reac hed (pres sure-c ycl ed) or a p res et vol ume de l i v ere d (vol ume -cyc l e d). Though the m ethod of c ycl i ng i s c l as si fi e d ac cordi ng to a s i ng l e constant, modern v ent i l a tors all ow a great er deg ree of control . In vol ume -cy cl e d m ode wi t h p res sure l i m i tati on, the up per pres sure alarm l i mi t i s set or the maxi m um i ns pi rat ory press ure control l ed . T he vent i l ator d el i vers a prese t t i d al vol ume (V T ) unl es s t he l ungs are non-c omp l i ant or ai rway re si s tance i s hi gh. Thi s i s use ful to av oi d hi gh peak ai rw ay p res sures . In v ol ume-c ycl ed mod e w i th a ti m e l i mi t , t he i ns pi rat ory fl ow i s reduced ; t he venti l ator d el i vers the prese t V T unl e ss i mp oss i bl e at t he set re spi ratory rat e. If pre ssure l i mi t ati on i s not av ai l abl e t hi s i s useful to l i m i t peak airw ay pre ssures . In t i me -cy cl e d m ode wi th pre ss ure control , prese t p res sure i s del i ve red throughout i ns pi rat i on (unl i ke pre ssure-cyc l ed ve nti l at i on), cyc l i ng bei ng det erm i ne d b y t i me . V T i s d epe nde nt on res pi ratory com pl i ance and ai rway re si s tance . He re, too, hi g h p eak ai rway press ures c an be avoi de d.

Setting up the mechanical ventilator Tidal volume Conventi onal l y set at 7–10m l /k g, t hough rec ent data sug ges t l owe r v al ues (6–7ml /kg ) may b e be tt er i n sev ere acute res pi rat ory failure, re duc i ng barot rauma and i m provi ng outc ome . In s eve re ai rfl ow l i mi tat i on (e .g. as thm a, acute bronchi t i s) sm al l er V T and mi nute vol um e may b e neede d t o allow p rol ong ed exp i rati on.

Respiratory rate Usual l y s et i n acc ordance w i t h V T t o provi de mi nut e ve nti l a ti on of 85–100ml /kg /mi n. In ti m e-c ycl ed or ti m e-l i mi ted mod es the se t resp i ratory rat e de termi nes the ti mi ng of t he venti l at or cyc l es .

Inspiratory flow Usual l y s et bet wee n 40–80l /mi n. A hi ghe r fl ow rate i s more c omfort abl e for alert pat i ents. Thi s al l ows for l ong er exp i rati on i n pat i ents wi t h s eve re ai rfl ow l i mi tat i on but m ay be ass oci ate d wi th hi ghe r p eak ai rway press ures. The fl ow p att ern may be ad jus ted on mos t vent i l ators. A square waveform i s oft en use d b ut dec el e rat i ng fl ow may re duc e peak airw ay p re ssure.

I:E ratio A func ti on of resp i ratory rat e, V T , i ns pi rat ory fl ow and i nspi rat ory ti me. Prol onge d e xpi rat i on i s us eful i n seve re ai rfl ow l i m i tati on w hi l e a prol onge d i nsp i ratory t i m e i s used i n AR DS to al l ow sl ow reac ti ng alve ol i ti me to fi l l . Al ert pat i ents are more com fortab l e wi t h s horter i nsp i ratory t i me s and hi g h i nsp i ratory fl ow rate s.

FIO 2 Set ac cordi ng to art eri al bl ood gas es. Us ual to st art at FIO 2 =0. 6–1 then adjust ac cordi ng t o arte ri a l b l ood g ase s.

Airway pressure In pre ss ure -control l ed or pre ssure-l i mi t ed mode s t he peak airw ay p re ssure (ci rcui t rathe r t han al veol ar press ure ) c an be set (usually ≤35–40cm H 2 O). PEEP i s us ual l y i ncre ase d t o m ai ntai n F RC w hen re spi rat ory compl i ance i s l ow. P.7

Initial ventilator set-up Che ck for l e aks

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Check oxygen is flowing FIO 2

0.6–1

VT

5–10ml/kg

Rate

10–15/min

I:E ratio

1:2

Peak pressure

≤35cmH 2 O

PEEP

3–5cmH 2 O

Key trial Ac ute Res pi rat ory Di stress Synd rom e Ne twork. Ve nti l a ti on wi th l ower ti dal vol um es com pared w i t h t rad i ti onal t i d al vol ume s for acute l ung i njury and the ac ut e resp i ratory d i st re ss syndrome. N Engl J Med 2000; 342:1301–8

See also: IPPV—m ode s of ve nti l a ti on, p8; IPPV—adjusti ng the ve nti l at or, p10; IPPV—failure to tol erate venti l at i on, p 12; IPPV—c omp l i cat i ons of ve nti l a ti on, p14; IPPV—w eani ng te chni ques, p16; IPPV—as ses sm ent of weani ng, p18; Hi gh fre que ncy ve nti l at i on, p 20; Pos i t i ve end ex pi ratory press ure (1), p 22; Pos i t i ve end ex pi rat ory press ure (2), p 24; Lung rec rui tm ent , p 28; Non-i nvas i ve re spi rat ory support, p32; CO 2 moni tori ng, p92; Bl ood gas anal ysi s, p100 P.8

IPPV—modes of ventilation Controlled mechanical ventilation (CMV) A p res et num ber of breat hs are de l i v ere d t o s upp l y al l the p ati ent 's venti l at ory re qui rem ent s. The se bre aths m ay be at a p res et V T (vol um e c ont rol l ed ) or at a prese t i nsp i ratory p res sure (press ure control l ed).

Assist control mechanical ventilation (ACMV) Pat i ents can tri g ger the v ent i l a tor to de termi ne t he res pi rat ory rate b ut , as wi th CMV, a prese t numb er of b re aths are del i ve red i f the s pontaneous resp i ratory rat e fall s b el ow t he p res et l e vel .

Intermittent mandatory ventilation (IMV) A p res et mandat ory rate i s set but p ati ent s are free t o b reathe sp ont ane ous l y bet ween se t v ent i l ator b reaths . Mandat ory breat hs may be synchroni se d wi th pat i e nts ' s pontaneous e fforts (SIMV) t o av oi d mandatory b reaths occ urri ng d uri ng a s pontaneous b reath. Thi s effect , k nown as ‘s tac ki ng’ may l e ad to exc ess i ve ti dal vol um es, hi gh ai rway press ure, i nc ompl et e ex hal ati on and ai r t rappi ng. Press ure support may be add ed to spontaneous bre aths t o ove rcome the work of b reathi ng ass oci ate d w i th op eni ng the ve nti l at or dem and valve .

Pressure support ventilation (PSV) A p res et i nspi rat ory press ure i s adde d t o the v ent i l ator c i rc ui t d uri ng i ns pi rat i on i n sp ont ane ous l y bre athi ng pati e nts . The prese t p res sure s houl d be adj ust ed to ens ure ad equate V T .

Choosing the appropriate mode Pre ssure control l ed venti l ati on avoi ds the d ang ers as soc i at ed wi t h hi gh pe ak ai rway press ure s, al t hough i t may re sul t i n marked chang es i n V T i f com pl i anc e alte rs . Al l owi ng t he pat i ent t o m ake som e s pontaneous resp i ratory e ffort may red uce se dat i on re qui re ment s, re train res pi rat ory muscl es and re duc e m ean ai rway press ures.

Apnoeic patient Use of IM V or ACMV i n pati e nts who are t ot al l y apnoe i c provi des the t otal m i nute vol ume req ui rem ent i f the pres et rat e i s hi g h enoug h (thi s i s effe cti vel y C MV) but allows spontaneous res pi ratory effort on re cov ery .

Patient taking limited spontaneous breaths A g uarant eed mi ni m um mi nute vol um e i s assured wi th bot h ACMV and IMV dep end i ng on the pres et rat e. T he work of spontaneous bre athi ng i s reduced by sup pl yi ng t he p re set V T for spontaneousl y t ri g gered bre aths w i th AC MV, or by add i ng press ure s upp ort to sp ont ane ous breat hs wi t h IMV. Wi th ACM V t he spontaneous ti d al vol ume i s guarante ed whe reas w i th IM V and pre ssure sup port s pontaneous t i dal v ol ume dep end s on l ung compl i ance and may be l e ss than the prese t t i d al vol ume. The advantage of IMV and press ure support i s that gradual reducti on of pre set rate, as spontaneous effort i ncre ase s, al l ows a smooth trans i ti on to pre ss ure support venti l ati on. Subs eque nt weani ng i s b y

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red uct i on of the p res sure s up port l eve l .

See also: IPPV—d esc ri pti on of vent i l ators, p6; IPPV—adjusti ng the ve nti l at or, p10; IPPV—failure to tol erate venti l at i on, p 12; IPPV—c omp l i cat i ons of ve nti l a ti on, p14; IPPV—w eani ng te chni ques, p16; IPPV—as ses sm ent of weani ng, p18; Hi gh fre que ncy ve nti l at i on, p 20; Pos i t i ve end ex pi ratory press ure (1), p 22; Pos i t i ve end ex pi rat ory press ure (2), p 24; Lung rec rui tm ent , p 28; Non-i nvas i ve re spi rat ory support, p32 P.9 P.10

IPPV—adjusting the ventilator Venti l at or adj ust ments are us ual l y mad e i n resp ons e t o bl ood gases , p ul s e oxi m etry or c apnography, pat i ent agi t ati on or di s comfort, or duri ng w eani ng . ‘ Mi g rat i on’ of t he endotracheal tube, ei the r d i st al l y t o t he cari na or be yond, or proxi m al l y s uc h t hat the c uff i s at voc al cord l eve l , may re sul t i n agi tat i on, e xces s coughi ng and a d ete ri orati on i n bl ood gas es. Thi s, and t ube ob struct i on, s houl d be consi dered and rec ti fi e d b efore c hangi ng vent i l ator or s edati on dos e s ett i ng s. The choi c e of v ent i l a tor mode depe nds up on the l e vel of consc i ousne ss, the numb er of s pontaneous b reaths be i ng tak en, and t he b l ood g as val ues . T he spontaneousl y b reathi ng pat i ent c an usual l y c ope ad equate l y wi t h p res sure sup port v ent i l ati on al one. How eve r, on occ asi on, a few i nt erm i t tent m andatory b reaths (SIMV) m ay be nec ess ary to ass i s t g as exchang e or s l ow an exc es si v e s pontaneous rate. The p aralys ed or heavi l y s edated pati e nt wi l l requi re mandat ory breat hs, ei the r v ol ume- or press ure -control l ed. The order of chang e wi l l be di ctated by the s everi t y of re spi ratory fai l ure and i ndi vi d ual op erator prefe rence. Earl i er use of i ncre ase d PEEP i s ad voc ated to re crui t col l a pse d alve ol i and t hus i m prove oxy genati on i n sev ere re spi rat ory fai l ure.

Low PaO 2 considerations Inc rease FIO 2 Revi ew V T and resp i ratory rate Inc rease PEEP (m ay rai se peak ai rway p res sure or reduce CO) Inc rease I:E rat i o Inc rease pre ssure sup port/p res sure c ont rol CMV, i ncreas e s edat i on ± mus cl e re l ax ant s Cons i de r t ol erati ng l ow l ev el (‘p erm i ss i ve hy pox aemi a’) Prone v ent i l ati on, i nhal ed ni t ri c ox i d e

High PaO 2 considerations Dec rease l eve l of p res sure c ont rol /p res sure s upp ort i f V T adeq uat e Dec rease PEEP Dec rease FIO 2 Dec rease I:E rat i o

High PaCO 2 considerations Inc rease V T (i f l ow and p eak ai rway pres sure allows) Inc rease res pi ratory rat e Reduce rat e i f t oo hi g h (to red uce i ntri nsi c PEEP) Reduce dead s pac e CMV, i ncreas e s edat i on ± mus cl e re l ax ant s Cons i de r t ol erati ng hi gh l e vel (‘ permi s si ve hype rcapni a’ )

Low PaCO 2 considerations Dec rease res pi ratory rat e Dec rease V T

See also: IPPV—d esc ri pti on of vent i l ators, p6; IPPV—m ode s of ve nti l a ti on, p8; IPPV—fai l ure to tol erate ve nti l at i on, p 12;

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IPPV—c omp l i cat i ons of ve nti l a ti on, p14; IPPV—w eani ng te chni ques, p16; IPPV—as ses sm ent of weani ng, p18; Hi gh fre que ncy ve nti l at i on, p 20; Pos i t i ve end ex pi ratory press ure (1), p 22; Pos i t i ve end ex pi rat ory press ure (2), p 24; Lung rec rui tm ent , p 28; Non-i nvas i ve re spi rat ory support P.11 P.12

IPPV—failure to tolerate ventilation Agi tati on or ‘ fi g hti ng the ve nti l at or’ m ay occur at any ti m e. Poor t ol e rance may al s o b e i ndi cated by hyp oxaemi a, hyp erc apni a, ve nti l at or al arm s or c ard i ov asc ul a r i ns tab i l i ty.

Poor gas exchange during initial phase of ventilation Inc rease FIO 2 t o 1. 0 and start manual ve nti l at i on. Chec k e ndotrache al tub e i s c orrec tl y posi t i oned and both l ungs are be i ng i nfl a ted . C ons i de r t ube re pl a cem ent , i nt rat rac heal obst ructi on or pne umot horax. Chec k v ent i l a tor ci rc ui t i s b oth i ntac t and pat ent and ve nti l at or i s funct i oni ng correct l y. Check venti l at or set ti ngs i nc l ud i ng FIO 2 , PEEP, I:E rati o, s et ti d al vol ume , resp i ratory rat e and/or p res sure control . Che ck ‘press ure l i mi t’ set ti ngs as the se may be set too l ow, causi ng the venti l at or to ti m e-c ycl e p rem aturel y.

Poor tolerance after previous good tolerance If agi tat i on oc curs i n a p ati ent who has p rev i ousl y tol erat ed m echani cal ve nti l a ti on, ei t her the p ati ent 's condi ti on has det eri orate d or t here i s a probl em i n the venti l at or ci rcui t (i ncl udi ng art i fi ci a l airway) or the v ent i l a tor i t sel f. The pat i ent s houl d be rem ove d from the ve nti l a tor and pl ac ed on m anual venti l ati on wi t h 100% ox ygen whi l e the probl e m i s resol ve d. Resort i ng to i ncre ase d s edati on ± mus cl e rel a xat i on i n thi s ci rcumst anc e i s d ang erous unt i l the cause i s re sol ved . Chec k p ate ncy of the endot rac heal t ube (e .g. wi th a suct i on cathe ter) and re-i nt ubat e i f i n d oub t. Cons i de r m al p osi ti on of t he end otracheal tube (e. g. cuff ab ove vocal cords , t ube ti p at c ari na, tube i n mai n bronchus). Seek and t reat and change s i n t he pat i ent's condi ti on, e.g . t ens i on pneum othorax, sputum pl ug, pain. Where p ati ent s are mak i ng sp ont ane ous re spi ratory effort c ons i d er i nc reasi ng p res sure sup port or addi ng mand atory bre aths. If p ati ent s fai l t o s ync hroni s e w i th IM V b y s tac ki ng s pontaneous and mand atory bre aths, i ncre asi ng pre ssure sup port and red uci ng mandat ory rate m ay hel p; al t ernati vel y, the us e of PSV may be app rop ri a te.

See also: IPPV—d esc ri pti on of vent i l ators, p6; IPPV—m ode s of ve nti l a ti on, p16; IPPV— adj ust i ng the v ent i l a tor, p 10; IPPV—c omp l i cat i ons of ve nti l a ti on, p14; IPPV—w eani ng te chni ques, p16; IPPV—as ses sm ent of weani ng, p18; Hi gh fre que ncy ve nti l at i on, p 20; Pos i t i ve end ex pi ratory press ure (1), p 22; Pos i t i ve end ex pi rat ory press ure (2), p 24; Lung rec rui tm ent , p 28; Non-i nvas i ve re spi rat ory support, p32; Sedati v es, p238; Mus cl e rel a xants, p240; Agi tati on/c onfusi on, p370 P.13 P.14

IPPV—complications of ventilation Haemodynamic complications Venous re turn i s dep end ent on pas si ve fl ow from central v ei ns t o ri ght atri um . As ri ght atri al press ure i ncreas es sec ond ary to the t ransmi tt ed i nc rease i n i nt rat horaci c pre ssure across compl i a nt l ungs, there i s a red uct i on i n ve nous ret urn. Thi s i s l ess of a probl e m i f l ung s are sti ff (e. g. ARD S) alt hough i t wi l l b e e xac erb ate d by the use of i nv ers e I:E rati o and hi gh PEEP. As l ung vol ume i s i ncrease d b y IPPV the p ul m onary vas cul ature i s constri c ted , t hus i nc re asi ng pul monary vas cul ar re si s tance . Thi s wi l l i nc re ase di ast ol i c v ol ume of t he ri ght ventri cl e and, by se ptal shi ft , i mped es fi l l i ng of the l e ft vent ri cl e . T hes e e ffec ts al l c ont ri b ut e to a red uce d s troke vol ume . T hi s re duc ti on c an be mi ni mi sed by re duc i ng ai rw ay p res sures , avoi di ng p rol ong ed i ns pi rat ory ti mes and maint ai ni ng b l ood vol ume.

Ventilator trauma The te rm barotraum a rel a tes to gas e scape i nt o c avi ti e s and i nt ers ti ti a l t i s sue s d uri ng IPPV. Barotrauma i s a mi s nom er si nce i t i s probabl y the d i st end i ng vol um e and hi g h s hear s tre ss that i s res ponsi b l e rat her than pre ss ure . It i s mos t l i k el y to occ ur wi th hi g h V T and hi gh PEEP. It occ urs i n IPPV and condi ti ons ass oc i at ed wi t h l ung ove ri nfl ati on (e. g. ast hma). T ens i on pneum othorax i s l i fe threateni ng and s houl d be sus pec ted i n any p ati ent on IPPV who bec ome s sud denl y agi tat ed, tachy cardi c, hyp otensi ve or e xhi bi ts sud den de teri orati on i n the i r bl ood gas es . An i mmed i ate c hes t drainage tub e s houl d be i ns ert ed i f tensi on p neumot horax dev el ops. Preventi on of v ent i l ator t rauma rel i es on avoi dance of hi gh V T and hi gh ai rway press ure s.

Nosocomial infection

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End otracheal i ntubat i on by pas ses normal d efence mec hani sm s. Ci l i ary act i vi ty and ce l l ul ar morphol ogy i n the tracheobronc hi al tre e are al t ere d. The re qui rem ent for e ndot rache al suc ti on furt her i ncreas es sus cep ti b i l i ty to i nfect i on. In addi ti on, the norm al heat and m oi s ture e xchang i ng me chani s ms are by pas sed re qui ri ng art i fi ci al hum i di fi cat i on of i nspi red gases . F ai l ure to provi de ade quate humi di fi c ati on i nc re ases t he ri s k of sp ut um ret ent i on and i nfec ti on. Mai ntaini ng venti l at ed pat i ents at 30° up ri g ht head t i l t has been shown to re duc e t he i nc i de nce of nos ocomi a l p neumoni a.

Acid–base disturbance Venti l at i ng pati e nts wi th chroni c res pi rat ory fai l ure or hyp erv ent i l a ti on m ay, by rap i d corre cti on of hyp erc apni a, cause res pi rat ory al kal osi s. Thi s reduces pul m onary b l ood fl ow and may c ont ri but e t o hy pox aem i a. A res pi rat ory aci dos i s due t o hy percap ni a may b e d ue t o i nap propri at e v ent i l a tor se tti ng s or may b e d esi red i n an at tem pt to avoi d hi g h V T and venti l at or trauma.

Water retention Vas opres si n re l eased from the ant eri or pi tui tary i s i nc reased due t o a red uc ti on i n i ntrathoraci c b l ood v ol ume and psy chol og i c al stress . R educed uri ne fl ow thus c ont ri b ute s t o w ate r rete nti on. In ad di t i on, t he use of PEEP red uce s l ym phati c fl ow wi t h c ons equent pe ri p heral oed ema, e spe ci a l l y affec ti ng t he upp er bod y. Hig h ai rw ay p res sure red uce s venous re turn, again contri buti ng t o oedem a.

Respiratory muscle wasting Prol onged ve nti l at i on may l ead to di sus e atrophy of the resp i ratory m usc l es .

See also: CO 2 moni t ori ng , p92; Bl ood g as analys i s , p 100; Central venous cat het er—us e, p 114; C ent ral ve nous cat het er—inserti on, p116; Bact eri ol ogy, p158; Acute che st i nfect i on (1), p288; Acut e c hes t i nfe ct i on (2), p 290; Ac ute res pi rat ory di stres s s ynd rom e (1), p292; Acut e resp i ratory di s tre ss syndrome (2), p294; Pne umot horax, p300 P.15 P.16

IPPV—weaning techniques Pat i ents may re qui re al l or part of the i r re spi rat ory support to be provi d ed by a me chani cal venti l at or. We ani ng from mec hani cal v ent i l ati on may fol l ow se veral pat terns. In pati e nts ve nti l a ted for s hort p eri ods (no more than a fe w days) i t i s common to al l ow 20–30mi n breat hi ng on a ‘T ’ p i ec e b efore removi ng t he end otracheal tube. For p ati ent s w ho hav e rece i ve d l ong er term v ent i l a ti on i t i s unl i ke l y that m echani cal support can be wi thd raw n s udd enl y; seve ral met hod s are com monl y used to we an the se p ati ents from me chani c al venti l at i on. T here i s no s trong evi dence that any tec hni que i s s upe ri or i n t erm s of w eani ng succe ss or rat e of we ani ng.

Intermittent ‘T’ piece or continuous positive airway pressure (CPAP) Spontaneous bre athi ng i s al l owed for i ncreas i ng l y prol onged pe ri ods wi t h a re st on mec hani cal v ent i l a ti on i n bet ween. The us e of a ‘T’ pi ec e for l ong er than 30mi n m ay l ead t o basal at el ect asi s s i nc e t he end otracheal tube byp ass es the phy si ol og i c al PEEP effec t of t he l arynx . It i s t herefore com mon to use 5c mH 2 O CPAP as spontaneous bre athi ng pe ri ods get l onge r. In the earl y st age s of we ani ng, me chani c al venti l at i on i s often conti nue d at ni ght t o e ncourage sl e ep, avoi d fat i gue and res t resp i ratory m usc l e s.

Intermittent mandatory ventilation (IMV) The se t m and atory rat e i s g rad ual l y red uce d as t he spontaneous rat e i ncreas es. Sp ont ane ous breat hs are us ual l y pre ss ure supporte d t o ov erc ome ci rc ui t and v ent i l a tor valve re si s tance. Wi th thi s tec hni que i t i s i mportant that t he pat i ent' s requi re d m i nute venti l ati on i s provi ded by the combi nat i on of mandatory b reaths and s pont ane ous breat hs wi t hout an e xce ssi ve spontaneous rat e. The red uc ti on i n m and atory rat e s houl d be s l ow enoug h t o m ai ntai n adeq uat e mi nute ve nti l at i on. It i s al s o i mportant that t he pat i ent c an synchroni se hi s own resp i ratory effort s wi th mandat ory venti l at or bre aths; m any cannot, parti c ul arl y w here t here are freq uent s pontaneous b reaths , s ome of whi ch may ‘st ac k’ w i t h mandatory b reaths causi ng hyp eri nfl at i on.

Pressure support ventilation Al l resp i ratory e fforts are s pontaneous b ut pos i ti ve pre ss ure i s ad ded to eac h b reath, the l eve l b ei ng c hos en to mai ntain an app rop ri ate ti dal vol um e. W eani ng i s pe rforme d b y a gradual red uct i on of the p res sure s upp ort l evel whi l e the re spi ratory rate i s <30/mi n. The pati e nt i s ext ubated or al l ow ed to bre athe wi th 5c mH 2 O CPAP w hen pre ss ure support i s mi ni mal (<10–15cmH 2 O wi th mod ern venti l at ors ).

Choice of ventilator Mod ern ve nti l at ors have enhanc ements to ai d we ani ng; howeve r, weani ng m ost pati e nts from vent i l ati on i s pos si bl e wi t h a basi c ve nti l at or and the i nt erm i tt ent ‘T ’ p i ec e t echni q ue, provi ded an ad equate fresh gas fl ow i s provi d ed. If IMV and/or p res sure s upp ort are used the v ent i l ator s houl d provi d e t he feat ures l i s ted op pos i te .

Key features in the choice of ventilator Venti l ator m ust al l ow pati e nt tri gg eri ng (i . e. not a m i nute vol ume di vi d er) Fres h g as fl ow m ust be great er than s pontaneous pe ak i ns pi rat ory fl ow

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Mi ni mum c i rc ui t resi stance (s hort, wi d e b ore , s moot h i nt ernal l um en) Low res i s tance-vent i l ator v al v es Sensi t i ve press ure or fl ow tri gg er (i d eal l y moni tored cl ose to the endot rac heal t ub e) Synchroni sed IM V (avoi ds ‘s tac ki ng’ mandat ory on sp ont aneous breaths)

See also: IPPV—m ode s of ve nti l a ti on, p8; IPPV—adjusti ng the ve nti l at or, p10; IPPV—as ses sme nt of weani ng , p 18; Conti nuous pos i t i ve ai rway press ure, p26; Non-i nvas i ve re spi rat ory support , p32 P.17 P.18

IPPV—assessment of weaning Assessment prior to weaning Pri or to weani ng i t i s i mp ort ant that the cause of res pi rat ory failure and any c ompl i c ati ons ari s i ng have b een corre cte d. Sep si s shoul d b e e rad i cated as shoul d othe r fact ors that i nc re ase oxy gen de mand . Att ent i on i s re qui re d t o nut ri ti onal st atus and fl ui d and el ect rol yt e balance. The d i ap hragm shoul d be al l ow ed to contract unhi nd ere d b y choosi ng the op ti m um pos i ti on for breat hi ng (si tti ng up unl ess the d i ap hragm i s paral ysed ) and ens uri ng that int ra-abd omi nal pres sure i s not hi g h. Ade quate analge si a must be provi d ed. Se dat i ve s are ofte n w i thdrawn by thi s poi nt but may s ti l l be need ed i n spe ci fi c si tuati ons, e. g. res i dual agi tati on, rai sed i ntracrani al pre ssure. We ani ng shoul d st art after ad equate ex pl a nat i on has b een gi ven to the pati e nt. Factors pre di cti ng weani ng s ucc ess are det ai l ed i n l i st opp osi te. Sp ont ane ous (p res sure-s upp ort ed) breat hi ng s houl d generall y st art as s oon as pos si bl e to al l ow red uct i on i n s edat i on l evel s, and maint ai n resp i ratory m usc l e functi on. We ani ng wi t h t he i nt ent i on of re mov i ng mec hani cal s upp ort i s unl i kel y t o b e s ucc ess ful whi l e FIO 2 >0. 4.

Assessment during weaning Conti nuous p ul s e oxi m etry and reg ul a r c l i ni c al rev i ew are e sse nti al duri ng we ani ng. Arte ri a l b l ood g ase s s houl d be tak en aft er 20–30m i n of s pontaneous b reathi ng. After s hort t erm ve nti l at i on, e xtubat e i f arte ri a l g ase s and res pi rat ory patte rn rem ai n sati s fac tory, the cough re fl e x i s adeq uat e and t he pat i ent c an cl ear sp utum. Pati ents bei ng weaned from l ong er term v ent i l ati on (>1 wee k) s houl d generall y be al l ow ed to bre athe s pontaneous l y wi t h C PAP for at l east 24h be fore e xtubat i on.

Indications for re-ventilation If spontaneous res pi rat i on i s di scoord i nate or the pati e nt i s exhaus ted , agi t ate d or c l am my, the v ent i l a tor shoul d b e rec onnect ed. Howev er, cl i ni cal moni tori ng shoul d avoi d e xhaust i on. Succ ess ful we ani ng i s more e asi l y acc omp l i s hed i f exc ess i ve fati g ue i s not al l ow ed to set i n. T achypnoea (>30/mi n), tachy cardi a (> 110/mi n), re spi rat ory ac i dosi s (p H <7. 2), ri si ng PaCO 2 and hyp oxaemi a (SaO 2 < 90%) shoul d all prompt reconnec ti on of t he venti l at or.

Factors associated with weaning failure Fai l ure t o w ean i s as soc i at ed wi t h: Inc reased oxy gen cost of bre athi ng Musc l e fat i g ue (hyp ophosp hat aem i a, hyp omagne sae mi a , hypok al a emi a, mal nut ri ti on, peri pheral neuropathy , myop athy and drugs, e. g. mus cl e re l ax ant s, ami nog l yc osi des ) Inad equate re spi ratory d ri v e (al k al osi s , opi a tes , s edati v es, malnutri ti on, ce reb rov asc ul a r acci dent, com a) Inad equate cardi ac re serve and heart fai l ure In the l a tte r c as e card i ac funct i on shoul d b e m oni tored duri ng sp ont ane ous breat hi ng p eri ods . Any det eri orati on i n cardi ac func ti on shoul d be treat ed aggres si v el y (e. g. opt i mal fl ui d the rap y, vasodi l at ors , i not rop es). P.19

Factors predicting weaning success PaO 2 > 11k Pa on FIO 2 =0. 4 (PaO 2 /FIO 2 rati o >27.5k Pa) Mi nute vol ume <12l /mi n Vi t al cap aci ty >10ml /kg Maxi mum i nspi ratory forc e (PImax) >20c mH 2 O Resp i ratory rat e/t i dal v ol ume < 100 Qs/Qt <15% Dead sp ace /ti dal vol um e < 60% Haem ody nam i c stabi l i t y A rat i o of resp i ratory rat e t o t i dal v ol ume (f/V T , s hal l ow breat hi ng i nde x) ≤v105 has bee n s how n t o have a 78%

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pos i t i ve predi cti ve val ue for succe ssful weani ng.

Key trial Yang K L, Tob i n MJ. A p rospe cti ve study of i nd exes predi ct i ng the outc ome of tri al s of we ani ng from m echani cal venti l at i on. N Eng l J Me d 1991; 324:1445–50

See also: IPPV—w eani ng te chni ques, p16; C O 2 moni tori ng, p92; Bl ood gas anal ysi s, p100; El e ctrol y tes , p 146; Calc i um , m agne si um and phosphate , p 148; Heart fail ure —as ses sme nt, p324; Acute weaknes s, p368; ICU neurom usc ul ar di s ord ers , p 388 P.20

High frequency ventilation High frequency jet ventilation (HFJV) A hi g h pres sure j et of g as ent rai ns further fre sh gas whi ch i s di rec ted by the j et towards t he l ungs. Res pi rat ory rates of 100–300/mi n ens ure mi nut e vol umes of about 20l /mi n althoug h t i dal v ol ume may be l ow er than d ead space. CO 2 el i mi nat i on i s us ual l y more e ffi ci e nt than c onv ent i onal IPPV. The met hod of gas e xchang e i s not ful l y el uci d ate d b ut i nc l udes turbul ent g as mi x i ng and c onv ect i on. Oxyg enati on i s d epe nde nt on m ean ai rway p res sure. Peak ai rway pre ss ure s are l owe r t han wi th conventi onal me chani c al venti l at i on but auto-PEEP and mean ai rway p res sures are mai ntaine d. SaO 2 ofte n fal l s w hen st art i ng on HF JV, thoug h usually i m proves wi th ti m e. The hi gh gas fl ow rate s emp l oy ed req ui re addi ti onal humi di fi cati on t o b e p rov i de d (30–100 ml /h); thi s i s usual l y nebul i sed wi th the jet .

Indications Bronc hop l eural fi stul a i s the onl y proven IC U i ndi cat i on for HFJV thoug h i t has bee n us ed to ass i s t we ani ng from mec hani cal v ent i l ati on as the ope n c i rcui t allows spontaneous bre aths w i thout the d raw bac ks of d emand val ves . HF JV al s o e nsures ad equate ve nti l at i on i f the p ati ent fails t o breat he ade quatel y. Reduci ng the dri vi ng pre ssure and i nc re asi ng the re spi rat ory rate may faci l i t ate weani ng furt her. In ARDS c onve nti onal v ent i l ati on can l e ad to v ent i l ator trauma i f a hi g h V T i s used . HFJV av oi d s p rob l em s associ a ted wi th hi g h V T b ut i s oft en unab l e to provi d e adeq uat e venti l at i on i n i s ol a ti on for pat i ents wi t h s eve re ARD S.

Setting up HFJV A j et mus t b e p rov i de d v i a a modi fi ed endot rac heal t ube or cathe ter mount . Entrai nment g as i s provi ded vi a a ‘T’ pi e ce. The t i dal v ol ume cannot be se t d i re ctl y. Rat her i t i s s et b y adjusti ng jet si ze, I:E rati o, dri vi ng pre ssure and res pi rat ory rate from an i n-bui l t algori t hm. The resp i ratory rat e i s usually se t b etw een 100–200/m i n. As resp i ratory rat e i nc reases at a c ons tant d ri vi ng p res sure t he PaCO 2 may i ncreas e as i ncreas i ng PEEPi i ncreas es the effect i v e phy si ol og i c al dead s pac e. T he I:E rati o i s us ual l y se t b etwe en 1:3 and 1:2. V T i s de termi ned by ai rway press ure and I:E rati o. D ri vi ng p res sure i s usual l y s et bet ween 1–2bar. The se pre ssures are m uch hi ghe r t han the 60–100c mH 2 O use d i n c onv ent i onal venti l at i on. PEEPi i s rel a ted to the d ri v i ng press ure, I:E rat i o and re spi ratory rate . Exte rnal PEEP may be add ed to i nc rease mean airw ay p re ssure shoul d thi s be nec ess ary to i m prove oxyg enati on.

Combined HFJV and conventional CMV May be us eful i n ARDS where HFJV alone c annot provi d e adequate gas e xchang e. Low fre que ncy press ure l i mi ted venti l at i on wi th PEEP provi des an ad equate mean airw ay pre ssure to ens ure ox yge nat i on whi l e CO 2 c l earance i s effect ed by HFJV. C are must be t ake n t o avoi d e xces si ve peak ai rway p res sure w hen HFJV and CMV breat hs stack.

High frequency oscillation (HFO) Thi s t ec hni que can be ap pl i ed ext ernal l y (see ‘N on-i nv asi ve res pi ratory sup port’) or vi a the e ndotrache al tub e. In the l at ter i nst anc e hi gh rates are appl i ed and t he dri vi ng p res sure gradually i ncre ase d. The FRC i ncrease s, rec rui ti ng al v eol i and i mp rov i ng ox yge nat i on. T he ai rway press ure can t hen be wound down, ofte n w i thout any s i gni fi cant det eri orati on i n oxyg enati on. P.21

Adjusting HFJV according to blood gases Increasing PaO 2 Inc re ase FIO 2 Inc re ase I:E rati o Inc re ase dri vi ng pre ssure Add ex ternal PEEP Consi d er red uci ng re spi rat ory rate

Decreasing PaCO 2 Inc re ase dri vi ng pre ssure Dec rease res pi rat ory rate

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See also: Venti l at ory support— ind i c ati ons , p 4; Pos i t i ve end ex pi rat ory press ure (1), p 22; Posi t i ve end e xpi rat ory press ure (2), p24; Acut e resp i ratory di s tre ss syndrome (1), p 292; Acute res pi rat ory di stres s s ynd rom e (2), p294 P.22

Positive end expiratory pressure (1) Pos i ti ve end ex pi ratory pre ss ure (PEEP) i s a modali ty use d i n p osi ti v e p res sure v ent i l ati on to pre vent t he alve ol i ret urni ng t o atmos pheri c p res sure d uri ng exp i rati on. It i s rout i ne l y set be twee n 3–5c mH 2 O; howe ver, i n s evere res pi rat ory failure i t wi l l oft en need to ex ceed 10cmH 2 O t o be ab ove the l ower i nfl exi on p oi nt of t he pre ssure–vol ume curve. Thi s has be en sug ges ted as be nefi ci al i n pat i ents wi t h s eve re ARD S. It rarel y need s t o ex cee d 20cm H 2 O t o avoi d cardi ores pi rat ory compl i cati ons and al veol ar ov er-di s tensi on (see be l ow ). It d oes not p rev ent nor atte nuate ARD S, or re duc e c api l l a ry l eak or l ung water.

Respiratory effects PEEP i mprove s oxyge nat i on by re crui t i ng col l aps ed alve ol i , red i st ri but i ng l ung wat er, de cre asi ng A–V mi smatc h and i nc re asi ng FRC.

Haemodynamics PEEP usually l owers b oth l e ft and ri ght ve ntri c ul a r p rel oad and i ncreas es RV aft erl oad . T hough PEEP may i ncreas e cardi ac out put i n l e ft heart fai l ure and fl ui d ove rl oad states by prel oad red uct i on, i n m ost ot her cases cardi ac out put fal l s , ev en at rel ati vel y l ow PEEP l evel s. PEEP m ay al s o c omp rom i se a poorl y funct i oni ng ri ght ve ntri c l e. Im proved PaO 2 resul t i ng from d ecreas ed venous ad mi x ture m ay s ome ti mes ari se sol el y from re duc ti ons i n cardi ac outp ut .

Physiological PEEP A s mal l degree of PEEP (2–3c mH 2 O) i s usual l y p rov i de d p hys i ol ogi cally by a c l osed l a rynx. It i s l os t w hen the pati ent i s i ntub ate d or t rac heostomi s ed and breat hi ng s pontaneousl y on a ‘ T’ pi ece wi t h no C PAP val ve (se e CPAP).

Intrinsic PEEP (auto-PEEP, air trapping, PEEPi) Inc re ased l evel of PEEP due to i ns uffi c i ent t i me for e xpi rat i on, l ead i ng to ‘air trapp i ng ’, CO 2 re tenti on, i ncre ase d ai rway press ures and i nc re ase d FR C. See n i n p athol ogi c al condi t i ons of i ncreas ed ai rfl ow res i st anc e (e.g. as thm a, emp hys ema) and w hen i nsuffi c i ent e xpi rat ory ti me i s set on the v ent i l a tor. Used cl i ni call y i n i nverse rati o ve nti l at i on to i nc re ase oxy genati on and dec re ase peak airw ay pre ssures . High l evel s of PEEPi c an, howeve r, sl ow w eani ng by an i nc re ase d work of bre athi ng ; use of e xtri nsi c PEEP may ove rcome thi s. PEEPi can be measured by tem porari l y occ l udi ng t he expi ratory outl et of v ent i l ator at e nd-e xpi rat i on for a fe w s econds to al l ow equi l i brati on of pre ssure bet wee n upper and l owe r airway and then readi ng t he vent i l ator p res sure g aug e (or pri nt-out ).

‘Best’ PEEP Ini ti al l y d esc ri bed as the l e vel of PEEP p roduc i ng the l owes t shunt val ue. Now ge neral l y c ons i de red to be the l owe st l ev el of PEEP t hat achi e ves SaO 2 ≥90% al l owi ng, where ver possi bl e , l owe ri ng of F IO 2 (i deal l y ≤0. 6) though not at t he exp ens e of pe ak ai rway press ure s > 35–40c mH 2 O or s i g ni fi cant red uct i ons i n D O 2 .

See also: IPPV—d esc ri pti on of vent i l ators, p6; IPPV—m ode s of ve nti l a ti on, p8; IPPV—adjusti ng the ve nti l at or, p10; IPPV—c omp l i cat i ons of ve nti l a ti on, p14; Pos i t i ve end ex pi ratory press ure (2), p 24; Conti nuous pos i ti ve ai rway pre ss ure , p 26; Lung recrui tment, p28 P.23 P.24

Positive end expiratory pressure (2) Adjusting PEEP 1. Meas ure bl ood gases and m oni tored haem ody nam i c vari ab l es . 2. If i nd i cated , alte r l eve l of PEEP by 3–5cmH 2 O i ncreme nts . 3. Re-m eas ure gas es and haemodynami c vari abl es aft er 15–20m i n. 4. Cons i de r furthe r c hanges as nec ess ary (i nc l ud i ng ad di t i onal change s i n PEEP, fl ui d c hal l e nge or vas oac ti v e drugs). A numb er of cl i ni cal tri al s have ad jus ted PEEP l eve l s ac cordi ng t o F IO 2 requi re ments (se e t abl e). Al though unl i k el y to consti tute ‘op ti m al PEEP’ for an i ndi v i dual pat i ent, thi s p rovi d es a us eful approxi mat i on and s tarti ng poi nt for further ti trati on of t herapy .

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FIO 2

0.3

0.4

0.4

0.5

0.5

0.6

0.7

0.7

0.7

0.8

0.9

0.9

0.9

1.0

PEEP (cmH 2 O)

5

5

8

8

10

10

10

12

14

14

14

16

18

≥18

Indications Hypoxae mi a re qui ri ng hi g h FIO 2 Opt i mi sat i on of press ure –vol um e c urv e i n s eve re res pi rat ory fai l ure Hypoxae mi a se condary t o l eft heart fai l ure Improve ment of c ard i ac output i n l eft he art failure Reduced work of b reathi ng duri ng w eani ng i n pat i e nts wi th hi g h PEEPi Neuroge ni c p ul m onary oede ma (i . e. non-cardi ogeni c pul monary oe dem a fol l owi ng rel i ef of up per ai rway obst ructi on)

Complications Reduced cardi ac out put . M ay nee d ad di ti onal fl ui d l oadi ng or eve n i not rop es. Thi s shoul d ge neral l y b e avoi ded unl ess hi ghe r PEEP i s ne ces sary t o m ai ntai n adeq uat e arteri a l oxyg enat i on. C aut i on shoul d b e e xerci s ed i n pati ents wi t h m yocard i al i s chaemi a. Inc reased ai rway pres sure (and pot ent i al ri sk of venti l at or trauma). Overi nfl a ti on l ead i ng to ai r t rap pi ng and rai se d PaCO 2 . Use wi th cauti on i n p ati ent s w i t h c hroni c ai rfl ow l i m i tati on or asthma. In press ure- c ont rol l e d ve nti l a ti on overdi s tensi on i s sug ges ted whe n an i ncreas e i n PEEP produc es a si gni fi cant fal l i n ti dal v ol ume. Hi g h l evel s wi l l d ecreas e v enous ret urn, rai s e i nt rac rani al press ure and i nc rease hepati c c ong est i on. PEEP may c hange t he are a of l ung i n whi ch a pul monary artery c athete r t i p i s pos i t i oned from We st Zone III to non-Zone III. Thi s i s sugge ste d b y a ri se i n wedg e p res sure of at l eas t hal f the i ncreas e i n PEEP and requi re s res i ti ng of the PA cathe ter.

See also: IPPV—d esc ri pti on of vent i l ators, p6; IPPV—m ode s of ve nti l a ti on, p8; IPPV—adjusti ng the ve nti l at or, p10; IPPV—c omp l i cat i ons of ve nti l a ti on, p14; Pos i t i ve end ex pi ratory press ure (1), p 22; Conti nuous pos i ti ve ai rway pre ss ure , p 26; Lung recrui tment, p28; Press ure–v ol ume rel ati ons hi p , p 96; Bl ood gas anal y si s , p 100; Inotrop es, p196; Fl ui d chall eng e, p 274; Atel ec tas i s and pul monary c ol l aps e, p284; Rai sed i ntracrani al press ure , p 382 P.25 P.26

Continuous positive airway pressure Conti nuous p osi ti ve airway pre ssure (CPAP) i s the addi ti on of p osi ti v e p res sure t o t he exp i ratory s i de of the b reathi ng ci rcui t of a s pontaneous l y venti l at i ng pati e nt who may or may not b e i nt ubat ed. Thi s se ts the bas el i ne up per ai rway pre ss ure above atm osp heri c pre ss ure , p rev ent s al veol ar c ol l aps e and pos si b l y rec rui ts al ready col l ap sed al veol i . It i s usual l y admi ni ste red i n i ncrements of 2.5cmH 2 O to a maxi mum of 10cmH 2 O and ap pl i ed vi a ei the r a ti ght-fi tt i ng face mas k (face CPAP), nasal mask (nasal CPAP) or exp i ratory l i m b of a ‘T’ pi ece breat hi ng c i rcui t. A hi g h fl ow (i . e. above peak i nsp i ratory fl ow ) i nsp i red air-oxy gen suppl y, or a l arg e rese rvoi r bag i n the i ns pi ratory ci rcui t, i s ne ces sary t o kee p t he val ve open. C PAP i m proves oxy genati on and may re duc e t he work of breat hi ng by reduci ng the al v eol ar-to-mouth pre ssure gradi e nt i n pat i ents wi th hi g h l eve l s of i nt ri nsi c PEEP. Trans i e nt peri od s of hi gh CPAP (e. g. 40c m H 2 O for 40s) may be a useful manoeuv re for re crui t i ng col l aps ed alve ol i and i mprovi ng oxy genati on i n ARD S.

Indications Hypoxae mi a re qui ri ng hi g h resp i ratory rate , e ffort and FIO 2 . Left he art fail ure to i m prove hypoxae mi a and c ard i ac output. Weani ng modal i t y. Reduci ng w ork of breat hi ng i n p ati ent s w i th hi gh PEEPi (e. g. ast hma, c hroni c ai rfl ow l i m i t ati on). NB: use wi t h caut i on and m oni tor c l os el y .

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Complications Wi t h m ask CPAP t here i s an i ncreas ed ri sk of aspi rati on as g ast ri c di l a tat i on may oc cur from swallowed ai r. Ins ert nasog ast ri c tube, es pec i al l y i f consc i ousne ss i s i mp ai red or gas tri c mot i l i ty i s re duc ed. Reduced cardi ac out put due t o reduced ve nous return (raise d i ntra-t horaci c pre ssure). M ay need ad di t i onal fl ui d or e ven i notrope s. Overi nfl a ti on l ead i ng to ai r t rap pi ng and hi gh PaC O 2 . Cauti on i s urged i n pati e nts wi th chroni c ai rfl ow l i mi tat i on or ast hma. Hi g h l evel s wi l l reduce venous re turn and i nc rease i nt racrani a l p res sure. Occ asi onal p oor pati e nt com pl i anc e w i th ti ght -fi tt i ng face m ask due t o feel i ng s of c l austrophobi a and di s com fort on b ri dge of nos e. Ins pi s sat ed sec ret i ons d ue to hi g h fl ow , d ry gas .

Management 1. Meas ure bl ood gases , m oni tor haemodynami c vari abl es and re spi rat ory rate. 2. Prep are ‘T ’ p i e ce c i rcui t w i t h a 5cm H 2 O CPAP valve on the e xpi rat ory l i mb. Conne ct i ns pi rat ory l i mb to fl ow gene rat or/l arge vol ume re servoi r bag. Adjus t ai r-oxy gen mi x t o obtain des i re d F IO 2 (measured by oxy gen anal yse r i n ci rcui t). Us e a he at–moi sture exc hanger to humi d i fy the i nhaled gas . If not i nt ub ated , c ons i d er ei t her nasal or face CPAP. At tac h m ask to fac e b y appropri at e harness and attach ‘T’ pi ece to mas k. Ens ure no ai r l eak around mas k. If usi ng a nasal m ask , encourag e t he pat i ent t o k eep thei r mouth cl ose d. 3. Meas ure gases , resp i ratory rat e, and hae mod ynami c s afte r 15–20mi n. 4. Cons i de r furthe r c hanges i n CPAP (by 2.5cmH 2 O i nc rem ent s) 5. Cons i de r need for (i ) fl ui d challe nge (or v asoact i ve drugs ) i f c i rc ul a tory c omp rom i s e and (i i ) nasog ast ri c t ube i f gast ri c atony p res ent .

See also: Pos i ti ve end ex pi ratory pre ss ure (1), p 22; Pos i t i ve end ex pi rat ory press ure (2), p 24; Inotrope s, p196; Fl ui d chall eng e, p 274; D ysp noe a, p278; Ai rway obs truct i on, p 280; Re spi rat ory failure, p282; At el e ctasi s and p ul m onary col l a pse , p284; Ac ute chest i nfec ti on (1), p288; Acute che st i nfect i on (2), p 290; Acut e resp i ratory d i s tre ss syndrome (1), p 292; Acut e resp i ratory di s tress sy ndrome (2), p 294; Pos t-operati ve i nt ens i ve care, p534 P.27 P.28

Lung recruitment The re has be en consi d erabl e i nterest i n rece nt years i n the conce pt of l ung recrui t ment. The rati onal e i s t hat reopeni ng of col l a pse d alve ol i wi l l re sul t i n i mprove d g as exc hange, wi t h res ul t i ng re duc ti ons i n ai rway p res sures and FIO 2 . Ti m i ng i s c ruc i al as col l aps ed alve ol i are m ore l i kel y t o b e recrui tab l e i n the earl y st age s of resp i ratory fai l ure. It app ears t hat be nefi t i s more l i ke l y i n non-re spi ratory c aus es of ARDS, rat her than i n cas es of d i rect pul monary pat hol ogy such as pne umoni a . Some ani mal st ud i es sugge st that recrui tment p roced ure s m ay e ven be pot ent i a l l y i nj uri ous i n t he l at ter si tuati on. Consi d erati on s houl d be gi v en to l ung recrui tme nt soon after i ntuba-t i on i n p ati ent s w i th se vere resp i ratory fai l ure, and proce dures causi ng d e-recrui tme nt, e. g. e ndotracheal sucti on and ai rway di sc onnect i on.

Recruitment techniques A numb er of tec hni que s are des cri bed to re crui t col l a pse d alve ol i , s uc h as ap pl y i ng 40cmH 2 O PEEP for 40s wi th no venti l at or bre aths; d el i ve ri ng a few l a rge -vol um e, vent i l ator-d el i vered bre aths; or by usi ng a c omb i nati on of varyi ng l ev el s of PEEP and i ncre asi ng pre ssure-del i ve red breat hs to obt ai n op ti mal gas ex change . Al though ane cdotal s ucc ess es are re ported , w i th oc cas i onal l y d ram ati c i mp rov ements i n l ung comp l i anc e and g as exc hange, no com parati ve tri al s have bee n p erform ed, and outc omes have not be en ass ess ed p rospe cti vel y. Hae mod ynam i c compromi se may occ ur duri ng t he proced ure , t hough thi s usually re cov ers on ce ssati on. P.29

Key trial Brower RG, et al for t he ARD S C l i ni c al Tri al s Ne twork. Effec ts of rec rui tme nt maneuv ers i n pati e nts wi th acute l ung i njury and acute res pi rat ory di stres s s ynd rom e ve nti l a ted wi t h hi g h p osi ti v e e nd-e xpi ratory p res sure. Cri t C are Me d 2003; 31:2592–7

P.30

Prone positioning Prone pos i ti oni ng i s us ed to tre at pat i ents wi t h acut e resp i ratory d i s tre ss syndrome (AR DS) to i m prove g as exc hange.

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A numb er of the ori es hav e b een propos ed to exp l ai n w hy t he prone pos i t i on hel ps . T hes e t heori e s i ncl ude : reducti on i n com pre ss i on at el e ctasi s of de pend ent l ung re gi ons (tem porary), red uct i on i n c hes t wall compl i ance i nc reasi ng i nt rathorac i c pre ss ure and al veol ar recrui t ment, bet ter re gi onal di aphragmat i c mov eme nt, be tte r V/Q mat chi ng, i mp rov ed sec ret i on c l earance and l es s al v eol ar di s tensi on l ead i ng to be tte r oxyg enati on.

Indications Prone pos i ti oni ng may be consi dered whe n: PaO 2 <8.5k Pa, FIO 2 ≥ 0.6, PEEP >10cmH 2 O des pi t e opti mi s at i on of other venti l at ory support.

Technique Pos i ti oni ng the p ati ent takes ti me and pre parati on. Four mem bers of s taff are requi red to t urn t he pat i ent and one person to se cure t he head and e ndotracheal tube. The turn i t sel f i s a tw o-st age proce dure v i a the l a teral pos i t i on. The arm on whi c h t he p ati ent i s t o b e rol l ed i s tuc ked under the hi p wi t h t he other arm l a i d across the c hes t. Pi l l ows are pl ace d unde r t he abd omen and c hes t p ri or to rot ati on to the l a teral pos i ti on. If st abl e, turn may be com pl e ted to prone. Pi l l ows are pl ace d unde r t he shoul d ers and p el v i s . The head of the be d i s rai sed and one arm i s ext end ed at the pati e nt' s s i d e whi l e t he othe r i s fl e xed wi t h t he head faci ng the op pos i te way .

Frequency of turns The re sponse to prone venti l at i on i s di ffi cul t to pre di c t. Som e p ati ent s m ay hav e no i m provem ent i n gas e xchang e; others may have a t emp orary benefi t, req ui ri ng freq uent t urns, and ot hers m ay have di ffi cul ty ret urni ng t o a supi ne pos i t i on. For c omp res si on atel ec tas i s i t i s l i kel y t hat be nefi t wi l l l ast up to 2h be fore resumpt i on of a s upi ne pos i t i on i s re qui red . For other condi t i ons, up to 18h prone pos i t i oni ng may b e requi re d. The head and arm s s houl d be rep osi ti one d 2-hrl y.

Complications The re are probl ems as soc i at ed wi t h p osi ti oni ng the pati e nt prone i nc l ud i ng: faci al oed ema, i ncorre ct pos i t i oni ng of l i mbs l e adi ng to nerve p al s y and acc i de ntal removal of drai ns and cat het ers , p res sure nec ros i s, my osi ti s os si fi c ans . The se probl e ms are preve ntabl e provi ded there i s aw are nes s of thei r p ote nti al .

Contraindications The re are tw o ab sol ut e c ont rai ndi cat i ons to p rone p osi ti on: sev ere he ad, sp i nal or abdomi nal i nj ury and s eve re hae mod ynam i c i nstabi l i t y. Rel a ti ve c ont raind i cati ons i ncl ude: Rece nt abd omi nal surge ry Large abdomen Preg nancy Spi nal i nstabi l i t y (though sp eci al bed s are avai l a bl e for t urni ng affec ted pat i e nts ) Freq uent s ei z ures Mul ti p l e trauma Rai s ed ICP P.31

Key trial Gat ti noni L, e t al for the Prone-Sup i ne Stud y Group. Effe ct of prone pos i ti oni ng on the survi val of pati e nts wi th acute res pi rat ory failure. N Eng l J Med 2001; 345:568–73

See also: Ac ute re spi rat ory di st res s s ynd rom e (1), p292; Acut e resp i ratory d i s tre ss syndrome (2), p294 P.32

Non-invasive respiratory support Dev i ce s of v ary i ng sophi sti cati on are avai l a bl e to aug ment s pontaneous b reathi ng i n the compl i ant p ati ent b y ei ther ass i s ti ng i nsp i rati on (i nspi rat ory support ) and/or p rov i di ng CPAP. Non-i nvas i ve support i s usual l y d el i vered by ti ght fi t ti ng fac e or nasal mask, thoug h a hel met may b e used and i nsp i ratory s upp ort can b e d el i vered by mouthp i ec e. Som e d evi ces al l ow conne cti on to an endotracheal tube for the i ntubat ed b ut spontaneousl y b reathi ng pat i e nt.

Indications Hypoxae mi a re qui ri ng hi g h resp i ratory rate , e ffort and FIO 2 Hype rc apni a i n a fati g ui ng pat i ent Weani ng modal i t y To avoi d e ndotrache al i nt ubati on w here d esi rab l e (e. g. sev ere chroni c ai rfl ow l i mi tati on, i mm unosup pre sse d pati ents) Reduces work of b reathi ng i n pati e nts wi th hi g h PEEPi (e.g . as thma, chroni c ai rfl ow l i mi tat i on). Use wi th cauti on

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and moni tor c l osel y Phys i ot herap y te chni q ue for i mp rovi ng FR C Sl e ep apnoea

Inspiratory support (IS) A p res et i nspi rat ory press ure i s g i ve n whi c h i s t ri ggered by the pati e nt' s b re ath. Thi s tri gg er can be ad jus ted acc ord i ng t o t he d egree of pat i ent e ffort. Some d evi ces wi l l de l i v er bre aths automat i call y at ad jus tab l e rat es and the I:E rati o may also be adj ust abl e. The ti dal vol um e d el i vered for a gi v en l ev el of i ns pi ratory sup port w i l l v ary acc ord i ng t o t he p ati ent 's re spi rat ory compl i a nce . An ex amp l e of an IS devi ce i s the Bi rd ve nti l a tor commonl y use d b y phy si othe rap i s ts for i m provi ng F RC and exp and i ng l ung bas es.

BiPAP (Bi-level Positive Airways Pressure) Thi s d evi ce del i v ers ad jus tab l e l ev el s of press ure support and PEEP. Del i v ere d b reaths can b e ei ther pat i ent-t ri g gered and /or mandat ory. Some Bi PAP d evi ces are dri v en by air; to i ncreas e t he F IO 2 , suppl eme ntal oxyg en c an be gi v en vi a a c i rcui t c onnect i on or through a p ort al i n the mask.

Management 1. Sel ect ty pe and del i v ery mod e of ve nti l a tory s upp ort . 2. Connect pati e nt as per de vi c e i nst ructi ons . 3. Use an app rop ri a te si zed mas k t hat i s comfortabl e and l eak -free. 4. A d el i vered pre ssure of 10–15c mH 2 O i s a usual start i ng poi nt whi ch can b e ad jus ted ac cordi ng to pat i ent res ponse (res pi rat ory rate, de gre e of fati g ue, comfort, bl ood gases …). 5. Expi ratory p res sure s upp ort l evel s are usual l y wi t hi n the 5–12cmH 2 O range. 6. Pati ent s i n res pi ratory di stress may have i ni ti al di ffi c ul ty i n cop i ng wi th the se devi ce s. Cons tant atte nti on and encouragem ent he l p to acc ust om the pati e nt to the de vi c e and/or m ask whi l e di ffe rent l eve l s of sup port, I:E rat i os et c. are be i ng te ste d t o fi nd the op ti mal se tti ng. Cauti ous ad mi ni st rat i on of l ow d ose subcutaneous opi a te i nj ect i ons (e.g. di amorphi ne 2. 5mg ) m ay hel p t o calm the pati e nt wi t hout d epress i ng resp i ratory d ri ve. The ti g ht-fi t ti ng m ask may be found i ncre asi ngl y c l a ust rop hob i c aft er a few d ays ' use. Thi s shoul d be pre-e mpt ed i f poss i b l e by al l owi ng the pat i e nt reg ul a r b reaks. Press ure areas such as the bri dg e of t he nos e s houl d be protec ted . P.33

Key trials Brochard L, et al . Noni nvas i ve venti l at i on for acut e e xac erb ati ons of chroni c obs truct i ve pul monary di se ase. N Engl J Med 1995; 333:817–22

Ant one l l i M, et al . A compari s on of noni nv asi ve p osi ti ve-pre ssure venti l ati on and conve nti onal m echani cal v ent i l ati on i n pat i ents wi t h acut e resp i ratory fai l ure. N Engl J M ed 1998; 339:429–35

P.34

Extracorporeal respiratory support The se tec hni que s have de cl i ned i n popul ari ty ove r rece nt years aft er sev eral t ri al s faile d t o d emonst rat e c l ear out com e b ene fi t i n ad ul t s w i th ve ry sev ere re spi rat ory failure . Surv i val rate s of 50–60% are rep ort ed but cl ear sup eri ori ty ov er convent i onal venti l at i on has not yet bee n d emonst rat ed i n control l ed studi e s. A l arge p ros pec ti ve random i se d s tud y (the ‘C ESAR’ tri al ) i s c urrent l y und er way i n the UK .

Extracorporeal CO 2 removal (ECCO 2 R) An ext rac orporeal veno-v enous ci rcul at i on al l ow s CO 2 cl earanc e v i a a g as exc hang e m emb rane. Bl ood fl ows of 25–33% cardi ac out put are t ypi cal l y us ed w hi c h onl y al l ow for p art i al ox yge nat i on support. Low freq uency (4–5/mi n) pos i t i ve press ure ve nti l at i on i s us ual l y us ed wi t h EC CO 2 R w i th conti nuous oxy genati on throug hout i ns pi rati on and exp i rati on. The l ungs are ‘ hel d open’ w i th hi gh PEEP (20–25c mH 2 O), l i m i te d p eak ai rway press ures (35–40c mH 2 O) and a c ont i nuous fresh gas s upp l y. Thus, ox yge nat i on i s effec ted wi t h l ung rest to ai d recovery. Ant i coagul at i on of the ext rac orp oreal ci rcui t can be re duc ed by usi ng hep ari n-b ond ed tub i ng and m embrane s.

Extracorporeal membrane oxygenation (ECMO) An ext rac orporeal veno-arte ri al ci rcul at i on wi th hi g h b l ood fl ows (approac hi ng c ard i ac outp ut) through a gas exc hange memb rane e nab l es most i f not al l of t he body 's gas ex change re qui rem ent s t o b e m et. The main di s adv ant age s c omp are d t o ECCO 2 R are the ne ed for l a rge bore art eri al punct ure wi th i ts conse que nt ri s ks , and hi gh ext rac orp oreal bl ood fl ows wi t h t he pot ent i al for c el l damag e.

Indications

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Fai l ure of m axi mum i ntensi v e t herapy and ve nti l a tory s upp ort to sustain ade quate gas exc hange as evi denced by the cri te ri a be l ow .

Contraindications Chroni c s yst emi c d i se ase i nvol vi ng any major organ s yst em (e. g. i rreve rsi bl e c hroni c CN S d i se ase , c hroni c l ung di s eas e wi th FEV 1 < 1l , FEV 1 /FVC <0. 3 of p red i ct ed, chroni c PaC O 2 >6. 0kPa, e mphyse ma or pre vi ous adm i ss i on for chroni c res pi rat ory i nsuffi c i ency, i ncurabl e or rap i dl y fatal m al i gnancy , c hroni c l e ft heart fai l ure, chroni c renal fai l ure, chroni c l i v er fai l ure, HIV re l at ed di seas e). Lung fail ure for >7 days (al though treat ment w i th ex tracorporeal re spi ratory s upp ort may pe rs i st for l ong er than 14 d ays ). Burns (>40% of b ody surfac e). More than 3 organ fai l ure s i n addi ti on to l ung fail ure .

Criteria for ECCO 2 R/ECMO i. Rapi d fai l ure of ve nti l at ory support : i mmed i at e use of the se tec hni que s s houl d be consi d ere d i n t hos e m eet i ng the fol l ow i ng cri t eri a for a p eri od >2h des pi te maxi mum i ntensi ve c are: PaO 2 <6.7k Pa FIO 2 1. 0 PEEP >5cmH 2 O ii. Sl ow fail ure of venti l at ory support: consi der us e afte r 48h maxi mum i ntensi ve c are for t hos e m eet i ng the fol l owi ng gas ex change and me chani cal pul monary func ti on c ri t eri a for a p eri od >12h:

PaO 2 <6.7kPa

PEEP >5cmH 2 O

Qs/Qt >30% on FIO 2 = 1.0

FIO 2 >0.6

PaO 2 /FIO 2 <11.2kPa

TSLC <30ml/cmH 2 O at 10ml/kg inflation

See also: Ant i c oag ul a nts , p 248; Prost agl and i ns , p 264; Acut e resp i ratory d i s tre ss syndrome (1), p292; Acute res pi rat ory di s tress sy ndrome (2), p 294 P.35 P.36

Endotracheal intubation Indications An art i fi ci al ai rway i s ne ces sary i n t he fol l ow i ng ci rc ums tances : Apnoea— Provi s i on of me chani c al venti l at i on, e .g. unc ons ci ous nes s, sev ere re spi rat ory muscl e w eak nes s, sel f-poi s oni ng Resp i ratory fai l ure—Prov i si on of mec hani cal v ent i l a ti on, e.g . ARDS, p neumoni a Ai rway prote cti on— Unc ons ci ousness , t rauma, as pi rat i on ri sk, poi soni ng Ai rway obs truct i on—Maint ai n ai rw ay p ate ncy , e .g. traum a, l aryng eal oed ema, t umour, burns Haem ody nam i c i ns tab i l i ty —Faci l i t ate mec hani cal v ent i l ati on, e. g. shock, cardi ac arrest

Choice of endotracheal tube Mos t adul ts req ui re a s tandard hi gh vol um e, l ow pre ssure cuffed endot rac heal t ube . T he average si ze d ad ul t wi l l req ui re a si ze 8. 0–9.0mm i d tube (si ze 7.5–8. 0mm i d for femal es ) cut t o a l e ngt h of 23cm (21cm for fe mal es). Parti cul ar probl e ms wi t h t he upp er ai rway , e .g. traum a, oede ma, may re qui re a s mal l er t ube . In s pec i fi c s i tuati ons non-st and ard tubes may be us ed, e. g. jet venti l at i on, armoure d t ube s t o avoi d ex ternal c ompres si on and d oub l e l um en tub es to i sol at e t he ri ght or l e ft l ung.

Route of intubation The us ual route s of i ntubat i on are oro-trache al and naso-t rache al . Oro-t rac heal i ntubat i on i s p referred. The nas o-t rac heal rout e has the ad vant age s of i ncreas ed pat i ent c omfort and t he pos si b i l i ty of eas i er b l i nd p l ac eme nt; i t i s al so e asi er to sec ure t he t ub e. Howe ver, t here are seve ral d i sadvantages . The t ube i s us ual l y sm al l er, there i s a ri sk of s i nusi ti s and oti t i s med i a and the rout e i s c ont raind i cated wi th concurrent c oag ul opat hy, CSF l eak and nasal fracture s.

Difficult intubation

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If a d i ffi cul t i ntub ati on i s pre di c te d, i t shoul d not b e at tem pte d b y an i nex peri enced op erator. D i ffi cul t y may b e pre di cte d i n t he pat i ent wi th a s mal l mout h, hi gh arc hed pal at e, l arge upp er i nc i sors , hy pog nat hi a , l arge t ong ue, ant eri or l a rynx, short nec k, i mm obi l e tem poro-mandi bul ar joi nt s, i mm obi l e cervi c al joi nts or morbi d obes i t y. If a di ffi c ul t i ntubat i on prese nts unexp ect edl y, the us e of a st yl e t, a st raight b l ad ed l aryng osc ope or a fi b reopti c l aryng osc ope may hel p . It i s i mportant not to pe rsi st for t oo l ong ; reve rt to bag and mask venti l at i on to ens ure ade quate oxyg enati on.

Complications of intubation Early complications Trauma, e. g. hae morrhage, med i as ti nal pe rforat i on Haem ody nam i c col l ap se, e. g. pos i ti ve pre ssure venti l at i on, v asodi l atati on, arrhyt hmi as or rapi d corre cti on of hype rc apni a Tube malposi t i on, e.g. fail ed i nt ubati on or e ndob ronchi al i ntub ati on

Later complications Infe ct i on i ncl udi ng m axi l l ary si nus i ti s i f nas al l y i ntubat ed Cuff press ure traum a (avoi d by m ai ntai ni ng cuff pres sure < 25c mH 2 O) Mout h/l i p traum a P.37

Equipment required Suc ti on (Yankauer ti p ) Oxyg en sup pl y , rebreat hi ng bag and mask Laryng osc ope (tw o c urv ed bl a des and s traight b l ad e) Sty l et /bougi e Endotracheal tubes (prefe rred s i z e and s mal l e r) Magi l l force ps Drugs (i nduc ti on agent, mus cl e re l ax ant , s edati v e) Syri ng e for cuff i nfl ati on Tape to se cure t ube Capnograph

See also: Venti l at ory support— ind i c ati ons , p 4; Op i oi d anal ges i cs , p 234; Se dat i ve s, p238; Mus cl e re l ax ant s, p240; Card i ac arres t, p272; Ai rw ay obs tructi on, p280; Res pi rat ory fai l ure, p282; Acute che st i nfect i on (1), p288; Acut e c hes t i nfect i on (2), p290; Acute res pi ratory di stress sy ndrome (1), p 292; Ac ute re spi rat ory di st res s s ynd rom e (2), p294; As thm a—ge neral manage ment, p296; Ast hma—venti l at ory manage ment, p298; Poi soni ng —ge neral pri nc i pl es, p452; Pos t-operati ve i nt ens i ve care, p534 P.38

Tracheotomy Indications To provi d e an arti fi c i a l airw ay i n pl a ce of oro- or naso-t rache al i nt ubati on. Thi s m ay be to p rovi d e be tt er pat i ent com fort, to avoi d voc al cord, mout h or nasal t rauma or, i n an em erg enc y, to byp ass ac ute upp er ai rway ob struc ti on. The op ti m al ti m e t o p erform a trache otomy i n an i nt ubat ed pat i ent i s not known; curre nt pract i ce sugge sts 10–16 day s, or sooner i f prol onge d i ntubat i on i s pred i ct ed, es pec i al l y i n cas es of di ffi c ul t i ntubat i on. Avoi di ng t he ri sks of voc al cord d amage may provi d e s ome ad vant age for a tracheos tom y. The red uc ed need for s edati on, the potenti a l t o eat , d ri nk and spe ak and the faci l i t ati on of mout h c are are all defi ni te adv ant age s.

Percutaneous tracheotomy A m ore rapi d proc edure w i t h l ess ti ssue t rauma and sc arri ng t han the st and ard op en surgi cal te chni que. It can be performed i n the ICU, avoi di ng the ne ed to transfer pat i ents to the atre. Coagul opathy shoul d b e ex cl ude d or t reated fi rst . Subc utaneous ti s sue s are i nfi l trated wi th 1% l i d ocaine and e pi nephri ne (adrenaline). After a 1–1.5c m mi dl i ne ski n c re ase i nci s i on, t he sub cut ane ous ti ss ue i s bl unt di s sec ted to the ante ri or t rache al wal l . The end otracheal tube ti p i s wi thdrawn to t he l ev el of the vocal cords . T he trache a i s t hen punct ure d i n t he mi d l i ne w i t h a 14G ne edl e bet wee n t he 1st and 2nd t rac heal c arti l age s (or l ow er), al l owi ng g ui d e wi re i nserti on. The st oma i s creat ed by di l at ati on to 32–36Fr (C i ag l i a te chni q ue) or by a g ui d ed forcep s d i l ati ng t ool (Schachner–Ov i l l te chni q ue). In the former case, the t rac heostomy tub e i s i ntroduced ov er an app rop ri a te si z ed di l at or and i n the l att er throug h t he ope n

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di l at i ng tool . End-t i dal CO 2 m oni tori ng c onfi rm s adequate ve nti l at i on d uri ng the proce dure. Fi b reopti c b ronchosc opy may be us ed t o c onfi rm correct tracheal pl ace ment and no t rauma to the poste ri or trache al wal l , though thi s may com promi s e v ent i l ati on.

Complications The main earl y com pl i cat i on i s haemorrhage from ves sel s ante ri or t o t he trachea. Thi s i s usual l y c ont rol l e d wi th di rec t p res sure or, occ asi onall y, s ut ure s. Bl e edi ng i nt o t he trachea m ay res ul t i n cl ot obs truct i on of the airw ay; end otracheal suct i on i s us ual l y effect i ve . Paratrache al pl a cem ent shoul d b e rare but p rom ptl y recogni sed by i nabi l i ty to venti l ate the l ung s. Lat er compl i cati ons i nc l ude trache ost omy di spl ace ment, stomal i nfec ti on and trache al ste nos i s. St enos i s i s often re l at ed to l ow grade i nfect i on and i s c l a i me d t o be more com mon wi t h open tracheot omy . R are com pl i cati ons i nc l ud e t rac heo-oe sop hag eal fi stul a due to traum a or pres sure necrosi s of t he pos teri or trac heal wall , or erosi on t hroug h t he l at eral t rac heal w al l i nto a b l ood v ess el .

Maintenance of a tracheotomy Si nce the up per ai r pas sag es have be en byp ass ed, arti fi ci al hum i d i fi cat i on i s requi re d. Coug h i s l es s e ffec ti ve w i thout a func ti oni ng l arynx so reg ul ar trache al suc ti on w i l l b e ne ces sary. Furthe rmore, the l arynx provi d es a s mal l amount of nat ural PEEP that i s l os t wi t h a tracheos tomy . T he ri s k of b asal atel ect asi s c an be ove rcome wi t h CPAP or att ent i on to res pi rat ory ex erc i se s t hat promote dee p breat hi ng. A safe fi st ul a forms wi thi n 3–5 day s, al l owi ng rep l ac eme nt of t he tracheotomy tub e. P.39

Tracheotomy tubes Standard high volume, low pressure cuff Fenest rat ed wit h or w ithout cuff Use ful where ai rway prot ect i on i s not a pri mary concern. May be cl ose d duri ng normal breat hi ng w hi l e p rov i di ng i nt ermi t tent s uct i on ac ces s.

Fenestrated with inner tube As above but wi th an i nner tub e t o faci l i t ate cl osure of the fe nes trati on d uri ng i ntermi t tent m echani cal ve nti l a ti on.

Fenestrated with speaking valve Ins pi rat i on al l ow ed throug h t he trache ost omy to re duc e de ad space and i nspi rat ory resi stance . Expi rat i on through the l arynx , v i a the fe nes trati on, al l owi ng spe ech and t he advantages of l a ryngeal PEEP.

Adjustable flange Ac comm odates ex tre me vari at i ons i n s ki n to trac hea dep th whi l e ens uri ng the cuff rem ai ns c ent ral i n t he trache a.

Pitt speaking tube A non-fenest rat ed, cuffe d t ube for conti nuous mec hani c al vent i l ati on and ai rway prot ect i on wi th a p ort to di rec t ai rfl ow abov e t he c uff to the l ary nx. When ai rfl ow i s d i re ct ed t hroug h t he l arynx som e p ati ent s are abl e t o v ocalis e.

Passy–Muir speaking valve Thi s i s an e xpi ratory oc cl usi ve val ve pl a ced ont o t he tracheost omy tube that p erm i ts i nsp i rati on t hrough the tracheost omy and e xpi rat i on through the gl ott i s . T he t rache ost omy tub e c uff must be fi rst defl at ed. The v al v e al l ows phonat i on, faci l i tat es swal l owi ng and m ay red uce as pi rati on. Smal l s tud i es have sug ges ted that i t may re duc e t he work of breat hi ng. The potenti al ti d al vol ume drop throug h c uff defl at i on makes thi s val ve onl y s ui t abl e i n t hos e pat i ents re qui ri ng no (or rel ati vel y l ow l ev el ) i nvas i ve venti l at ory support.

Silver tube An unc uffed tub e used oc cas i onal l y i n ENT practi ce to mai nt ai n a t rache ost omy fi s tul a.

See also: Venti l at ory support— ind i c ati ons , p 4; Op i oi d anal ges i cs , p 234; Se dat i ve s, p238; Mus cl e re l ax ant s, p240; Card i ac arres t, p272; Ai rw ay obs tructi on, p280; Res pi rat ory fai l ure, p282; Acute che st i nfect i on (1), p288; Acut e c hes t i nfect i on (2), p290; Acute res pi ratory di stress sy ndrome (1), p 292; Ac ute re spi rat ory di st res s s ynd rom e (2), p294; As thm a—ge neral manage ment, p296; Ast hma—venti l at ory manage ment, p298; Poi soni ng —ge neral pri nc i pl es, p452. Pos t-operati ve i nt ens i ve care, p534 P.40

Minitracheotomy A 4mm di a met er unc uffed pl a sti c t ube i nserte d t hrough the c ri c othyroi d mem brane und er l oc al anaest het i c.

Indications Removal of ret ai ned sec re ti ons, us ual l y i f pat i ent' s c oug h i s we ak Emergency acc ess to l ower ai rway i f uppe r airw ay obs tructe d

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Contraindications/cautions Coag ul opat hy Non-com pl i ant , agi t at ed p ati ent (unl e ss sed ate d)

Technique Som e c omm erc i al ki ts re l y on b l i nd i ns ert i on of a bl unt i nt rod uc er; others us e a Se l di ng er tec hni que where a gui dew i re i s i nse rte d v i a the cri cothy roi d memb rane i nto the t rac hea. An i nt rod uce r p ass ed over t he w i re di l a tes the track al l owi ng eas y p ass age of the tube. 1. Use ase pti c t ec hni que . Cl eanse si te w i t h anti sep ti c . Locate cri cothy roi d m emb rane (m i dl i ne ‘ spongy ’ area betw een cri c oi d and thyroi d carti l ag es). 2. Infi l t rat e l ocal s ki n and s ubc ut aneous ti ssues wi t h 1% l i docai ne ± ep i ne phri ne (adre nal i ne). Adv anc e need l e i nt o deep er ti ssues, as pi rati ng to confi rm abse nce of bl ood then i nfi l t rat i ng wi th l i doc ai ne unti l c ri cot hyroi d memb rane i s p i erce d and air can be easi l y aspi rated . 3. (If usi ng Sel di nge r t echni q ue i ns ert g ui d ewi re throug h m embrane i nto trachea. ) Te the r t hyroi d c art i l a ge wi t h one hand , i nc i se sk i n and ti ssues verti c al l y i n mi d l i ne (al ongs i de wi re) wi th short-bl a ded guard ed scalpe l p rov i de d wi t h pack. Insert scalpe l t o b l ad e g uard l eve l t o make ade quate hol e through cri cothy roi d m emb rane. Remove scalpe l . 4. Ins ert bl unt i ntroducer through i nc i s i on si te i nt o t rac hea (or over gui de wi re). Angl e caudal l y . Re l at i v el y l i ght res i st anc e w i l l be fe l t duri ng c orrect passage—do not force i ntroduc er i f res i s tance p roves exc ess i ve . 5. Lub ri c ate pl ast i c tube wi t h g el . Sl i de tube ove r i ntroducer i nto trachea. 6. Remove i nt rod uce r (+ wi re ), l eav i ng pl ast i c tube in sit u. 7. Confi rm correct posi t i on by pl aci ng own hand over tube and fe el i ng ai rfl ow d uri ng bre athi ng. Suc ti on d own tube to aspi rate i nt rat rac heal c ont ent s (che ck pH i f i n doubt). Cap openi ng of tube. Suture t o s ki n. 8. Perform CXR (unl ess ve ry smooth i nserti on and no c hange i n cardi o-resp i ratory v ari abl es). 9. O 2 can be ent rai ned through the tube, or an ap propri ate conne ctor (provi d ed i n pac k) pl a ced to al l ow bag gi ng, use of the Bi rd venti l at or and /or short te rm ass i st ed venti l ati on.

Complications Punc ture of b l ood v ess el at cri cothy roi d m embrane may c aus e s i gni fi cant i nt rat rac heal or e xte rnal b l ee di ng. App l y l oc al pre ssure i f thi s occ urs after bl ade i nci s i on. If b l e edi ng conti nues , i nse rt mi ni t rac heotom y t ube for a tamp onadi ng e ffe ct. If bl eed i ng pe rsi st s, i ns ert de ep sut ure s e i ther si de of m i ni tracheot omy; i f thi s fai l s , c ont act surgeon for assi st anc e Perforati on of oesophagus Medi ast i ni ti s (rare) Pneumot horax P.41

See also: Che st phy si othe rap y, p48; Atel ect asi s and pul monary col l aps e, p 284; Acute che st i nfec ti on (1), p288; Acut e c hes t i nfect i on (2), p290 P.42

Chest drain insertion Indications Drai nage of ai r (p neumot horax), fl ui d (e ffusi on), bl ood (haemothorax ) or pus (emp yem a) from the p l eural sp ace .

Insertion technique 1. Use 28Fr d rai n (or l arger) for hae mot horax or e mpy ema; 20Fr wi l l suffi c e for a pure pne umothorax . Sel di nger-ty pe drains wi th an i nt egral gui dew i re are now al s o avai l ab l e. The d rai n i s usuall y i nse rte d t hrough the 5th i nte rcostal s pac e i n t he mi d -ax i l l ary l i ne , fi rs t anae stheti si ng s ki n and p l eura wi t h 1% l i docai ne. Ensure that ai r/fl ui d/bl ood/p us i s as pi rate d. 2. Make a 1–1.5c m s ki n creas e i nci si on, creat e a track wi t h g l ov ed fi nger (or forc eps ) t o s eparat e muscl e fi b res and open pl eura. 3. Ins ert drai n through ope n p l eura wi t h t roc har wi thd rawn t o e nsure ti p i s b l unt t o avoi d l ung dam age . Angl e and i ns ert drai n to correct pos i t i on (t owards l ung apex for a pneum othorax and l ung base for a haem othorax/e ffus i on). Connec t d rai n t o t he und erw ate r s eal . CT sc an or ul trasound may be use ful for d i re cti ng pl a ceme nt for focal /sm al l col l ect i ons.

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4. Sec ure drai n to chest wall by properl y pl a ced sutures. 5. Perform CXR t o e nsure correc t s i t i ng and l ung re i nfl at i on. 6. Pl ac e on 5–10cmH 2 O (0. 5–1.3k Pa) neg ati ve pre ssure (l ow p res sure w al l sucti on) i f l ung has not ful l y e xpande d.

Subsequent management Drains shoul d not be cl a mpe d p ri or t o removal , or t ransport of pat i ent. Drains may be re mov ed when the l ung has re-e xpanded and t here i s no air l eak (no res pi ratory swi ng i n fl ui d l eve l or air l e ak on c oug hi ng). Unl ess l ong term ve nti l a ti on i s nece ssary, a drain i ns erted for a pne umothorax shoul d usually be l e ft in si tu duri ng IPPV. Remove d rain at end-exp i rati on. Cov er hol e w i th thi ck gauze and El as top l as t; a p urs e-s tri ng sut ure i s not usual l y nece ss ary . Re peat C XR i f i nd i cated by det eri orati ng cl i ni cal si gns or b l ood gas anal ysi s.

Complications Morb i d i ty as soc i at ed wi t h c hes t d rai nag e m ay be up t o 10%. Punc ture of i nt erc ost al ves sel may c aus e si gni fi cant b l ee di ng. Consi d er (i ) corre cti ng any coagul op athy, (i i ) pl a ci ng d eep tensi on sut ure s around drain or (i i i ) rem ovi ng drain, i nse rti ng a F ol e y cathe ter, i nfl at i ng the bal l oon and appl yi ng t racti on to tam ponade bl e edi ng ves sel . If t hes e m eas ure s fai l , c ont act (t horaci c) surgeon. Punc ture of l ung ti ss ue may cause a b ronchopl e ural fi s tul a. If che st drain suc ti on (up to 15–20c mH 2 O) fai l s, cons i d er (i ) pl eurode si s (e .g. wi t h t et rac ycl i ne ), (i i ) hi gh frequenc y je t v ent i l ati on ± doubl e-l ume n e ndobronchi al tub e, or (i i i ) s urgery. Ext ubate i f feas i bl e. Perforati on of m ajor v ess el (oft en fat al )—cl amp but d o not remove drain, re sus ci tat e w i th bl ood , c ont act surgeon, c ons i d er doubl e -l umen end otrac heal t ube. Infe ct i on—take c ul tures; anti b i ot i c s (s tap hyl oc occ al ± anaerobi c c ove r); consi der re mov i ng /re si t i ng d rai n. Loc al di s com fort/p ai n from pl e ural i rri tati on m ay i mp ai r cough. C ons i de r s i mp l e analge si a , s ubc utaneous l i d ocaine , i nst i l l i ng l ocal anae stheti c, l ocal or re gi onal anaes the si a , e tc. Drain di s l od gem ent —i f ne ede d, rep l ac e/resi te new drai n, d ependi ng on c l e anl i ne ss of si t e. Don't adv anc e ol d drain (i nfec ti on ri sk ). Lung entrapm ent /i nfarcti on—avoi d mi l ki ng d rai n i n p neumot horax. P.43

See also: IPPV—c omp l i cat i ons of ve nti l a ti on, p14; Hi gh freq uency venti l at i on, p 20; Pl e ural aspi rat i on, p 44; Bas i c res us ci t ati on, p270; Pne umot horax, p300; Haemothorax , p 302 P.44

Pleural aspiration Drai nage of fl ui d from t he pl e ural s pac e usi ng e i t her a need l e, cannul a or fl e xi b l e small -bore d rai n. Incre asi ngl y bei ng performed under ul trasound gui dance. Bl ood/pus usuall y requi re s l arg e-b ore drai n i nserti on.

Indications Improve ment of b l ood g ases Symp tom ati c i mp rov ement of d ysp noe a Di a gnosti c ‘ tap ’

Contraindications/Cautions Coag ul opat hy

Complications Punc ture of l ung or subdi ap hragmat i c vi sce ra Bl e edi ng

Fluid protein level Protei n > 30g /l (thi s shoul d be vi ewe d i n t he c ont ext of the p l as ma protei n l eve l )-exud ate —cause s: i nfl am mat ory e. g. pne umoni a , p ul m onary embol us, neop l as m, col l a gen vas cul ar di seases

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Protei n < 30g /l -transudat e—c aus es: (i ) i ncreas ed venous press ure (e. g. heart fai l ure, fl ui d ove rl oad ), (i i ) de cre ase d col l oi d osm oti c p res sure (e.g . c ri t i c al i l l nes s l eadi ng t o reduced pl asm a prot ei n from c api l l ary l e ak and hep ati c dys functi on, he pat i c fai l ure, ne phroti c s ynd rom e)

Technique 1. Confi rm prese nce of effus i on by CXR or ul trasound. 2. Sel ect drai nage si te ei t her by maxi m um are a of st ony dul l ness under pe rc uss i on or under ul trasound gui dance. 3. Use ase pti c t ec hni que . Cl ean area wi t h anti sep ti c and i nfi l t rat e l ocal s ki n and s ubc ut aneous ti ssues wi t h 1% l i d ocaine . Advance i nto dee per ti ssues, as pi rat i ng to confi rm abs enc e of bl ood then i nfi l t rati ng w i th l ocal anae stheti c unt i l pl e ura i s pi erced and fl ui d c an be aspi rated . 4. Adv anc e drai nag e ne edl e/c annul a /drai n sl owl y, app l yi ng gentl e suct i on, t hrough chest wal l and i ntercos tal sp ace (above upp er border of ri b t o av oi d ne urovas cul ar bundl e) unti l fl ui d can be as pi rate d. 5. Wi t hdraw 50ml for m i c rob i ol ogi cal (M , C &S, TB st ai n, e tc. ), bi oche mi c al (prote i n, gl uc ose, et c.) and hi s tol ogi cal /cy tol ogi cal (p neumoc yst i s , mali gnant cel l s, et c.) anal y si s as i ndi cat ed. 6. Ei t her l e ave drai n in s it u conne cte d t o d rai nag e b ag or connec t needl e/c annul a by 3-way tap to drai nage apparat us . 7. Cont i nue aspi rati on/d rai nag e unti l no furt her fl ui d can b e w i thdrawn or i f pat i ent b ecomes sy mpt omat i c (pai n/d ysp noe a). Dys pnoea or hae mody nam i c change s m ay occ ur due to re moval of l arg e v ol umes of fl ui d (>1–2l ) and s ubs equent fl ui d shi ft s; i f thi s i s consi d ere d t o b e a pos si bi l i ty , remove no m ore than 1l at a t i me ei t her by cl amp i ng /dec l a mpi ng drain or rep eat i ng ne edl e aspi rat i on after an eq ui l i b rat i on i nterval (e .g. 4–6h). 8. Remove need l e/drain. Cover punct ure si te wi t h fi rml y app l i ed gauze d re ssi ng.

See also: Che st drain i ns erti on, p42; Ac ute chest i nfec ti on (1), p288; Acute c hes t i nfect i on (2), p 290; Pul monary e mbol us , p308; Heart fai l ure—asse ssm ent , p 324; He art failure —manage ment, p326; Rheumat i c di s orders, p492; Vasc ul i ti des , p494 P.45 P.46

Fibreoptic bronchoscopy Indications Diagnostic Col l ec ti on of mi crobi ol ogi c al ± c ytol og i cal s pec i m ens (by bronc ho- al veol ar l a vag e, p rotec ted brush sp eci men, bi opsy ). Caus e of b ronchi al obs truct i on (e. g. cl ot, forei gn b ody , neop l as m). Exte nt of i nhal a ti on i njury . Di a gnosi s of ruptured trachea/bronchus.

Therapeutic Cl earance of sec ret i ons, i nhal ed v omi tus , e tc . Removal of l umen-obs truct i ng matte r (e.g. mucus pl ug , bl ood cl ot , food, tooth). Proxi m al obs tructi on rat her t han cons ol i dati on i s s ugg est ed by the radi ol og i c al appe arance of a col l ap sed l ung/l ob e and no air bronc hog ram . Cl eansi ng —re movi ng soot or othe r t oxi c m ate ri al s , i rri gati on w i th saline. Di rect ed phy si othe rap y ± saline t o l oos en sec ret i ons. Di rect ed pl a cem ent of bal l oon c at het er to arrest pul monary b l ee di ng. To aid di ffi c ul t e ndotrache al i nt ubati on.

Contraindications/cautions Coag ul opat hy Seve re hyp oxaemi a

Complications Hypoxae mi a —from suc ti on, l os s of PEEP, part i al ob struct i on of endot rac heal t ube and non-d el i ve ry of t i d al vol ume.

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Haem ody nam i c di s turbance i ncl udi ng hype rte nsi on and tachy cardi a (rel a ted to hy pox aemi a, agi tat i on, t rache al sti mul ati on, et c.). Bl e edi ng. Perforati on (unusual t hough more c omm on i f b i opsy tak en).

Procedure It i s di ffi cul t t o p erform fi bre opt i c bronc hos cop y i n a nas al l y i nt ubated pat i e nt. A narrow -l umen sc ope can be us ed but suc ti on i s l i m i t ed. 1. Pre-oxy genate wi t h FIO 2 1.0. Moni t or wi t h p ul s e oxi m etry. 2. Inc rease pre ssure al a rm l i m i t on venti l at or. 3. Lub ri c ate sc ope wi th l ub ri cant g el /sal i ne . 4. If uni ntubat ed, app l y l i doc ai ne g el to nares ± sp ray to phary nx. 5. Cons i de r s hort-term IV s edati on ± paral ysi s. 6. Ins ert sc ope nasal l y (i n a non-i nt ubated pati e nt) or through cat het er mount port i n an i ntubat ed pat i ent. An ass i st ant shoul d s upp ort the e ndotrache al tub e d uri ng the proc edure t o m i ni mi se trauma to bot h t rache a and scope. 7. Inje ct 2% l i doc ai ne i nto trachea to p re vent coughi ng and haem ody nami c effe cts from trache al /cari nal sti mul ati on. 8. Perform thorough i nsp ect i on and any nece ssary proced ure s. If SpO 2 ≤85% or haem odynami c d i s turbance occ urs , remove scope and al l ow re -oxy genati on before conti nui ng. 9. Bronchoal veol ar l a vag e i s p erform ed b y i ns ti l l at i on of at l e ast 60ml of (preferabl y w arm ) i sot oni c s al i ne i nto affe cte d l ung area wi t hout s uct i on, fol l owe d b y as pi rat i on i nto a s teri l e c athete r t rap . Al l bronc hos cop i c sam pl e s shoul d be sent p rom ptl y t o t he l ab . 10. Reducti on of effect i ve end otrac heal t ube l umen and sucti on may affec t t he t i d al vol ume , l eadi ng to hyp oxaemi a and/or hyp erc apni a. 11. Aft er proced ure , rese t v ent i l a tor as ap propri at e. P.47

Chest physiotherapy The ai m i s t o e xpand c ol l ap sed al veol i , mobi l i se chest se creti ons or re -i nfl a te col l ap sed l ung seg ments. No sc i enti fi c val i dati on of e ffe cti veness has b een rep orted . The c urrent v i ew i s that routi ne ‘ prophy l ac ti c’ suc ti oni ng/ bag gi ng shoul d be av oi d ed i n the cri ti cally i l l .

Indications Mobi l i sat i on of se cre ti ons. Re-e xpansi on of c ol l ap sed l ung/l ob es. Prop hyl axi s agai ns t alve ol a r c ol l aps e and sec ond ary i nfec ti on.

Contraindications/cautions Agg res si v e hype ri nfl a ti on i n alread y hy peri nfl a ted l ungs , e .g. ast hma, e mphyse ma—though can be ve ry use ful i n removi ng m ucus p l ugs. Undrai ned pne umothorax . Rai s ed i nt racrani a l p res sure.

Techniques Hyperinflation Hyp eri nfl at i ng to 50% ab ove venti l at or-del i ve red V T , ai mi ng to e xpand col l ap sed al veol i and mobi l i s e s ecreti ons . V T i s rarel y m easure d, s o e i t her exc ess i v e or i nad equate hyp eri nfl at i ons m ay b e g i ve n d epe ndi ng on l ung c ompl i a nce and ope rat or tec hni que. Pres sure-l i m i ti ng dev i ce s (‘bl ow-off val ves ’) or manomet ers c an avoi d e xce ssi ve ai rway pre ss ure s. A recomme nded te chni q ue i s sl ow i nsp i rati on, a 1–2s pl ate au phase and then rap i d rel eas e of the b ag to si mul ate a ‘ huff’ and mobi l i se se creti ons . Pre-oxyg enati on m ay b e need ed as PEEP may b e l ost and t he d el i vered V T may be i nadeq uat e. Cardi a c outp ut oft en fal l s wi t h v ari abl e b l ood p res sure and heart rat e resp ons es. Sedat i on may bl unt the haemodynami c resp ons e. Ful l d efl ati on avoi ds ai r t rap pi ng.

Suction Rem ovi ng sec ret i ons from trachea and mai n b ronchi (usual l y ri ght). A cough refl ex may be st i m ul a ted to mob i l i se

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sec ret i ons furthe r. Tenaci ous se cre ti ons may be l oose ned by i ns ti l l a ti on of 2–5 ml 0.9% s al i ne. Fal l s i n SaO 2 and cardi ovas cul ar di sturb anc e may b e av oi d ed by pre -ox ygenati on.

Percussion and vibration Drummi ng and shaki ng act i ons over chest wall to mob i l i se se cre ti ons.

Inspiratory pressure support (Bird ventilator) The ai m i s t o i ncreas e FRC and exp and col l a pse d alve ol i .

Postural drainage Pat i ent p osi ti oni ng to ass i st drai nage —de pends on affe ct ed l ung area(s).

See also: End otracheal i ntubat i on, p 36; Ches t p hys i othe rap y, p 48; At el ect asi s and pul monary col l a pse , p 284; Haem opt ysi s, p304; Inhal a ti on i njury, p306 P.48

Complications Hypoxae mi a —from suc ti on, l os s of PEEP, et c. Haem ody nam i c di s turbance affect i ng cardi ac out put, heart rat e and b l ood p res sure whi ch may be rel ate d t o hi gh V T , ai rway pres sure, hyp oxae mi a , agi t ati on, trac heal s ti m ul a ti on, etc . Di rect traum a from sucti oni ng. Barotraum a/vol ut rauma i ncl udi ng p neumot horax.

General Ade quat e humi di fi c ati on avoi ds te nac i ous s put um and mucus pl ugs . Pai n rel i ef i s i mp ort ant to encourag e g ood che st exc ursi on and c oug h. Mobi l i sat i on and e ncouragi ng d eep breat hi ng m ay avoi d i nfe cti on.

When to request urgent physiotherapy Col l aps ed l ung/l obe wi th no ai r bronc hog ram vi si bl e , i .e. sugge sti ng proxi m al obs truct i on rathe r t han cons ol i dati on. Mucus p l uggi ng causi ng s ubs egm ent al col l ap se e.g . asthma.

When not to request urgent physiotherapy Cl i ni c al si g ns of che st i nfect i on wi th no sec ret i ons bei ng produc ed. Radi ol ogi cal consol i d ati on wi t h air bronc hog ram but no se creti ons prese nt. P.49

See also: Venti l at ory support— ind i c ati ons , p 4; Endot rac heal i ntubat i on, p 36; Trache otomy, p38; Mi ni tracheot omy , p 40; Fi b reopti c bronchosc opy , p 46; Ate l ec tas i s and pul monary c ol l aps e, p284; Ac ut e chest i nfec ti on (1), p288; Acute c hes t i nfect i on (2), p290

Ovid: Oxford Handbook of Critical Care

Ed itors:

Si nge r, M ervyn; We bb, An dre w R.

Ti tle : O xf ord Ha ndbook of Cr itic al Car e, 2nd Ed ition Cop yri ght © 1997,2005 M. Si nge r and A. R. W ebb , 1997, 2005. Publ i shed i n the Uni te d Stat es by Oxford Uni ve rsi ty Press Inc > Tab le of Co n te n ts > Car dio vasc u la r Th e r ap y T ech n i qu e s

Cardiovascular Therapy Techniques Defibrillation El e ct ri c al conversi on of a tachy arrhyt hmi a t o rest ore normal s i nus rhy thm . Thi s may be an eme rg enc y proc edure (when t he ci rcul at i on i s ab sent or s eve rel y c omp rom i s ed), se mi -el e cti ve (when t he ci rcul at i on i s c ompromi se d t o a

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l es ser d egree), or el ect i ve (w hen synchroni se d c ard i ov ers i on i s p erform ed t o rest ore s i nus rhyt hm for a non-compromi si ng s uprave ntri c ul a r t achycardi a). Sy nchroni s ati on req ui res i ni ti al connec ti on of ECG l eads from t he pat i ent t o t he defi bri l l at or so that t he shock i s del i ve red on the R wav e t o mi ni mi s e t he ri s k of v ent ri c ul a r fi b ri l l at i on. New er, bi phasi c de fi b ri l l a tors req ui re approxi mat el y half the ene rgy se tti ng of monophasi c d efi bri l l ators.

Indications Comp rom i se d c i rcul ati on, e. g. VF, VT Rest orati on of s i nus rhy thm and more effect i ve cardi ac out put Les sens ri sk of cardi ac thromb us format i on

Contraindications/cautions Aware p ati ent Seve re coagul opathy Caut i on wi th rec ent thrombol ys i s Di g oxi n l eve l s i n tox i c range

Complications Surfac e b urn Peri cardi al tam ponade El e ctrocuti on of b yst and ers

Technique (se e algori t hm opp osi te). The chance s of m ai ntai ni ng s i nus rhy thm are i ncreas ed i n el e cti ve cardi oversi on i f K + >4.5mmol /l and p l as ma Mg 2+ l evel s are normal . Pri or to defi bri l l at i on, e nsure sel f and onl ooke rs are not i n c ont act wi th pat i ent or b ed frame. To reduce the ri sk of sup erfi c i al burns , repl ace ge l /g el l ed pad s afte r e very 3 shocks . Cons i de r res i ti ng pad dl e posi t i on (e .g. anteroposte ri or) i f defi bri l l at i on fails . The ri sk of i nt rac tab l e VF fol l ow i ng de fi b ri l l a ti on i n a pat i e nt rec ei v i ng di gox i n i s small unl es s t he pl a sma di g oxi n l evel s are i n the t oxi c rang e or t he p ati ent i s hypovol aemi c. P.53

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Figure. No Caption Available.

See also: Chronotropes , p 206; Sedati v es, p238; Cardi ac arrest , p 272; Tachy arrhyt hmi as, p316; Hyp okalae mi a , p422 P.54

Temporary pacing (1) Whe n t he heart' s i ntri nsi c pacem aki ng abi l i ty fai l s, te mporary i nte rnal or e xte rnal p aci ng can be i nsti tuted . Inte rnal el e ctrod es c an be end ocardi al (i nserte d vi a a ce ntral vei n) or epi cardi al (pl ace d on the e xte rnal s urface of the he art at thorac otomy). T he e ndocardi al wi re m ay b e p l ac ed und er fl uoroscopi c c ont rol or ‘b l i nd’ us i ng a b al l oon fl ot ati on cat het er. Ex ternal paci ng can be rap i d l y performed by pl a cem ent of two el ect rodes on the front and rear chest wall whe n asys tol e or t hi rd d egree heart bl ock has produced ac ute haemod ynami c compromi se. It i s often us ed as a b ri d ge to tem porary i nternal paci ng. It can al so be use d as a prophyl a cti c m eas ure , e .g. for M obi tz Typ e II s econd-d egree heart bl ock.

Indications Thi rd-deg ree heart bl ock Mobi tz Typ e II s econd-deg ree he art bl ock when t he ci rcul at i on i s compromi sed or an ope rat i on i s p l anned Overpac i ng (rarel y ; more suc ces sful wi t h i nte rnal p aci ng) Asy stol e

Complications Internal pacing As for ce ntral venous cathe ter i nserti on Arrhyt hmi as Infe ct i on (i ncl udi ng end ocardi ti s) Myoc ard i al p erforati on (rare)

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External pacing Di s com fort

Troubleshooting Fai l ure t o p ace may be due t o: 1. No p ace mak er spi kes se en—che ck connec ti ons, check batte ry. 2. No c apt ure (p aci ng spi kes but no QRS com pl e x fol l owi ng)—poor pos i ti oni ng/di s l odgem ent of wi re. Te mporari l y i nc rease out put as thi s may re gai n c apt ure . Re pos i t i on/re pl a ce i nt ernal pac i ng wi re.

General 1. Chec k t hre shol d dai l y as i t wi l l ri s e s l owl y ove r 48–96h, probabl y due t o fi brosi s occurri ng around t he el ec trode s. 2. Overpac i ng i s occasi onal l y i ndi c ate d for a tachy cardi a not res pondi ng t o anti arrhyt hmi c t herapy or cardi ove rs i on. For SVT, pac i ng i s us ual l y att emp ted wi th the wi re si t ed i n the ri ght at ri um. Pace at rat e 20–30bpm ab ove pati ent's he art rate for 10–15s, the n ei ther dec rease rat e i mme di a tel y t o 80bp m or sl owl y, by 20b pm every 5–10s. 3. If overpac i ng fail s, und erp aci ng may be att emp ted wi th the wi re si t uat ed i n ei t her at ri um (for SVT) or, us ual l y , vent ri cl e (for ei t her SVT or VT). A pac ed rat e of 80–100b pm m ay produc e a re fractory peri od suffi ci e nt to sup pre ss the i ntri ns i c tac hyc ard i a. 4. Epi cardi a l p aci ng performed duri ng c ardi a c s urg ery re qui re s s i ti ng of ei t her tw o e pi c ard i al el ect rodes or one epi cardi a l and one ski n el e ctrode (us ual l y a hypodermi c ne edl e). The p aci ng threshol d of ep i cardi al wi res ri ses qui ckl y and m ay bec ome i neffe cti ve aft er 1–2 days. 5. In asys tol e, an el e ctri c al rhy thm produced by paci ng d oes not g uarant ee an adeq uat e c ard i ac output i s b ei ng gene rat ed. P.55

See also: Tem porary paci ng (2), p56; Chronot ropes , p 206; Cardi ac arres t, p272; Brad yarrhy thm i as , p 318 P.56

Temporary pacing (2) Technique (for endocardial electrode placement) 1. If usi ng fl uoroscopy, mov e p ati ent to X-ray sui te or pl ace l e ad shi el d s around bed area. Pl ace pati e nt on ‘sc ree ni ng t abl e’. St aff shoul d w ear l e ad aprons . 2. Use ase pti c t ec hni que throughout. Insert 6Fr she ath i n i nternal jugul ar or subcl avi an vei n. Sut ure i n posi t i on. 3. Connect paci ng w i re el ect rodes to pac i ng box (bl a ck = ne gat i ve pol ari t y = di s tal, red = p osi ti ve pol ari ty = proxi m al ). Set p ace mak ert o d emand. Che ck box i s worki ng and bat tery c harge ade quate. Turn pac i ng rate to ≥30b pm above p ati ent 's i ntri ns i c rhy thm . Set vol tag e t o 4V. 4. Ins ert paci ng w i re through she ath i nto central v ei n. If usi ng b al l oon c atheter, i ns ert to 15–20cm dep th the n i nfl at e b al l oon. Advance cat het er, vi ewi ng ECG moni t or for chang e i n ECG morphol og y and c apt ure of paci ng rat e. If usi ng screeni ng , d i re ct wi re t oward the ap ex of t he ri ght ventri cl e. App rox i mate i ns erti on d ept h from a neck ve i ni s 35–40c m. 5. If p aci ng i m pul ses not c apt ure d, (defl at e b al l oon), wi t hdraw wi re t o 15cm i nserti on d ept h t hen re peat s tep 4. 6. Onc e paci ng cap tured, de cre ase vol tage b y d ecreme nts to de termi ne t hre shol d at whi ch pac i ng i s no l onge r capt ured. Id eal pos i t i on de termi ned by a t hre shol d ≤0. 6V. If not ac hi eved , re-p osi ti on w i re. 7. If p oss i b l e, as k pati ent to cough to che ck that w i re does not di sl odge . 8. Set vol tage at 3 × threshol d and s et des i re d heart rate on ‘d emand’ mod e. Tap e wi re se curel y to pati e nt to pre vent di sl odg ement.

Technique (for external pacing) 1. Connect paci ng w i re ge l l ed e l ec trode s t o pacem ake r. Pl a ce bl a ck (= negati v e p ol a ri t y) el e ctrode on the ante ri or ches t wal l t o t he l eft of the l owe r s ternum and red (= p osi ti ve p ol a ri ty) el e ct rod e t o the c orres pondi ng p osi ti on on t he pos teri or hemi thorax . 2. Connect EC G e l ec trodes from ECG moni t or to exte rnal pac emak er and another set of el e ct rod es from pacem ake r to p ati ent

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3. Set pac emaker to de mand. T urn p aci ng rat e t o ≥30bp m abov e pati ent 's i nt ri nsi c rhyt hm. Se t c urrent t o 70mA. 4. Start pac i ng . Increas e c urrent (b y 5mA i nc re ment s) unt i l paci ng rate captured on moni t or. 5. If p aci ng rate not cap tured at curre nt of 120–130mA re si t e e l ec trodes and repe at ste ps 3–4. 6. Onc e paci ng cap tured, se t c urrent at 5–10m A abov e t hre shol d. P.57

See also: Tem porary paci ng (1), p54; Chronot ropes , p 206; Cardi ac arres t, p272; Brad yarrhy thm i as , p 318 P.58

Intra-aortic balloon counterpulsation Principle A 30–40ml ball oon i s pl ace d i n t he des cendi ng aort a. The bal l oon i s i nfl at ed wi t h hel i um duri ng di ast ol e, t hus i nc re asi ng di a stol i c b l ood pres sure above the b al l oon. T hi s se rve s t o i nc rease c oronary and cerebral perfusi on. The bal l oon i s d efl ate d d uri ng sy stol e, thus dec reasi ng p eri phe ral resi stance and i ncreas i ng s troke v ol ume. No pharmacol ogi cal t echni q ue exi sts whi ch can i ncreas e c oronary b l ood fl ow whi l e re duc i ng pe ri p heral re si s tance. Int ra-aorti c b al l oon count erp ul s ati on may i m prove cardi a c p erform anc e i n s i tuati ons where drugs are i neffec ti ve.

Indications The most obv i ous i ndi cat i on i s t o s upp ort the c i rc ul ati on where a st ruc tural cardi ac defect i s to be re pai red surg i cally . How ever, i t may be use d i n acut e c i rcul atory fai l ure i n any si t uat i on where re sol uti on of the cause of the card i ac dys functi on i s exp ect ed. In ac ute my ocardi al i nfarc ti on, re sol uti on of peri -i nfarct oe dem a may allow s pontaneous i mp rov eme nt i n myocardi a l func ti on; the us e of i ntra-aort i c bal l oon c ounterpul sati on m ay p rov i de te mporary ci rcul at ory support and promote myoc ardi a l heal i ng by i m provi ng m yoc ard i al bl ood fl ow. Ot her i ndi c at i ons i ncl ude acute myocardi t i s and poi s oni ng wi t h my ocardi al de pre ssants . Intra-aort i c bal l oon c ounterpul sati on s houl d not be use d i n aort i c re gurgi t ati on si nce the i ncreas e i n d i as tol i c bl ood press ure woul d i ncre ase re gurgi t ant fl ow.

Insertion of the balloon The us ual route i s vi a a fe moral art ery . Perc utaneous Sel di nger cathe teri s ati on (wi th or wi t hout an i ntroducer sheat h) provi d es a rapi d and safe t echni q ue wi t h m i ni mal arteri a l t rauma and bl eedi ng . Open surgi cal cathe teri s ati on may be nec ess ary i n el derl y pat i e nts wi th atheromat ous di sease. The ball oon pos i t i on shoul d b e c hec ked on a C XR t o e nsure that t he rad i o-opaque ti p i s at t he l ev el of t he 2nd i ntercostal s pac e. Ens ure the l eft radi a l p ul s e i s not l ost.

Anticoagulation The prese nce of a l arge fore i g n body i n the aorta re qui res s yst emi c anti coagul ati on to pre vent t hrombosi s . T he bal l oon s houl d not be l e ft defl at ed for l onge r t han a m i nute whi l e in si tu othe rwi se thromb osi s m ay occ ur des pi t e ant i c oagul at i on.

Control of balloon inflation and deflation Hel i um i s used to i nfl a te t he bal l oon, i t s l ow d ens i t y faci l i t ati ng rapi d trans fer from pum p t o ball oon. Infl ati on i s com monl y ti m ed to the ‘R’ wave of t he ECG, althoug h t i mi ng may be taken from an arte ri a l p res sure wave form. Mi nor adj ust ment m ay b e m ade to the t i mi ng to ens ure that i nfl at i on oc curs i mme di atel y afte r c l osure of the aort i c val ve (after the d i croti c not ch of t he art eri al press ure waveform) and d efl ati on occ urs at the e nd of d i as tol e. The fi l l i ng vol ume of the ball oon can be vari e d up t o t he maxi mum balloon vol ume . T he g re ater t he fi l l i ng v ol ume, the g reater the ci rc ul a tory augm ent ati on. The rate at whi ch bal l oon i nfl at i on oc curs m ay coi nci de wi t h e very c ard i ac be at or eve ry 2nd or 3rd c ard i ac be at. Sl owe r rate s are nec ess ary i n tachy arrhyt hmi as . W eani ng of i nt ra-aorti c b al l oon counte rpul s ati on may be achi ev ed by red uci ng aug mentat i on or the rate of i nfl at i on. P.59

See also: Hyp ote nsi on, p312; He art fai l ure—ass ess ment, p324; Heart fai l ure—manag eme nt, p326; Pos t-operati ve i nt ens i ve care, p534

Ovid: Oxford Handbook of Critical Care

Ed itors:

Si nge r, M ervyn; We bb, An dre w R.

Ti tle : O xf ord Ha ndbook of Cr itic al Car e, 2nd Ed ition Cop yri ght © 1997,2005 M. Si nge r and A. R. W ebb , 1997, 2005. Publ i shed i n the Uni te d Stat es by Oxford Uni ve rsi ty Press Inc > Tab le of Co n te n ts > Ren al Th e r ap y Tec h n i qu e s

Renal Therapy Techniques Haemo(dia)filtration (1)

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The se are al ternat i ve s t o d i al ysi s that requi re a pre ssuri sed , p uri fi e d w ate r s upp l y, more expe nsi ve equi pm ent and ope rat or exp ert i s e, and a g reater ri sk of hae mody nam i c i nstabi l i t y due t o rapi d fl ui d and osm oti c s hi fts . Hae mo(d i a)fi l trati on can be arteri ov enous, us i ng the p ati ent 's bl ood pre ss ure to dri ve bl ood through the hae mofi l t er, or pum ped ve no-v enous. The l att er i s adv ant age ous i n that i t i s not de pendent on t he p ati ent 's bl ood press ure and the pump sys tem i ncorporate s alarms and safet y feature s. Veno-ve nous haem o(di a)fi l t rati on i s i ncreas i ngl y the tec hni que of choi c e. Bl ood i s us ual l y drawn and ret urned vi a a 10–12F r d oub l e l um en central v enous cat het er.

Indications Azotae mi a (uraem i a) Hype rkalae mi a Anuri a /ol i guri a; t o m ake sp ace for nutri ti on Seve re met abol i c ac i d osi s of non-t i s sue hyp ope rfusi on ori gi n Fl ui d overl oad Drug removal Hypothe rmi a/hype rtherm i a

Techniques Num erous i nc l udi ng haemofi l trati on, haemodi a fi l trati on, ul trafi l trati on, conti nuous ul t rafi l trati on w i th i ntermi tte nt di a l ys i s (CUPID ). Fi l trate i s us ual l y rem oved at 1–2l /h and fl ui d bal anc e adjuste d b y varyi ng the fl ui d repl ace ment rat e. Hi g h v ol ume hae mofi l t rat i on i nvol ves much hi g her cl earances (e. g. 35l i n a 4h peri od ) t hough vari ab l e out com es are re ported i n randomi s ed st udi es. Cre ati ni ne and pot ass i um cl earanc es are hi gher wi t h d i afi l t rat i on t houg h fi l trati on alone i s usuall y suffi ci ent provi ded an ade quate ul t rafi l t rate v ol ume i s achi ev ed (1000m l /h = c reati ni ne c l earance of 16ml /mi n).

Membranes Usual l y p ol y acryl oni tri l e , pol yami d e or p ol y sul phone. May b e hol l ow fi bre or fl at -pl at e i n de si gn. Surface are a us ual l y 0.6–1m 2 .

Replacement fluid A b uffere d b al a nce d e l ec trol yt e s ol uti on i s gi v en to buffer aci dae mi a and achi eve the d esi red fl ui d balance. Buffe rs i nc l ude l ac tat e (m etabol i s ed b y l i v er to b i c arb onate), ac etate (me tab ol i sed by mus cl e), and bi carbonat e. Ace tat e causes the m ost haemod ynami c i nst abi l i t y and i s rarel y used i n the c ri t i c al l y i l l . Bi carbonat e s ol uti ons may be more effi ci ent than l ac tat e at reve rsi ng se vere me tab ol i c aci dos i s, but outc ome benefi t has yet to be de mons trate d from i t s use and c are i s ne ede d wi th co-adm i ni st ere d c al c i um si nc e calc i um bi carbonate may crys tal l i s e. In l i ver fai l ure a l ac tat e b uffer may not be ad equate l y met abol i s ed. Si mi l arl y, i n poor perfus i on st ate s, the muscl e m ay not be abl e t o met abol i s e an acet ate buffer. An i ncre asi ng met abol i c al kal osi s m ay be due to exc ess i ve buffe r. In thi s c ase , use a ‘ l ow l a ctate’ (i .e. 30mmol /l ) rep l ac eme nt fl ui d . Potas si um c an be add ed, i f ne ces sary, to mai ntain normokalae mi a . Havi ng 20m mol KCl i n a 4.5l bag provi des a concentrati on of 4.44mmol /l . K + cl earanc e i s i ncreas ed by dec reasi ng t he concentrati on wi t hi n the rep l ac eme nt fl ui d or the di al ysate. P.63

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Figure. No Caption Available.

Key trials Ronco C, e t al. Effect s of d i ffere nt dos es i n conti nuous v eno-venous haemofi l trati on on outc ome s of ac ute re nal fai l ure: a p ros pec ti ve rand omi sed tri a l . Lancet 2000; 356:26–30 Bouman CS, e t al. Effe ct s of earl y hi gh-vol ume conti nuous venovenous he mofi l t rati on on s urv i val and rec overy of renal functi on i n i ntensi v e c are pati e nts wi th acute renal fai l ure: a p ros pec ti v e, random i ze d t ri al . Cri t C are Me d 2002; 30:2205–11

See also: Hae mo(d i a)fi l trati on (2), p64; Coagul ati on moni t ori ng, p156; Ant i c oagul ants , p 248; Ol i guri a, p 330; Ac ute re nal fai l ure—di a gnosi s , p 332; Ac ute re nal fail ure —manage ment, p334; M etabol i c aci dos i s , p 434; Met abol i c alkalos i s, p436; Poi soni ng —ge neral pri nc i pl es p324; Me tab ol i c aci d osi s, p434; Metabol i c al kal osi s, p436; Poi s oni ng—general pri nc i pl es, p452; Rhab dom yol ysi s, p528 P.64

Haemo(dia)filtration (2) Anticoagulation Ant i coagul at i on of the c i rc ui t i s usually wi th unfrac ti onat ed hep ari n (200–2000IU/h), or a pros tanoi d (prost acyc l i n or PG E 1 ) at 2–10ng/kg /mi n, or a c omb i nati on of t he two. Li tt l e exp eri enc e i s avai l ab l e on the us e of l ow mol ecul ar we i ght hepari n, c i t rat e and othe r anti coagul ants suc h as hi rudi n. No anti coagul ant may b e neede d i f t he pat i ent i s auto-anti c oag ul a ted . Prem ature cl ott i ng may be due t o m echani cal ki nki ng/obs truct i on of the ci rc ui t , i nsuffi ci ent anti c oag ul a ti on,

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i nadequate bl ood fl ow rat es or to l ac k of endog enous ant i coagul ants (anti t hrombi n III, hepari n cofac tor II). Usual fi l ter l i fes pan shoul d b e at l eas t 2 days but i s often dec re ased i n s ept i c pat i ents due to de cre ase d endogenous anti c oag ul a nt l ev el s . In t hi s s i tuati on, consi der use of fres h froz en pl a sma, a sy ntheti c p rot eas e i nhi bi tor such as aproti ni n, or ant i throm bi n III rep l ac eme nt (cos tl y).

Filter blood flow Fl ow t hrough the fi l t er i s us ual l y 100–200ml /mi n. Too sl ow a fl ow rat e promotes cl ot ti ng. Too hi gh a fl ow rat e w i l l i nc re ase trans memb rane p res sures and d ecreas e fi l t er l i fesp an wi t hout s i gni fi cant i mp rov eme nt i n cl e arance of ‘mi ddl e m ol e cul es ’ (e .g. urea).

Complications Di s connec ti on l ead i ng to haemorrhage . Infe ct i on ri sk (st eri l e tec hni que must be emp l oy ed). El e ctrol y te, ac i d–bas e or fl ui d i mbalance (ex ces s i nput or removal ). Haem orrhag e (vas cul ar acc ess si te s, pept i c ul cers) rel ate d t o anti coagul ati on therapy or c ons ump ti on coag ul opat hy. He pari n-i nd uc ed t hrombocyt ope ni a may rare l y occ ur.

Cautions Haem ody nam i c i ns tab i l i ty re l at ed to hyp ovol aem i a (es pec i al l y at start ). Vas oac ti v e d rug re moval b y t he fi l ter (e .g. catec hol ami nes ). Memb rane b i oc omp ati bi l i t y p rob l em s (esp eci al l y w i th cuprophane). Drug d osages may ne ed to b e revi sed (c ons ul t pharmaci st ). Ami no aci d l oss es throug h t he fi l ter. Heat l oss l e adi ng to hypothe rmi a. Mask i ng of py rex i a P.65 P.66

Peritoneal dialysis A s l ow form of di a l ys i s, ut i l i si ng the pe ri toneum as the di al y si s me mbrane . Sl ow correct i on of fl ui d and el ect rol yt e di s turbance may be be tte r t ol e rat ed by cri ti cal l y i l l p ati ent s and the te chni que d oes not requi re compl ex equi pm ent . How ever, tre atm ent i s l a bour i nte nsi ve and there i s consi derab l e ri s k of p eri toneal i nfec ti on. It has be en l argel y sup ers ede d b y haem ofi l trati on i n mos t i nt ens i ve care uni ts.

Peritoneal access For ac ute pe ri t one al di a l ys i s a t rochar and cannul a are i ns ert ed throug h a sm al l sk i n i nc i s i on under l ocal anaes the ti c . The sk i n i s prepared and drape d as for any st eri l e proced ure . T he com mone st app roach i s through a s mal l m i dl i ne i nc i s i on 1c m b el ow t he umbi l i cus . T he sub cut ane ous ti ssues and pe ri t one um are punct ure d b y t he trocar whi ch i s wi t hdrawn sl i g htl y b efore t he cannul a i s advance d t owards the p ouc h of Dougl as . In order t o av oi d damag e t o i nt ra-abd omi nal st ructures 1–2l warmed pe ri t one al di a l ys ate may b e i nfused i nto the peri t one um b y a st and ard , s hort i nt ravas cul ar cannul a p ri or t o p l ac eme nt of the trocar and cannul a s yst em. If the mi dl i ne ac ces s s i te i s not avai l ab l e an al t ernati ve i s to use a l at eral approac h, l at eral to a l i ne joi ni ng the umb i l i cus and the anteri or superi or i l i a c s pi ne (av oi d i ng the i nfe ri or e pi g ast ri c v ess el s ).

Dialysis technique Warmed pe ri t one al di a l ys at e i s i nfused i nto the peri t one um i n a vol um e of 1–2l at a t i m e. D uri ng the acut e p has e, fl ui d i s fl ushed i n and drai ned conti nuousl y (i .e. wi th no dwel l ti m e). Onc e b i oc hem i c al control i s achi eve d i t i s usual to l eave fl ui d i n the pe ri t one al cav i ty for 4-6h be fore drai ni ng. Hep ari n (500IU/l ) m ay be adde d t o t he fi rst 6 c ycl es to pre vent fi bri n cat het er bl ock age. There aft er, i t i s onl y nec es sary i f t here i s b l ood or c l oudi ness i n the d rai nag e fl ui d .

Peritoneal dialysate The di al y sat e i s a st eri l e balanced el ect rol yte sol ut i on wi th gl ucose at 75mm ol /l for a s tandard fl ui d or 311m mol /l for a hype rtoni c fl ui d (used for g reater fl ui d remov al ). T he fl ui d i s usual l y p otassi um free s i nce p otass i um exc hanges sl owl y i n pe ri toneal di al y si s , althoug h p otassi um may be add ed i f nec ess ary .

Complications Fl ui d l eak Poor drai nage

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Steroi d therapy Obes e or el de rl y pati e nt Cathete r b l oc kag e Bl ee di ng Omental encas ement Infe ct i on W hi t e c el l s > 50/ml , cl oud y d rai nag e fl ui d Hype rgl yc aemi a Absorpt i on of hy perosm oti c g l uc ose Di a phragm sp l i nti ng

Treatment of infection It i s pos si bl e to st eri l i se the pe ri t one um and cat het er by add i ng ap propri at e anti bi oti c s t o t he di a l ys at e. Sui tab l e reg i me ns i ncl ude: Cefurox i me 500mg /l for 2 c ycl es then 200m g/l for 10 d ays Gent ami ci n 8mg/l for 1 cy cl e dail y P.67

See also: Ol i guri a , p 330; Ac ute re nal failure—di a gnosi s, p332; Ac ute re nal fail ure —manage ment, p334 P.68

Plasma exchange Indications Pl a sma ex change may be us ed to remove ci rcul at i ng toxi ns or t o repl ace mi ss i ng pl asm a fact ors . It m ay b e used i n sep si s (e .g. me ni ngoc occ aem i a). In p ati ent s w i th i m mune me di ated di se ase, pl as ma e xchang e i s usually a tem porary measure w hi l e s yst emi c i mmunos upp res si on take s e ffe ct. There are s ome i mm une me di a ted di seases (e .g. Gui l l ai n–Barré s ynd rom e, t hromboti c t hrombocyt ope ni c purpura) where an i s ol a ted rathe r t han a c ont i nuous ant i body–ant i ge n reac ti on c an be tre ate d w i th earl y pl asm a e xchang e and no fol l ow-up i mmunos upp re ssi on. Most di s eas es req ui re a dail y 3–4l pl asm a ex change re peated for at l eas t 4 further occ asi ons ov er 5–10 d ays .

Techniques Cell separation by centrifugation Bl ood i s se parate d i nto component s i n a ce ntri fuge . Pl as ma (or other spe ci fi c bl ood com ponent s) are di scarde d and a pl a sma re pl a cem ent fl ui d i s i nfused i n eq ual vol ume . C ent ri fugati on m ay be conti nuous w here bl ood i s wi thdrawn and ret urned by sep arate nee dl e s, or i nt erm i t tent where bl ood i s wi thdrawn, sep arated and t hen re turned vi a t he sam e nee dl e .

Membrane filtration Pl a sma i s conti nuous l y fi l tered throug h a l a rge pore fi l ter (m ol e cul ar wei ght cut-off typ i cally 1, 000,000Da). The pl a sma i s di sc ard ed and re pl a ced by i nfus i on of an equal vol ume of rep l ac eme nt fl ui d. The t echni q ue i s si mi l ar to hae mofi l t rat i on and uses the s ame eq ui p ment.

Replacement fluid Mos t p ati ent s w i l l t ol e rat e repl ace ment w i th a pl a sma subst i tute. Our p refere nce i s t o repl ace pl asm a l oss wi th equal vol ume s of 6% hy droxy-ethyl starch and 5% al bumi n. Howev er, some use parti al cry stall oi d re pl a cem ent and ot hers use al l albumi n repl ace ment . Some fresh froze n p l as ma wi l l b e nece ssary aft er the ex change to rep l ac e c oag ul a ti on fac tors. The onl y i nd i c ati on to rep l ac e p l as ma l os s wi th al l fres h frozen pl a sma i s where pl asm a ex change i s be i ng performed to re pl a ce mi s si ng p l asma fac tors.

Complications Ci rcul atory i ns tab i l i ty Intravascul ar vol um e c hanges Re mov al of ci rcul at i ng catec hol ami nes Hypoc al cae mi a Reduced i ntravas cul ar COP If repl ace ment wi th cryst al l oi d

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Infe ct i on Re duc ed pl a sma op soni sati on Bl e edi ng Re mov al of coag ul ati on fac tors P.69

Indications Autoimmune disease Goodpasture' s s ynd rome Gui l l ai n–Barré s ynd rom e Myastheni a g rav i s Pem phi gus Rap i dl y p rog res si ve g l omerul onep hri ti s SLE Thromb oti c t hromb ocyt ope ni c p urp ura

Immunoproliferative disease Cry ogl obul i naem i a Mul ti pl e mye l om a Wal denstrom' s macrog l ob ul i nae mi a

Poisoning Paraquat

Others Meni ng ococcal s ept i c aemi a (pos si bl e benefi t) Sep si s (p oss i b l e benefi t) Rey e's sy ndrome

See also: Coagul ati on moni tori ng, p156; Ant i coagul ants, p248; Gui l l ai n–Barré s yndrome , p 384; Myastheni a g rav i s , p 386; Pl a tel et di sorders, p406; Poi s oni ng—general p ri nci pl e s, p452; Vascul i ti d es, p494

Ovid: Oxford Handbook of Critical Care

Ed itors:

Si nge r, M ervyn; We bb, An dre w R.

Ti tle : O xf ord Ha ndbook of Cr itic al Car e, 2nd Ed ition Cop yri ght © 1997,2005 M. Si nge r and A. R. W ebb , 1997, 2005. Publ i shed i n the Uni te d Stat es by Oxford Uni ve rsi ty Press Inc > Tab le of Co n te n ts > Gas tr oi n te sti n al Th er a py Te ch n iqu es

Gastrointestinal Therapy Techniques Sengstaken-type tube Use d t o m anag e oesophageal v ari ceal haem orrhag e t hat conti nue s d esp i te pharm acol og i cal ± pe r-e ndoscopi c therapy. The de vi c e (Sengst ake n– Bl a kemore or si mi l ar) i s a l arge-bore rubb er tub e usually containi ng two balloons (oe sop hag eal and gastri c ) and t wo furthe r l ume ns (oe sop hag eal and gastri c ) t hat ope n abov e and b el ow t he bal l oons. Thi s d evi ce works usual l y b y t he gas tri c bal l oon al one compress i ng t he vari ce s at t he cardi a . Infl ati on of the oes ophage al bal l oon i s rare l y nec ess ary .

Insertion technique The tubes are usually ke pt i n the fri dg e t o p rov i de ad ded st i ffnes s for easi er i nserti on. 1. The pat i ent ofte n requi res j udi ci ous se dat i on or me chani c al venti l ati on (as warrante d b y c ons ci ous state/l ev el of agi tat i on) pri or t o i nse rti on. 2. Chec k b al l oons i nfl ate prope rl y be forehand. Lubri cate end of tub e. 3. Ins ert vi a m out h. Pl ac e t o d ept h of 55–60cm , i .e. to ens ure gast ri c balloon i s i n st omac h p ri or to i nfl at i on. 4. Infl at e gast ri c balloon wi t h w ate r t o v ol ume i ns tructe d b y m anufact urer (us ual l y ♠200ml ). A s mal l amount of

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rad i o-opaq ue contrast may be add ed. Ne gl i gi bl e re si s tance to i nfl at i on s houl d be fel t . C l am p g ast ri c b al l oon l um en. 5. Pul l t ube bac k unti l res i st anc e i s fel t, i .e . g ast ri c ball oon i s at cardi a. Fi x tub e i n p l ac e b y appl yi ng counter-t rac ti on at t he mout h. Ol d-fashi oned m ethods , s uch as at tac hi ng t he tub e t o a free-hang i ng l i tre b ag of sal i ne , have bee n s upe rse ded by more m anageabl e te chni ques. For e xamp l e, tw o w oode n t ong ue dep res sors, ‘thi ck ene d’ by havi ng El ast opl ast wound around them, are p l ac ed ei t her si de of the tube at t he mouth and then att ached t o e ach ot her at both end s b y more El a stopl ast . T he t ube re mai ns gri pp ed at t he mouth/che ek by t he att ached t ong ue dep res sors b ut can be re tract ed unt i l ade quate b ut not ex ces si ve t rac ti on i s bei ng app l i e d. 6. Perform X-ray to check sati s fac tory p osi ti on of g ast ri c b al l oon. 7. If b l ee di ng c ont i nues (c ont i nued l arge asp i rates from gas tri c or oesophageal l ume ns), i nfl ate oe sop hage al bal l oon (approx 50m l ).

Subsequent management 1. The gas tri c bal l oon i s usuall y ke pt i nfl at ed for 12–24h and defl at ed p ri or to end osc opy ± s cl erothe rap y. T he tracti on on the tube s houl d be tes ted hourl y b y t he nursi ng staff. The oe sop hag eal l umen shoul d b e pl ac ed on cont i nuous d rai nag e whi l e e nte ral nutri ti on and adm i ni st rat i on of drugs can b e g i ve n vi a t he gas tri c l um en. 2. If t he oes ophage al bal l oon i s used , d efl ate for 5–10m i n eve ry 1–2h t o reduce the ri sk of oes ophageal p res sure necros i s. Do not l eav e oe sop hag eal balloon i nfl at ed for l onge r t han 12h after s cl e rot herapy . 3. The tub e m ay need to st ay in si tu for 2–3 days though peri ods of d efl ati on shoul d t hen be al l owe d.

Complications Asp i rati on Perforati on Ul c erati on Oes ophageal necrosi s P.73

See also: Upp er gas troi ntes ti nal hae morrhage, p344; Bl ee di ng v ari ce s, p346 P.74

Upper gastrointestinal endoscopy Oes ophago-gastro-d uod enos cop y i s i de nti cal i n ve nti l at ed and non-v ent i l a ted pati e nts , t hough a p rot ect ed ai rway ± sed ate d s tat us usual l y faci l i tat es the proce dure.

Indications Inve st i gati on of up per gast roi nte sti nal s i gns/s ymp toms . e .g. bl eed i ng , p ai n, m ass , obst ructi on Therape uti c, e. g. s cl erothe rap y for vari ce s, l oc al epi nep hri ne (ad renal i ne) i njec ti on for di s crete bl eed i ng poi nt s, e.g. i n ul ce r b ase Pl ac eme nt of nas ojej unal t ube (w hen gas tri c atony pre vents ent eral feedi ng ) or pe rc utaneous g ast rostomy (PEG) ERCP—unusual i n the IC U p ati ent

Complications Loc al trauma causi ng hae morrhage or p erforati on Abd omi nal di ste nsi on com promi s i ng resp i ratory func ti on

Contraindications/cautions Seve re coagul opathy shoul d i deall y be correct ed

Procedure Upp er gas troi ntes ti nal end osc opy shoul d b e p erform ed b y an e xperi e nce d operator t o mi ni mi s e t he durati on and trauma of the p roc edure, and t o mi ni mi s e g ase ous di ste nsi on of the gut . 1. The pat i ent i s usual l y p l ac ed i n a l ate ral posi t i on t houg h c an be sup i ne i f i ntub ate d. 2. Inc rease FIO 2 and v ent i l ator p res sure alarm s ett i ng s. Consi d er i ncre asi ng sed ati on and ad jus ti ng v ent i l a tor mode .

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3. Moni tor ECG, SPO 2 , ai rway press ures and hae mod ynami c vari a bl e s t hroughout . If p ati ent i s on press ure s upp ort or p re ssure control v ent i l atory m ode s also moni t or ti dal vol ume s. The op erator shoul d c eas e t he proced ure , at leas t temp orari l y, i f the p ati ent be com es comp romi s ed. 4. At the end of the p roc edure the op erator shoul d aspi rat e as m uch ai r as p oss i bl e out of the gastroi ntes ti nal tract to d ecompress the abdomen. P.75

See also: Pul se oxi met ry, p90; Upp er gas troi nt est i nal haem orrhag e, p344; Bl ee di ng v ari ces , p 346

Ovid: Oxford Handbook of Critical Care

Ed itors:

Si nge r, M ervyn; We bb, An dre w R.

Ti tle : O xf ord Ha ndbook of Cr itic al Car e, 2nd Ed ition Cop yri ght © 1997,2005 M. Si nge r and A. R. W ebb , 1997, 2005. Publ i shed i n the Uni te d Stat es by Oxford Uni ve rsi ty Press Inc > Tab le of Co n te n ts > Nu t r iti on

Nutrition Nutrition—use and indications Mal nut ri ti on l ead s t o p oor wound healing, pos t-operati ve com pl i cat i ons and sep si s. Ade quate nut ri t i onal support i s i mp ort ant for c ri ti c al l y i l l pati e nts and s houl d be provi d ed earl y duri ng t he i l l nes s. Evi dence for i m proved outcome from e arl y nutri t i onal sup port e xi s ts for pati e nts wi th traum a and b urns. Ent eral nut ri t i on i s i ndi cat ed whe n swallowi ng i s i nadequate or i m pos si bl e but g ast roi nte sti nal func ti on i s othe rwi se i nt act . Pare nte ral nutri ti on i s i nd i c ate d where the g ast roi nt est i nal t rac t c annot be use d t o p rov i de ad equate nut ri ti onal support , e. g. obs truct i on, i l eus , hi gh sm al l bowel fi stul a or mal abs orp ti on. Parent eral nutri t i on may b e us ed to sup pl e ment e nte ral nutri ti on whe re gas troi nt est i nal functi on al l ows parti al nut ri ti onal support .

Consequences of malnutrition Underfeeding

Overfeeding

Loss of muscle mass Reduced respiratory function Reduced immune function Poor wound healing Gut mucosal atrophy Reduced protein synthesis

Increased VO 2 Increased VCO 2 Hyperglycaemia Fatty infiltration of liver

Calorie requirements Vari ous formul ae e xi s t to c al cul ate the p ati ent 's bas al met abol i c rate but are m i sl ead i ng i n c ri t i c al i l l nes s. Met abol i c rat e c an be meas ured by i nd i re ct cal ori met ry but most pat i e nts are as sumed to req ui re 2000–2700Cal / day, or l es s i f starve d or unde rwe i ght.

Nitrogen requirements Ni t rogen exc ret i on c an b e c al c ul ate d i n t he abs enc e of re nal failure acc ordi ng t o t he 24h urea e xcreti on: Ni t rog en (g/24h) = 2 + Uri nary urea (m mol /24h) × 0. 028 How ever, as w i t h most formul ae, thi s met hod l a cks ac curac y. M ost pati e nts requi re 7–14g /day .

Other requirements The normal requi rements of sub strat es, vi tami ns and t rac e el eme nts are t abl ed opp osi te. Most l ong-t erm cri t i call y i l l pat i ents re qui re fol i c aci d and vi t ami n s upp l em ent ati on duri ng nutri ti onal s up port, e.g . Sol v i to. T rac e e l em ent s are usual l y s up pl e ment ed i n parent eral formul ae b ut shoul d not b e requi red duri ng enteral nut ri ti on. P.79

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Normal daily requirements (for a 70kg adult) Water

2100ml

Energy

2000–2700Cal

Nitrogen

7–14g

Glucose

210g

Lipid

140g

Sodium

70–140mmol

Potassium

50–120mmol

Calcium

5–10mmol

Magnesium

5–10mmol

Phosphate

10–20mmol

Vitamins Thiamine

16–19mg

Riboflavin

3–8mg

Niacin

33–34mg

Pyridoxine

5–10mg

Folate

0.3–0.5mg

Vitamin C

250–450mg

Vitamin A

2800–3300iu

Vitamin D

280–330iu

Vitamin E

1.4–1.7iu

Vitamin K

0.7mg

Trace elements

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Iron

1–2mg

Copper

0.5–1.0mg

Manganese

1–2µg

Zinc

2–4mg

Iodide

70–140µg

Fluoride

1–2mg

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P.80

Enteral nutrition Routes i ncl ude nas o-g ast ri c , naso-duode nal /jej unal, gas trost omy and je junost omy. Nasal tube fee di ng s houl d be vi a a soft, fi ne-b ore tube to aid pat i e nt comfort and avoi d ul ce rat i on of the nose or oes ophagus. Prol onged enteral fee di ng may be acc omp l i she d v i a a pe rc utaneous/p eroperati ve gas trost omy or perope rat i ve je junost omy . Enteral fee di ng provi d es a m ore compl ete di et than p are nte ral nutri ti on, mai nt ai ns s truct ural i nte gri ty of the gut, i mp rov es bow el adaptati on afte r rese cti on and re duc es i nfect i on ri sk .

Feed composition Mos t p ati ent s t ol erate i so-osm ol a r, non-l a ctose fee d. Carbohy drates are p rov i d ed as s ucros e or gl uc ose pol yme rs ; protei n as w hol e p rot ei n or ol i g opep ti des (may b e b ett er abs orb ed than free ami no aci ds i n ‘el eme ntal’ fee ds); fats as med i um chai n or l ong chain tri gl yce ri d es. Me di um c hai n t ri gl y ceri de s are bet ter ab sorbed . Standard feed i s formul ate d at 1Cal /ml . Spec i al fe eds are av ai l ab l e, e.g . hi g h fi bre, hi g h p rot ei n-calori e, re st ri c ted salt, hi gh fat or concentrated (1.5 or 2Cal/ml ) for fl ui d re stri ct i on. Immune-enhanc ed feed s (e.g . g l ut ami ne-enri ched or Imp act ®, a formul a s upp l em ent ed wi t h nucl eot i de s, arg i ni ne and fi sh oi l ) may red uce nosoc omi al i nfect i ons b ut no evi dence of out com e b ene fi t has b een shown from l arg e p ros pec ti v e s tud i es .

Management of enteral nutrition Onc e a de ci s i on i s made to start ent eral nut ri t i on, 30ml /h ful l s treng th standard feed may b e s tarted i m med i at el y . St art er reg i me ns i nc orp orati ng di l ute fe ed are not ne ces sary. Aft er 4h at 30m l /h the feed shoul d b e st opp ed for 30m i n pri or to as pi rati on of the st omac h. Si nce gastri c jui ce producti on i s i nc re ased by the p res enc e of a nas ogastri c tub e, i t i s re asonabl e t o acce pt an asp i rate of <200ml as evi dence of gas tri c empt yi ng and the refore to i ncrease the i nfusi on rate t o 60ml /h. Thi s proces s i s rep eat ed unt i l the targe t feed rate i s achi ev ed. There afte r, asp i rati on of the stomac h c an be red uce d t o 8hrl y. If the gas tri c asp i rate vol ume i s >200m l t he i nfusi on rat e i s not i ncre ase d b ut the fee d i s c ont i nued. If as pi rate s remain at hi g h v ol ume des pi t e m eas ure s t o p rom ote gas tri c emp tyi ng (e. g. met ocl oprami de or ery thromy ci n) t hen ei the r b owe l rest , nasoduodenal /nas ojej unal feed i ng or parenteral nut ri ti on shoul d be consi dered.

Complications Tube pl ace ment: trache obronc hi a l i nt ubati on, nas ophary nge al perforati on, i ntracrani al penetrati on (bas al sk ul l frac ture), oe sop hag eal pe rforat i on Refl ux Pul monary asp i rati on Naus ea and vomi t i ng Abd omi nal di ste nsi on i s occ as i onal l y reporte d w i th fe atures i ncl udi ng a te nde r, di ste nde d ab dom en and an i nc reasi ng m etabol i c aci dos i s . Laparot omy and bowel re sec ti on m ay be nece ss ary i n se vere cases Di a rrhoea: l arg e vol ume, bol us fee di ng, hi g h osmol al i t y, i nfect i on, l act ose i ntol erance , anti bi oti c t herapy , hi gh fat content Cons ti pat i on Metabol i c : de hyd rat i on, hype rgl yc aemi a, el e ctrol yte i m bal anc e P.81

Key trial At ki nson S, et al . A prosp ect i ve , rand omi zed , d oub l e-bl i nd, control l ed cl i ni cal t ri a l of e nte ral i m munonutri ti on i n the cri ti cal l y i l l . Cri t C are Me d 1998; 26:1164–72

See also: Nut ri ti on—use and i ndi c ati ons , p 78; El e ctrol ytes , p 146; Calc i um , m agne si um and phosphate , p 148; Gut mot i l i ty age nts , p 226; Vomi t i ng/gast ri c st asi s, p338; Di arrhoe a, p 340; Bowel pe rforat i on and obst ructi on, p348; Hyp ernatraem i a, p416; Hyp onatraemi a, p418; Hyp erk al a emi a, p420; Hypokal aem i a, p422; Hy pom agnesae mi a , p 424; Hypocal cae mi a , p 428; Hypophos phatae mi a , p430 P.82

Parenteral nutrition Feed composition Carbohydrate i s normally provi ded as conce ntrate d g l uc os e. 30–40% of tot al cal ori es are us ual l y gi ven as l i pi d (e. g. soy a b ean emul s i on). T he ni t rogen sourc e i s s ynt het i c, cryst al l i ne L-am i no ac i ds whi ch shoul d c ont ai n ap propri at e quanti ti es of all es senti a l and mos t non-e sse nti al ami no aci ds . Carbohyd rat e, l i pi d and ni troge n s ources are usually mi x ed i nt o a l a rge bag i n a st eri l e pharmacy uni t. Vi tam i ns , t rac e e l em ent s and approp ri a te el e ctrol y te concentrati ons can b e ac hi eved i n a si ngl e i nfus i on, thus avoi di ng m ul t i pl e c onnect i ons. Vol um e, p rotei n and c al ori e content of t he feed shoul d b e d ete rmi ned on a dai l y bas i s i n conjuncti on wi t h t he di e ti ti a n.

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Choice of parenteral feeding route Central venous A d edi cat ed cat het er (or l umen of a m ul ti -l um en cat het er) i s pl ace d unde r s teri l e condi ti ons . F or l ong-t erm fee di ng a sub cut ane ous tunne l i s ofte n used to se parate sk i n and vei n ent ry si t es. Thi s probab l y red uce s t he ri sk of i nfe cti on and cl earl y i d ent i fi es the sp eci al purpos e of t he cat het er. Id eal l y, bl ood sampl es shoul d not b e t aken nor othe r i nj ect i ons or i nfusi ons gi ven vi a t he feed i ng l umen. T he central v enous route al l ows i nfus i on of hy perosm ol a r sol ut i ons, provi d i ng ad equate ene rg y i ntake i n reduced vol um e.

Peripheral venous Parent eral nutri t i on vi a t he peri pheral rout e requi res a s ol uti on w i th os mol al i ty <800mOsmol /k g. Ei t her the v ol ume mus t b e i ncreas ed or the energ y c ont ent (p art i cul arl y from c arbohy drate) re duc ed. Pe ri p heral cannul ae si tes must be change d freq uentl y .

Complications Catheter related

Misplacement Infection Thromboembolism

Fl ui d exce ss Hype ros mol ar hyp erg l y caem i c st ate El e ctrol y te i mb al a nce Hypophosphataemi a

Metabolic acidosis

Hyperchloraemia Metabolism of cationic amino acids

Rebound hy pog l yc aemi a High endog enous i ns ul i n l eve l s

Vitamin deficiency

Vitamin excess

Folate Thiamine Vitamin K

Vitamin A Vitamin D

Pancytopenia Encephalopathy Hypoprothrombinaemia

Dermatitis Hypercalcaemia

Fatt y l i ve r P.83

See also: Nut ri ti on—use and i ndi c ati ons , p 78; El e ctrol ytes , p 146; Calc i um , m agne si um and phosphate , p 148; Hypernat raemi a, p 416; Hyponat rae mi a , p 418; Hy perkal aem i a, p420; Hyp okal aem i a, p422; Hy pom agnesaemi a, p424; Hyp ocalcaemi a, p428; Hypophosphataemi a, p430; Met abol i c aci dos i s , p 434

Ovid: Oxford Handbook of Critical Care

Ed itors:

Si nge r, M ervyn; We bb, An dre w R.

Ti tle : O xf ord Ha ndbook of Cr itic al Car e, 2nd Ed ition Cop yri ght © 1997,2005 M. Si nge r and A. R. W ebb , 1997, 2005. Publ i shed i n the Uni te d Stat es by Oxford Uni ve rsi ty Press Inc > Tab le of Co n te n ts > Spe cial Su pp or t Su r fa ces

Special Support Surfaces Special support surfaces Pressure sores Pre ssure sores oc cur due t o c ompres si on of ti ss ue bet ween bone and the support surface and due to sheari ng force s, fri ct i on and macerat i on of ti ssues agai ns t t he sup port s urface . T he use of spe ci al beds at tem pts t o reduc e t he pre ss ure at the contact i ng sk i n surfac e t o a l e vel l ower than t he cap i l l ary occl usi on pre ss ure . In t he m ajori t y of c ase s i t i s suffi ci e nt to mi ni mi se the ti me that t he sup port s urfac e contact s any one are a of sk i n by pos i ti on change s.

Factors suggesting the need for a special bed

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Pati ent s wi t h s everel y rest ri c ted mobi l i t y d ue t o t racti on or cardi ores pi rat ory i nstabi l i t y c annot be t urned freq uentl y, i f at all . Pati ent s wi t h d ecreas ed s ki n i nte gri ty, e. g. burns, press ure s ore s alre ady prese nt, chroni c ste roi d use , di ab etes mel l i t us. Pati ent s on v asoact i ve drug i nfusi ons.

Types of special support surface Air mattress Thi s e i t her re pl a ces or i s pl ace d on t op of a st and ard hospi tal b ed m att re ss. They p rov i d e mi ni mum red uc ti on i n contac t p res sure but shoul d b e c ons i de red as mi ni m um sup port for any pat i e nt wi t h t he abov e fact ors .

Low air loss bed The se purpos e-b ui l t p res sure-rel i ev i ng be ds al l ow eas i er pati e nt mob i l i ty than othe r s upp ort s urface s. Cont act pre ss ure may st i l l b e hi gher than c api l l ary occ l usi on p res sure s o p osi ti oni ng i s sti l l re qui red . Pati ent s w ho are hae mod ynam i c al l y unst abl e s houl d usual l y b e m anaged on a l ow ai r l oss bed , p art i c ul a rl y i f re cei vi ng v asoconstri c tor drugs . The p res enc e of p res sure s ore s w i th i ntact ski n i s an i ndi cat i on for a l ow air l os s b ed. Rotat i onal l ow ai r l oss bed s allow automat ed l at eral rotati on at v ari abl e t i me i nterval s to faci l i tat e c hes t d rai nag e. The se may al s o b e useful whe re manual pos i t i oni ng i s i mpract i cal.

Air fluidised bed Thi s i s the onl y s up port s urface that consi s tentl y l owers c ont act pres sure t o b el ow capi l l a ry occ l us i on pres sure. Conseq uentl y , p ati ent s w i th se vere c ard i oresp i ratory i ns tab i l i ty , w ho c annot be turned , and pat i ents wi t h p res sure sores wi t h b rok en ski n b ene fi t most. The addi ti onal ab i l i ty to control the te mperat ure of the i m med i at e e nvi ronment i s an adv ant age i n hy pot hermi c pati e nts and t hos e wi th l a rge surface are a b urns. Any ex udat e from the s ki n i s ads orb ed i nt o t he si l i c one be ads on whi ch the pati e nt fl oats . T hi s dryi ng effe ct i s parti cul arl y use ful i n maj or burns (al though i t must be tak en i nt o account for fl ui d repl ace ment t herapy ). T he ai r fl ui di s ed bed al so has a rol e i n p ai n rel i e f.

Ovid: Oxford Handbook of Critical Care

Ed itors:

Si nge r, M ervyn; We bb, An dre w R.

Ti tle : O xf ord Ha ndbook of Cr itic al Car e, 2nd Ed ition Cop yri ght © 1997,2005 M. Si nge r and A. R. W ebb , 1997, 2005. Publ i shed i n the Uni te d Stat es by Oxford Uni ve rsi ty Press Inc > Tab le of Co n te n ts > Resp ir a tor y M on itor in g

Respiratory Monitoring Pulse oximetry Conti nuous non-i nv asi ve moni tori ng of arte ri a l oxyg en sat urati on b y p l ac eme nt of a probe em i tt i ng red and near-i nfrare d l i g ht over t he p ul se on d i gi t, earl obe, cheek or bri dg e of nose. It i s unaffect ed by s ki n p i gm ent ati on, hyp erb i l i rubi naem i a or anaemi a (unl ess profound).

Physics The col our of b l ood v ari es wi t h oxyge n s aturat i on d ue t o t he opt i cal p roperti e s of t he haem moi et y. As the Hb mol ecul e gi v es up O 2 i t bec ome s l ess pe rme abl e t o red l i g ht and takes on a b l ue ti nt . Saturat i on i s de termi ned spe ctrop hot omet ri cal l y by meas uri ng the ‘ bl uene ss’ , uti l i s i ng the abi l i t y of compound s t o absorb l i g ht at a s pec i fi c wav el e ngt h. The us e of tw o wavel eng ths (650 and 940nm) pe rmi ts the rel a ti v e q uant i t i es of re duc ed and oxy hae mogl obi n to b e c al c ul ate d, the reb y de termi ni ng s aturat i on. T he art eri al pul se i s us ed to provi d e t i me poi nt s t o al l ow sub tract i on of the const ant ab sorpt i on of l i ght by ti ssue and venous bl ood. The accurac y of p ul s e oxi m etry i s wi t hi n 2% ab ove 70% SaO 2 .

Indications Cont i nuous moni t ori ng of art eri al ox ygen saturat i on.

Cautions As onl y t wo w ave l engths are use d, pul se oxi met ry meas ures func ti onal rather than frac ti onal ox yhaemog l ob i n sat urati on. Errone ous l y hi g h read i ng s are gi ven wi t h c arb oxy hae mog l ob i n and met hae mog l ob i n. Wi t h p oor peri p heral perfus i on or i ntense vas oconst ri cti on the re adi ng may be i nacc urate (‘fail soft’ ) or, i n newe r mode l s, ab sent (‘fail hard’). Moti on art efacts and hi gh l evel s of ambi ent l i ght i ng m ay affe ct readi ngs.

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Errone ous si gnal m ay b e p rod uce d b y s i gni fi cant venous pul sati on from tri cuspi d reg urg i tati on or v enous cong est i on. Venous pul sati l i t y ac count s for di fferenc es bet ween ear and fi nger SpO 2 i n t he sam e subje ct. Ens ure a g ood LED s i g nal i ndi c ator or a pul se waveform (i f av ai l abl e) i s see n on t he m oni tor. Vi t al dye s (e.g. me thy l thi oni ni um chl ori d e (m ethyl e ne bl ue), i ndoc yani ne green) may affec t SpO 2 re adi ngs . P.91

See also: Oxy gen therapy, p2; Vent i l a tory s upp ort —i ndi cat i ons, p4; IPPV—ad jus ti ng t he venti l ator, p10; Conti nuous pos i ti ve ai rway press ure, p 26; End otrac heal i ntubat i on, p 36; Trache otomy, p38; F ibreop ti c bronchoscopy, p46; Chest phy si othe rap y, p48; Uppe r g ast roi nte sti nal e ndos copy, p74; Bl ood gas anal ysi s, p100; Basi c res usc i tati on, p270; Dys pnoea, p278; Res pi rat ory fai l ure, p282; Acute che st i nfect i on (1), p288; Acut e c hes t i nfe cti on (2), p 290; Ac ute res pi rat ory di stres s s ynd rom e (1), p292; Acut e resp i ratory di s tre ss syndrome (2), p294; Ast hma—ge neral manage ment , p 296; Ast hma—ve nti l at ory manag ement, p298; Pne umothorax , p300; Poi s oni ng—general p ri nci pl e s, p452; Pos t-op erati ve i nt ens i ve care, p534 P.92

CO 2 monitoring Capnography For capnography , resp i ratory g ase s m ust be sampl ed conti nuousl y and m eas ure d b y a rap i d re sponse dev i c e. Si nce CO 2 has an absorpt i on band i n the i nfrared sp ect rum , m eas ure ment i s faci l i tat ed i n gas mi xtures . Othe r g ase s c an i nt erfere wi th i nfrared ab sorpti on by CO 2 . Thi s m ay b e overcom e b y cali brati ng t he i ns trume nt wi t h known concentrati ons of CO 2 i n the requi re d m eas ure ment rang e, d i l ute d wi th a g as mi x ture s i m i l a r t o e xhaled gas.

The capnogram The CO 2 c onc ent rat i on of exhal ed g as consi sts of 4 p has es (se e fi gure). T he p res enc e of s i gni fi cant concentrati ons of CO 2 i n phase 1 i mp l i e s rebreat hi ng of e xhaled gas. Fai l ure of an ex pi ratory val ve to ope n i s t he most l i ke l y cause of reb reathi ng duri ng m anual vent i l ati on, al though an i nade quate fl ow of fresh gas i nto a reb reathi ng bag i s a com mon cause. The s l op e of phase 3 i s dep end ent on the rate of al v eol ar gas ex change . A st eep sl ope may i ndi cat e venti l at i on-perfus i on mi sm atc h s i nc e alve ol i that are poorl y v ent i l a ted but w el l pe rfused di scharge l at e i n t he res pi rat ory cy cl e . A st eep sl ope i s se en i n pat i ents wi t h s i g ni fi cant aut o-PEEP.

Colorimetric devices The underl yi ng pri nc i pl e i s t hat t he c hange i n pH produc ed by di fferent CO 2 c onc ent rat i ons i n sol uti on wi l l c hange the col our of an i ndi c ator. The se are sm al l de vi c es that fi t ont o an e ndotrache al tub e or t he vent i l ator c i rcui t and res pond rap i d l y (up to 60 bre aths/m i n). T hey can be affec ted by exc ess i ve humi d i t y and g ene ral l y onl y w ork i n the rang e 0–4% C O 2 . They are use ful to confi rm trache al i ntub ati on, duri ng p ati ent trans fer and i n t he cardi ac arrest si tuati on.

End-tidal PCO 2 End -ti dal PC O 2 app rox i mates PaCO 2 i n pati e nts wi th normal l ung funct i on. In ICU p ati ent s pul monary funct i on i s rarel y normal, thus end-ti dal PCO 2 i s a poor approxi mat i on of PaC O 2 . Larg e d i ffere nce s m ay repres ent an i nc re ase d dead s pac e t o t i dal v ol ume rat i o, poor pul monary perfusi on or i ntrapul monary s hunti ng. A progre ssi ve ri s e i n end -ti dal PC O 2 may rep re sent hypov ent i l ati on, ai rway ob st ruc ti on or i ncreas ed C O 2 produc ti on d ue to i nc reased met abol i c rate. End-t i dal PCO 2 falls wi th hyp erv ent i l ati on and i n l ow card i ac output s tat es. It i s ab sent w i th venti l at or di s connec ti on and duri ng cardi ac arres t b ut ri s es wi t h e ffe cti ve CPR or res torat i on of a s pontaneous ci rcul at i on.

Dead space to tidal volume ratio The arteri al t o end-t i dal PCO 2 di fferenc e m ay be use d t o calc ul a te the physi ol ogi c al dead s pac e t o t i dal v ol ume rat i o vi a the Bohr eq uat i on:

In health a val ue bet ween 30 and 45% s houl d be exp ect ed. P.93

The components of the normal capnogram

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Figure. No Caption Available.

Phase 1 Duri ng t he earl y part of the e xhaled breat h anat omi cal de ad s pac e and sam pl i ng dev i ce de ad space gas are s ampl ed. The re i s neg l i gi b l e CO 2 i n phas e 1.

Phase 2 As al veol ar gas be gi ns t o b e s amp l ed there i s a rap i d ri se i n CO 2 conce ntrati on.

Phase 3 Phase 3 i s k nown as the alve ol a r p l at eau and represe nts the CO 2 c onc ent rat i on i n mi xed ex pi red al v eol ar gas . T here i s normal l y a s l i ght i ncrease i n PCO 2 duri ng p has e 3 as al veol ar gas e xchang e conti nues duri ng ex pi rati on. Ai rw ay obs truct i on or a hi g h rate of CO 2 producti on wi l l i nc rease t he sl ope. End-t i dal PCO 2 w i l l b e l ess than t he PCO 2 of i d eal al v eol ar gas si nc e the s amp l ed ex hal ed gas i s mi xed wi th al v eol ar dead sp ace gas.

Phase 4 As i nspi rat i on be gi ns t here i s a rapi d fal l i n sampl e PCO 2 .

See also: Venti l at ory support— ind i c ati ons , p 4; IPPV—adj ust i ng the v ent i l a tor, p 10; End otracheal i ntub ati on, p36; T rac heotom y, p38; F i breop ti c bronc hos cop y, p46; Bl ood gas anal ysi s, p100; Bas i c res usc i t ati on, p270 P.94

Pulmonary function tests Few of the numerous pul monary func ti on t est s c urrentl y avail abl e i mpact upon c l i ni c al managem ent of the cri t i call y i l l , parti c ul arl y i f t he pat i ent has to be m ove d t o a l ab oratory. A numb er of other tes ts req ui re hi g hl y sp eci al i se d equi pm ent and ful fi l a p red omi nant rese arc h rol e.

Clinically relevant tests

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Measurement

Test

Common clinical use

PaO 2 , SaO 2 , PaCO 2

Arterial blood gases

SpO 2

Pulse oximetry

End-tidal PCO 2

Capnography

Vital capacity, tidal volume

Spirometry, electronic flowmetry

Serial measurement of borderline function (VC <10–15ml/kg) e.g. Guillain–Barré syndrome

Peak expiratory flow rate FEV 1 , FVC

Wright peak flow meter Spirometry, electronic flowmetry

(Spontaneous ventilation) asthma (Spontaneous ventilation) asthma, obstructive/restrictive disease

Lung/chest wall compliance (see equations opposite)

Pressure–volume curve

Ventilator adjustments, monitoring disease progression

Flow-volume loop, pressure-volume loop

Pneumotachograph manometry

Ventilator adjustments

Research tests (examples) Measurement

Test

Research use

Diaphragmatic strength (transdiaphragmatic pressure)

Gastric and oesophageal manometry

Respiratory muscle function, weaning

Pleural (intrathoracic) pressure

Oesophageal manometry

Ventilator trauma, work of breathing, weaning

Functional residual capacity

Closed circuit helium dilution, (bag-in-a-box) open circuit N 2 washout

Lung volumes, compliance

Ventilation–perfusion relationship

Multiple inert gas elimination technique, isotope techniques

Regional lung ventilation–perfusion, pulmonary gas exchange

Pulmonary diffusing capacity

Carbon monoxide uptake

Pulmonary gas exchange

P.95

Notes Comp l i ance eq ual s t he change i n press ure duri ng a l i ne ar i nc rease of 1l i n vol ume above FRC. The al v eol ar–art eri al ox ygen di ffe rence i s <2k Pa i n youth and <3. 3kPa i n ol d age. The Bohr e quati on c al cul ate s p hys i ol ogi cal de ads pac e, V D . The normal value i s be l ow 30%. The shunt equati on est i mates the p rop ort i on of bl ood shunt ed pas t p oorl y venti l ate d alve ol i (Q S ) c omp are d t o tot al l ung b l ood fl ow (Q T ). Thes e e quati ons al l ow est i mati on of v ent i l a ti on/p erfusi on mi s mat ch: V/Q=1, venti l at i on and pe rfusi on are wel l -m atc hed . V/Q>1, i nc re ase d de ads pac e (where alve ol i are p oorl y perfus ed but we l l venti l at ed). V/Q<1, i nc re ase d ve nous admi xture or shunt (where al veol i are perfused but poorl y v ent i l ate d). The normal range i s <15%.

Lung volumes and capacity

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Figure. No Caption Available.

Equations Alveolar gas equation P A O 2 = FIO 2 -(PaCO 2 /re spi ratory q uot i ent) [RQ oft en app rox i mated to 0.8]

Alveolar-arterial oxygen difference (A-a) d i fferenc e = FIO 2 × 94.8 - PaCO 2 - PaO 2

Bohr equation: V D /V T = (PaCO 2 - ex pi red PCO 2 )/PaC O 2

Shunt equation Q S /Q T =(Cc O 2 -CaO 2 )/(Cc O 2 -CvO 2 ) whe re CcO 2 = end -capi l l a ry O 2 c ont ent , a = art eri al , v = mi xed ve nous

See also: Venti l at ory support— ind i c ati ons; IPPV—adjusti ng the ve nti l at or; IPPV—w eani ng te chni ques; IPPV—asse ssm ent of weani ng; Pul se oxi metry; CO 2 moni t ori ng; Bl ood gas anal y si s; C hroni c ai rfl ow l i m i t ati on; Ast hma—ge neral manage ment ; Ast hma—ve nti l at ory manag eme nt; Ac ute weakne ss; Gui l l ai n–Barré s ynd rom e; My ast heni a gravi s ; Rhe umati c di sorders; Vas cul i t i de s P.96

Pressure–volume relationship Thi s i s det erm i ne d b y t he c omp l i anc e of the l ung s and che st wal l . The i nspi ratory p res sure–v ol ume rel ati ons hi p contai ns three com ponent s: an i ni ti al i nc rease i n pre ssure wi t h no s i gni fi cant vol ume change ; a l i near i ncreas e i n vol ume as press ure i ncreas es (the sl ope of whi ch re pre sents res pi rat ory sy ste m c ompl i a nce ); and a furt her pe ri od of pre ss ure i ncre ase wi th no vol ume i nc re ase . These three phase s are sep arated by two i nfl exi on z one s, the l ower rep res ent i ng t he openi ng pres sure of t he s yst em aft er fl ow resi stance has b een ove rc ome i n small er ai rway s and t he upp er app rox i mati ng t o t otal l ung c apac i t y. The exp i ratory p re ssure–vol ume re l at i onshi p s houl d normal l y app rox i mate the i nspi ratory c urv e, ret urni ng to funct i onal res i d ual capac i ty . In p ati ent s w i th sm al l ai rw ay c ol l ap se, sep arati on of t he i ns pi rat ory and ex pi rat ory curve s oc curs (hy ste res i s) as gas i s t rap ped i n sm al l er ai rway s at t he end of exp i rati on.

Dynamic measurement A p res sure–vol ume l oop m ay be vi e wed on mos t m odern m echani cal ve nti l a tors. A s quare wav e i nsp i ratory w ave form (const ant fl ow) and no i nspi ratory p aus e are nece ssary for waveform i nterpre tat i on. St ati c m eas ure ment Small i ncre mental l ung vol ume s (200ml ) are de l i vered w i th a cal i b rat ed syri ng e. The press ure me asurem ent aft er eac h i ncreme nt i s tak en und er zero fl ow condi ti ons, al l ow i ng const ructi on of a pres sure–v ol ume curve. A quasi s tat i c curve can be const ruc ted by se tti ng i ncre mental ti dal vol um es (e. g. b etw een 100 and 1000ml ) for s ucc ess i v e venti l at or bre aths and m eas uri ng the pres sure d uri ng an i ns pi rat ory pause .

Use of pressure volume curves Si nce re spi rat ory muscl e acti vi ty can al ter i ntrathorac i c press ure , t he pre ssure vol ume curve i s more eas i l y ob tai ned i n the re l ax ed, ful l y ve nti l at ed pat i ent. Both stati c and d ynami c re spi rat ory sy st em c omp l i anc e can b e d ete rmi ned as the sl ope of the l i ne ar porti on of t he curve, i . e. where i nc rem ent al pre ssure i nfl at es the l ungs . Bel ow t he l ow er i nfl ex i on zone the sm al l ai rways are cl ose d and exp i rati on d oes not reac h func ti onal re si d ual c apac i t y. The l ow er i nfl ex i on zone the refore re pre sents the ap propri at e s ett i ng for e xternal PEEP to avoi d gas trapp i ng . Abov e t he upp er i nfl ex i on zone the l ungs cannot i nfl ate further. The uppe r i nfl exi on zone t herefore rep res ent s t he max i mum s ett i ng for

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peak airw ay p re ssure.

Compliance: calculations Lung c omp l i anc e (l /cm H 2 O) = ΔV L /ΔP L w here L, t he l i t re above FRC, i s the s l op e of t he l i near porti on of the curve . Tot al res pi rat ory sy ste m c omp l i ance i s de ri v ed from t he equati on: (1/tot al com pl i anc e) = (1/l ung com pl i anc e) + (1/chest wall com pl i anc e) Tot al com pl i anc e c an be cal cul at ed i n w el l s edat ed, ve nti l at ed pat i ents as : ti dal vol ume /(e nd-i ns pi ratory pause pre ssure - PEEP). P.97

Figure. No Caption Available.

See also: Venti l at ory support— ind i c ati ons; IPPV—adjusti ng the ve nti l at or, p10; Posi ti v e e nd expi ratory p res sure (1), p22; Pos i ti ve end ex pi ratory pre ss ure (2), p 24; Chroni c ai rfl ow l i mi tat i on, p 286; Asthma—general m anag eme nt, p286; As thm a—ve nti l a tory m anag eme nt, p298 P.98

Blood gas machine A s mal l amount of hep ari ni s ed bl ood i s ei t her i nje cte d from a s yri ng e or as pi rat ed from a cap i l l ary t ube i nto the mac hi ne. The bl ood comes i nto contac t wi th three el ect rod es whi ch measure p H, PO 2 and PCO 2 . pH—m eas ure d b y t he pot ent i al ac ros s a pH-se nsi ti ve g l as s m emb rane s eparat i ng a sam pl e of known pH and the tes t s ampl e. PO 2 —the part i al ox ygen press ure, i s meas ured by appl yi ng a pol ari s i ng vol tage bet ween a pl a ti num cat hod e and a si l v er anod e (Cl a rk el e ctrode ). O 2 i s red uce d, generati ng a curre nt proporti onal t o t he PO 2 . PCO 2 —the p art i al p res sure of c arb on di oxi d e, uti l i s es a p H e l ec trode wi t h a Te fl on m embrane (Seve ri nghaus el ec trode ) whi ch al l ows t hroug h uncharg ed m ol e cul es (CO 2 ) but not c harged i ons (H + ). C O 2 al one thus c hanges the pH of a b i carbonat e e l ec trol yt e s ol uti on, the chang e b ei ng l i nearl y rel ate d t o t he PCO 2 . Hb—e st i mated photom etri c al l y; thi s i s not as acc urate as co-oxi met ry (see be l ow ). Bi c arb onate— cal cul at ed b y t he Henderson–Hasse l bach equati on

Act ual HC O 3 - i nc l udes bi carbonate , c arb onate and carbam ate . Act ual base exc ess (de fi c i t )—t he d i fferenc e i n c onc ent rat i on of st rong b ase (ac i d) i n whol e bl ood and t hat ti t rat ed to pH 7.4, at PCO 2 5.33kPa and 37°C . Standard bas e ex ces s (defi ci t)—a c al c ul ate d in viv o b ase exc ess (d efi ci t). Standard bi c arb onate— the pl asm a c onc ent rat i on of hy drogen carbonat e eq ui l i b rat ed at PC O 2 5.33kPa, PO 2 13.33kPa and tem perature 37° C. Bl ood gas value s c an be gi v en ei t her as ‘p Hst at’ or ‘alphast at’ , t he former correct i ng for b ody tem perature by shi ft i ng the calcul a ted Bohr oxyhaem ogl obi n d i ss oc i at i on curve (hypertherm i a to the ri ght , hypothe rmi a t o t he l eft). Al phastat measures true b l ood g as l ev el s i n the s amp l e.

Co-oximeter Thi s d i ffers from a b l ood g as mac hi ne i n t hat the b l ood i s haemol ys ed to cal cul at e (i ) t otal Hb and fet al Hb and (i i ) oxy Hb, carboxyhaemogl obi n (C OHb ), methaem ogl obi n and sul phaemogl obi n by ut i l i si ng abs orb anc e at s i x wav el e ngt hs (535, 560, 577, 622, 636, 670nm ).

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Taking a good blood gas sample Use a 1ml sy ri nge contai ni ng p referabl y a dry he pari n sal t (i f not , l i q ui d sodi um hepari n 1000i u/m l s ol uti on j ust fi l l i ng the hub). Tak e s amp l e, ex pel ai r, mi x sampl e t horoug hl y and i nse rt wi t hout d el a y.

Cautions Too muc h hepari n cause s d i l uti on errors and i s aci d i c . Ni t rous oxi d e or hal othane anae sthesi a m ay gi v e unre l i a bl e PO 2 value s. Int rav enous l i p i d adm i ni st rat i on may affec t p H v al ues. Abnorm al (hi gh/l ow) pl asm a p rot ei n conce ntrati ons affec t b ase de fi c i t. P.99

See also: Bl ood gas anal y si s , p 100; Invas i v e bl ood gas m oni tori ng, p 102 P.100

Blood gas analysis A hepari ni s ed (arteri al , v enous, capi l l ary) bl ood sam pl e can b e i nse rte d i nto a bl ood gas mac hi ne and/or co-oxi met er for me asurem ent of gas te nsi ons and s aturat i ons, and ac i d –base s tatus .

Measurements Identi fi c ati on of art eri al hyp oxaemi a and hype rox i a, hy percap ni a and hypocap ni a —enabl i ng moni t ori ng of di s eas e progre ssi on and effi c acy of tre atm ent . Vent i l ator and FIO 2 adj ust ments can be mad e p rec i s el y . pH, PaC O 2 and base defi ci t (or bi c arbonate) value s c an be revi ewe d i n p arall el for di agnosi s of ac i d osi s and al kalos i s , w het her i t i s re spi ratory or m etab ol i c i n ori gi n, and whe the r any comp ens ati on has oc curre d. (Se e fi g ure opp osi te ). Usi ng a co-ox i me ter, accurat e m eas ure ment c an be m ade of hae mog l ob i n oxy gen saturati on and al so the total Hb l eve l . The more sop hi s ti cat ed co-oxi m ete rs permi t me asurem ent of the frac ti on of me tHb , C OHb , d eox yHb and fetal Hb. Meas ure ment of m i xe d ve nous oxyg en s at urati on—for cal cul ati on of oxy gen consumpt i on and moni t ori ng of oxyg en sup pl y :de mand balance.

Causes of acid–base disturbances Resp i ratory aci dos i s— exc ess CO 2 product i on and /or i nade quate exc ret i on, e .g. hy pove nti l a ti on, exc ess narcoti c Resp i ratory al k al osi s —re duc ti on i n PaCO 2 due t o hype rve nti l at i on Metabol i c ac i dosi s —us ual l y l a cti c, ket o, renal or tub ul a r. Consi d er ti ssue hypop erfusi on, i nge sti on of aci ds (e.g . aspi ri n), l oss of al k al i (e .g. di arrhoe a, renal tub ul a r aci d osi s), di abe ti c k etoaci dos i s and hy perchl oraemi a (e.g. from ex ces s norm al sal i ne ad mi ni s trati on) Metabol i c al kal osi s. Consi d er exc ess al kal i (e.g . b i carbonat e or b uffe r i nfusi on), l oss of aci d (e.g . l arg e g ast ri c aspi rates , renal), hy pokalae mi a , d rug s (e.g . d i ureti cs )

Normal values

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pH

7.35–7.45

PCO 2

4.6–6kPa

PO 2

10–13.3kPa

HCO 3 -

22–26mmol/l

ABE

-2.4 to +2.2

Arterial O 2 saturation

95–98%

Mixed venous oxygen saturation

70–75%

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P.101

Figure. No Caption Available.

See also: Oxy gen therapy, p2; Vent i l a tory s upp ort —i ndi cat i ons, p4; IPPV—ad jus ti ng t he venti l ator, p10; IPPV— as ses sme nt of weani ng, p18; Posi ti v e e nd e xpi ratory p res sure (1), p22; Posi ti v e e nd expi ratory p res sure (2), p24; C ont i nuous pos i t i ve ai rway press ure, p26; Non-i nvas i ve re spi rat ory support , p32; Extracorporeal resp i ratory sup port, p34; Hae mo(d i a)fi l trati on (1), p62; Haemo(di a )fi l trat i on (2), p 64; Pe ri t one al di al y si s , p 66; Parent eral nutri t i on, p 82; Bl ood gas machi ne, p98; Inv asi ve b l ood g as moni tori ng, p102; Art eri al cannul at i on, p 112; Pul monary art ery c atheter— use , p118; Gut tonom etry, p130; Lac tat e, p 170; Basi c res usc i tati on, p270; Re spi rat ory fail ure , p 282; Chroni c ai rfl ow l i mi t ati on, p286; Acute che st i nfec ti on (1), p288; Acut e c hes t i nfe ct i on (2), p 290; Ac ute re spi ratory d i st res s syndrome (1), p292; Acut e resp i ratory d i s tre ss syndrome (2), p294; Ast hma—ge neral managem ent , p 296; As thm a—ve nti l a tory m anag eme nt, p298; Heart fai l ure—ass ess ment, p324; Gene ral ac i d–bas e m anageme nt, p432; Met abol i c ac i d osi s, p434; M etabol i c al k al osi s , p 436; Di ab eti c k etoaci dos i s, p442; Poi s oni ng —ge neral pri nci pl es, p452 Sal i c yl a te poi soni ng , p 454; Inhal ed p oi sons, p466; Post -op erati v e i nte nsi ve care, p534 P.102

Invasive blood gas monitoring Conti nuous b l ood g as moni tori ng c an be achi ev ed vi a an i nt ra-arteri al he pari n-bonded cathe ter wi th on-l i ne d i sp l ay of di rec tl y me asured and computed bl ood gas v ari abl es. Re sul ts are up dat ed every 20–30s . Re cal i b rat i on i s ge neral l y rec omm end ed at 12-hrl y i nte rvals.

Technology Sys tem s uti l i s e ei ther el e ctrode , t onometri c or op tod e t echnol ogy . El e ctrode te chnol ogy i s si m i l ar to t hat de sc ri b ed for bl ood gas machi ne measureme nt. Op ti c al se nsors uti l i se ei t her ab sorbance or fl uore sce nce sp ect rop hot ome try to measure t he si gnal from the chemi cal i nte rac ti on betw een the anal yte (O 2 , CO 2 and H + ) and an i nd i cator phase .

Problems Damp i ng of the arte ri al pre ssure wave form c an occ ur throug h t he pre sence of the cathe ter wi thi n t he art eri al cannul a. A d edi cat ed, non-taperi ng 20G c annul a reduces thi s dam pi ng e ffec t. An i nc reasi ng d ri ft i n acc uracy i s rec ogni s ed afte r s eve ral days. P.103

See also: Bl ood gas anal y si s , p 100 P.104

Extravascular lung water measurement St andard met hod s of asse ssi ng pul monary oe dem a are i ndi re ct. The CXR all ows quali tat i ve as ses sme nt onl y and i s sl ow t o c hange i n res ponse to cl i ni cal treat ment. Ass ess ment of c ard i ac fi l l i ng press ure s d oes not t ake i nto acc ount the de gre e of c api l l a ry permeabi l i t y or l ymphati c adap tat i on. Cons equent l y, a rel ati vel y l ow CVP or PAWP may be ass oci at ed w i th pul monary oede ma form ati on and hi gh fi l l i ng pre ssures i n c hroni c he art failure may be as soc i at ed wi t h no oede ma and be ent i re l y app rop ri ate. Ex travas cul ar l ung wat er (EVLW) measureme nt provi d es a t echni q ue for quanti fyi ng pul monary oe dem a and m oni tori ng t he res ponse t o t re atme nt.

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Measurement technique The normal v al ue of 4–7ml /kg for e xtravascul ar l ung wat er has be en d eri ve d by gravi met ri c t echni q ues pe rforme d pos t-m ort em. A doubl e i ndi c ator t ec hni que may be us ed i n l i v i ng pati ent s. Two i nd i c ators are i njec ted vi a a central vei n; one di stri butes wi thi n the vas cul ar sp ace and t he othe r t hroug hout t he i nt ra- and ex travas cul ar sp ace. The vol ume of di stri buti on of t he i nd i c ators i s deri ve d from the d i l uti on c urves det ect ed at the fe moral art ery . C ool ed 5% gl ucos e i s use d as a the rmal i ndi cator for i ntra- and ext ravasc ul ar vol ume and i ndoc yani ne green bound to al bum i n as a c ol ori metri c i ndi c at or for i ntravas cul ar vol ume . D ete cti on at the fe moral art ery i s by a fi b reopti c c athete r w i th a the rmi st or ti p . T he cardi a c outp ut i s measured by the rmodi l ut i on at the fe moral art ery . T he rat e of ex ponent i al de cay of the therm odi l ut i on curv e al l ows t he deri vati on of t he vol ume of di s tri buti on b etw een the i nje cti on and det ec ti on si tes (the heart and l ungs). Pul monary therm al vol ume = t hermod i l uti on CO × rate of exp onenti al dec ay of t hermod i l uti on curve (i ntra- and ext rav asc ul a r v ol ume) Si mi l ar pri nc i pl es may be app l i ed t o t he dye di l ut i on c urv e prod uce d on i njec ti on of i ndocyani ne g ree n w hi c h i s ass ume d t o d i st ri but e wi thi n the vascul ar sp ace onl y. Pul monary bl ood vol um e = dye di l ut i on CO × rat e of ex ponent i al de cay of dye di l uti on c urv e (i nt rav asc ul a r v ol ume) EVLW may be cal cul ate d b y s ubt rac ti ng pul monary bl ood vol ume from pul monary therm al vol ume .

Limitations of EVLW measurement Si nce i t i s known that alb umi n c an e xchang e across cap i l l ary m embranes, pul monary bl ood vol um e i s overest i mated by thi s t echni que and ex travas cul ar l ung wate r i s the refore und erest i mated . Howev er, the c orresp ond i ng error i s small and not p art i c ul a rl y si gni fi cant c l i ni c al l y. A m ore se ri ous drawback i s i n the l i mi tat i on of treat ment op ti ons . Tre atm ent of pul monary oe dem a b y d i uresi s and ul t rafi l trati on has bee n s how n t o be l e ss effect i ve at re duc i ng EVLW i n cap i l l ary l eak , c omp are d t o conge sti ve heart fai l ure. Si mi l arl y, the s trateg y of preve nti ng oed ema format i on by di ure si s whi l e maint ai ni ng the c i rcul ati on wi t h c ate chol am i ne i nfus i ons appe ars t o be futi l e; vas oconst ri cti on so produc ed i nc re ase s EVLW . P.105

See also: Cardi a c outp ut— the rmodi l ut i on, p 122; Cardi ac out put —ot her i nvas i ve , p 124; Acut e resp i ratory di s tre ss syndrome (1), p292; Acute res pi rat ory di stress s yndrome (2), p294; He art failure—ass ess ment, p324

Ovid: Oxford Handbook of Critical Care

Ed itors:

Si nge r, M ervyn; We bb, An dre w R.

Ti tle : O xf ord Ha ndbook of Cr itic al Car e, 2nd Ed ition Cop yri ght © 1997,2005 M. Si nge r and A. R. W ebb , 1997, 2005. Publ i shed i n the Uni te d Stat es by Oxford Uni ve rsi ty Press Inc > Tab le of Co n te n ts > Car dio vasc u la r Mon ito r in g

Cardiovascular Monitoring ECG monitoring Conti nuous ECG moni tori ng i s routi ne i n e very i nte nsi ve care uni t . T he standard tec hni que i s to di spl ay a t hre e l ead ECG (c ommonl y l ead II). Othe r l i m b l ead s may b e used al though the el ec trodes are p l ac ed at the shoul ders and l eft si de of t he abd omen. Othe r l ead confi gurat i ons c an be used for s pec i fi c purpos es:

Chest–Shoulder–V5

Early detection of left ventricular strain

Chest–Manubrium–V5

Early detection of left ventricular strain

Chest–Back–V5

P wave monitoring

Mod ern, c ont i nuous moni t ors i ncl ude al arm funct i ons for bradyc ard i a and tachy cardi a moni t ori ng , and s oft ware routi nes for arrhythmi a de tec ti on or ST s egm ent anal y si s .

Causes of changes in heart rate or rhythm Change s i n heart rate or rhythm m ay b e an i ndi cat i on of: Symp atheti c act i vi ty

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Ci rc ul a tory i ns uffi ci enc y Pai n Anxi ety Hypox aem i a Hypercapni a Adv ers e d rug effect s Anti arrhy thm i cs Sedati v es El e ctrol y te i mb al a nce Feve r P.109

See also: Defi bri l l at i on, p 52; Temp orary pac i ng (1), p54; T emp orary pac i ng (2), p 56; Card i ac arres t, p272; T achyarrthythmi as, p316; Bradyarrhythmi as, p318; Acute coronary syndrome (1), p320; Ac ute coronary sy ndrome (2), p 322; Hyp erk al a emi a, p420; Hypokal aem i a, p422; Poi soni ng—g ene ral pri nci p l e, p452; T ri c yc l i c anti d epress ant poi s oni ng, p460; Hyp otherm i a, p518; Pai n, p532 P.110

Blood pressure monitoring Non-invasive techniques Non-i nvas i ve te chni ques are i ntermi tte nt but automated . T hey i ncl ude osc i l l ot onomet ry (det ect i on of cuff pul sat i on as the sy stol i c p res sure), de tec ti on of arte ri a l t urbul enc e under t he c uff, ul t ras oni c d ete cti on of art eri al wal l m oti on und er the cuff and det ec ti on of bl ood fl ow di s tal to the c uff. Any cuff s yst em s houl d us e a cuff l arg e e nough to cove r two-thi rd s of t he surfac e of t he uppe r arm.

Invasive (direct) arterial monitoring Bl ood press ure i s most use ful l y moni tored from l arger l i mb art eri es , e .g. fem oral or b rac hi al . Howeve r, the potenti a l for damag e t o these arteri e s i s c ons i de rab l e and most consi d er i t safer to use the radi al or dorsalis pe di s arteri e s, the press ure i n whi c h i s hi gher. The arte ri a l c annul a i s c onnect ed to an appropri a te t ransd uce r s yst em vi a a s hort l ength of non-c ompl i a nt manomet er tub i ng. The trans duc er shoul d be mat ched t o t he moni tor, i . e. as recomme nde d by the manufact ure r of t he m oni tor. T he trans duc er mus t b e zeroed t o atmospheri c p re ssure. The t ransducer shoul d be pos i ti one d at t he l ev el of the 4t h i nte rcostal s pac e i n t he mi d -ax i l l ary l i ne . T he t ransd uce r, manomet er tub i ng and cannul a s houl d be conti nuousl y fl us hed wi t h 3ml /h hepari ni s ed sal i ne (1000IU/l ).

Damping errors It i s i m portant t hat the m oni tori ng sy ste m i s c orrec tl y damped . An unde rd ampe d s yst em wi l l overest i mate sys tol i c and underest i mate di a stol i c b l ood p res sure. The conve rse i s true for an ove rd ampe d s yst em. Moreover, i t i s not pos si bl e to corre ctl y i nte rp ret wav eform shape i f damp i ng i s not correc t. A c orrec tl y damped sy st em w i l l return i mm edi ate l y to the press ure waveform aft er fl ushi ng . Re turn i s sl ow i n an ov erd amp ed sys tem and t here i s ofte n res onance around t he bas el i ne before re turn t o t he pre ssure wav eform i n an unde rdampe d s yst em.

Interpretation of waveform The shape of the arteri a l p res sure w ave form gi ves us eful q ual i t ati ve i nform ati on about the st ate of the he art and ci rcul at i on: Short sys tol i c ti me Hypov ol a emi a High pe ri p heral res i s tance Mark ed res pi rat ory sw i ng Hypov ol a emi a Peri cardi a l e ffusi on Ai rw ays ob struct i on High i ntra-thoraci c p res sure Sl ow s yst ol i c upst rok e Poor myocardi al contracti l i ty High pe ri p heral res i s tance

Limitations of blood pressure monitoring

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It i s i m portant not to rel y on arte ri a l b l ood p res sure m oni tori ng alone i n t he c ri ti c al l y i l l . A normal b l ood p res sure doe s not guarantee ade quate org an bl ood fl ow. C onv ers el y , a l ow b l ood pres sure m ay b e acce ptabl e i f pe rfusi on pre ss ure and bl ood fl ow i s ade quate for al l organs. Measureme nt of cardi a c outp ut, i n ad di ti on t o b l ood pres sure, i s nec ess ary where there i s doubt ab out the ad equacy of the c i rc ul ati on. P.111

Examples of arterial waveform shape

Figure. No Caption Available.

See also: Arteri al cannul at i on, p 112; Hyp ote nsi on, p312; Hy pertensi on, p314 P.112

Arterial cannulation Indications Performed corre ctl y, arteri al cannul at i on i s a safe t echni q ue al l owi ng conti nuous m oni tori ng of bl ood pres sure and fre que nt sam pl i ng of bl ood. It i s i ndi cat ed i n any pat i ent w i t h unst abl e or p otenti al l y unst abl e haem o-dy nam i c or res pi rat ory st atus.

Radial artery cannulation The radi a l art ery i s mos t fre quentl y c hos en b ecause i t i s acce ssi bl e and has good c ol l ate ral bl ood fl ow. Al l en's tes t, use d t o c onfi rm the ul nar arte ri al bl ood sup pl y , i s not rel i ab l e .

Technique of cannulation The wri st i s hyperext end ed and the t hum b ab duc te d. Aft er ski n c l eansi ng l oc al anaest het i c (1% pl ai n l i docai ne) i s i nj ect ed i nt o t he ski n and sub cut ane ous ti ss ue over the m ost promi nent p ul s ati on. The c ourse of the artery i s note d and a 20G Te fl on c annul a i s i nserted al ong the l i ne of the ve ss el . The us ual t echni q ue i s to ent er the ves sel i n t he sam e w ay as an i ntrave nous c annul a woul d be i nserted . T here i s usually some res i st anc e t o s ki n punct ure. To avoi d acc i d ent al l y p unc turi ng the p ost eri or wal l of t he art ery, t he ski n and art ery shoul d b e p unc tured as two di sti nc t manoeuvre s. Al t ernati vel y, a s mal l s ki n ni ck may be made t o faci l i tat e s ki n entry . In the case of el d erl y p ati ent s w i th mobi l e, atheromat ous ve sse l s a t echni q ue that i nvol ve s d el i berate trans fi xati on of the artery m ay be used . T he cannul a i s p ass ed throug h t he ant eri or and poste ri or wal l s of the ves sel , t hus

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i mm obi l i si ng i t. The ne edl e i s removed and the c annul a wi thd raw n s l ow l y i nt o t he l um en ves sel , b efore bei ng adv anc ed forward. Sel di nge r-t ype ki ts are al so avai l a bl e for arte ri a l c annul a ti on. A g ui dewi re i s fi rst i nse rte d t hrough a ri g i d ste el nee dl e . T he i nd wel l i ng p l as ti c c annul a i s then pl a ced ov er the gui de wi re. The cannul a shoul d be conne cte d t o a conti nuous fl ushi ng dev i ce after succe ssful puncture . Fl us hi ng wi th a s yri ng e shoul d be av oi d ed si nce the hi gh pre ssures ge nerate d m ay l ead t o a ret rograde c erebral emb ol us.

Alternative sites for cannulation Brachial artery End artery s upp l yi ng a l arge v ol ume of ti s sue . T hus throm bos i s has potenti al l y s evere c ons equenc es.

Ulnar artery Shoul d be av oi d ed i f the radi a l arte ry i s occ l uded .

Femoral artery May be di ffi cul t t o k eep cl ean. Al so suppl i es a l arge vol ume of ti ssue. A l ong er cat het er shoul d be us ed to avoi d di s pl ace ment .

Dorsalis pedis artery Bl ood press ure wi l l be at l east 10–20m mHg hi ghe r t han i n the c ent ral ci rc ul a ti on.

Complications Di g i tal i sc haem i a due to arteri al s pas m, t hromb osi s or e mbol us Bl e edi ng i n cas es wi t h alte red coagul at i on st atus Infe ct i on i s a ri s k i n p rol ong ed cannul ati on Fal s e aneurys m P.113

See also: Bl ood gas anal y si s , p 100; Invas i v e bl ood gas m oni tori ng, p 102; Bl ood p res sure m oni tori ng , p 110; Routi ne c hanges of di s pos abl es , p 478 P.114

Central venous catheter—use Types of catheter Si ngl e , d oub l e, tri pl e or q uad rupl e l umen. She aths for i ns ert i on of pul monary arte ry cat het er or pac i ng wi re. Tunnel l ed cathe ter for l ong te rm use . Mul ti l ume n c athete rs al l ow mul ti p l e i nfus i ons t o b e gi ven se parate l y ± c ont i nuous press ure moni tori ng . Mi ni mi ses ac ci d ent al bol us ri sk. Large-b ore doubl e l ume n c athete rs use d for venovenous di al ysi s/fi l t rat i on. Comm on routes are i nte rnal j ugul ar, s ubc l a vi a n and femoral . ‘Long’ cathe ters c an be i ns ert ed vi a brachi al or ax i l l ary v ei ns t hough are generall y not used due t o t he ri s k of thromb osi s.

Uses Invasi ve haem ody nami c moni tori ng. Infusi on of d rug s t hat c an c aus e p eri pheral p hl e bi t i s or ti ssue necrosi s i f t i s sue ext ravas ati on occ urs (e .g. TPN , epi nephri ne, ami od arone). Rapi d v ol ume i nfusi on. NB the rate of fl ow i s i nv ers el y proporti onal t o t he l ength of the c annul a . Acc ess , e .g. for p aci ng wi re i nse rti on. Emergency acc ess when peri pheral c i rcul ati on i s ‘s hut down’ . Renal repl ace ment t herapy , p l as map heresi s, exc hange transfusi on.

Contraindications/cautions

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Coag ul opat hy. Undrai ned pne umothorax on contral a teral si de. Agi tat ed, re stl ess pati ent .

Complications Art eri al punct ure . Haem orrhag e. Arrhyt hmi as. Infe ct i on (us ual l y sk i n, oc cas i onal l y s eps i s or end ocardi ti s). Pneumot horax. Ai r em bol i sm , v enous thromb osi s, hae mot horax, chyl othorax (rare).

Central venous pressure measurement Use of an el e ct roni c pre ssure trans duc er i s pre ferabl e t o m anometry w hi c h i nc orp orates a three-way tap , a fl ui d res ervoi r b ag and a fl ui d-fi l l ed verti cal col um n, the he i ght of whi c h c orresp ond s t o C VP. The pres sure t ransducer shoul d be pl ace d and ‘ze roe d’ at the l e vel of the l e ft atri um (approxi mat el y mi d-axi l l ary l i ne) rat her than t he st ernum whi ch i s more affe cte d b y pati ent pos i t i on (s upi ne/sem i -erec t/p rone). Venous pul s ati on and som e resp i ratory swi ng shoul d be se en i n the trace but not a RV pres sure w aveform (i .e. cathe ter i nserted too far).

Troubleshooting Exc ess i ve bl eed i ng at the i nse rt i on si te i s usual l y c ont rol l e d b y d i re ct com pre ssi on. If not c ont rol l e d, correc t any coagul opathy , If p ost -throm bol ysi s, consi der trane xami c aci d. The i nci denc e of l ocal i nfe cti on (us ual l y coagul as e ne gat i ve St aphyl ococ ci or S. aureus) ri ses aft er 5 d ays . R out i ne change of cathe ter at 5–7 days i s not ne ces sary t hough change ov er a wi re may be suffi ci e nt i f the pati e nt dev el ops an une xpl ai ned pyrexi a or neut rop hi l i a. Howev er, re moval ± chang e of s i te i s ne ede d i f t he s i t e i s c el l ul i ti c or b l ood cul tures taken through the cat het er are posi ti v e. P.115

See also: Hae mo(d i a)fi l trati on (1), p62; Haemo(di a )fi l trat i on (2), p 64; Parenteral nut ri ti on, p82; Te mporary p aci ng (1), p54; Tem porary paci ng (2), p56; Cent ral v enous c athete r—ins ert i on, p 116; Pul monary artery c at het er—i ns ert i on, p 120; Fl ui d chall eng e, p 274; R out i ne chang es of d i s pos abl es, p478 P.116

Central venous catheter—insertion Ul t rasound-g ui ded pl acem ent shoul d b e c ons i de red , e spe ci al l y for di ffi c ul t pl ace ments. The t echni q ue wi t h ul tras ound gui dance i s di fferent from the l a ndm ark te chni que; ope rat ors shoul d t o b e abl e to i d ent i fy a p ate nt vei n and mani pul at e b oth probe and c annul a si mul taneousl y . T here w i l l be many si t uat i ons w here an ul trasound de vi c e m ay b e unavai l ab l e so pl a cem ent us i ng anatomi c al l andmarks al one shoul d s ti l l be l earnt .

Landmarks Vari ous l andmarks have b een de scri be d. For ex ampl e: Int ernal jug ul a r: Hal fway be twe en m ast oi d proc ess and s ternal notch, l ate ral to carot i d pul sati on and medi al to medi al border of st ernoc l ei dom ast oi d . Ai m tow ard i p si l at eral ni pp l e, ad vanci ng unde r b ody of ste rnocl e i domas toi d unti l vei n entered. Sub cl a vi a n: 3 c m be l ow junct i on of l a teral thi rd and me di a l t wo thi rd s of cl avi cl e. Turn head to contral a teral si d e. Ai m for p oi nt b etw een jaw and contral ate ral shoul der ti p. Ad vanc e need l e sub cut ane ous l y to hi t cl avi cl e. Scrape ne edl e under c l av i cl e and advance further unt i l ve i n ent ere d. Femoral : Locate femoral arte ry i n groi n. Insert need l e 3cm me di a l l y and angl ed ros trall y. Adv anc e unti l v ei n ente red .

Insertion technique The Se l di ng er tec hni que (de sc ri b ed bel ow) i s safer than t he ‘cathe ter-ov er-nee dl e ’ t echni q ue and shoul d g eneral l y be use d i n ICU pat i ents. 1. Use ase pti c t ec hni que throughout. Cl ean are a w i th anti s ept i c and s urround w i th st eri l e drapes . Anaest het i se l oc al are a wi th 1% l i doc ai ne. F lus h l um en(s ) of c athete r wi th saline. 2. Use met al nee dl e to l ocat e c ent ral ve i n. 3. Pass wi re (wi th ‘J’ or fl opp y e nd l ead i ng) t hroug h ne edl e i nt o ve i n. Onl y mi ni m al res i st anc e at m ost shoul d b e fel t . If not, re mov e wi re and c onfi rm nee dl e ti p i s sti l l l ocat ed wi t hi n ve i n l um en. Moni t or for arrhy thm i as . If

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thes e occur, wi re i s probab l y at tri cus pi d v al v e. Usuall y resp ond s t o retract i ng wi re a few c m. 4. Remove need l e l eavi ng w i re ex trudi ng from sk i n punct ure si te. 5. Depe ndi ng on si ze/t ype of cathe ter to be i nserted , a ri gi d di l a tor (± pre ced ed by a s cal pel i nci s i on t o enl arge punc ture si t e) may be pas sed ov er the wi re t o form a track throug h t he sub cut ane ous ti ss ues to the ve i n. Remove d i l ator. 6. Thread cat het er ove r w i re . Ensure end of wi re ext rud es from c atheter t o preve nt acc i d ent al l os s of wi re i n vei n. Ins ert cathe ter i nto vei n t o d ept h of 15–20cm. Re move wi re. 7. Chec k for fl a shb ack of bl ood dow n e ach l umen and re spi ratory s wi ng, the n fl us h wi th saline. 8. Sut ure cathe ter to sk i n. Cl ean and dry area. C over wi th st eri l e trans parent se mi p erm eabl e d re ssi ng. 9. A CXR i s usual l y p erform ed t o v eri fy corre ct pos i ti on of ti p (j unc ti on of s uperi or v ena cav a and ri g ht atri um) and to e xcl ude a pne umothorax . Unl es s i n an e mergency si t uat i on, a sati sfactory pos i ti on shoul d ge neral l y b e confi rmed before us e of t he c at het er. P.117 P.118

Pulmonary artery catheter—use Though i n cl i ni cal use for 30 years , retrosp ect i ve data analys es sug ges ted an ass oc i at i on be twee n c athete r use and i nc re ase d mort al i ty that has not bee n c onfi rmed by prospe cti ve tri al s. Studi es have al so found an i nad equate knowl e dge bas e regard i ng i nserti on and dat a i nte rpret ati on so p roper trai ni ng i n i ts use i s mandat ed.

Uses Pres sure moni tori ng—R A, RV, PA, PAWP Fl ow moni t ori ng— (ri ght v ent ri c ul a r) cardi ac out put Oxyg en sat urati on— ‘mi xed venous ’ (i .e . i n R V outfl ow tract /PA), det erm i nati on of l eft to ri ght shunt s (ASD , VSD ) Deri ve d vari abl es— SVR , PVR, LVSW , RVSW , DO 2 , VO 2 , O 2 ER Temp orary pac i ng Ri ght v ent ri cul ar eje cti on fracti on and end-d i as tol i c vol ume

Specialised catheters Cont i nuous mi xed ve nous oxyge n s aturat i on me asurem ent Cont i nuous card i ac output m easure ment RV e nd-di a stol i c v ol ume, RV eje cti on fracti on cal cul at i on Ventri cul ar (±atri al ) paci ng

Management Moni tor PA p res sure conti nuousl y to re cog ni s e forw ard cathe ter mi grati on and pul monary arteri a l occl usi on. If so, corre ct i mm edi ate l y by p arti a l c athete r w i thdrawal to preve nt i nfarc ti on. The ri sk of l oc al i nfect i on (usuall y Staph. aureus or c oag ul a se negati ve s tap hyl oc occ i ) ri s es aft er 5 d ays . A cathe ter change ov er a gui d ewi re may be suffi c i ent i f unex pl a i ne d p yre xi a or ne utrophi l i a deve l op s. Rem oval ± change of si te i s nee ded i f the s i te i s ce l l ul i ti c, or pos i ti ve cul tures are grown from ei t her l i ne ti p or b l ood. Wi t hd raw sam pl e s of p ul m onary art ery bl ood sl owl y from the di st al l um en to pre vent ‘ art eri al i zati on’, i . e. pul monary venous sampl i ng .

Wedge pressure measurements Infl at e b al l oon sl owl y, moni tori ng the wav eform to avoi d overwed gi ng and pot ent i al ve sse l rupt ure es pec i al l y i f el d erl y and/or pul monary hy pertensi v e. The trace shoul d onl y ‘w edg e’ afte r ≥ 1.3ml ai r has b een i njec ted . Measure at e nd-e xpi rati on when i nt rathorac i c pre ss ure i s cl ose st to atm osp heri c press ure . For v ent i l ate d p ati ent s e nd exp i rati on ≡ l owes t w edg e readi ng ; duri ng spontaneous b reathi ng end ex pi rat i on ≡ hi ghest readi ng . Me asurem ent i s di ffi c ul t i n t he dys pnoei c pati e nt; a ‘ mean’ wed ge readi ng m ay b e used i n thi s i nstance . The PAWP cannot be hi ghe r t han the PA di as tol i c pre ss ure . CVP, PAWP and CO shoul d not be measured duri ng rapi d vol um e i nfusi on b ut aft er a p eri od of equi l i brati on (5-10 mi n). The PAWP doe s not e qual t he LVEDP i n mi tral s tenosi s. In mi t ral regurgi tat i on me asure PAW P at t he end of the ‘A’ w ave .

West's zones The cathe ter ti p s houl d l i e i n a zone III re gi on where PA pres sure >PV p re ssure >al veol ar press ure and b el ow l eft

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atri a l l eve l on a l at eral CXR. Sus pec t a non-z one III p osi ti on i f (i ) fol l ow i ng a ri s e i n PEEP, t he PAW P ri se s b y > 50% of the i ncre ment, (i i ) t he wed ge trace shows no d ete ctabl e cardi ac pul sati on and/or exce ss re spi rat ory vari a ti on. A non-zone III pos i ti on i s more l i k el y wi th PEEP and/or hypovol aemi a. P.119

Normal values Stroke volume

70–100ml

Cardiac output

4–6l/min

Right atrial pressure

0–5mmHg

Right ventricular pressure

20–25/0–5mmHg

Pulmonary artery pressure

20–25/10–15mmHg

Pulmonary artery wedge pressure

6–12mmHg

Mixed venous oxygen saturation

70–75%

Derived variables

Key trials and studies Connors AF Jr e t al . The effect i ve nes s of ri ght heart c athete ri zat i on i n the i ni t i a l c are of cri ti cal l y i l l p ati ent s. JAM A 1996; 276:889–97 Ri c hard C et al . Earl y use of t he pul monary artery c athete r and out com es i n pat i ents wi t h s hoc k and acute res pi rat ory di s tress sy ndrome : a random i ze d c ont rol l e d t ri a l . JAM A 2003; 290:2713–20 Ibe rt i T J et al . A mul t i ce nte r s tud y of p hys i ci ans ' k now l ed ge of t he pul monary artery c athete r. JAM A 1990; 264:2928–32

See also: Pos i ti ve end ex pi ratory pre ss ure (1), p 22; Pos i t i ve end ex pi rat ory press ure (2), p 24; Bl ood gas anal ysi s, p100; Ext rav asc ul ar l ung water me asurem ent , p 104; Ce ntral venous cathe ter—us e, p114; Cent ral ve nous cat het er— inserti on, p116; Pul monary arte ry cat het er—i nserti on, p120; Cardi ac out put—t hermod i l uti on, p122; C ard i ac out put —ot her i nvas i v e, p 124; Flui d c hal l enge, p274; He art failure—ass ess ment, p324; R out i ne chang es of di s pos abl es , p 478

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P.120

Pulmonary artery catheter—insertion Insertion 1. Ins ert 8Fr c ent ral ve nous i ntroducer sheat h unde r s tri ct as ept i c tec hni que. Pul monary art ery cathe teri s ati on i s easi er vi a i nte rnal j ugul ar or subcl avi an vei ns. 2. Prep are cathe ter pre-i ns ert i on—3-way tap s on all lum ens , fl us h l ume ns wi t h c ry stalloi d, i nfl ate bal l oon w i th 1.6m l air and c hec k for c onc ent ri c i nfl ati on and l e aks , p l ac e t ransparent s l ee ve ove r c athete r t o m ai ntai n future ste ri l i t y, p re ssure transd uce di st al l um en and zero t o a re ferenc e p oi nt (usual l y m i d-axi l l a ry l i ne). De pendi ng on cat het er typ e, othe r p re-i ns erti on c al i brati on ste ps may be req ui red, e. g. oxy gen sat urati on. 3. Ins ert cathe ter 15cm (i . e. beyond the l e ngt h of t he i nt rod uce r s heath) be fore i nfl ati ng bal l oon. Adv anc e c athete r smoothl y t hroug h t he ri g ht heart chambe rs. Pause to rec ord p res sures and note wave form s hap e i n RA, R V and PA. Whe n a characte ri sti c PAWP waveform i s obt ai ned, st op adv anc i ng cathe ter, d efl ate balloon and ensure t hat PA w ave form reap pears. If not , w i thdraw c athete r b y a fe w cm . 4. Sl owl y re -i nfl a te bal l oon, obs erv i ng wav eform trace. The we dge re cordi ng shoul d not b e ob tai ned unti l at l eas t 1.3m l of air has be en i nj ect ed i nt o t he bal l oon. If not , wi thdraw c atheter 1–2c m and repe at. If ‘overwed ged’ (pre ss ure conti nue s t o c l i m b on i nfl ati on), c athete r i s i ns ert ed too far and b al l oon has i nfl ate d forw ard ov er di s tal l umen. Imme di a tel y d efl ate , wi thdraw cathe ter 1–2c m and repe at. 5. Aft er i ns ert i on, a CXR i s usually pe rforme d t o v eri fy cat het er pos i ti on and to ex cl ude pne umot horax.

Contraindications/cautions Coag ul opat hy Tri cus pi d valve prost hes i s or di sease

Complications Prob l e ms of c ent ral ve nous c athete ri sat i on Arrhyt hmi as (es pec i al l y whe n t rav ers i ng tri c usp i d val ve) Infe ct i on (i ncl udi ng end ocardi ti s) Pul monary art ery rupt ure Pul monary i nfarc ti on Knot ti ng of c athete r Val ve d amage (do not wi thd raw cathe ter unl es s b al l oon de fl a ted )

Troubleshooting Exc ess i ve cathe ter l engt h i n a he art chamb er causes coi l i ng and a ri sk of k not ti ng. No more t han 15–20cm shoul d be pas sed be fore t he wave form c hanges . If not, defl at e b al l oon, w i thdraw c athete r, rep eat . A knot can be manage d b y (i ) ‘unknott i ng ’ w i th an i ntral umi nal wi re, (i i ) p ul l i ng taut and re mov i ng cathe ter + i nt rod uce r s heath tog ether, or (i i i ) surgi cal or angi ographi c i nt erv ent i on. If cat het er fai l s to adv anc e t o next chambe r, consi der ‘s ti ffeni ng ’ c athete r b y i nje cti ng i c ed cry stalloi d through di s tal l um en, rol l i ng pati e nt to l eft l ate ral posi t i on or ad vanci ng c at het er sl owl y wi th bal l oon d efl ated . The cathe ter shoul d neve r b e wi thdrawn wi t h t he b al l oon i nfl ate d. Arrhy thm i as on i nserti on usuall y oc cur w hen the cathe ter ti p i s at the tri cuspi d val ve. The se usual l y resol ve on wi t hdrawi ng the cathe ter or, occasi onal l y , after a sl ow b ol us of 1.5m g/kg l i docai ne. P.121

Waveforms

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Figure. No Caption Available.

See also: Central v enous cat het er— ins erti on, p116; Pul monary arte ry cat het er—use , p 118; Pneum othorax, p300; Hae mot horax, p302; Tac hyarrhythmi a s, p316 P.122

Cardiac output—thermodilution The rmodi l ut i on i s the t echni q ue uti l i sed by the pul monary arte ry cat het er to measure ri g ht vent ri cul ar cardi ac out put . The pri nc i p l e i s a m odi fi c ati on of the Fi ck p ri nci pl e where by a b ol us of cool e d 5% g l uc ose i s i njec ted through the proxi m al l umen i nt o t he central ci rcul at i on (ri ght atri um) and t he t emp erature c hange i s det ect ed by a t hermi s tor at the cathe ter ti p, som e 30cm di stal. A modi fi cat i on of the Hami l ton–Stew art eq uat i on, uti l i s i ng the vol ume, tem perature and sp eci fi c he at of the i njec tat e, enab l e s c ard i ac output t o b e c al c ul a ted by an on-l i ne c omp ute r from a curve measuri ng te mpe rat ure chang e i n t he pul monary artery. Conti nuous t hermod i l uti on meas urement uses a mod i fi ed cat het er that e mi t s heat pul se s from a the rmal fi l a ment l yi ng wi t hi n t he ri g ht ventri cl e and ri g ht atri um , 14–25cm from the ti p. 7.5W of he at are ad ded to the bl ood i nt ermi t tentl y ev ery 30–60s and t hes e t emp erature c hanges are m eas ure d b y a the rmi st or 4cm from the ti p. Though upd ate d freq uentl y , t he cardi a c outp ut di s pl ayed i s usually an ave rag e of t he pre vi ous 3–6mi n.

Thermodilution injection technique The computer const ant must be set for t he vol ume and te mpe rat ure of the 5% gl ucose use d. 10m l of i ce-col d g l uc ose provi d es the most acc urate measure. 5ml of room t emp erature i nje ct ate i s suffi ci e ntl y p rec i s e for norm al and hi gh out put st ate s howe ver i t s accurac y d oes worse n at l ow outp ut val ues . 1. Pres s ‘St art ’ b utt on on com put er. 2. Inje ct fl ui d sm oot hl y ove r 2–3s . 3. Repe at at l east twi ce more at rand om p oi nts i n the resp i ratory c ycl e. 4. Averag e 3 measureme nts falli ng wi t hi n 10% of e ach ot her. Re jec t outp uts gaine d from curve s t hat are i rregul ar/non-s mooth.

Erroneous readings Val ve l es i ons—t ri cus pi d re gurgi tat i on wi l l al l ow som e of the i nje ctate to refl ux back i nt o t he ri g ht atri um. Aorti c i nc omp etence produc es a hi gher l e ft v ent ri cul ar out put as a proporti on w i l l regurgi tat e b ack i nto the l e ft vent ri cl e . Sep tal de fect s. Los s of i njec tat e. Che ck that c onnect i ons are ti g ht and do not l eak .

Advantages Most commonl y us ed and fam i l i ar IC U t echni q ue, computer warni ngs of poor c urves .

Disadvantages Non-conti nuous (by i nj ect i on te chni que). 5–10% i nte r- and i ntraobs erver vari a bi l i ty . Errone ous re adi ngs wi th tri cuspi d regurgi tat i on, i nt rac ard i ac s hunts. Freq uentl y repeated me asurem ent s m ay res ul t i n consi derabl e v ol umes of 5% gl ucose b ei ng i nj ect ed. P.123

See also: Pul monary artery c athete r—use, p118; Cardi ac out put —ot her i nvas i ve , p 124; Cardi ac out put—non-i nvasi ve (1), p146; Cardi a c outp ut— non-i nvas i ve (2), p 146; Fl ui d challe nge , p 274; Hy pot ens i on, p 312; Heart fai l ure —as ses sme nt, p324; Sys tem i c i nfl a mmat i on/mul t i -organ fail ure , p 484; Burns —fl ui d manag ement, p510 P.124

Cardiac output—other invasive Dye dilution Mi x i ng of a gi v en vol ume of i nd i cator t o an unknown v ol ume of fl ui d al l ows calcul at i on of thi s vol ume from the de gre e of i nd i cator di l uti on. The ti me el a pse d for the i ndi c ator t o p ass some di s tance i n the cardi ovascul ar s yst em y i el ds a

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cardi ac out put val ue, calc ul a ted as :

…where I i s the amount of i ndi c at or i nj ect ed, C m i s the me an c onc ent rati on of the i ndi cator and t i s the t otal d urati on of the curve . T he t radi t i onal dye di l ut i on t echni q ue i s to i nj ect i ndoc yani ne green i nto a c ent ral ve i n fol l ow ed b y rep eat ed sam pl i ng of art eri al bl ood to enabl e const ruc ti on of a ti me–concentrati on curve wi t h a rap i d up stroke and an exp one nti al dec ay. Pl ott i ng the d ye dec ay c urve s emi l og ari thmi c al l y and ext rap ol a ti ng v al ues to the ori gi n p roduc es the cardi ac out put . T he COLD-Pul s i on de vi c e m eas ure s t he concentrati on d ecay d i rect l y from an i ndwe l l i ng arteri al probe, thus com put i ng card i ac output. Al t ernati vel y, thi s dev i ce may us e t he the rmodi l ut i on app roach, av oi d i ng pul monary artery c athete ri sat i on. T he Li D CO dev i ce i s based on a s i m i l a r p ri nci pl e us i ng l i thi um as the ‘ dye’ .

Advantages Reasonabl y ac curat e, l es s i nvasi v e t han pul monary arte ry cat het er pl a cem ent .

Disadvantages Inv asi ve, re ci rcul at i on of dy e preve nts mul t i pl e repe ate d m easure ment s, l e ngt hy, und erest i mates l ow output v al ues. Inaccurate w i t h moderate / s eve re val vul ar reg urg i tati on. Use of paral ysi ng age nts may i nte rfe re wi t h l i thi um measureme nt.

Direct Fick The am ount of subst anc e p ass i ng i nto a fl ow i ng sy st em i s e qual t o t he di fferenc e i n c onc ent rat i on of the s ubs tance on eac h s i de of the s yst em m ul ti p l i e d b y t he fl ow wi thi n the sy ste m. C ard i ac output i s thus usually calcul a ted by di v i d i ng total body oxyg en consum pti on by the di fference i n oxyg en content b etw een art eri al and m i xe d ve nous bl ood. Al te rnati v el y , CO 2 p rod uct i on can b e used i nste ad of VO 2 as t he i ndi c ator. Art eri al C O 2 can be deri v ed non-i nvas i ve l y from e nd-t i d al CO 2 whi l e mi xed venous CO 2 c an b e d ete rmi ned by rapi d re breathi ng i nto a b ag unt i l CO 2 l e vel s have eq ui l i brate d.

Advantages ‘Gol d st and ard ’ for cardi a c outp ut est i mati on.

Disadvantages For VO 2 : Invasi ve (req ui res measureme nt of mi x ed v enous bl ood), requi re s l eak -free open ci rc ui t or an unwi e l dy cl osed ci rc ui t te chni q ue. Oxy gen consumpt i on me asurem ent s v i a met abol i c cart unrel i ab l e i f FIO 2 i s hi g h. Lung oxy gen consumpt i on not me asured by pul monary arte ry cat het er tec hni que (m ay be hi g h i n ARDS, p neumoni a…). For CO 2 : Non-i nv asi ve but re qui re s norm al l ung func ti on and i s thus not generally ap pl i cab l e i n ICU pati e nts . P.125

See also: CO 2 moni t ori ng , p92; Bl ood g as analys i s , p 100; Ext ravas cul ar l ung w ate r m eas ure ment , p 104; Pul monary arte ry cat het er—us e, p 118; C ard i ac output—t hermod i l uti on, p122; Cardi a c outp ut— non-i nvas i ve (1), p 126; C ard i ac out put —non-i nvasi v e (2), p128; Indi rect calori m etry, p168; Fl ui d chal l enge, p274; Hyp ote nsi on, p312; Heart fai l ure— ass ess ment, p324; Syst emi c i nfl amm ati on/mul ti -org an fai l ure, p484; Burns—fl ui d m anagem ent , p 510 P.126

Cardiac output—non-invasive (1) Doppler ultrasound An ul trasound beam of known fre que ncy i s re fl e ct ed b y m ovi ng red bl ood corpuscl es wi t h a shi ft i n frequenc y proporti onal t o t he b l ood fl ow ve l oc i ty . T he act ual ve l oc i ty can b e c al c ul a ted from the Doppl er equati on whi ch req ui res the c osi ne of t he vec tor be twe en the di rec ti on of t he ul t ras ound b eam and that of bl ood fl ow. T hi s has b een app l i ed t o b l ood fl ow i n the asce ndi ng aorta and aorti c arch (v i a a suprast ernal app roach), d esc end i ng thoraci c aorta (oe sop hag eal app roach) and i ntracard i ac fl ow (e.g . t ransmi tral from an ap i cal approac h). Sp ect ral anal ysi s of t he Dop pl e r freq uency shi ft s p rod uce s v el oci t y–t i me waveforms , t he are a of whi c h represe nts the ‘ stroke di stance ’, i .e . the di st anc e trave l l ed by a col um n of b l ood wi th eac h l eft ve ntri c ul a r s yst ol e (s ee fi g ure op pos i te ). The produc t of stroke di st anc e and aort i c (or mi tral val ve) cross -sec ti onal area i s st rok e v ol ume. Cross -sec ti onal area can be measured echocardi ographi c al l y; howe ver, as b oth op erator exp erti s e and equi pm ent i s re qui red , t hi s ad di ti onal measureme nt can be ei the r i gnored or as sum ed from nomog ram s t o p rov i de a reasonabl e es tim ate of st rok e vol um e.

Advantages Qui ck , s afe, mi ni m al l y i nv asi ve, re asonabl y accurate, conti nuous (vi a oe sop hag eal ap proach), othe r i nform ati on on contract i l i ty, prel oad and afterl oad from wav eform shape (see fi gure opposi t e).

Disadvantages Non-conti nuous (unl es s v i a oes ophagus), l earni ng curve , operator d ependent.

Echocardiography Com bi nes struct ural as wel l as d ynam i c ass es sment of t he heart usi ng ul t rasound refl ec ted off vari ous i nterfac es. Transt horac i c or transoesophageal p rob es provi d e i nformati on on v al v e i nte gri ty, gl obal (di a stol i c and s yst ol i c) and

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reg i onal ventri cul ar funct i on, w al l thi c kne ss, pe ri c ard i al fl ui d or t hi c keni ng , aort i c di sse cti on, ve ntri c ul a r v ol umes and eje cti on fracti on, and p ul m onary pre ssures . Oft en c omb i ne d w i th i nteg ral D opp l er ul trasound for cardi ac out put est i mati on d eri ve d from com bi ned measureme nt of aort i c di ame ter pl us fl ow at vari ous si tes , e .g. l e ft vent ri cul ar out fl ow t rac t, aorta, trans mi tral. Analyt i c software or formul ae can al so enabl e comput at i on of cardi ac out put from est i mati ons of ventri cul ar vol um es.

Advantages Non-i nvas i ve , s afe , rel a ti v el y qui ck . Prov i de s othe r useful i nform ati on on cardi a c s truct ure and func ti on.

Disadvantages Exp ens i ve eq ui p ment, l engthy l earni ng c urve and i nt erobse rve r v ari ab i l i ty. Body hab i tus or p athol ogy (e. g. emp hys ema) may i mpair i mage qualit y. P.127

Doppler blood flow velocity waveform variables

Figure. No Caption Available.

Changes in Doppler flow velocity waveform shape

Figure. No Caption Available.

See also: Cardi a c outp ut— the rmodi l ut i on, p 122; Cardi ac out put —ot her i nvas i ve , p 124; Card i ac output—non-i nv asi ve (2), p128; Fl ui d chall eng e, p 274; Hypotensi on, p312; Heart fai l ure—asse ssm ent , p 324; Sy ste mi c i nfl ammati on/m ul t i -org an fai l ure, p484; Burns— fl ui d manage ment, p510 P.128

Cardiac output—non-invasive (2) Pulse contour analysis The conce pt of thi s t echni q ue i s that t he contour of t he art eri al press ure wav eform i s proporti onal t o s troke vol ume. How ever, i t i s al s o i nfl uenced by aorti c i mpe dance so anothe r c ard i ac output m eas uri ng tec hni que (e .g. comme rci al dev i ce s uti l i s i ng COLD -Pul si on or Li D CO) must be used i n t ande m for i ni ti al cal i brat i on. Al thoug h i t c an the n b e used as a m eans of conti nuous cardi ac out put moni t ori ng, frequent re -calib rat i on s houl d be p erformed agains t t he refere nce te chni que. Thi s i s parti c ul arl y i mportant whe n c hang es i n i m pedance oc cur, e .g. wi th change s i n c ard i ac

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out put , v asc ul a r t one , b ody te mpe rat ure .

Advantages Conti nuous fl ow moni t ori ng, us es dat a from arteri al cannul a al read y in si tu for press ure moni t ori ng.

Disadvantages Change s i n v asc ul a r c omp l i ance wi l l affect ac curac y requi ri ng fre que nt rec al i brati on. Req ui res a good qual i ty , non-ob struct ed and non-d ampe d arte ri al wave form. The re i s deb ate about the re l at i v e qual i ty of si gnal from radi a l v s. fem oral arte ry.

Thoracic bioimpedance Imp edance chang es ori gi nate i n the t horaci c aorta w hen bl ood i s ej ect ed from t he l eft ve ntri c l e. Thi s effect i s us ed to det erm i ne st roke v ol ume from formul a e ut i l i si ng the el ect ri cal fi el d si ze of the thorax, bas el i ne thorac i c i m ped anc e and fl uct uat i on rel a ted to sys tol e, and ve ntri c ul a r e jec ti on t i me . A corre ct i on fac tor for s ex, he i ght and wei ght i s al so i nt roduc ed. The te chni q ue s i m pl y ut i l i se s four pai rs of el ect rod es pl a ced i n prosc ri bed pos i t i ons on t he nec k and thorax ; t hes e are connec ted to a d edi cat ed moni tor w hi c h m eas ure s t horaci c i mp edance to a l ow ampl i t ude , hi gh (70kHz) freq uenc y 2.5m A c urrent appl i ed ac ros s t he el e ctrode s.

Advantages Qui ck , s afe, total l y non-i nvas i ve , reas onabl y ac curate i n normal, spontaneousl y b reathi ng sub jec ts.

Disadvantages Di screpanci es i n cri ti cal l y i l l p ati ent s (esp eci al l y t hos e w i th arrhythmi a s, tac hyc ard i as , i ntrat horaci c fl ui d s hi fts , anatom i cal d eformi ti es, aorti c regurgi tat i on), met al wi t hi n t he t horax, i nabi l i ty to veri fy si gnal. P.129

See also: Cardi a c outp ut— the rmodi l ut i on, p 122; Cardi ac out put —ot her i nvas i ve , p 124; Card i ac output—non-i nv asi ve (1), p126; Fl ui d chall eng e, p 274; Hypotensi on, p312; Heart fai l ure—asse ssm ent , p 324; Sy ste mi c i nfl ammati on/m ul t i -org an fai l ure, p484; Burns— fl ui d manage ment, p510 P.130

Gut tonometry A g as permeabl e si l i cone b al l oon at tac hed to a s amp l i ng t ube i s pass ed i nt o t he l ume n of t he gut . D evi ces ex i st for tonome try i n the s tom ach or si gmoi d col on. The t onomet er al l ows i ndi rect me asurem ent of the PCO 2 of t he g ut muc osa and c al c ul a ti on of t he pH of t he muc osa.

Indications Gut mucos al hyp ope rfusi on i s an e arl y c ons equenc e of hypov ol a emi a. Cove rt ci rcul at ory i nad equacy due to hyp ovol ae mi a may be de tec ted as gut mucos al ac i dosi s and has been rel a ted to pos t-operati ve com pl i cat i ons aft er maj or surgery. In cri ti cal l y i l l p ati ent s t here i s s ome ev i de nce that pre venti on of gut m ucosal ac i d osi s i mprove s out com e. The si gmoi d col on tonomet er i s us eful t o d ete ct i sc hae mi c col i ti s earl y (e .g. aft er abd omi nal vascul ar surgery).

Technique Saline tonometry In the ori gi nal t echni q ue the tonome ter ball oon was prepared by de gas si ng and fi l l i ng w i t h 2. 5ml 0. 9% sal i ne. T he sal i ne was w i thdrawn i nt o a sy ri nge connec ted to the s amp l i ng t ube pri or to i nserti on. After i nserti on the saline w as pas sed back i nt o t he bal l oon. The PCO 2 of t he sal i ne i n the b al l oon eq ui l i b rat ed wi t h t he PC O 2 of t he gut l umen ov er a peri od of 30–90mi n. At s teady state i t was as sum ed that t he PC O 2 of t he gut l umen and g ut muc osa were i n equi l i bri um . T i me corre ct i on fac tors were de ri ved for parti al eq ui l i brat i on bet wee n t he bal l oon s al i ne and the g ut l um en. The m eas ure ment was c omp l et ed by sam pl i ng the saline from the b al l oon and an arteri a l b l ood s amp l e for measureme nt of art eri al [HC O 3 - ].

Gas tonometry Usi ng ai r i n t he tonomet ry bal l oon all ows more rapi d e qui l i brati on b etw een the t onom ete r and the l umi nal PCO 2 . A mod i fi ed cap nom ete r automat i cally fi l l s t he bal l oon wi th ai r and samp l e s t he PCO 2 afte r 5–10mi n eq ui l i b rat i on. Sub seq uent c ycl es of bal l oon fi l l i ng d o not use fresh ai r s o CO 2 equi l i brati on i s qui ck er. Tonome tri c PCO 2 m ay be com pared wi t h e nd-ti d al PCO 2 (m eas ure d w i th the s ame capnom ete r) as an est i mate of art eri al PCO 2 . Wi t h a normal cap nog ram , a balloon PCO 2 si gni fi cantl y hi ghe r t han end-t i dal PCO 2 i mpl i e s g ut muc osal hypop erfusi on.

pH versus regional PCO 2 The pH of the gut m ucosa (pHi) may be cal cul at ed usi ng a modi fi ed He nde rson–Hass el b ach eq uat i on:

whe re K i s t he ti m e d ependent e qui l i brati on c ons tant. How ever, most of the v ari ati on i n the me asurem ent i s due t o vari at i on i n regi onal PCO 2 . Com pari ng re gi onal PCO 2 w i th PaCO 2 gi ves as much i nform ati on as mak i ng the c al c ul a ti on

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of pHi and overcome s t he probl emat i c as sum pti on that arte ri a l [HCO 3 - ] i s equi valent t o m ucosal capi l l a ry [HCO 3 - ]. P.131

See also: CO 2 moni t ori ng , p92; Bl ood g as analys i s , p 100 Ovid: Oxford Handbook of Critical Care

Ed itors:

Si nge r, M ervyn; We bb, An dre w R.

Ti tle : O xf ord Ha ndbook of Cr itic al Car e, 2nd Ed ition Cop yri ght © 1997,2005 M. Si nge r and A. R. W ebb , 1997, 2005. Publ i shed i n the Uni te d Stat es by Oxford Uni ve rsi ty Press Inc > Tab le of Co n te n ts > Neu r ol ogi cal Mo n it or i n g

Neurological Monitoring Intracranial pressure monitoring Indications To confi rm t he di a gnosi s of raise d i nt rac rani al press ure (ICP) and moni t or treat ment. May be use d i n c ase s of he ad i nj ury part i cul arl y i f venti l at ed, Gl asg ow C oma Sc ore ≤8, or wi th an abnorm al CT scan. Al s o used i n encep hal opathy , pos t-neurosurge ry and i n se l ec ted cases of i ntracrani al hae morrhage. Al though a rai sed IC P c an b e rel ated to poor prognosi s after he ad i nj ury , t he converse i s not true. Sust ai ned red uct i on of raise d ICP (or mai nte nance of cerebral perfus i on pres sure) i n head i njury m ay i mp rov e outc ome al t hough l arge control l ed tri al s are l ac ki ng.

Methods of monitoring intracranial pressure Ventricular monitoring A c athete r i s i ns ert ed i nt o t he l at eral v ent ri cl e vi a a burr hol e. The cathe ter may be conne cte d t o a press ure trans duc er or may contai n a fi bre opt i c press ure moni t ori ng dev i ce . F ibreop ti c c athete rs req ui re regul ar c al i brati on acc ord i ng t o t he m anufac turer' s i ns truct i ons. Bot h s yst ems shoul d b e t est ed for pat enc y and dam pi ng b y t emp orari l y rai si ng i nt rac rani a l p res sure (e.g . wi th a c oug h or b y occl udi ng a j ugul ar ve i n). C SF may be draine d t hrough the ventri cul ar cathe ter to re duc e i ntrac rani al press ure.

Subdural monitoring The dura i s ope ned vi a a burr hol e and a hol l ow b ol t i nserte d i nto the s kul l . The bol t may be connec ted to a p re ssure trans duc er or admi t a fi breop ti c or hi -fi del i t y pres sure m oni tori ng de vi c e. A s ubd ural b ol t i s e asi er to i ns ert than ventri cul ar moni t ors . T he mai n d i sadvantages of sub dural moni t ori ng are a tendency t o unde res ti mat e ICP and dam pi ng e ffe cts . Agai n c al i brati on and pat enc y t est i ng s houl d be performed reg ul arl y.

Complications Infect i on—part i cul arl y aft er 5 d ays Hae morrhage— parti c ul arl y w i th coagul op athy or d i ffi cul t i nserti on

Using ICP monitoring Normal IC P i s < 10m mHg . A raise d ICP i s usual l y t reated when > 25m mHg i n he ad i nj ury . As ICP i nc reases , t here are oft en sus tai ned ri se s i n ICP t o 50–100m mHg l a sti ng for 5–20m i n, i ncreas i ng wi th fre que ncy as the basel i ne ICP ri s es. Thi s i s ass oci ate d w i th a 60% mortal i t y. Cere bral perfus i on press ure (C PP) i s the di ffe rence bet ween me an BP and mean ICP. Treatm ent ai med at re duc i ng IC P m ay als o reduc e m ean BP. It i s i mport ant to mai ntain CPP >50–60mmHg. P.135

See also: Int racrani a l haem orrhag e, p376; Subarachnoi d haem orrhag e, p378; R ai s ed i nt rac rani a l p res sure, p382; He ad i nj ury (1), p 504; Head i njury (2), p506 P.136

Jugular venous bulb saturation Ret rog rad e p ass age of a fi bre-opti c c athete r from the i nte rnal jugul a r v ei n i nto the jug ul ar bul b e nab l es conti nuous moni tori ng of j ugul ar ve nous b ul b saturati on (SjO 2 ). Thi s can be us ed i n conjuncti on wi t h othe r m oni tors of c ere bral hae mod ynam i c s s uch as mi ddl e c ere bral b l ood fl ow , c ere bral arte ri ovenous l a ct ate di fferenc e and i nt rac rani a l pre ss ure to di rec t m anageme nt.

Principles of SjO 2 management Normal value s are app rox i matel y 65–70%. In the ab sence of anae mi a and w i th maint enance of normal SaO 2 value s, val ues of Sj O 2 >75% sugge st l uxury pe rfusi on or gl obal i nfarcti on wi t h oxyg en not bei ng ut i l i sed ; v al ues <54% corre spond t o c erebral hyp operfus i on whi l e values < 40% sugge st gl obal i s chaemi a and are us ual l y ass oci ate d w i th

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i nc re ase d c ere bral l act ate producti on. Knowl edg e of SjO 2 allows opt i mi sat i on of brai n bl ood fl ow to avoi d (i ) ei t her exc ess i ve or i nade quate perfus i on and (i i ) i a trogeni call y i nduced hyp ope rfusi on t hroug h t reati ng rai s ed i nt racrani a l pre ss ure agg re ssi vel y w i th di ure ti cs and hyp erv ent i l ati on. St udi es i n traum a pati ent s have found (i ) a hi gher mortal i t y wi th epi sodes of jug ul a r v enous des aturat i on and (i i ) a si g ni fi cant rel at i onshi p b etw een cereb ral pe rfusi on pre ss ure (CPP) and Sj O 2 whe n t he C PP was <70mmHg. A fal l i ng SjO 2 may b e an i ndi cat i on to i ncreas e CPP t hough no prospe ct i ve random i s ed t ri al has ye t b een performed to st udy the e ffec t on outc ome . App roxi m atel y 85% of cerebral venous drai nage passe s d own one of the i nte rnal j ugul ar ve i ns (usually the ri ght). SjO 2 usuall y represe nts drai nage from bot h hemi sphere s and i s equal on b oth si des ; howe ver, after focal i njury, thi s pat tern of d rai nag e m ay alt er.

Insertion technique 1. Ins ert i ntroduc er sheath rost ral l y i n i nt ernal jugul ar vei n. 2. Cal i brate fi bre opt i c cat het er pre -i nserti on. 3. Ins ert cathe ter vi a i ntroducer s heat h; adv anc e t o jugul ar bul b. 4. Wi t hdraw i nt rod uce r s heath. 5. Confi rm (i ) free as pi rati on of bl ood vi a cat het er, (i i ) sat i s fac tory l i ght i nt ens i ty re adi ng, (i i i ) sati s fac tory posi ti oni ng of cat het er ti p by l a teral cervi cal X-ray (hi gh i n jug ul ar bul b, above l eve l of 2nd cervi c al verteb ra). 6. Perform in vi vo cal i brat i on, repe at c al i brati on 12-hrl y.

Troubleshooting If the cathe ter i s si te d t oo l ow i n the jugul ar bul b, erroneous SjO 2 v al ues may re sul t from mi xi ng of i ntrace reb ral and ext rac ere bral venous bl ood. Thi s coul d be parti cul arl y p ert i nent whe n c ere bral b l ood fl ow i s l ow. Ens ure l i ght i nte nsi ty readi ng i s sat i sfact ory ; i f t oo hi g h t he cat het er may be abutti ng agains t a wall, and i f l ow the cat het er may not b e patent or have a smal l cl ot over the t i p. Be fore t reati ng t he pat i ent, al w ays confi rm the ve rac i ty of l ow re adi ngs ag ai nst a b l ood s ampl e d rawn from the c athete r and meas ured i n a co-ox i me ter. P.137

Formulae

where

SjO 2 = jugular bulb oxygen saturation SaO 2 (%) = arterial oxygen saturation CMRO 2 = cerebral metabolism of oxygen CBF = cerebral blood flow

cerebral perfusi on p res sure = mean sy st emi c BP -i nt rac rani al pres sure

See also: Int racrani a l p res sure m oni tori ng, p134; Other neurol ogi cal m oni tori ng , p 140; Int rac rani a l haemorrhag e, p 376; Sub arachnoi d haemorrhage , p 378; Raise d i ntrac rani al press ure, p 382; Head i njury (1), p504; He ad i nj ury (2), p506 P.138

EEG/CFM monitoring EEG monitoring The EEG refl ect s c hanges i n cort i cal e l ec tri cal func ti on. Thi s, i n turn, i s de pendent on ce reb ral p erfusi on and oxy genati on. EEG m oni tori ng can b e useful to ass ess ep i l e pti form acti vi ty as w el l as ce reb ral we l l -bei ng i n pat i e nts who are s edat ed and paral yse d. The conve nti onal EEG can be us ed i nt erm i tt ent l y but data red uct i on and arte fac t sup press i on are neces sary to all ow s uc ces sful use of EEG rec ordi ngs i n the IC U.

Bispectral index (BIS) monitor BIS i s a st ati sti cal i nde x d eri ved from t he EEG and e xpress ed as a s core b etwe en 0 and 100. Scores bel ow 50 have bee n rel i abl y associ ate d wi th anaest hes i a-i nd uc ed unconsc i ousness . Asse ssm ent i n the c ri ti c al l y i l l pati e nt may be com pl i cated by vari ous c onfoundi ng fact ors such as sep ti c e nce phal op athy, head traum a and hypoperfus i on. A l ow score i s re l at ed to deep or ex ces si v e s edati on, and may al l ow dose red uct i on (or c ess ati on) of se dat i ve age nts , esp eci al l y i n paral y sed pati e nts .

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Cerebral function monitor (CFM) The CFM i s a si ngl e c hannel , fi l t ere d t rac e from 2 rec ord i ng el ect rodes pl ace d ov er the pari e tal regi ons of the sc al p. A thi rd el ect rod e m ay b e used i n the m i dl i ne to he l p wi t h i nt erfere nce det ect i on. The pari e tal re cordi ng e l ec trodes are usual l y p l aced cl ose to wat ers hed areas of the b rai n i n orde r t o allow m axi mum sensi ti v i ty for i schaem i a det ect i on. Vol tage i s di s pl a yed ag ai nst ti m e on a chart runni ng at 6–30cm /h.

Figure. No Caption Available.

Use of CFM The CFM may d ete ct cerebral i sc hae mi a ; b urs t s upp re ssi on (peri ods of i nc reasi ngl y prol onge d e l ec tri cal s i l enc e) provi d e an e arl y w arni ng . Sed ati on produc es a fal l i n basel i ne t o <5µV, eq ui val ent to burst suppress i on. T hi s i s e qui val ent to max i mum red uct i on i n c ere bral VO 2 and no furt her be nefi t woul d be gai ned from addi ti onal s edat i on. Sei zure act i vi ty may be det ect ed i n pat i ents des pi te app are ntl y adequate cl i ni cal c ont rol or where muscl e rel axants hav e b een use d. P.139

Typical CFM patterns

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Figure. No Caption Available.

P.140

Other neurological monitoring Cerebral blood flow (CBF) CBF can b e me asured by radi oi s otop i c te chni ques uti l i si ng t rac ers s uch as xenon-133 gi ven i ntravenous l y or by i nhal ati on. Thi s rem ai ns a re search tool i n vi e w of the radi oac ti vi t y e xpos ure and t he usual nee d t o m ove the pati e nt to a g amma-camera. Howe ver, p ort abl e m oni tors are now av ai l abl e. Mi d dl e ce reb ral arte ry (MCA) b l ood fl ow can be det erm i ne d non-i nv asi vel y b y t ranscrani al Doppl er ul t ras onography . T he pul sat i l i ty i ndex (PI) rel a tes to cerebrovascul a r resi stance wi th a ri s e i n PI i ndi cat i ng a ri s e i n res i st anc e and cerebral vas osp asm . Vas osp asm can also be de si g nat ed when the M CA bl ood fl ow ve l oc i t y ex cee ds 120cm/s and sev ere vas osp asm when vel oci ti es >200cm/s. Low value s of c ommon c aroti d end-d i as tol i c bl ood fl ow and vel oci ty hav e b een shown to be hi g hl y di sc ri m i nati ng pre di c tors of b rai n d eat h. Imp ai red reacti vi ty of C BF to change s i n PC O 2 (i n normal s 3–5% pe r mmHg PCO 2 chang e) i s anot her marke r of p oor out com e.

Near-infra red spectroscopy (NIRS) Near-i nfrare d (700–1000nm ) l i ght p rop agated ac ros s t he head i s absorbe d b y haemogl obi n (oxy- and de -oxy ), myog l ob i n and ox i di sed cy toc hrome aa 3 (t he t ermi nal part of t he res pi ratory chain i nv ol v ed i n oxi dat i ve

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phos phoryl at i on). The sum of (ox y- + de oxy -) haem ogl obi n i s c ons i d ere d an i ndex of ce reb ral bl ood vol um e (C BV) chang e, and the di fferenc e as an i ndex of change i n haemogl obi n saturati on ass umi ng no vari at i on oc curs i n CBV. C BV and fl ow can be quanti fi e d b y c hangi ng t he FIO 2 and meas uri ng the resp ons e. Cere bral b l ood fl ow i s me asured by a m odi fi cat i on of the Fi ck pri nc i pl e. Oxy hae mogl obi n i s the i ntravas cul ar non-di ffus i bl e t racer, i ts acc umul at i on be i ng prop ort i onal to the arteri al i nfl ow of t rac er. Good correl at i ons have been found wi th the xenon-133 te chni que. Cytochrome aa 3 c annot be quanti fi e d b y N IRS but i ts red ox status may b e fol l owed to provi de som e i ndi cat i on of mi t ochond ri a l func ti on. Move ment arte fac t m ust be avoi de d and som e de vi c es re qui re red uct i on of am bi e nt l i g hti ng .

Lactate The brai n normall y ut i l i se s l act at e as a fue l ; howe ver, i n s tat es of sev ere l y i mp ai red cerebral perfus i on t he b rai n may bec ome a net l ac tate p roduc er wi t h t he venous l ac tat e ri s i ng ab ove the arteri a l v al ue. A l act ate ox ygen i ndex can b e deri ve d b y d i vi di ng t he venous –arteri a l l act ate di ffe rence by t he art eri o-jugul a r v enous oxyg en di fferenc e. Val ues >0. 08 are consi ste ntl y s een wi th cerebral i s chaemi a. P.141

See also: Lac tat e, p170; Int rac rani a l haem orrhag e, p376; Subarachnoi d haem orrhag e, p378; R ai s ed i nt rac rani al p res sure, p382; Head i njury (1), p504; He ad i nj ury (2), p 506; Brain ste m d eat h, p548

Ovid: Oxford Handbook of Critical Care

Ed itors: Si nge r, M ervyn; We bb, An dre w R. Ti tle : O xf ord Ha ndbook of Cr itic al Car e, 2nd Ed ition Cop yri ght © 1997,2005 M. Si nge r and A. R. W ebb , 1997, 2005. Publ i shed i n the Uni te d Stat es by Oxford Uni ve rsi ty Press Inc > Tab le of Co n te n ts > Lab or a tor y M on i tor in g

Laboratory Monitoring Urea and creatinine Measured i n bl ood, uri ne and, occ asi onall y, i n othe r fl ui ds such as abd omi nal drai n fl ui d (e .g. urete ri c di srupt i on, fi s tul ae )

Urea A p rod uc t of the urea cy cl e re sul ti ng from am moni a bre akd own, i t d epends upon adeq uat e l i ve r func ti on for i ts synthe si s and adeq uat e renal func ti on for i ts ex cre ti on. Low l e vel s are thus s een i n ci rrhos i s and hi gh l ev el s i n renal fai l ure. Uraemi a i s a cl i ni cal s ynd rom e i ncl ud i ng l e thargy , d row si ness , c onfusi on, pruri tus and peri cardi ti s resul t i ng from hi gh pl asm a l eve l s of ure a (or, more c orrec tl y , ni troge nous w ast e p rod uct s—azot aem i a). The rati o of uri ne :pl asm a urea may be us eful i n d i st i ngui shi ng ol i guri a of re nal or pre-renal ori g i ns . Hig her rati os (>10:1) are s een i n pre-renal c ond i ti ons , e .g. hy pov ol a emi a, w hereas l ow l eve l s (<4:1) occ ur wi t h d i rect re nal causes . 24-h m eas ure ment of uri nary urea (or ni t rogen) ex cre ti on has bee n p rev i ousl y us ed as a gui d e t o nutri ti onal p rot ei n rep l ac eme nt but i s c urrent l y not consi dered a useful routi ne t ool .

Creatinine A p rod uc t of creat i ne break dow n, i t i s predom i nantl y d eri ve d from ske l et al mus cl e and i s als o renal l y exc re ted . Low l ev el s are found w i th malnutri ti on and hi gh l eve l s wi th mus cl e break down (rhab dom yol ysi s) and i m pai red exc re ti on (re nal failure). In t he l at ter case, a cre ati ni ne v al ue > 120 µm ol /l s ugg est s a creat i ni ne cl earanc e <25ml /mi n. The us ual rati o for p l as ma ure a (mmol /l ) to creat i ni ne (µm ol /l ) i s app rox i matel y 1:10. A much l ow er rat i o i n a cri ti cal l y i l l p ati ent i s s ugg est i ve of rhabdomyol ys i s whe reas hi gher rat i os are s een i n ci rrhos i s , malnutri ti on, hyp ovol ae mi a and he pat i c fai l ure. The rati o of uri ne :pl asm a c reati ni ne may hel p di sti ng ui s h b etw een ol i guri a of re nal or pre-renal ori g i ns . Higher rati os (>40) are see n i n p re-renal condi t i ons and l ow l e vel s (<20) wi th di rec t renal c aus es. Cre ati ni ne c l e arance i s a m eas ure of gl ome rul ar fi l trati on. Once fi l tered, onl y small amount s of c reati ni ne are reabsorbe d. Normal l y i t exc eed s 100m l /m i n.

Normal plasma ranges

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Urea

2.5–6.5mmol/l

Creatinine

70–120µmol/l (depends on lean body mass)

P.145

See also: Hae mo(d i a)fi l trati on (1), p62; Haemo(di a )fi l trat i on (2), p 64; Pe ri t one al di al y si s , p 6; Nut ri t i on—us e and i nd i c ati ons ; Uri nal ys i s, p166; Ac ute failure renal fai l ure—di a gnosi s , p 332; Acut e renal fai l ure—m anag eme nt, p334; Rhabdomyol ys i s, p528 P.146

Electrolytes (Na + , K + , Cl - , HCO 3 - ) Measured acc uratel y b y d i re ct -readi ng i on-spe ci fi c el ect rod es from p l as ma or uri ne, thoug h are sensi t i ve to i nt erferenc e by ex ces s l i q ui d he pari n.

Sodium, potassium Pl a sma l e vel s m ay be e l ev ate d b ut poorl y re fl e ct i nt racel l ul ar (ap proxi m ate l y 3–5mmol /l for N a + , 140–150mmol /l for K + ) or total body l eve l s . Pl as ma p otassi um l e vel s are affe cte d b y p l as ma H + l ev el s ; a me tab ol i c aci d osi s red uce s uri nary pot ass i um exc re ti on w hi l e an al kal os i s wi l l i nc rease excret i on. Ol der measuri ng d evi ces such as fl a me p hot ome try or i ndi rec t-read i ng i on-s pec i fi c e l ec trodes gave spuri ous l y l ow pl a sma Na + l eve l s wi t h c onc urrent hyperprote i naemi a or hypertri gl yce ri dae mi a . Uri nary e xcret i on dep end s on i ntake, total body bal anc e, aci d–b ase bal ance, hormones (i ncl udi ng ant i –d i ureti c hormone, al d ost erone, corti cos te roi ds, at ri a l natri uret i c pep ti de), drugs (p art i c ul a rl y di ureti cs, non-s teroi d al ant i -i nfl amm atori es and ACE i nhi bi t ors ), and re nal funct i on. In ol i guri a , a uri nary Na + l ev el <10m mol /l sug ges ts a p re-renal cause whe reas >20mm ol /l i s s een wi th di rec t renal dam age . T hi s does not app l y i f di ure ti c s have be en g i ve n p rev i ousl y.

Chloride, bicarbonate Bi carbonate l e vel s v ary wi t h aci d–b ase bal anc e. In the ki dne y, Cl - re abs orp ti on i s i nc reased whe n HCO 3 - re abs orp ti on i s d ecreas ed, and v i ce ve rsa. Pl as ma [Cl - ] thus tends to vary i nve rse l y wi t h p l as ma [HCO 3 - ], k eep i ng the t otal ani on c onc ent rat i on normal. A rai sed [Cl - ] (p roduc i ng a hype rchl oraem i c met abol i c ac i d osi s) may be see n wi th ad mi ni st rat i on of l a rge vol um es of i sotoni c sal i ne or i sot oni c sal i ne-containi ng col l oi d sol ut i ons. Hyp erc hl orae mi a i s al so found wi t h e xperi m ent al sal t w ate r d row ni ng b ut rarel y see n i n actual cas es.

Anion gap The ani on gap i s t he di fferenc e b etwe en une sti mat ed ani ons (e .g. phosphate , k etones , l act ate ) and c at i ons. In met abol i c ac i d osi s an i ncreas ed ani on gap occ urs w i th re nal failure, i nges ti on of aci d , k etoaci dos i s and hyp erl act at aemi a, whe reas a normal ani on gap (usual l y associ ated wi th hyp erc hl oraemi a) i s found w i th de cre ase d aci d e xcreti on (e. g. Add i s on' s d i se ase , renal t ubul ar ac i dosi s) and l os s of b ase (e. g. di a rrhoe a, p anc reati c/b i l i ary fi s tul a, ac etaz ol ami de, urete ros i gm oi d ost omy ).

Normal plasma ranges Sodium

135–145mmol/l

Potassium

3.5–5.3mmol/l

Chloride

95–105mmol/l

Bicarbonate

23–28mmol/l

Anion gap = plasma [Na + ] + [K + ] - [HCO3 - ] - [Cl - ]

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Normal range

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8–16mmol

P.147

See also: Hae mo(d i a)fi l trati on (1), p62; Haemo(di a )fi l trat i on (2), p 64; Pe ri t one al di al y si s , p 66; Nut ri ti on—use and i ndi c ati ons , p78; Uri nal y si s, p166; Crys tal l oi ds, p176; Di ure ti c s, p212; T achyarrhy thm i as , p 316; Brady arrhyt hmi as , p318; Ac ute renal fai l ure— di a gnosi s , p 332; Ac ut e renal fail ure —manage ment, p334; Vomi ti ng/g ast ri c s tas i s , p 338; D i a rrhoea, p340; Acute l i ver fai l ure, p360; Hy pernat raemi a, p 416; Hyponat rae mi a , p 418; Hy perkal aem i a, p420; Hyp okalae mi a , p422; Met abol i c ac i dosi s , p 434; Me tab ol i c al k al osi s , p 436; Di abe ti c ke toaci d osi s, p442; Hype ros mol ar di a bet i c eme rge nci es, p444; Hy poad re nal cri si s, p448; Poi s oni ng—general p ri nci pl e s, p452; Rhabd omyol ys i s , p 528 P.148

Calcium, magnesium and phosphate Calcium Pl a sma calci um l ev el s have bee n t rad i ti onall y c orrect ed to pl a sma al bum i n l ev el s ; t hi s i s now c ons i de red i rre l ev ant , parti cul arl y at t he l ow al bum i n l ev el s se en i n cri ti cal l y i l l p ati ent s. Measureme nt of t he i oni s ed frac ti on i s now consi dered m ore pe rti ne nt si nce i t i s the i oni sed fract i on that i s res ponsi b l e for the e xtrace l l ul a r acti ons of calci um, wi t h c hanges i n the i oni sed fract i on b ei ng resp ons i bl e for the sy mpt omat ol ogy. Hi g h c al ci um l eve l s occ ur wi t h hype rparat hyroi d i s m, certai n m al i gnanci es and sarcoi d osi s w hi l e l ow l ev el s are s een i n renal fai l ure, se vere pancreat i t i s and hy pop arathy roi di s m.

Magnesium Pl a sma l e vel s p oorl y refl ec t i nt rac el l ul ar or whol e b ody st ore s, 65% of whi ch i s i n bone and 35% i n ce l l s . T he i oni s ed fracti on i s ap proxi m ate l y 50% of the total l e vel . Hi g h m agnesi um l ev el s are s een wi th renal fai l ure and exc ess i ve ad mi ni st rat i on; t hi s rare l y req ui res treat ment unl e ss seri ous cardi a c c ond uct i on probl ems or ne urol og i c al com pl i cat i ons (res pi rat ory paral ysi s, com a) i nt erv ene . Low l e vel s occur fol l owi ng sev ere di arrhoea, di ure ti c therapy, al cohol abuse, and ac com pany hypocal cae mi a . Mag nes i um i s us ed the rap eut i c al l y for a numbe r of c ond i ti ons i ncl udi ng ventri cul ar and s uprave ntri cul ar arrhythmi a s, ecl amp si a, s ei zures, as thm a and afte r m yoc ard i al i nfarct i on. Supranormal p l as ma l ev el s of 1. 5–2.0m mol /l are oft en sought .

Phosphate Hi g h l eve l s are se en wi t h renal fai l ure and i n t he pre sence of an i sc hae mi c bowel . Low l eve l s (somet i me s <0. 1mm ol /l ) occ ur wi t h c ri t i c al i l l nes s, chroni c al c ohol i sm and di ure ti c us age and may p oss i bl y res ul t i n muscl e weaknes s, fai l ure to wean and m yoc ard i al dy sfunct i on.

Normal plasma ranges Calcium

2.2–2.6mmol/l

Ionised calcium

1.05–1.2mmol/l

Magnesium

0.7–1.0mmol/l

Phosphate

0.7–1.4mmol/l

P.149

See also: IPPV—asse ss ment of we ani ng, p18; Pl as ma exc hange, p68; Nut ri t i on—use and i nd i c ati ons , p 78; T achyarrhythmi a s, p316; Pancre ati ti s , p 354; G eneral i se d s ei z ure s, p372; Hypom agnesaemi a, p424; Hyp erc al c aem i a, p426; Hyp ocalcaemi a, p428; Hypophosphataemi a, p430; Pre -ec l am psi a and ecl amp si a , p 538 P.150

Cardiac function tests The i m portance of bi oche mi c al markers of m yocard i al ne crosi s has b een em phas i s ed by a conse nsus d ocument from the Europ ean Soci e ty of Cardi ol og y and Ameri c an Col l eg e of Cardi ol ogy. The d i ag nos i s of myoc ardi a l i nfarct i on was red efi ned as a typ i cal ri s e and fal l i n t rop oni n, or a more rap i d ri se and fal l i n CK-M B, wi t h at l eas t one of t he fol l ow i ng :

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Isc hae mi c sy mpt oms Deve l op ment of p athol ogi c al Q w aves on EC G ECG ST el e vat i on or de pre ssi on Coronary i nte rve nti on

Troponins Troponi ns are b ound t o t he act i n fi l ame nt wi t hi n muscl es and are i nvol ve d i n e xci tat i on–c ont rac ti on c oup l i ng. Both cardi ac troponi n T and t roponi n I are cod ed b y s pec i fi c gene s and are i m munol ogi c al l y d i s ti nct from t hos e i n s kel etal mus cl e. N ei t her i s d ete ctabl e i n normal heal thy i ndi v i dual s b ut bot h are rel eas ed i nt o t he b l oodst re am from cardi omyocyt es dam age d b y ne crosi s, tox i ns and i nfl amm ati on. They b ecome det ect abl e b y 4–6h aft er myocardi a l i nj ury, p eak at 14–18h, and persi st for up to 12 day s. Current assays are hi ghl y s pec i fi c as the y us e rec ombi nant hum an cardi a c t rop i ni n T as a st andard . Due to thei r hi gh sensi ti v i ty , p l as ma l ev el s ri se wi th other cardi a c i nsul t s, e.g . t achycardi a (SVT /VT ), peri cardi ti s, myocardi t i s , s eps i s, he art failure, se vere e xerti on and pul monary emb ol i sm . T he d egree of ri s e p ost -MI or duri ng cri ti cal i l l ness correl a tes wi th a worse outcome. A p osi ti ve tes t i s w hen the card i ac troponi n T or I v al ue ex cee ds the 99th percenti l e of v al ues for a control g roup on ≥1 occ asi on duri ng the fi rst 24h aft er the i ndex cl i ni cal e vent. For cardi ac troponi n T t hi s i s q uot ed as 0.05–0. 1ng /ml though many l ab s now c ons i d er val ues >0. 03ng/m l as p osi ti v e. Val ues for c ard i ac t rop oni n I de pend on the p art i c ul a r ass ay use d (usual l y > 0.5–1. 5ng /ml ). T he neg ati ve pre di c ti v e v al ue afte r an ac ut e MI i s prob abl y s tronge st aft er 6h. Sensi ti v i ty pe aks at 12h but at t he exp ens e of a l ow er spe ci fi c i ty . W i th re nal dy sfunct i on, hi gher l e vel s are need ed to di a gnose myocardi a l d amage due to i mp ai red exc ret i on.

Cardiac enzymes Cre ati ne ki nase (CK ) i s d ete ctabl e i n pl asm a w i thi n a few hours of m yoc ard i al i njury. The cardi ac -sp eci fi c i s oform (CK-MB) can b e me asured i f there i s c onc urrent sk el e tal muscl e i njury . CK and as partate ami not ransfe ras e (AST ) peak b y 24h and fal l over 2–3 d ays whe reas t he ri se and sub seq uent fal l i n pl as ma l ac tat e de hyd rog enase tak es 1–2 day s l ong er.

Brain (or B-type) natriuretic peptide (BNP) Cardi omyocyt es produc e and sec ret e c ard i ac natri ureti c p ept i de s. Pl a sma l e vel s ri s e i n a vari et y of c ond i ti ons but hi g h l eve l s are predomi nant l y ass oc i at ed wi t h heart fail ure , and i nc rease i n rel ati on to sev eri ty. A sensi ti v i ty of 90–100% i s c l ai med , w hereas sp eci fi c i t y i s approxi mat el y 70–80%. N ume rous c omm erc i al as say s for B-t ype nat ri ure ti c pe pti de (BN P) or proBNP are now avai l ab l e, each wi t h t hei r own di a gnosti c rang e. The y are use ful as a screeni ng t ool for pati ent s p res ent i ng wi th dys pnoea, for prog nos ti c ati on, and for ti t rat i on of therapy. Le vel s ri s e i n the el derl y, i n renal fail ure , and i n pul monary di seases causi ng ri g ht ventri cul ar ov erl oad (e .g. pul monary em bol us). P.151

Figure. No Caption Available.

Key paper Ant man E et al . My ocardi al i nfarc ti on red efi ned —a c ons ens us doc ume nt of The Joi nt Europ ean Soc i e ty of Cardi ol og y/Ameri c an C ol l ege of Cardi ol ogy comm i t tee for the rede fi ni t i on of myocardi a l i nfarc ti on. J Am Col l Cardi ol 2000; 36:959–69 McC ul l oug h PA, et al . B-typ e natri uret i c pep ti d e and cl i ni c al jud gme nt i n eme rge ncy di agnosi s of heart fai l ure : analys i s from Bre athi ng Not Prop erl y (BNP) Mul ti nati onal St udy . C i rc ul ati on 2002; 106:416–22

See also:

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Ac ute coronary syndrome (1), p 320; Ac ut e c oronary s yndrome (2), p322; Heart fai l ure—as se ssm ent , p 324 P.152

Liver function tests Hep ati c m etabol i s m proc eeds vi a Phas e I enzym es (oxi dat i on and p hos phoryl ati on) and t hen subse que ntl y t o Phase II enzyme s (gl ucuroni dat i on, s ul phati on, ace tyl ati on). Phase I enzyme re act i ons i nvol ve cy toc hrome P450.

Markers of hepatic damage Al a ni ne ami notrans ferase (ALT) Asp art ate am i notransferase (AST) Lac tat e d ehyd rog enase (LD H) Pat terns and rati os of v ari ous enzym es are vari a bl e and unre l i a bl e di agnost i c i ndi c ators. Me asurem ent of ALT alone i s usual l y s uffi c i ent. It i s more l i ve r-s pec i fi c but l e ss sensi t i v e than AST and has a l ong er hal f-l i fe . AST i s not l i v er-spe ci fi c but i s a sensi ti v e i ndi cat or of hep ati c d amage. The pl as ma l eve l i s p roporti onal to the d egree of hep atocel l ul ar dam age . Low l eve l s oc cur i n ex trahep ati c obst ruc ti on and i nact i ve ci rrhos i s. LD H i s i nse nsi ti ve and non-sp eci fi c . Isoe nzy me el e ctrophore si s i s need ed t o d i s ti ngui sh cardi ac, erythroc yte , s kel etal mus cl e and l i ve r i nj ury . Ac ute phase reactants s uch as C-reac ti v e p rot ei n (C RP) are al so produc ed by the l i ver. Leve l s i nc re ase duri ng c ri t i c al i l l ne ss and fol l owi ng hepat oc el l ul a r i njury.

Markers of cholestasis Bi l i rubi n Al k al i ne phosphatase Gamm a-g l ut amy l t ransfe ras e (γ-GT) Bi l i rubi n i s deri ve d from Hb re l eased from e ryt hrocyt e b reakdown and conjug ate d w i th gl ucuroni d e b y the hep atocyt es. The c onj ugat ed fract i on i s wat er-sol ub l e whereas the unconjugat ed fracti on i s l i pi d -sol ub l e. Le vel s are i nc re ase d wi th i ntra- and e xtrahe pat i c bi l i a ry obs truct i on (pred omi nant l y conjug ate d), he pat oce l l ul ar damag e and hae mol ysi s (usual l y m i xe d p i ct ure). Jaundi ce i s det ect ed whe n l evel s >45µ mol /l . Al kal i ne phosp hat ase i s re l eased from b one , l i ve r, i ntes ti ne and pl a centa. In the ab sence of bone d i se ase (check Ca 2+ and PO 4 3- ) and p reg nancy, rais ed l eve l s us ual l y i nd i cate bi l i a ry tract dys functi on. A rai sed γ-G T i s a hi ghl y s ens i t i ve marke r of he pat obi l i ary di sease. Incre ase d s ynt hes i s i s i nduc ed by obst ructi ve chol es tas i s , alcohol , v ari ous drugs and t oxi ns, ac ute and c hroni c he pat i c i nfl a mmat i on.

Markers of reduced synthetic function Al b umi n Cl ot ti ng fac tors Chol i nest erase Al bum i n l ev el s fall duri ng cri t i cal i l l nes s d ue to protei n c atabol i s m, c api l l ary l e ak, de cre ase d s ynt hes i s, di l ut i on wi th art i fi ci al col l oi ds . Coagul ati on fac tors II, VII, IX and X are l i ver-sy nthesi sed . Over 33% of funct i onal hep ati c mas s must be l os t before any ab normal i ty i s se en.

Indicators of function Li d ocaine me tab ol i tes (M egX)

Indicators of hepatic blood flow Ind ocyani ne g ree n c l earance Bromos ul p hthal e i n cl earanc e P.153

Normal plasma ranges

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Albumin

35–53g/l

Bilirubin

3–17µmol/l

Conjugated bilirubin

0–6µmol/l

Alanine aminotransferase

5–50U/l

Alkaline phosphatase

100–280U/l

Aspartate aminotransferase

11–55U/l

Cholinesterase

2.3–9.0KU/l

γ-glutamyl-transferase

5–37U/l

Lactate dehydrogenase

230–460U/l

See also: Parent eral nutri t i on, p 82; Jaundi ce, p358; Ac ute l i ver failure, p360; C hroni c l i ver fail ure , p 364; Parace tam ol poi soni ng, p 456; HELLP s ynd rom e, p540 P.154

Full blood count Haemoglobin A rai sed hae mog l ob i n occ urs i n p ol y cyt hae mi a (pri m ary and se condary t o c hroni c hypox aem i a) and i n hae moc onc ent rat i on. Anae mi a may be due t o reduced re d c el l mass (de cre ase d red cel l p rod uct i on or s urv i val) or hae mod i l uti on. The l a tte r i s com mon i n cri ti cal l y i l l p ati ent s. In sev ere anaem i a the re may be a hyperdy nami c ci rcul at i on whi ch, i f s eve re, may de com pensat e t o c ard i ac failure . In t hi s case, bl ood trans fus i on must be performed wi t h e xtreme care to avoi d fl ui d overl oad, or i n as soc i at i on wi th pl a smaphe res i s. Di ffe renti al di a gnosi s of anaemi a i nc l udes : Reduced MC V Iron de fi c i ency (ani socyt osi s and poi ki l ocy tos i s ) Rai s ed MCV Vi tami n B 1 2 or fol a te d efi ci enc y Al cohol ex ces s Li ve r d i se ase Hypot hyroi di s m Normal MCV Anae mi a of chroni c di s eas e Bone marrow fail ure (e. g. acute fol ate de fi c i ency) Hypot hyroi di s m Haemol ys i s (i ncreas ed ret i cul oc yt es and bi l i rubi n)

White blood cells A rai sed whi te cel l count i s ext rem el y common i n c ri t i c al i l l nes s. Causes of chang es i n the di fferent i a l c ount i ncl ude :

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Neutrophilia

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Lymphocytosis

Eosinophilia

Bacterial infection

Brucellosis

Asthma

Trauma and surgery

Typhoid

Allergic conditions

Burns

Myasthenia gravis

Parasitaemia

Haemorrhage

Hyperthyroidism

Inflammation

Leukaemia

Steroid therapy Leukaemia Neutropenia

Lymphopenia

Viral infections

Steroid therapy

Brucellosis

SLE

Typhoid

Legionnaire's disease

Tuberculosis

AIDS

Sulphonamide treatment Severe sepsis Hypersplenism Bone marrow failure

Barri er nursi ng may be use d for neut ropeni a <1.0 ×10 9 /l .

Platelets Correc t i nt erp ret ati on of pl a tel et counts re qui re s b l ood t o be taken by a v ene puncture. Arte ri a l b l ood i s c omm onl y tak en from an i ndwe l l i ng cannul a but i s not i deal. Thromb ocy top eni a i s d ue to dec reased pl ate l et producti on (bone marrow failure, vi tam i n B 12 or fol at e d efi ci e ncy ), d ecreas ed pl atel et survi val (ITP, TT P, i nfe ct i on, hypersp l eni sm , hep ari n t herapy ), i nc reased pl ate l et c ons umpt i on (haem orrhag e, DIC ) or in vi vo aggreg ati on gi v i ng an app arent thromb ocy top eni a; thi s s houl d be che cke d on a bl ood fi l m. Sp ont aneous bl e edi ng i s as soc i at ed wi t h p l at el e t c ounts <20 ×10 9 /l and p l at el et c ove r i s req ui red for proce dures or traumati c bl eed s at c ounts <50 ×10 9 /l . P.155

Normal ranges

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Haemoglobin

13–17g/dl (men), 12–16g/dl (women)

MCV

76–96fl

White cell count

4–11 ×10 9 /l

Neutrophils

2–7.5 ×10 9 /l

Lymphocytes

1.3–3.5 ×10 9 /l

Eosinophils

0.04–0.44 ×10 9 /l

Basophils

0–0.1 ×10 9 /l

Monocytes

0.2–0.8 ×10 9 /l

Platelets

150–400 ×10 9 /l

See also: Bl ood trans fus i on, p 182; Bl ood products , p 252; Haemothorax , p 302; Haemopty si s, p304; Uppe r g ast roi nt est i nal hae morrhage, p344; Bl eed i ng vari c es, p346; Lowe r i nt est i nal b l ee di ng and col i t i s, p348; Bl ee di ng d i sorde rs , p 396; Anaemi a, p400; Si c kl e ce l l di sease, p402; Haem ol y si s , p 404; Pl at el e t d i sorde rs, p406; Neutropeni a, p408; Leukae mi a , p 410; Malari a , p 490; Vasc ul i ti des , p494; Mul ti p l e trauma (1), p 500; M ul t i p l e trauma (2), p 502; Burns —fl ui d manag ement, p510; Post -partum haem orrhag e, p542 P.156

Coagulation monitoring Basic coagulation screen The basi c sc re en c ons i s ts of a pl at el e t c ount, prothromb i n ti m e, act i vated parti al throm bopl as ti n ti me and throm bi n ti me. Cl ose att ent i on to bl ood sampl i ng te chni que i s v ery i m portant for corre ct i nt erp ret at i on of coagul ati on tes ts . Drawi ng b l ood from i ndwe l l i ng cat het ers s houl d, i d eal l y, be av oi d ed s i nce sam pl e s m ay b e d i l uted or contami nate d wi t h hepari n. T he correc t vol ume of bl ood mus t b e pl ac ed i n the sam pl e tube to avoi d di l uti on errors. Lab oratory coagul ati on tes ts are us ual l y pe rforme d on ci trate d p l as ma samp l e s t aken i nto gl ass tubes .

Specific coagulation tests Activated clotting time (ACT) Sam pl e tube contai ns cel i t e, a di at omac eous e art h, whi ch act i vates the c ont act sy st em; thus t he ACT predomi nant l y tes ts the i ntri ns i c pat hway. The AC T i s p rol ong ed by hepari n t herapy , t hrombocyt openi a , hy pot hermi a, haem odi l ut i on, fi b ri nol ysi s and hi g h d ose ap rot i ni n. Normal i s 100–140s.

Thrombin time (TT) Sam pl e tube contai ns l yophi l i sed throm bi n and c al c i um. T hrombi n b ypasse s t he i nt ri nsi c and ext ri nsi c p athways s uch that t he coagul ati on ti me t est s t he com mon pathw ay w i th conve rsi on of fi b ri noge n t o fi bri n. T he T T i s p rol onged by fi b ri nog en d epl et i on, e. g. fi b ri nol ysi s or t hrombol ys i s , and hepari n v i a ant i throm bi n III d epe nde nt i nt eract i on wi th thromb i n. A hi gh dos e TT i s more sensi ti v e t o hepari n anti c oag ul a ti on t han fi bri nog en l ev el s . N orm al range i s 12–16s .

Prothrombin time (PT) Sam pl e tube contai ns ti ssue fact or and cal ci um. Ti ssue fact or act i vates the e xtri ns i c pathw ay. The PT i s prol onge d wi t h c oum ari n anti coagul ants, l i ver di sease and vi tam i n K d efi ci e ncy . N orm al range i s 12–16s . T he Int ernati onal Normal i s ed R ati o (INR ) rel a tes PT to control and i s normally 1.

Activated partial thromboplastin time (APTT) Sam pl e tube contai ns kaol i n and c ephal i n as a pl ate l et subst i t ute to ac ti v ate the i ntri ns i c pathw ay. The APTT i s prol onged by he pari n the rap y, DIC , s eve re fi b ri nol y si s, von Wi l l e brand fac tor, fact or VIII, fac tor X1 or factor XIII defi ci enc i e s. Normal range i s 30–40s.

D-dimers and fibrin degradation products (FDPs) Fi b ri n frag ment s are rel eas ed by pl a smi n l ys i s. FD Ps can be ass aye d b y an i mmunol ogi cal met hod ; t hey are often measured i n the cri t i cally i l l to confi rm d i ss emi nat ed i nt ravasc ul ar coagul ati on. A l ev el of 20–40µ g/ml i s c omm on

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pos t-operati vel y, i n sep si s, trauma, renal fail ure and D VT. Rai se d l evel s do not di sti ngui sh fi bri nogenol y si s and fi b ri nol ysi s. As say of the d-di m er fragment i s more s pec i fi c for fi b ri nol ysi s, e.g . i n D IC, si nce i t i s onl y rel eas ed aft er fi b ri n i s form ed.

Coagulation factor assays As says are avai l ab l e for al l c oag ul ati on fact ors and m ay be use d for d i agnos i s of sp eci fi c de fec ts. As he pari ns i nhi bi t fac tor Xa ac ti vi t y, the fac tor Xa as say i s t herefore t he mos t s pec i fi c method of control l i ng l ow mol ec ul ar wei ght hep ari n t herapy . Si nce thi s assay i s not dep end ent on contac t s yst em act i vati on, i t al so avoi ds the effec ts of aproti ni n when moni tori ng hepari n t herapy . P.157

The coagulation cascade – new concept

Figure. No Caption Available.

The tradi ti onal c oag ul a ti on c asc ade consi sti ng of ext ri nsi c, i nt ri nsi c and com mon pat hways i s now consi dered out mod ed, i nconsi s tent w i t h c l i ni cal obse rvati ons , and i nad equate to ex pl a i n the pathw ays l eadi ng t o haem ost asi s i n viv o. Thi s s che ma has be en repl ac ed rec ent l y by a ce l l -bas ed mod el wi t h t he major i ni ti a ti ng haem ost asi s e vent in viv o b ei ng t he act i on of fac tor VIIa and t i ss ue fac tor (T F) at t he si t e of i njury.

See also: Hae mo(d i a)fi l trati on (1), p62; Haemo(di a )fi l trat i on (2), p 64; Anti coagul ant s, p248; T hrombol yt i cs , p 250; Bl ood produc ts , p 252; Coagul ant s and ant i fi bri nol yt i cs , p 254; Ap rot i ni n, p256; Haem othorax, p 302; Haem opt ysi s, p304; Ac ute coronary syndrome (1), p 320; Ac ut e c oronary s yndrome (2), p322; Uppe r g ast roi nt est i nal haem orrhag e, p344; Bl eedi ng vari c es, p346; Lowe r i nte st i nal b l ee di ng and col i ti s, p348; Acut e l i ve r fai l ure , p 360; Bl e edi ng di sorders, p396; Cl otti ng di s orders, p398; Pl ate l et di sorde rs, p406; Parace tam ol poi soni ng , p 456; Post-operat i ve i ntensi v e c are , p534; HELLP syndrome, p540 P.158

Bacteriology Mi c robi ol og y s ampl es shoul d, i f pos si b l e, be taken pri or to commencem ent of anti m i crobi al therapy. In se vere i nfect i ons, broad sp ect rum anti m i crobi al s s houl d be starte d w i thout await i ng re sul ts . Sampl i ng s i te s i nc l ud e t hos e sus pec ted cl i ni call y of harbouri ng i nfec ti on or, i f a s pec i fi c s i te cannot b e i denti fi ed cl i ni call y, b l ood, uri ne and sputum sampl es. In se vere i nfe cti on, i ndwe l l i ng i ntravas cul ar cat het ers s houl d be rep l ac ed and the cathe ter t i ps se nt for cul t ure . Samp l es shoul d b e s ent to the l aborat ory prompt l y to al l ow earl y i ncub ati on and to prevent p ote nti al l y mi s l e adi ng growth. Swabs must be sent i n t he app rop ri ate trans port m edi a.

Blood cultures In ord er to avoi d ski n c ont ami nat i on, t he ski n s houl d be cl e ane d w i th al cohol and al l ow ed to d ry thoroughl y before venepunct ure . A 5–20m l b l ood s amp l e i s wi t hdrawn and d i vi ded i nto anaerobi c and aerobi c cul ture bot tl es. In add i ti on, c ul t ure s s houl d be tak en throug h i ndw el l i ng i ntravas cul ar cathe ters i f c athete r-rel ated se psi s i s sus pec ted . Al l s amp l es must be cl e arl y l abe l l e d. Cul ture b ott l e s are i nc ubated and ex ami ned frequent l y for bacte ri a l g row th. Pos i ti ve cul tures must be i nt erp ret ed i n l i ght of the cl i ni cal p i c ture; an e arl y p ure growt h from mul ti pl e bott l es i s l i kel y t o be si gni fi cant, al t hough cul tures from c ri ti c al l y i l l pati e nts may appe ar l at er or not at al l d ue to anti bi oti c the rap y. Any Gram neg ati ve i sol at es or Staph. aureus are usual l y t ake n as si gni fi cant.

Urine Cat het er spe ci m ens are usually ob tai ned from the cri ti cally i l l . The sampl i ng s i te shoul d b e p rep are d asep ti c al l y p ri or to sam pl i ng. The s pec i me n s houl d be sent t o t he l ab oratory i mme di a tel y and exam i ne d m i cros cop i cally for organi s ms, cas ts and crys tal s. Uri ne i s pl a ted onto cul ture m edi um wi t h a calib rated l oop and i nc ubated for 18–24h pri or to exami nati on. Bacte ri a >10 8 /l (or a pure growth of 10 5 /l ) re pre sent a si gni fi cant g row th. Al l c athete r s pec i m ens show bac teri a l g row th i f the cat het er has be en i n pl a ce for >2day s. Isol at i on of the s ame org ani sm from b l ood c onfi rm s a si gni fi c ant cul ture .

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Sputum Sputum sampl es are easi l y c ont ami nat ed duri ng c ol l ect i on, p art i c ul a rl y sp eci mens from non-i ntubat ed pat i ents. Suc ti on spe ci m ens from i nt ubated pati e nts can b e t aken vi a a st eri l e sucti on cat het er, prote cte d c athete r b rus h or from s pec i fi c l ung s egme nts vi a a bronc hos cop e. Gram negati v e b act eri a are fre que ntl y i sol ate d from tracheal asp i rate s of i ntubat ed p ati ent s; onl y d eep sucti on spe ci mens are s i g ni fi cant. Bl ood cul t ure s s houl d acc omp any sputum spe ci mens i n t he d i ag nos i s of pne umoni a . Samp l es shoul d b e s ent to the l aborat ory i m med i at el y .

Pus samples and wound swabs As pi rate d p us mus t b e s ent to the l aborat ory i m medi at el y or a s wab sampl e m ay b e t ake n and s ent i n t ransport med i um . Pus i s pre ferabl e for bac teri al i sol ati on.

Typical ICU-acquired nosocomial infections Pne umoni a due t o Pseudom onas ae rug inosa, St aph. aure us, Kl ebs iel la sp p., Enterobacte r s pp. Uri nary i nfe cti on wi t h E. coli, Ps . ae ruginosa, Kl ebs iel la spp ., Proteus s pp. Cathete r rel ated se psi s—Stap h. aureus , c oag ul a se neg ati ve staphy l oc occ i P.159

See also: Pl e ural aspi rati on, p44; Fi b reopti c bronchosc opy , p 46; Ches t p hys i othe rap y, p 48; Vi rol og y, s erol og y and ass ays , p160; Uri nal ysi s, p166; Ant i mi crobi al s , p 260; At el e ctasi s and p ul m onary col l ap se, p284; Acut e c hes t i nfe cti on (1), p288; Acute che st i nfect i on (2), p290; Abdomi nal sep si s , p 350; Pancreat i ti s, p354; Meni ngi ti s, p374; T etanus , p 390; Neutropeni a, p408; Infec ti on—d i ag nos i s , p480; Infect i on—t reatme nt, p482; Sep si s and s ept i c shock—treat ment , p486; HIV re l at ed di s eas e, p488; M al a ri a, p 490; Burns—gene ral manag eme nt, p512; Pyrexi a (1), p518; Py rex i a (2), p520 P.160

Virology, serology and assays Antibiotic assays Ant i b i ot i c ass ays are usuall y pe rforme d for drugs wi t h a narrow t herape uti c rang e, suc h as ami nogl ycosi d es and vancom yci n. It i s not us ual to re que st an ass ay on day 1 of t reatme nt. There aft er, sampl es are tak en dai l y pri or to gi v i ng a dos e and at 1h afte r an i ntrave nous i nje cti on or i nfus i on.

Serology A c l otte d b l ood s pec i me n al l ows anti bodi e s t o vi ral and aty pi c al ant i ge ns to be ass ayed . It i s usual to send ac ut e and conval esc ent (14 d ays ) se rum to de termi ne ri s i ng anti b ody ti tres. Si ngl e s amp l e ti t res may b e used to det ermi ne pre vi ous exp osure and carri er st atus.

Hepatitis B Serol ogy i ncl udes he pat i ti s B s urface ant i g en as a sc ree ni ng t es t and hepati t i s B core anti gen to de termi ne i nfect i v i ty . T here i s a 10% carri er rate i n South Eas t Asi ans . Serol og y s houl d be sent i n all hi g h ri s k p ati ent s, e.g . jaundi ce, IV drug abuse, homos exual s , p ros ti t ut es, those wi t h t at toos or unexp l ai ned he pat i c enz yme ab normal i ti es . In add i ti on, he pat i t i s B s tat us shoul d be known i n st aff who suffe r acci dental ex pos ure to body fl ui ds , e .g. through nee dl e sti ck i njury. Thos e w ho are not i mmune m ay be tre ate d wi th i m munogl obul i n.

HIV Si nce HIV p osi ti v e s tat us carri es conseq uences for l i fe sty l e and i nsuranc e, i t shoul d rare l y be ass ess ed wi t hout p ri or counse l l i ng and c ons ent . T he C D4 count may be use d t o asse ss the l i kel i hood of sym tom atol og y b ei ng AIDS-re l at ed, al t hough thi s wi l l fal l further wi t h acut e c ri ti c al i l l ne ss; ag ai n, c ons ent shoul d usually be sought p re-tes ti ng. Hi g h ri s k pat i ents shoul d b e consi de red for t est i ng , e .g. hom ose xual m al e s, i nt rav enous drug abus ers , haem ophi l i ac s, Cent ral Afri c an ori gi n. In c ri ti c al l y i l l pati e nts such consent c an rarel y b e ob tai ned and unconse nte d t est i ng may b e us ed whe re managem ent may c hange s i g ni fi cantl y w i th knowl edg e of the HIV st atus, or where organ d onati on i s b ei ng consi dered. Mos t AID S-rel a ted i nfec ti ons can be ad equate l y tre ate d wi thout knowl e dge of the HIV status . Pati ent s or staff who are reci pi e nts of a need l es ti ck i nj ury can b e t reated wi t h anti re trovi ral therapi e s i f ri sk i s hi gh.

Viral culture Mos t c omm onl y used for CM V. Sam pl e s of b l ood, uri ne or bronchi al as pi rat e m ay b e s ent for D EAF F (d ete ct i on of earl y ant i ge n fl uores cent foci ). Herpes vi rus i nfe cti ons may be de tec ted by el ect ron mi crosc opy of sam pl e s (i nc l ud i ng pus tul e fl ui d) and ad enovi rus i n i mm unosup press ed p ati ents wi t h a chest i nfec ti on.

Fungi Candid a and Asp ergil lus can be ass ess ed by cul ture ± anti g en tes ts . Cry ptococ cus can b e d ete cte d b y Indi an i nk st ai n i n bi ops y sampl es.

Other tests

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Other tes ts avail abl e t o make mi c rob i ol og i cal d i ag nos es i nc l ude anti gen te st i ng for c ert ai n bacte ri a (e .g. pne umococ cus ), and PCR (p ol y merase chain re act i on) whi c h am pl i fi es the mi crobi a l D NA. PC R i s an e xtremel y sensi ti v e t est for s pec i fi c organi s ms. Howev er, i t i s prone to envi ronm ent al contam i nati on (e.g . from ai rborne sp ore s) and i t cannot d i st i ngui sh bet wee n c ol oni s ati on and i nfec ti on. P.161

Common serology for critically ill patients Hep ati ti s A Hep ati ti s B Hep ati ti s C HIV CMV Myc opl asm a p neumoni ae Leg ionell a p neumop hil a

Antibiotic therapeutic levels Trough (mg/l)

Peak (mg/l)

Amikacin

<8

30

Gentamicin

<2

4–10*

Tobramycin

<2

4–10

Vancomycin

<8

20–30

*Seek microbiological advice if once daily gentamicin is used

See also: Bac teri ol og y, p158; Uri nal y si s , p 166; Anti mi c rob i als, p260; Acute c hes t i nfect i on (1), p 288; Ac ut e c hes t i nfe cti on (2), p290; Jaundi ce, p358; Ac ute l i ver failure, p360; T etanus , p 390; Botul i s m, p392; HIV rel at ed d i s eas e, p 488; Py rex i a (1), p 518; Pyre xi a (2), p 520 P.162

Toxicology Purpose Sam pl e s t ake n from bl ood , uri ne, vomi tus or g ast ri c l avag e (dep end i ng on drug or poi son i nges ted ) for: Moni tori ng of t herapeuti c d rug l e vel s (usual l y p l as ma) and av oi d anc e of t oxi ci t y, e.g . d i goxi n, ami nogl ycosi d es, l i t hi um, phe nyt oi n Identi fi c ati on of unk nown toxi c subst anc es (e. g. cyani d e, amp het ami nes , op i at es ) causi ng sym ptomat ol ogy and/or pat hol ogy . Al ways tak e a uri ne sam pl e for anal ysi s. Confi rm ati on of tox i c pl a sma l e vel s and moni tori ng of t reatme nt effe ct , e. g. parace tam ol , as pi ri n Medi col eg al , e.g . alc ohol , rec reati onal drugs fol l owi ng road traum a

Samples Confi rm w i th chemi stry l aborat ory ± l oc al poi sons uni t as t o whi c h, how, and when bod y fl ui d s amp l es shoul d b e tak en for anal y si s , e .g. pe ak/t rough l ev el s for ami nogl ycosi des , uri ne s amp l es for out-of-hosp i tal p oi s oni ng , repeat parace tam ol l ev el s to moni t or effi cacy of tre atm ent P.163

See also: Vi rol ogy, se rol ogy and assays, p160; Poi soni ng—g eneral pri nc i pl es , p 45

Ovid: Oxford Handbook of Critical Care

Ed itors:

Si nge r, M ervyn; We bb, An dre w R.

Ti tle : O xf ord Ha ndbook of Cr itic al Car e, 2nd Ed ition

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Cop yri ght © 1997,2005 M. Si nge r and A. R. W ebb , 1997, 2005. Publ i shed i n the Uni te d Stat es by Oxford Uni ve rsi ty Press Inc > Tab le of Co n te n ts > Misc ell an e ou s Mo n it or i n g

Miscellaneous Monitoring Urinalysis Techniques Bi oche mi c al /met abol i c : i. c ol ori m etri c ‘d i ps ti cks ’ read manual l y from refe rence chart or by aut omated mac hi ne w i t hi n 15s—2mi n of d i pp i ng i n uri ne (s ee manufac turer's i ns truct i ons). Us ual l y performed at the b eds i de . ii. s odi um and pot ass i um l evel s can be measured i n mos t anal yse rs use d for pl a sma el ect rol yte me asurem ent . Re cal i b rat i on of the machi ne or sp eci al di l uti on tec hni ques may be req ui red. iii. l aborat ory anal y si s Haem atol og i cal—ei t her by di pst i ck or l a boratory tes ti ng Mi c rob i ol ogi cal —mi crosc opy , c ul t ure, s ens i t i vi ty; anti g en tes ts Renal d i se ase —us ual l y by mi c roscopy + l a boratory tes ti ng

Associated tests Som e of t he abov e i nve sti gat i ons are performed i n conjunct i on wi th a b l ood t est , e .g. uri ne :pl asm a rati os of ure a, creati ni ne and osm ol a l i ty to di s ti ngui sh re nal from p re -renal causes of ol i guri a, 24h uri ne col l e cti on pl us pl a sma creati ni ne for creat i ni ne cl e arance es ti mati on.

Cautions Whi te bl ood c el l s, prote i nuri a and m i xe d b act eri al growt hs are routi ne fi ndi ngs i n cat het eri se d p ati ent s and do not nec ess ari l y i ndi c ate i nfec ti on. A ‘ pos i ti ve’ di pst i c k t est for b l ood d oes not di ffe renti ate bet wee n haematuri a , haemogl obi nuri a or myog l ob i nuri a. Onl y c onjugat ed bi l i rubi n i s excret ed i nt o t he uri ne. Uri nary s odi um and pot ass i um l evel s are i ncre ase d b y d i ureti c usag e. P.167

Urinalysis tests

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Biochemical/metabolic: pH

dipstick

glucose

dipstick

ketones

dipstick

protein

dipstick, laboratory

bilirubin

dipstick

sodium, potassium

electrolyte analyser, laboratory

urea, creatinine, nitrogen

laboratory

osmolality

laboratory

specific gravity

bedside gravimeter, laboratory

myoglobin

laboratory, positive dipstick to blood

drugs, poisons

sent to Poisons Reference Laboratory

Haematological: red blood cells

microscopy, positive dipstick to blood

haemoglobin

laboratory, positive dipstick to blood

neutrophils

dipstick, laboratory

Microbiological: bacteriuria

microscopy, culture

TB

microscopy, culture (early morning specimens)

Legionnaire's disease

laboratory

Nephro-urological: haematuria

microscopy

granular casts

microscopy

protein

laboratory

sodium, potassium

electrolyte analyser, laboratory

malignant cells

cytology

See also: Nut ri ti on—use and i ndi c ati ons , p 78; Bac teri ol og y, p 158; Vi rol og y, s erol og y and ass ays , p 160; Acut e renal fai l ure— di a gnosi s , p 332; Hy pernat rae mi a , p 416; Hy ponatraem i a, p418; Hy perkal aemi a, p420; Hyp okal aem i a, p422; Di abet i c ket oac i d osi s, p442; Poi soni ng—gene ral p ri nci p l e s, p452; Infect i on—d i ag nos i s, p480; Rhabdom yol ysi s, p528 P.168

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Indirect calorimetry Cal ori met ry refers t o the m eas ure ment of energ y p rod uct i on. Di rect calori m etry i s t he meas urement of heat produc ti on i n a s eal ed c ham ber but i s i mp rac ti c al for cri t i call y i l l pat i ents. Indi rec t c al ori metry m eas ure s t he rat e of oxi dat i on of me tab ol i c fuel s b y d ete cti ng the vol um e of O 2 consumed and CO 2 p rod uce d. The rati o of CO 2 producti on to O 2 uti l i sat i on (resp i ratory q uot i e nt or RQ) defi ne s w hi c h fuel s are bei ng uti l i sed (se e t abl e). Knowl e dge of the oxy gen ut i l i sat i on b y the v ari ous fuel s al l ows t he cal cul at i on of ene rgy product i on. Carbohyd rat e and fat are ox i d i se d to CO2 and water produci ng 15–17 and 38–39k J/g re spe cti vel y. Protei n i s oxi d i s ed t o C O2, water and ni troge n (subse que ntl y e xcrete d as urea) prod uci ng 15–17k J/g.

Technique of indirect calorimetry Ins pi rat ory and mi xed ex pi rat ory gas es mus t b e s amp l ed . O 2 conce ntrat i on may be me asured by a fuel ce l l sensor or a fast re sponse , p aramag net i c sensor. C O 2 i s usual l y m eas ure d b y i nfrare d absorpt i on. Sens ors may b e c al i brated wi t h refe rence to known c onc ent rati ons of s tandard gas or by burni ng a pure fue l w i th a pre di c tab l e O 2 c ons ump ti on. Measureme nts are usually made at ambi ent te mpe rat ure, p res sure and hum i d i ty pri or to conve rsi on to standard tem perature, press ure and humi di ty. In order to calcul at e m etabol i c rat e (ene rgy exp end i t ure ) i nsp i re d and expi re d mi nute vol um es are re qui red . It i s comm on for one mi nute vol ume to be meas ured and the ot her de ri ved from a Hal dane t ransformati on:

The ni trogen conce ntrat i ons are ass umed to be the c onc ent rat i on of gas whi c h i s not O 2 or CO 2 . C al c ul a ti on of e nergy exp end i ture uti l i ses a mod i fi cat i on of the d e We i r formul a Energy exp end i ture = (3.94 VO 2 + 1. 11 VCO 2 ) × 1.44 Al though i t i s possi bl e t o calc ul a te the rate of p rot ei n me tab ol i sm by refere nce to the uri nary urea concentrati on, and the refore to se parate non-prot ei n from p rotei n e nergy e xpe ndi ture, the resul ti ng mod i fi cat i on of the above formul a i s not us ual l y cl i ni cal l y si gni fi c ant .

Errors associated with indirect calorimetry Underestimate VCO 2

H + ion loss, haemodialysis, haemofiltration

Overestimate VCO 2

hyperventilation, HCO3 - infusion

Underestimate VO 2

free radical production, unmeasured O 2 supply

FIO 2 > 0.6

small difference between inspired and expired O 2

Loss of volume

circuit leaks, bronchopleural fistula

Use of indirect calorimetry Hel ps to mat ch nut ri ti onal i ntak e t o e nergy e xpe ndi ture. It i s i m portant t o feed cri ti cal l y i l l p ati ent s approp ri a tel y, avoi di ng bot h unde rfe edi ng and ove rfe edi ng (se e t abl e). Indi rect calori m etry m ay also be us ed to ass ess the work of bre athi ng by as ses si ng the change i n VO 2 duri ng w eani ng from m echani cal ve nti l a ti on. The VO 2 change may al so be use d t o asse ss app rop ri ate l ev el s of se dat i on and anal ges i a. P.169

Respiratory quotients for various metabolic fuels Ketones

0.63

Fat

0.71

Protein

0.80

Carbohydrate

1.00

The whol e bod y R Q d epe nds on the fuel or com bi nati on of fue l s bei ng uti l i sed . N orm al l y a combi nat i on of fat and carbohydrate are uti l i s ed wi t h a RQ of 0.8. Li pog enes i s as soc i at ed wi t h b oth se psi s and overfee di ng m ay gi v e a RQ of 1.1–1. 3

See also: IPPV—asse ss ment of we ani ng, p18; N utri t i on—us e and i nd i cati ons , p78; Ente ral nutri ti on, p80; Parenteral nut ri ti on,

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p82; C O 2 moni tori ng, p92; Cardi ac out put —ot her i nvas i ve , p 124; Opi oi d analge si c s, p234; N on-opi oi d analg esi cs, p236; Sed ati ves , p 238; Py rex i a (1), p 518; Pyre xi a (2), p 520; Pai n, p 532 P.170

Lactate Measurement of blood lactate Analys ers are avai l a bl e to al l ow rap i d measureme nt of bl ood or pl a sma l a ctate on s mal l sam pl e s, usi ng enz yme -bas ed met hod s. The enzymati c c onv ers i on of l a ctate to p yruvat e i s an oxyg en uti l i s i ng reac ti on. The ext racti on of oxyg en from t he sam pl e can b e de tec ted by a sensi t i ve ox yge n fuel cel l sensor and i s d i re ctl y p roporti onal to the s amp l e l ac tat e c onc ent rati on. A w hol e bl ood sampl e (venous or arteri al si nc e t here i s no prac ti c al di fferenc e) i s col l ec te d i nto a hepari n fl uori d e tube to pre vent c oag ul a ti on and gl y col ysi s (l ac tat e p rod uc i ng ). N i t ri t e m ay be used i n t he s amp l e tub e t o c onv ert haemog l obi n to the me t form , t hus av oi d i ng up tak e of ox yge n d uri ng the enzym e reac ti on. The enzymati c me thod i s s pec i fi c for the L-i s omer and w i l l not, there fore, d ete ct D-l act at e (e .g. i n short bowel syndrome). N orm al art eri al whol e bl ood l ac tat e c onc ent rat i on i s <1.5m mol /l . Lactate may al so be m eas ure d from reg i onal si tes as an ai d t o the asse ssm ent of re gi onal pe rfusi on (e.g . arte ri a l –j ugul ar b ul b di ffe rence).

Biochemistry of lactate production Pyruvate i s the end p rod uct of gl ycol ys i s. Most i s the n m etabol i se d b y p yruvat e d ehyd rogenase to ace tyl CoA, the maj or sub strate for t he Kre bs cyc l e. Howeve r, i n condi ti ons of mi t ochond ri a l d ysfunc ti on (e.g . c el l ul ar hypoxi a , sep si s) m ore py ruv ate i s conve rte d t o l act ate by l a ctate dehydroge nas e. Lac tat e i s a buffe r not an aci d s o a hi gh bl ood l ac tat e i s not, there fore, synonym ous wi th l ac ti c aci d osi s. In conti nuous haem ofi l trat i on the repl ace ment fl ui d i s usuall y buffe red wi th l ac tat e at 35–45mm ol /l ; t hus b l ood l act ate l ev el s wi l l ri se wi t hout aci d osi s.

Causes of lactic acidosis Lac ti c aci d osi s occurs whe n p rod uct i on of l a ct i c aci d i s i n e xce ss of rem oval . The maj or source s are ske l et al mus cl e, brain and re d b l ood c el l s. Rem oval i s m ai nl y by met abol i s m t o g l uc ose i n the l i ve r and ki d ney . Hepat i c re mov al i s i mp ai red by poor p erfusi on and ac i dosi s . Lac ti c ac i dosi s i s t rad i ti onal l y c l as si fi ed as ty pe A or t ype B. Ty pe A refe rs to exc ess producti on whe n t i ss ue oxy genati on i s i nadeq uat e. Typ e B occ urs w here t here i s no s yst emi c t i ss ue hyp oxi a. Epi nep hri ne the rap y m ay cause acc el e rat ed aerobi c g l yc ol y si s and p yruvat e p rod uct i on i n ex ces s of mi t ochond ri al nee ds; thi s may produc e an i ncreas i ng me tab ol i c aci dos i s oft en out of proporti on to the pat i e nt' s cl i ni cal st atus. In sep si s, hyp erl act at aem i a i s mai nl y due t o i ncreas ed mus cl e Na + K + -ATPase act i vi ty . Treat ment of met abol i c ac i d osi s w i th sodi um b i carbonat e s ol uti on m ay i nc rease l ac tat e p rod uct i on. A s evere and persi ste nt typ e A l ac ti c aci d osi s i s ass oci ate d wi th a p oor outcome.

Identifying type A lactic acidosis Evi dence of poor t i ss ue perfus i on may b e ob vi ous cl i ni cal l y. Calcul at i on of arteri a l D O 2 may confi rm i nadeq uat e t i ss ue oxy gen del i v ery but a normal D O 2 doe s not guarantee ad equacy of sup pl y . P.171

Key trial Tot aro RJ, Raper RF. Ep i nephri ne-i nduced l a cti c aci dos i s fol l ow i ng cardi opul monary b ypass. Cri t Care M ed 1997; 25:1693–9

See also: Hae mo(d i a)fi l trati on (1), p62; Haemo(di a )fi l trat i on (2), p 64; Bl ood gas anal ysi s, p100; Art eri al cannul at i on, p 112; Other neurol og i cal m oni tori ng , p 140; Met abol i c ac i dosi s, p434; Syst emi c i nfl amm ati on/mul ti org an fai l ure, p484 P.172

Colloid osmotic pressure Col l oi d osmoti c pres sure (COP) i s the p res sure req ui red to pre vent net fl ui d move ment b etw een two sol ut i ons sep arated by a sel ect i ve l y permeabl e mem brane whe n one c ont ai ns a great er col l oi d concentrati on t han the othe r. The se l ec ti vel y pe rme abl e m emb rane s houl d i mp ede the passage of col l oi d m ol e cul es but not s mal l i ons and w ate r. COP i s de termi ned by num ber of mol ecul es rather than t ype. Howev er, mos t sol uti ons ex hi b i t non-i d eal be hav i our d ue to i nt ermol ecul ar i nteract i ons and el e ct ros tat i c effect s. Hence COP cannot be i nferred from pl a sma prote i n concentrati ons ; i t m ust be measured.

Measurement of COP In a m emb rane oncom ete r t he pl a sma sampl e i s s eparat ed from a re ferenc e 0. 9% sal i ne sol ut i on b y a mem brane wi t h a m ol e cul ar wei ght ex cl usi on b etw een 10,000 and 30,000D a. The re ferenc e s ol uti on i s i n a cl os ed c ham ber containi ng a p res sure t ransd uce r. Sal i ne wi l l pas s to t he sam pl e chamb er by col l oi d osmosi s c reati ng a neg ati ve press ure i n the refere nce chamb er. When the neg ati ve press ure preve nts any furt her fl ow across the me mbrane , i t i s e qual t o t he COP of the sampl e. Normal pl asm a C OP i s 25–30m mHg .

Clinical use of COP measurement Assessing significance of reduced plasma proteins

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Pl a sma al bum i n l ev el s are almost i nv ari abl y red uce d i n c ri t i c al l y i l l pat i e nts . Cause s i nc l ud e i nte rst i t i al l e akage, fai l ed sy nthesi s and i ncre ase d me tab ol i sm . Howev er, the s ame group of pat i ents oft en hav e rai s ed l ev el s of acute phase protei ns whi ch contri bute to COP. Si nc e t here i s no e vi d enc e t hat corre cti on of pl a sma al bum i n l ev el s i s benefi ci a l , many c l i ni c i ans c orrec t p l as ma v ol ume defi ci t w i t h arti fi c i al c ol l oi d . T hes e wi l l contri b ute to COP whi l e al s o reduci ng hepati c albumi n sy nthesi s. If COP i s maint ai ned >20mmHg i t i s l i ke l y that reduced pl asm a albumi n l ev el s are of no s i gni fi cance.

Avoiding pulmonary oedema It has be en sug ges ted that a d i ffere nce bet wee n C OP and pul monary artery w edg e p res sure > 6mmHg m i ni mi ses the ri sk of p ul m onary oed ema. Howev er, i n the face of sev ere capi l l ary l eak i t i s unl i kel y t hat pul monary oedem a c an be avoi de d i f p l as ma vol umes are t o b e m ai ntai ned compati b l e wi t h c i rcul atory ade quacy. Conversel y, a norm al COP woul d not ne ces sari l y preve nt pul monary oe dem a i n s evere c api l l ary l e ak; the contri b uti on of COP to fl ui d dynami cs i n thi s si t uat i on i s much red uc ed.

Selection of appropriate fluid therapy It i s di ffi cul t not to sup port t he use of col l oi d fl ui ds i n hypo-onc oti c p ati ent s. In pat i e nts wi th renal fai l ure t he rep eat ed use of col l oi d fl ui d may l e ad to a hy peronc oti c s tate. Thi s i s ass oci ate d w i th ti ss ue d ehy drati on and fai l ure of gl omerul a r fi l trati on (thus p rol ong i ng the renal fai l ure). Measureme nt of a hi gh COP i n pati e nts who have bee n treate d w i th arti fi c i al col l oi d s s houl d di rect t he use of cry stall oi d fl ui d s. It i s i m portant t o note that e xce ssi ve di ure si s may al so l e ad t o a hy per-oncot i c state for whi ch cryst al l oi d repl ace ment m ay b e nece ssary. P.173

See also: Hae mo(d i a)fi l trati on (1), p62; Haemo(di a )fi l trat i on (2), p 64; Li ver func ti on t est s, p152; Fl ui d c hal l enge, p274

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Ed itors: Si nge r, M ervyn; We bb, An dre w R. Ti tle : O xf ord Ha ndbook of Cr itic al Car e, 2nd Ed ition Cop yri ght © 1997,2005 M. Si nge r and A. R. W ebb , 1997, 2005. Publ i shed i n the Uni te d Stat es by Oxford Uni ve rsi ty Press Inc > Tab le of Co n te n ts > F lu ids

Fluids Crystalloids Types Sal i ne : e. g. 0.9% s al i ne, Ri nge r's l act ate , Hart mann's sol ut i on, 0.18% s al i ne i n 4% gl ucos e Gl ucos e: e .g. 5%, 10%, 20%, 50% Sod i um bi carbonate : e. g. 1.26%, 8. 4%

Uses Crys tal l oi d fl ui ds – to provi d e t he dai l y req ui reme nts of water and el ec trol yt es. They shoul d be gi ven to cri ti cal l y i l l pati e nts as a conti nuous b ack ground i nfus i on to suppl eme nt fl ui d s g i ve n duri ng feed i ng, or to c arry drugs. Hi g her conce ntrati on gl ucos e i nfusi ons – t o p rev ent hy pog l yc aem i a. Potassi um chl ori de – to sup pl e ment c rys tal l oi d fl ui ds . Sod i um bi carbonate – for corre cti on of met abol i c ac i dosi s , uri nary alkalini sati on, etc

Routes IV

Notes A s i g ni fi cant pl a sma vol um e d efi ci t shoul d b e repl ace d w i th col l oi d sol ut i ons s i nc e c rys talloi ds are rapi dl y l ost from the pl asm a, parti c ul arl y d uri ng peri ods of i nc reased cap i l l ary l eak , e .g. se psi s. As mos t p l as ma sub sti tutes are carri ed i n sal i ne sol ut i ons, any ad di t i onal 0. 9% s al i ne cryst al l oi d i nfus i on i s onl y ne eded to re pl a ce exc ess sodi um l os ses . The sodi um c ont ent of 0. 9% s al i ne i s eq ui v al e nt to that of ex tracel l ul ar fl ui d . A dail y requi re ment of 70–80mmol sod i um i s normal alt hough t here m ay be exc ess l oss i n swe at and from t he gas troi nt es ti nal tract. Ri nger's l a ctate or Hartmann' s s ol uti on have no pract i cal advantage over 0. 9% sal i ne for fl ui d m ai ntenanc e. The y

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may , howev er, be us eful i f l arg e v ol umes of cryst al l oi d are used to av oi d hyp erchl oraemi c aci d osi s. Hyp erc hl oraemi c aci dos i s may ad versl y affec t c oag ul a ti on and renal functi on. 5% gl ucos e i s used to suppl y i ntrave nous w ate r requi rements. The 50g/l g l uc ose conte nt ens ure s an i sot oni c s ol uti on but onl y provi d es 200Cal /l . Normal requi rement i s approxi mat el y 1. 5–2l /d ay. Water l oss i n exc ess of el ect rol yte s i s unc omm on but oc curs i n e xce ss swe ati ng, fe ver, hyperthyroi di sm, di abe tes i nsi pi d us and hy percal cae mi a . Pot ass i um chl ori d e m ust be gi ven sl owl y si nc e rapi d i nje cti on may cause fat al arrhy thm i as . N o more than 40mm ol /h shoul d be gi ven al though 20mmol /h i s more usual . The frequenc y of i nfusi on i s d i c tat ed b y p l as ma pot ass i um measureme nts . P.177

Ion content of crystalloids (mmol/l) Na + 0.9% saline

150

Hartmann's

131

0.18% saline in 4% glucose

30

K+

HCO3 -

Cl -

Ca 2+

150 5

29

111

2

30

Ion content of gastrointestinal fluids (mmol/l) H+ Gastric

40–60

Na +

K+

HCO3 -

Cl -

20–80

5–20

150

100–150

Biliary

120–140

5–15

30–50

80–120

Pancreatic

120–140

5–15

70–110

40–80

Small bowel

120–140

5–15

20–40

90–130

Large bowel

100–120

5–15

20–40

90–130

See also: Nut ri ti on—use and i ndi c ati ons , p 78; Ure a and c re ati ni ne, p144; El ec trol yt es , p 146; Sodi um bi c arb onate, p178; Col l oi ds , p 180; Hy pernat rae mi a , p 416; Hy ponatraem i a, p418; Hyp erkal aemi a, p420; Hyp okal aem i a, p422; Me tab ol i c aci dos i s, p434; Di a bet i c ket oac i d osi s, p442; Hy perosm ol a r d i ab eti c eme rge nci es, p444; Mul ti pl e trauma (1), p500; Mul ti pl e traum a (2), p502; Burns—fl ui d manage ment, p510; Pos t-operati ve i nt ens i ve care, p534 P.178

Sodium bicarbonate Types Isotoni c sod i um bi carbonate 1. 26% Hype rt oni c s odi um bi c arb onate (1mm ol /ml ) 8. 4%

Uses Correc ti on of me tab ol i c aci dos i s. Al k al i ni s at i on of uri ne . Al k al i ni s at i on of bl ood, e. g. for treat ment of tri c ycl i c ant i d epress ant ov erd ose .

Routes IV

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Notes Isotoni c (1. 26%) s odi um bi c arb onate may be use d t o c orrect ac i d osi s associ a ted wi th renal fai l ure or t o i nduce a forced al kal i ne di uresi s. The hy pertoni c (8. 4%) sol uti on i s rarel y requi red i n i nt ens i ve care practi ce to rai se bl ood pH i n sev ere me tab ol i c aci d osi s. Bi carbonate therapy i s i nappropri a te when ti ss ue hypoperfus i on or ne crosi s i s p res ent . Adm i ni st rat i on may b e i ndi cat ed as ei t her sp eci fi c t herapy (e. g. al k al i ne di ures i s for s al i cyl ate ov erd ose ) or i f t he pat i ent i s symp tom ati c (usual l y dys pnoe i c ) i n t he abse nce of ti ssue hypoperfus i on (e .g. re nal fai l ure). The PaCO 2 may ri se i f mi nut e v ol ume i s not i ncre ase d. Bi c arbonate cannot cros s t he c el l m embrane wi thout di s soci a ti on s o t he i nc rease i n PaCO 2 m ay res ul t i n i ntrace l l ul ar ac i d osi s and depres si on of my ocardi al ce l l functi on. The de cre ase i n pl asm a i oni sed calci um may al so cause a d ecreas e i n my ocardi al contract i l i ty . Si gni fi cantl y w ors e hae mod ynam i c effect s have be en rep ort ed wi t h b i carbonat e c omp are d t o eq ui m ol a r s al i ne i n pati e nts wi th sev ere heart fai l ure. Convi nci ng human e vi d enc e t hat bi carbonate i m proves myocardi al contracti l i ty or i nc reases resp ons i ve nes s t o ci rcul at i ng catec hol ami nes i n s evere aci dos i s i s l ac ki ng, though anecd otal s ucc ess has b een re ported . Aci dos i s rel at i ng to myocardi al dep res si on i s rel ated to i ntrace l l ul ar c hang es that are not ac curate l y refl ec te d by arteri a l b l ood che mi s try. Exc ess i ve ad mi ni s trati on m ay c aus e hype ros mol al i ty , hypernat raemi a, hypokal aem i a and sodi um ov erl oad . Bi carbonate may de cre ase ti ss ue oxyg en avai l a bi l i t y by a l eft s hi ft of t he oxyhaem ogl obi n d i ss oci at i on curve . Sod i um bi carbonat e does hav e a pl ace i n the manag eme nt of aci d rete nti on or al k al i l oss, e. g. chroni c renal fai l ure, renal tub ul ar aci dos i s, fi st ul a e, d i arrhoea. Fl ui d and/or p otassi um defi c i ts shoul d b e c orrect ed fi rst . P.179

Ion content of sodium bicarbonate (mmol/l) Na +

K+

HCO3 -

1.26% sodium bicarbonate

150

150

8.4% sodium bicarbonate

1000

1000

Cl -

Ca 2+

See also: Bl ood gas anal y si s , p 100; El ec trol yt es ), p146; Crys tal l oi ds , p 176; Cardi ac arrest , p 272; Me tab ol i c aci dos i s, p434; Sal i c yl a te poi soni ng , p 454 P.180

Colloids Types Al b umi n: e.g . 4. 5–5%, 20–25% human al b umi n s ol uti on Dext ran: e .g. 6% De xtran 70 Gel ati n: e.g. 3. 5% pol yge l i ne, 4% suc ci nyl a ted ge l at i n Hydroxy ethyl starc h: e .g. 6% he tas tarch, 6% hex ast arch, 6 and 10% pe ntastarch, 6% t etrast arc h

Uses Repl ace ment of p l as ma v ol ume defi ci t/p erc ent age Short term v ol ume e xpansi on (ge l at i n, de xtran) Medi um term v ol ume exp ans i on (al bum i n, pe ntast arc h) Longer te rm vol ume exp ans i on (hetastarch)

Routes IV

Side-effects

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Di l uti on coagul opathy Anaphyl axi s Int erfere nce wi th bl ood c ross-mat chi ng (De xtran 70)

Notes Small er vol umes of col l oi d are requi re d for res usc i t ati on wi t h l ess contri buti on to oede ma. Mai nt enance of pl a sma col l oi d osm oti c p res sure (COP) i s a use ful effec t not see n wi th cryst al l oi ds, but c ol l oi d s c ont ai n no cl ott i ng fact ors or other pl a sma enzym e s yst ems . Al bum i n i s the main provi d er of COP and has s eve ral ot her rol es . T here i s no e vi d enc e t hat mai nt ai ni ng pl asm a al b umi n l eve l s , as op pos ed to pl a sma COP wi th art i fi ci al pl asma subst i t ute s, i s bet ter. Al bum i n 20–25% and Pe ntaspan 10% are hyp eroncoti c and used to provi de col l oi d w here s al t rest ri c ti on i s nec ess ary . Thi s i s rarel y ne ces sary i n i nte nsi ve care as p l as ma vol ume exp ans i on i s rel a ted to the we i ght of c ol l oi d i nfused rat her t han the conce ntrat i on. Arti fi ci a l c ol l oi ds use d wi th ul trafi l trati on or di ures i s are just as effect i ve i n oe dema states . Pol yge l i ne i s a 3. 5% sol uti on contai ni ng cal ci um (6.25mmol /l ). Thi s p re vent s use of the same g i v i ng se t for bl ood trans fus i ons. Suc ci nyl ated ge l at i n i s a 4% s ol uti on wi t h a l arge r m ol e cul ar si z e t han pol yg el i ne gi v i ng a sl i ghtl y l onger effec t. Thi s, and the l ack of cal ci um i n sol uti on, make i t more useful than p ol y gel i ne for s hort t erm pl asm a vol ume ex pans i on. In pat i ents wi t h c api l l ary l e ak al b umi n and smalle r m ol e cul ar wei ght col l oi d s l eak to the i nte rst i ti um . In t hes e cases i t i s pe rhaps bet ter to us e l arg er mol ecul ar we i ght c ol l oi ds suc h as hydroxye thy l s tarch, t hough concl usi v e e vi d enc e i s l a cki ng. Het ast arc h and hex ast arc h are usual l y 6% s ol uti ons wi t h a hi gh deg ree of prote cti on from m etabol i sm due t o a hi g h deg ree of subst i tuti on (proporti on of g l uc os e uni t s s ubs ti t ut ed w i th hy droxye thy l g roups—DS) or a hi g h rati o of C 2 t o C6 carbon at oms subst i tuted (C 2:C6 rati o). The mol ec ul a r w ei g ht ranges vary but mol ec ul a r s i ze s are l arge enough to ens ure a prol onged effec t. Thes e are the most use ful col l oi d s i n c api l l a ry l eak. Prol onged i t chi ng re l at ed to i nt radermal de pos i ti on and i nterferenc e w i th coagul at i on are c omp l i c ati ons i f ex ces si ve d ose s are use d. Pentas tarch and te trast arc h p rov i de onl y a short t erm effect si mi l ar to succi nyl at ed g el a ti n. P.181

Unique features of albumin Transp ort of vari ous mol ecul es . Free radi c al sc avengi ng. Bi ndi ng of t oxi ns. Inhi bi ti on of p l at el e t aggregati on.

Relative persistence of colloid effect Albumin

+++

Dextran 70

++

Succinylated gelatin

++

Polygeline

+

Hetastarch (high MW, high DS, low C2:C6 ratio)

++++

Hexastarch (medium MW, high DS, high C2:C6 ratio)

++++

Pentastarch (medium MW, low DS, low C2:C6 ratio)

++

Tetrastarch (low MW, low DS, high C2:C6 ratio)

++

Pers i s tence i s dep end ent on mol ecul a r s i ze and p rot ect i on from met abol i s m. Hi g h D S and hi g h C2:C6 rati o prote ct hyd rox yet hyl st arc h from me tab ol i sm. Al l arti fi c i al col l oi d s are pol ydi spe rse (i .e. there i s a range of m ol e cul ar si zes ).

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Key trial The SAFE study i nv est i g ators. A com pari son of al bumi n and s al i ne for fl ui d re sus ci tat i on i n the i nte nsi ve care uni t . N Eng l J Me d 2004; J50:2247-56.

See also: Cry stall oi d s, p176; Bl ood t ransfusi on, p182; Bl ood p roduc ts, p252; Bas i c res us ci t ati on, p270; F l ui d c hal l enge, p274; Di abet i c ket oac i d osi s, p442; Syst emi c i nfl amm ati on/mul ti organ fai l ure , p 484; Seps i s and se pti c s hoc k t re atme nt, p550; Anaphy l ac toi d reac ti ons , p 496; Burns —fl ui d manage ment, p510; Post -op erati v e i nte nsi ve care, p534 P.182

Blood transfusion Blood storage Bl ood cel l s are e vent ual l y des troye d due t o oxi d ant damag e duri ng storag e of whol e bl ood . Si nc e w hi t e c el l s and pl a sma enzym e s yst ems are of i m portance i n thi s cel l ul ar des truct i on, e ffe cts are c orresp ond i ng l y l es s seve re for pac ked re d c el l s. Bl ood us ed for trans fus i on i n mos t of Europe i s now routi nel y l euk ode pl e ted . M i croag gre gat e format i on i s as soc i a ted wi t h p l atel ets , w hi t e c el l s and fi b ri n and rang e i n s i z e from 20–170µm. The ri sk of mi c roaggreg ate dam age i s re duc ed wi t h p ack ed red ce l l s . In addi ti on t o s phe roc ytosi s and haem ol y si s , p rol onged storag e d epl ete s ATP and 2, 3-D PG l ev el s thus i nc reasi ng the oxy gen affi ni ty of the red c el l s. If whol e bl ood i s to be use d i n c ri ti c al l y i l l pati e nts i t s houl d be as fres h as p oss i b l e.

Compatibility In an eme rge ncy , wi th mas si ve b l ood l os s t hat threatens l i fe , i t i s p erm i s si b l e to transfuse O neg ati ve pac ked cel l s but a sam pl e must be take n for groupi ng pri or to trans fus i on. W i th modern l aborat ory proce dures i t i s possi bl e to obt ai n ABO com pat i bi l i ty for group spe ci fi c trans fus i on wi thi n 5–10mi n and a ful l cross -mat ch i n 30m i n.

Hazards of blood transfusion Ci t rat e t oxi ci t y—hypocal cae mi a i s rarel y a probl em and the p rop hyl act i c use of calci um sup pl ementat i on i s not rec omme nde d. Potassi um l oad—p otass i um re turns to cel l s rapi d l y but hy perkal aemi a m ay be a prob l em i f bl ood i s st ore d at room te mpe rat ure . Sod i um l oad— from ci trate i f the t ransfusi on i s m ass i ve . Hypothe rmi a—c an be avoi de d b y warmi ng bl ood as i t i s trans fus ed. Jaundi c e—haem ol y si s of i ncom pat i bl e or ol d bl ood. Pyre xi a —i mmunol ogi cal trans fus i on re act i ons t o i nc ompati bl e re d or whi t e c el l s or p l at el e ts . DIC— parti al act i vati on of c l ot ti ng fact ors and d est ructi on of stored ce l l s , e i ther i n ol d b l ood or when transfusi on i s i nc omp ati bl e . Anaphyl ac toi d reac ti on—urt i cari a i s common and probab l y due to a reac ti on t o t ransfused pl asm a p rot ei ns; i f seve re i t may be treat ed by s l owi ng t he t ransfusi on and gi vi ng c hl orpheni rami ne 10mg IV/IM. In se vere anap hyl axi s, i n add i t i on to st and ard treat ment, the trans fus i on shoul d b e s top ped and s aved for l ate r anal ysi s and a s amp l e tak en for further cross-mat chi ng. Transm i ss i on of di sease— i nc l ud i ng vi ruses , p arasi t es (malari a), p ri ons. Transfusi on-rel ate d acut e l ung i njury (TRALI) and ot her i mmune reac ti ons . A mul t i ce ntre t ri al sug ges ted l i beral trans fus i on i n the c ri t i c al l y i l l produced l e ss fav ourabl e outc omes , parti c ul a rl y i n young er, l ess si ck pat i ents, than usi ng a t ri gger haemogl obi n of 7g /dl . P.183

Key trial Heb ert PC , W el l s G , Bl aj chm an MA et al , for t he Tranfusi on R equi re ments i n Cri ti c al Care Inve sti gat ors. A mul ti center, rand omi zed , c ont rol l ed cl i ni cal t ri al of transfusi on req ui reme nts i n c ri t i c al care. N Engl J M ed 1999; 340:409–17

See also: Cal ci um, mag nes i um and p hos phate, p148; Ful l b l ood c ount, p154; Coag ul a ti on m oni tori ng, p156; Basi c res usc i tati on, p270; Hae mothorax, p302; Hae mop tys i s, p304; Up per gastroi ntes ti nal haemorrhage , p344; Bl e edi ng vari c es, p346; Low er i nt est i nal bl e edi ng and col i t i s , p 348; Bl e edi ng di s ord ers , p 396; Anaem i a, p400; Hae mol ysi s, p404; Mal ari a, p490; Anaphy l ac toi d reac ti ons , p 496; Pos t-operati ve i nt ens i ve care, p534; Pos t-p art um haem orrhag e, p542

Ovid: Oxford Handbook of Critical Care

Ed itors:

Si nge r, M ervyn; We bb, An dre w R.

Ti tle : O xf ord Ha ndbook of Cr itic al Car e, 2nd Ed ition Cop yri ght © 1997,2005 M. Si nge r and A. R. W ebb , 1997, 2005. Publ i shed i n the Uni te d Stat es by Oxford Uni ve rsi ty

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Press Inc > Tab le of Co n te n ts > Resp ir a tor y d r u gs

Respiratory drugs Bronchodilators Types β 2 agoni st s: e.g . s al b utamol , e pi nephri ne, terbutal i ne Ant i chol i nergi cs: e. g. i pratropi um Theophy l l i ne s: e .g. am i nophy l l i ne Ste roi ds: e. g. hydroc ort i sone, predni sol one Others : e. g. ket ami ne, i s ofl urane, halot hane

Uses Rel i ef of bronc hos pas m

Routes Inhal e d (s al b ut amol , e pi nephri ne, te rbutal i ne , i pratropi um, i s ofl urane, halot hane) Nebul i sed (s al b utamol , ep i nephri ne, terbut al i ne, i pratropi um) IV (sal butam ol , epi ne phri ne , t erb utali ne, i p rat rop i um , ami nophyl l i ne , hydrocort i sone, ket ami ne) PO (ami nop hyl l i ne, predni sol one)

Side-effects CNS st i mul at i on (s al b utamol , e pi nephri ne, terbut al i ne , am i nophy l l i ne ) Tachycard i a (sal butamol , epi nep hri ne , t erb utaline, ami nop hyl l i ne, ket ami ne) Hypotensi on (sal but amol , terbut al i ne , ami nophyl l i ne , i sofl urane , hal othane) Hype rgl yc aemi a (sal but amol , epi nep hri ne , t erb utaline, hyd roc ort i s one, predni s ol one) Hypokal aem i a (salbutam ol , ep i ne phri ne , t erb utali ne, hyd roc orti s one , p red ni s ol one) Lac ti c ac i dosi s (s al but amol )—rare

Notes Sel ec ti v e β 2 ag oni sts are usuall y gi ven by i nhal ati on vi a a pre ssuri sed aeros ol or a ne bul i z er. Inhal ati on oft en gi v es rap i d re l i e f of bronc hos pas m, al t hough the ae ros ol i s of l es s b ene fi t i n se vere asthma. Neb ul i ze d drug s requi re a mi ni mum v ol ume of 4ml and a dri vi ng g as fl ow of 6–8l /mi n. In ext rem is , ep i ne phri ne may b e used IV, SC or i nje cte d d own the endot rac heal t ube . As e pi nephri ne i s not se l ec ti v e, arrhyt hmi as are more l i kel y. Howe ver, t he α ag oni st effect may reduce muc osal s wel l i ng b y v asoconstri c ti on. Iprat rop i um bromi de has no sys tem i c effect s and doe s not dep res s m ucoci l l i ary cl earanc e. It i s synerg i s ti c wi th β 2 agoni s ts but has a sl owe r onse t of ac ti on. Ami nop hyl l i ne i s synerg i s ti c wi th β 2 agoni s ts . D osages mus t b e adjuste d accordi ng to pl a sma l e vel s (range 10–20m g/l ) s i nc e t oxi c e ffe cts may be se vere. Dos e requi re ments are re duc ed by heart fai l ure, l i v er di seas e, chroni c ai rfl ow l i m i tati on, fev er, ci met i di ne, erythrom yci n. Dos e requi rements are i ncreas ed i n chi l dren, s moke rs and those wi t h a moderate to hi gh al c ohol i ntake.

See also: St eroi ds , p 262; Chroni c ai rfl ow l i mi tati on, p286; Asthma—general m anageme nt, p296; As thm a—v ent i l a tory manage ment , p 298 P.187

Drug dosages

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Aerosol*

Nebuliser*

Salbutamol

100–200µg

2.5–5mg

Terbutaline

250–500µg

5–10mg

Epinephrine

0.5mg

Ipratropium

250µg

IV bolus

IV infusion 3–20µg/min

1.5–5µg/min

Aminophylline

5mg/kg over 20min

Hydrocortisone

200mg qds

0.5mg/kg/h

*Aerosols and nebulisers are usually given 4–6 times daily but may be given more frequently if necessary.

In ext rem is , ep i ne phri ne may b e g i ve n as 0.1–0.5mg s ubc ut aneousl y, i njec ted dow n t he end otracheal tube or by IV i nfusi on. P.188

Respiratory stimulants Types Drug antagoni st s: e.g . nalox one , fl um aze ni l CNS st i mul ants: e. g. d oxapram Al m i tri ne

Uses Acute res pi ratory fai l ure due to fai l ure of v ent i l a tory d ri ve. Drug i nduced ve nti l at ory failure, e. g. as a resul t of exc ess i ve se dat i on or post-operat i ve l y.

Routes IV

Modes of action Nal oxone—s hort acti ng opi at e antag oni st . Fl um aze ni l —s hort acti ng benzod i azepi ne ant agoni s t. Doxapram—g ene ral i s ed c ent ral nerv ous sy ste m s ti m ul a nt wi t h p red omi nant resp i ratory sti mul ati on at l ow er dose s. St i mul at i on of carot i d che morece ptors at very l ow dos es w i t h i ncreas ed ti d al vol ume s. Al m i tri ne—i ncreas es the se nsi ti vi t y of carot i d chemorec ept ors to hyp oxaemi a and hype rc apni a.

Side-effects Sei zures (fl umazeni l , doxap ram ) Tachyarrhythmi a s (nal oxone, fl umazeni l ) Hal l uc i nati ons (doxap ram )

Notes Res pi ratory st i mul ants are mainl y used i n pati e nts wi th chroni c ai rfl ow l i mi tat i on who d evel op acute hyp erc apni c res pi rat ory failure. Effec ts of doxapram are short-l i ved so i nfusi on i s nec es sary. Aft er about 12h i nfus i on the effec ts on venti l atory dri ve are re duc ed. Nal oxone may be use d i n resp i ratory depres si on d ue to opi ate drugs . Si nc e i t reve rse s all opi at e effec ts, i t may b e bet ter to re verse res pi rat ory de pre ssi on wi t h non-spe ci fi c res pi rat ory st i mul ants , l eavi ng pai n rel i ef i ntac t. It may nee d t o b e repeated when l ong acti ng opi ate s are i nv ol v ed.

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As mos t b enz odi aze pi nes are l ong act i ng c ompared to fl umazeni l , repeated doses may b e ne ces sary. Al mi t ri ne d oes not p rod uce ce ntral res pi rat ory st i mul at i on but i t does i mprove venti l at i on–pe rfusi on m atc hi ng b y aug menti ng hypoxi c pul monary v asoconstri ct i on. Effe cts c ont i nue for s eve ral hours after i njec ti on. P.189

Drug dosages IV Infusion

IV bolus

Naloxone

0.1–0.4mg

Flumazenil

0.2mg over 15min (0.1mg/min to max 2mg)

Doxapram

1–1.5mg/kg over 30s

Almitrine

0.25–0.5mg/kg over 30min

IV

2–3mg/min

Key paper Greens tone M , Lass ers on TJ. Doxap ram for ve nti l a tory fai l ure due t o ex ace rbati ons of chroni c obs tructi ve pul monary di s eas e. Coc hrane Dat abase Sys t R ev. 2003; CD000223. Rev i ew

See also: Opi oi d anal ges i cs , p 234; Sed ati ves , p 238; R esp i ratory fai l ure, p 282; Sedat i v e poi s oni ng, p458; Pos t-op erati ve i nt ens i v e c are , p534 P.190

Nitric oxide Ni t ri c oxi d e i s now rec ogni se d as a fundam ent al med i at or i n many p hys i ol ogi cal proc ess es. One of i t s m ost i mportant effect s i s s mooth mus cl e re l ax ati on; ni tri c oxi de i s the maj or l oc al control l er of vas cul ar tone v i a effe ct s on cy cl i c GMP.

Inhaled nitric oxide Ni t ri c oxi d e i s p rov i de d for i nhal a ti on from cy l i nders (1000pp m ni t ri c ox i de i n ni trogen). It i s di l ut ed wi t h i nsp i ratory gas es, ei the r at t he gas suppl y t o t he venti l ator or i n t he i ns pi rat ory l i mb of the venti l at or ci rcui t, to provi de an i nhal ed c onc ent rati on of 1–40p pm, al though most pat i ents req ui re l es s t han 20ppm . Inhal at i on produces vas odi l at ati on at the si te of gas ex change , and m ay i mp rov e ve nti l a ti on–p erfusi on mat chi ng and re duc e p ul m onary art ery pres sures. Random i s ed m ul t i -centre st udi es i n pat i ents wi t h acut e l ung i njury have re vealed no l ong-t erm benefi t or outc ome i m provem ent .

Side-effects Ni t ri c oxi d e i s i mme di a tel y b ound t o haemogl obi n ensuri ng l ocal e ffe cts onl y. There i s no tol eranc e b ut pat i ents can bec ome de pend ent on conti nue d i nhalat i on wi th re bound p ul monary hyp ert ens i on and hypoxae mi a on wi t hdrawal. For thi s reason, wi thdrawal mus t b e g rad ual . Exce ssi ve hum i di fi cat i on of i nspi red gases may form ni tri c aci d wi th NO; the use of he at–moi sture exc hangers rather than w ater b aths i s recomme nded .

Monitoring Ni t ri c oxi d e and ni t rog en di oxi d e c onc ent rat i ons m ay be moni tored conveni entl y wi th portabl e fuel cel l anal yse rs or by che mi l umi nes cence. It i s i mportant to moni tor c onc ent rat i ons of b oth gases i n the i nsp i ratory l i m b of t he venti l at or ci rcui t. Moni t ori ng of ni t rog en di oxi d e i s i mportant to ens ure that tox i c dos es are not form ed wi t h t he oxy gen i n the i nsp i re d g as and subse que ntl y i nhaled by the p ati ent . Al thoug h i t i s ext rem el y rare to s ee tox i c ni t rogen di oxi de c onc ent rati ons (>5p pm) i t i s poss i bl e t o remove ni t rog en d i oxi d e from the i nspi re d g as by usi ng a sod a l i me ad sorber. M ethaem ogl obi n i s form ed when ni tri c oxi de bi nds to hae mogl ob i n. Prol onge d i nhalat i on at hi ghe r dos es may rarel y p rod uce si gni fi cant me thaemogl obi naem i a (>5%) and thi s s houl d the refore be moni t ore d d ai l y.

Achieving the correct dose App roxi m atel y 50% of pat i ents wi t h s eve re res pi ratory fai l ure res pond t o ni tri c oxi de. Howeve r, the most effect i ve dos e v ari es. It i s us ual t o s tart at 1ppm for 10mi n and m oni tor the c hange i n PaO 2 /FIO 2 rati o. An i ncre ase shoul d b e fol l ow ed by an i nc rease i n ni t ri c ox i d e conce ntrat i on to 5p pm for a furt her 10mi n. T hereafter, t he dos e i s adjuste d acc ord i ng t o resp ons e at 10mi n i nte rvals unt i l the most effect i ve dose i s found. Si nce the underl y i ng pathophy si ol og y may chang e, i t i s i mp ort ant to as ses s t he dos e resp ons e at d ai l y i nte rvals, ai mi ng t o k eep the d ose at the l owes t effect i ve l e vel .

Scavenging Si nce the c onc ent rat i ons used are s o s mal l , di l uti on of exhal e d g ase s i nto the at mos phe re i s unl i k el y to produce i mp ort ant envi ronment al concentrati ons . In t he ai r-condi ti oned i ntensi ve c are envi ronment ai r changes are s o

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fre que nt as to make sc ave ngi ng unnece ssary. P.191

Key trials Del l i nge r R P et al , for the Inhal ed Ni t ri c Oxi d e i n ARDS Stud y Group. Effe cts of i nhal ed ni t ri c oxi d e i n p ati ent s w i th acute res pi rat ory di stress s yndrome : resul t s of a random i ze d p has e II t ri a l . Cri t Care Me d 1998; 26:15–23 Lundi n S et al , for t he The Europ ean St udy Group of Inhal ed Ni t ri c Oxi d e. Inhal a ti on of ni tri c oxi de i n acute l ung i nj ury: resul t s of a Europe an mul ti c ent re st udy . Inte nsi ve Care Me d 1999; 25:911–19

See also: Vas odi l a tors, p198; Acut e resp i ratory di s tress sy ndrome (1), p 292; Acute res pi rat ory di stres s s ynd rom e (2), p294 P.192

Surfactant In ARD S t here i s dec reased surfactant produc ti on, bi oche mi c al abnormal i ty of the surfact ant produced and i nhi bi t i on of surfac tant func ti on. The ne t resul t i s al veol ar and sm al l ai rw ay c ol l ap se. Surfactant al s o c ont ri but es to host defenc e agai nst mi cro-organi sm s. Surfac tant rep l ac eme nt woul d b e e xpe cte d t o ex ert t herapeuti c e ffec ts on l ung mec hani cs , g as exc hange and hos t d efe nce . Ins ti l l a ti on of s urfact ant (e i ther as a l i qui d or neb ul i se d) v i a the endot rac heal t ube i nto the l ungs i s as soci a ted wi th i mp rov ed out com e i n neonatal resp i ratory d i s tre ss syndrome. Pot ent i a l i ndi cat i ons i n adul ts i ncl ude ARD S, pne umoni a , c hroni c ai rfl ow l i mi t ati on and as thm a. Mul ti p l e studi es i n ARD S have yet to de monstrate mortalit y benefi t, though thi s may be re l at ed to the typ e of s urfact ant , t he vol ume us ed, or the de l i very s yst em. St udi es have de monstrate d i mprove d oxyg enat i on wi th re comb i nant surfactant protei n C and a trend to i mp rov ed survi val i n pati e nts wi th di rect l ung i njury. Furthe r s tud i es are unde rway usi ng recombi nant s urfact ant prote i n C w i th phosphol i pi ds, and wi th surfactant protei ns B and C. The surfactant i s i ns ti l l e d i nto the l ung s v i a an end otracheal cat het er. Com pl i cat i ons of s urfact ant treat ment have i ncl uded i ncreas ed c oug h, sputum product i on, b ronchospasm, i ncre asd peak airw ay p re ssure and adv ers e e ffe cts on pul monary func ti on. The se can be mi ni mi se d b y ad equate se dat i on and neurom usc ul ar bl ockade b efore i ns ti l l i ng surfac tant. P.193

Key trial Sprag g RG , Lewi s JF, Wal mrath HD et al . Effect of re com bi nant surfact ant prote i n C-based surfactant on the ac ute res pi rat ory di stres s s ynd rom e. N Engl J M ed 2004; 351:884–92

See also: Ac ute re spi rat ory di st res s s ynd rom e (1), p292; Acut e resp i ratory d i s tre ss syndrome (2), p294

Ovid: Oxford Handbook of Critical Care

Ed itors: Si nge r, M ervyn; We bb, An dre w R. Ti tle : O xf ord Ha ndbook of Cr itic al Car e, 2nd Ed ition Cop yri ght © 1997,2005 M. Si nge r and A. R. W ebb , 1997, 2005. Publ i shed i n the Uni te d Stat es by Oxford Uni ve rsi ty Press Inc > Tab le of Co n te n ts > Car dio vasc u la r Dr u gs

Cardiovascular Drugs Inotropes Types Cate chol am i ne s: e.g . e pi nephri ne, norepi nep hri ne, dobut ami ne, dopam i ne Phos phodi e st erase (PDE) i nhi bi tors: e.g. mi l ri none, enoxi mone Dope xam i ne Cal c i um s ens i ti sers: e.g . l evosi m end an Card i ac gl yc osi des : e. g. di goxi n (weak)

Modes of action Inc rease force of m yoc ard i al contrac ti on, ei t her by st i mul at i ng c ard i ac β 1 ad renore cep tors (cat echol a mi nes), decreas i ng c AMP break down (PDE i nhi bi tors), i ncreas i ng calci um sensi ti v i ty (C a s ens i ti sers), di re ctl y i ncreas i ng cont racti l i ty (di goxi n), or i nhi bi t i ng ne uronal re upt ake of norad renal i ne (dop exami ne). Al l agents exc ept di gox i n

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have , t o g reater or l e sse r d egrees , associ ated di l a tor or const ri ctor p rop ert i es vi a β 1 and β 1 adrenorec ept ors , dopami nerg i c re cep tors, or K AT P channel s . Di g oxi n m ay c aus e s pl a nchni c v asoc ons tri ct i on and, for an i notropi c e ffe ct, re qui re s p l as ma l eve l s at the top of the the rap eut i c range . The i nc re ase i n cardi ac work i s p art i al l y offset i n those drugs posse ss i ng as soc i at ed di l ator e ffe cts . Other than ep i nephri ne (when us ed for i t s v asoconstri c tor effec t i n c ard i op ul m onary res usc i t ati on) or di gox i n (for l ong t erm us e i n c hroni c he art failure), i not rop es are us ual l y gi ven by conti nuous IV i nfusi on ti t rat ed for effec t.

Uses Myoc ard i al fail ure , e .g. pos t-m yoc ard i al i nfarct i on, c ard i om yop athy Myoc ard i al d epress i on, e .g. se psi s Aug ment at i on of oxy gen del i v ery i n hi gh-ri s k s urgi c al pat i ents

Side-effects Arrhyt hmi as (us ual l y ass oci at ed w i th concurrent hy povol ae mi a ) Tachycard i a (usual l y ass oci ate d wi th concurre nt hyp ovol ae mi a ) Hypotensi on (rel ate d t o d i l ator p rop ert i es ± concurrent hypovol aem i a) Hype rt ens i on (rel a ted to const ri c tor prope rt i es ) Ang i nal c hes t p ai n, or ST-s egm ent and T -wav e c hanges on ECG

Notes Epi nep hri ne , nore pi nephri ne, dob utami ne and d opami ne s houl d be gi v en vi a a c ent ral v ei n as ti ssue necrosi s m ay occ ur sec ond ary to pe ri pheral ext ravas ati on. P.197

Drug dosages Epinephrine

Infusion starting from 0.05µg/kg/min

Norepinephrine

Infusion starting from 0.05µg/kg/min

Dobutamine

Infusion from 2.5–25µg/kg/min

Dopamine

Infusion from 2.5–50µg/kg/min

Dopexamine

Infusion from 0.5–6µg/kg/min

Milrinone

Loading dose of 50µg/kg over 10min followed by infusion from 0.375–0.75µg/kg/min

Enoximone

Loading dose of 0.5–1mg/kg over 10min followed by infusion from 5–20µg/kg/min

Digoxin

0.5mg given PO or IV over 10–20min. Repeat at 4–8h intervals until loading achieved (assessed by clinical response). Maintenance dose thereafter is 0.0625–0.25mg/day depending on plasma levels and clinical response.

Levosimendan

12–24µg/kg over 10min followed by 0.1µg/kg/min for 24h

See also: Int ra-aorti c b al l oon count erp ul s ati on, p58; Card i ac output—t hermod i l uti on, p122; Card i ac output—other i nv asi ve, p124; Cardi a c outp ut— non-i nvas i ve (1), p 126; C ard i ac output— non-i nvas i ve (2), p 128; Bas i c res usc i t ati on, p270; Cardi a c arrest , p 272; Fl ui d chal l eng e, p274; Hypotensi on, p312; Sep si s and s ept i c shock —treat ment, p486; Care of the potenti a l organ d onor, p552 P.198

Vasodilators

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Types Ni t rat es: e. g. g l y ceryl tri ni trate, i s osorbi de di ni t rat e Ang i ot ens i n converti ng e nzy me (AC E) i nhi bi tors: e.g . c apt opri l Smooth mus cl e rel a xant s: e.g . s odi um ni t roprussi de, hy dralazine α-ad renerg i c ant agoni sts : e. g. phe ntol am i ne β 2 -adre nergi c ag oni st s: e.g. salb utamol Cal c i um antag oni st s: e .g. ni fed i pi ne , di l t i azem Dopami nergi c ag oni sts : e .g. dop exami ne Phos phodi e st erase i nhi bi tors: e.g . e nox i mone, mi l ri none, si l denafi l Pros tagl a ndi ns: e. g. e pop ros tenol (PGI 2 ), al prost adi l (PGE 1 ) B-t ype nat ri ure ti c pe pti de analog ues , e .g. ne si ri t i de

Modes of action Inc rease cyc l i c GM P c onc ent rat i on (b y ni tri c oxi de donati on or by i nhi b i ti ng cGM P b reakdown), or ac ts di rec tl y on dopami nerg i c re cep tors l ead i ng to vasod i l atat i on Reduce (to varyi ng degrees ) v ent ri cul ar pre l oad and/or afte rl oad . Reduce cardi a c w ork .

Uses Myoc ard i al fail ure , e .g. pos t-m yoc ard i al i nfarct i on, c ard i om yop athy Ang i na/i s chaemi c heart d i se ase Sys tem i c hyp ert ens i on (s pec i fi c c aus es, e. g. phaeoc hromoc ytoma) Vas oconst ri c ti on Peri pheral v asc ul a r d i se ase /hy pop erfusi on Spl anc hni c p erfusi on (dopex ami ne, dop ami ne) Pul monary hyp ert ens i on (i nhaled NO, p ros tag l andi ns, si l de nafi l )

Side-effects/complications Hypotensi on (oft en ass oci ate d w i th concurre nt hyp ovol ae mi a ) Tachycard i a (oft en ass oci ate d w i th concurrent hyp ovol ae mi a ) Symp tom s i nc l ud e headache , fl us hi ng, pos tural hy pot ens i on Renal fai l ure (ACE i nhi bi tors)—es pec i al l y wi t h renal art ery st enos i s , hypovol aemi a, non-st eroi dals

Notes Gl yceryl tri ni trate and i sos orb i de di ni t rate red uce bot h p re l oad and afte rl oad. At hi gher dos e the afte rl oad effect bec ome s m ore promi nent. Tol erance to ni trate s usually commences wi thi n 24–36h unl es s i nte rmi tt ent oral dos i ng i s us ed. Progress i ve i ncreas es i n dos e are req ui red to achi ev e t he sam e effec t. Prol onged (> 24–36h) dose-rel ate d admi ni s trati on of s odi um ni troprussi de can rarel y p roduc e a met abol i c ac i d osi s rel at ed t o c yani de ac cum ul a ti on. ACE i nhi bi t or tab l et s c an be crushe d and gi v en ei t her SL or vi a a nasog ast ri c t ube. Dop ami nergi c d rug s i mprove sp l anchni c bl ood fl ow t hough cl i ni cal be nefi ts are unproved . Hyd ral azi ne has an unpre di c tabl e effect on bl ood press ure and, i f gi v en IV, shoul d b e used wi th cauti on. P.199

Drug dosages Nitrates

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Sodium nitroprusside

20–400µg/min

Hydralazine

5–10mg by slow IV bolus, repeat after 20–30min. Alternatively, by infusion starting at 200–300µg/min and reducing to 50–150µg/min

ACE inhibitors

Captopril: 6.25mg test dose increasing to 25mg tds Enalapril: 2.5mg test dose increasing to 40mg od Lisinopril: 2.5mg test dose increasing to 40mg od

Nifedipine:

5–20mg PO. Capsule fluid can be injected down nasogastric tube or given sublingually

Phentolamine

2–5mg IV slow bolus. Repeat as necessary.

Dopexamine

Infusion from 0.5–6µg/kg/min

Milrinone

Loading dose of 50µg/kg over 10min followed by infusion from 0.375–0.75µg/kg/min

Enoximone

Loading dose of 0.5–1mg/kg over 10min followed by infusion from 5–20µg/kg/min

Epoprostenol, alprostadil

Infusion from 2–30ng/kg/min

Nitric oxide

By inhalation: 2–40ppm

Nesiritide

2µg/kg bolus followed by infusion of 0.01–0.03µg/kg/min

Sildenafil

50mg tds PO

See also: Bl ood press ure moni t ori ng, p110; Card i ac output—the rmodi l uti on, p122; Cardi a c outp ut—other i nvasi ve, p124; Cardi a c outp ut— non-i nvas i ve (1), p 126; Card i ac outp ut—non-i nvasi ve (2), p 128; Hypotensi v e agent s, p202; Ant i a ngi nal ag ent s, p208; N i tri c oxi de , p190; Bas i c res us ci t ati on, p270; F lui d c hal l enge, p274; Hy pertensi on, p314; Ac ute coronary syndrome (1), p 320; Ac ut e c oronary s yndrome (2), p322; Heart fai l ure—as se ssm ent , p 324; Heart fai l ure— managem ent , p 326; Pre-e cl a mps i a and ec l am psi a, p538 P.200

Vasopressors Types α-ad renerg i c : e. g. norepi nep hri ne , ep i nephri ne, dop ami ne, ephedri ne, p henyl e phri ne, m ethoxami ne Drugs red uci ng produc ti on of c ycl i c GM P (i n s ept i c shock ): e .g. me thy l thi oni ni um chl ori de (m ethyl e ne b l ue) Vas opress i n or synthe ti c anal ogue s, e.g . t erl i p res si n

Modes of action Act i ng on pe ri p heral α-adre nergi c or vasop res si n V1 rece ptors Bl ocki ng cGM P p rod uct i on (m ethyl e ne bl ue) Inc rease afte rl oad , mainl y b y arte ri ol a r v asoconstri c ti on and res torati on of vasc ul ar reacti vi t y Venoconst ri c ti on

Uses To i nc rease org an p erfusi on press ure s, parti c ul arl y i n hi gh output, l ow pe ri p heral re si s tance states , e .g. se psi s, anap hyl axi s To rai se c oronary p erfus i on press ure s i n c ard i opul monary re sus ci t ati on (ep i ne phri ne, v asopre ssi n)

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Side-effects/complications Inc reased cardi ac work Dec reased cardi ac out put , e spe ci a l l y wi th age nts where press or effect s p red omi nat e Myoc ard i al and s pl anc hni c i schaem i a Inc reased myocardi al i rri t abi l i t y, esp eci al l y wi t h c onc urrent hy pov ol a emi a, l eadi ng t o arrhythmi a s and tac hyc ard i a Dec reased peri p heral perfus i on and d i st al i s chaemi a/ne crosi s

Notes Pre ssor agents shoul d be av oi d ed, i f possi bl e , i n l ow cardi ac outp ut st ate s as t hey may further com promi s e t he ci rcul at i on. Met hox ami ne and phe nyl ephri ne are the ‘p urest ’ p res sor ag ent s; other α-ad renergi c ag ent s have i notropi c p rop ert i es to gre ate r or l ess er deg re es. Ephedri ne i s s i mi l ar t o ep i nephri ne b ut i ts effec ts are more p rol onged as i t i s not met abol i s ed by monoami ne oxi das e. Effect s of p res sor ag ent s on s pl a nchni c , renal and cerebral ci rcul at i ons are vari a bl e and unpredi ctabl e . Pul monary vascul ar re si stance i s al so rai sed by these ag ent s. Met hyl thi oni ni um chl ori de (me thy l ene b l ue ) i nhi bi t s t he NO–cGM P p athway . It i s c urrent l y unl i c ens ed as a pres sor age nt and i t s use has onl y been reporte d i n a few sm al l case seri es . A mul t i ce ntre s tud y of a NO synthase i nhi b i tor (L-NMM A) was pre mat ure l y di sconti nue d d ue to adve rse outcomes . Vas opres si n (s hort hal f-l i fe, i nfus i on ne ede d) and terl i pre ssi n (l onger half-l i fe, can be gi ven by bol us) may b e effect i ve i n treat i ng catec hol ami ne-res i s tant v asodi l atory shock. Parad oxi cal l y, such pat i ents res pond t o s mal l d ose s that have no press or effe ct i n healt hy p eop l e. Mul ti ce ntre outc ome st udi es are ongoi ng. Exc ess i ve dosi ng of any pre ssor agent m ay l ead to re gi onal i s chaemi a, e.g . c ard i ac , s pl anc hni c. Di g i t al i sc hae mi a may re spond to prompt adm i ni st rat i on of i ntravenous prost anoi ds (e .g. PGE 1 , PGI 2 ). P.201

Drug dosages Norepinephine

Infusion starting from 0.05µg/kg/min

Epinephrine

Infusion starting from 0.05µg/kg/min

Dopamine

Infusion from 5–50µg/kg/min

Methoxamine

3–10mg by slow IV bolus (rate of 1mg/min)

Ephedrine

3–30mg by slow IV bolus

Methylthioninium chloride (methylene blue)

1–2mg/kg over 15–30min

Vasopressin

0.01–0.04U/min

Terlipressin

0.25–0.5mg bolus, repeated at 30min intervals as necessary to maximum 2mg.

Key paper Lop ez A, et al. Mul ti pl e -ce nte r, random i ze d, pl a ceb o-c ont rol l ed , d oub l e-bl i nd study of the ni tri c oxi de s ynt has e i nhi bi tor 546C88: effe ct on survi v al i n pat i e nts wi th sep ti c shock . C ri t Care Med 2004; 32:21–30

Landry DW , et al . Vas opress i n defi ci enc y c ont ri but es to the vas odi l a ti on of se pti c shock. Ci rcul at i on 1997; 95:1122–5

P.202

Hypotensive agents Types

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Vas odi l at ors α- and β-ad re nergi c bl ock ers In routi ne ICU p rac ti ce β-b l oc kers are use d rel a ti v el y i nfre que ntl y b ecause most hav e a l ong hal f-l i fe and the negati ve i not ropi c effect s are generall y undes i rabl e. Exc ept i ons are esm ol ol and l ab etalol , b oth of whi ch hav e short hal f-l i ve s and v asodi l at i ng prope rti es.

Modes of action Vas odi l at ors re duc e p rel oad and afte rl oad to vari ab l e deg ree s d ependi ng on t ype and d ose β-bl ock ers reduce t he force of myoc ardi a l c ont rac ti l i t y

Uses Hype rt ens i on—sy ste mi c and p ul m onary Heart fai l ure—t o reduce aft erl oad ± p rel oad (c aut i on wi th β-b l oc kers) Cont rol of bl ood press ure, e .g. di ss ect i ng aorti c aneurys m

Side-effects/complications Exce ss i ve hyp ote nsi on Heart fai l ure (w i t h β-bl ocke rs ) Peri pheral hypoperfus i on (wi th β-b l oc kers) Bronchosp asm (wi th β-b l oc kers) Dec reased sym pat het i c re sponse to hyp ogl ycaemi a (wi t h β -bl ock ers )

Notes In cri ti cal l y i l l p ati ent s i t i s oft en advi sab l e to use short -ac ti ng β-bl oc kers b y i nfus i on. P.203

Drug dosages

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Glyceryl trinitrate 2–40mg/h Isosorbide dinitrate 2–40mg/h

Sodium nitroprusside

20–400µg/min.

ACE inhibitors

Captopril: 6.25mg test dose increasing to 25mg tds Enalapril: 2.5mg test dose increasing to 40mg o.d Lisinopril: 2.5 mg test dose increasing to 40mg o.d

Nifedipine:

5–20mg PO. Capsule fluid can be injected down nasogastric tube or given sublingually.

Phentolamine

2–5mg IV slow bolus. Repeat as necessary

Esmolol

A titrated loading dose regimen is commenced followed by an infusion rate of 50–200µg/kg/min.

Propranolol

Initially given as slow IV 1mg boluses repeated at 2min intervals until effect is seen (to maximum 5mg)

Labetalol

0.25–2mg/min

Hydralazine

5–10mg by slow IV bolus, repeat after 20–30min. Alternatively, by infusion starting at 200–300µg/min and reducing to 50–150µg/min.

See also: Bl ood press ure moni t ori ng, p110; Card i ac output—the rmodi l uti on, p122; Cardi a c outp ut—other i nvasi ve, p124; Cardi a c outp ut— non-i nvas i ve (1), p 126; Card i ac outp ut—non-i nvasi ve (2), p 128; Vasodi l at ors , p 198; Basi c res us ci t ati on, p270; Fl ui d challe nge , p 274; Hy pertensi on, p314; Pre -ec l am psi a and ecl amp si a , p 538 P.204

Antiarrhythmics Onl y anti arrhy thm i cs l i kel y t o b e used i n the ICU set ti ng are des cri bed . For supraventri cul ar tachy arrhyt hmi as: adenosi ne, ve rap ami l , ami odarone, di g oxi n, β-b l oc kers, mag nes i um For ve ntri cul a r t achyarrhy thm i as : ami odarone , l i d ocai ne , fl ec ai ni de , b ret yl i um, β-bl ocke rs, magne si um

Uses Correc ti on of supraventri cul ar and v ent ri c ul ar tac hyarrhythmi a s w hi c h e i ther com promi se t he ci rcul at i on or coul d pote nti al l y do so. Di fferent i at i on be twe en s uprave ntri c ul a r and ventri cul ar arrhy thm i as us i ng ad enosi ne

Notes Al l anti arrhyt hmi c agents hav e s i de -effec ts; other than d i g oxi n t hey are ne gat i ve l y i notropi c t o great er or l e sse r deg ree s and may i nduc e profound hy pot ens i on (e .g. verapami l , β-bl oc kers) or b rad ycard i a (e.g . β -bl ock ers , ami odarone, di g oxi n, l i d ocaine). β-b l oc kers i n p art i c ul a r s houl d be use d w i th cauti on bec aus e of these effec ts. Al l A-V bl ocke rs are contrai ndi cat ed i n re-ent ry tac hyc ard i a (e. g. W ol ff–Park i ns on–Whi te sy ndrome). Ade nos i ne : ve ry short-act i ng; m ay rev ert parox ysm al SVT to si nus rhythm. Ine ffe cti ve for at ri a l fl ut te r and fi b ri l l at i on, VT. Contrai ndi c ate d i n 2° and 3° heart bl ock, si ck si nus sy ndrome , as thma. May cause fl ushi ng , bronchosp asm and oc cas i onal sev ere brady cardi a.

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Ami odarone: e ffe cti ve agains t all typ es of tac hyarrhythmi a . Usually gi ven by IV i nfus i on for rapi d e ffe ct but req ui res i ni ti al l oadi ng d ose . W hen converti ng from IV t o oral dosi ng, i ni ti al hi g h oral dosi ng (200mg tds ) i s s ti l l req ui red. Contrai ndi c ate d i n p ati ent s w i t h t hyroi d dy sfunct i on. Has l ow acute tox i c i ty , t hough may cause sev ere bradyc ard i a and bot h c hroni c and acute p ul monary fi b rosi s . Avoi d w i th ot her Cl ass III agents (e. g. sot al ol ). Must be g i ve n v i a central v ei n as cause s p eri phe ral p hl e bi t i s. β-bl ock ers : for SVT, e smol ol i s p referred due to i t s s hort hal f-l i fe though may cause vasod i l atat i on. Ini ti a l l y, i nc reasi ng l oad i ng doses re qui re d; an i nfusi on m ay be need ed the reafte r. Propranol ol can be gi ven by sl ow IV bol use s of 1m g repe ate d at 2mi n i nterval s t o a max i mum of 5mg). Do not g i ve β-bl ocke rs wi t h v erapam i l . Bre tyl i um : m ay t ake 15–20mi n to take e ffe ct; now us ed pre dom i nantl y for res i s tant VF/VT. CPR shoul d be cont i nued for at l east 20mi n. Di g oxi n: s l ow-ac ti ng, re qui res l oadi ng (1–1.5g) t o achi eve therapeuti c pl as ma l eve l s whi ch can be moni t ore d. Load i ng i deally gi ven ove r 12–24h but can b e d one ove r 4–6h. C ont rai ndi cated i n 2° and 3° heart b l oc k. May caus e s eve re bradyc ard i a. Low K + and M g 2+ and marke dl y rai s ed Ca 2+ i ncreas e my ocardi al se nsi ti v i t y to di gox i n. Ami odarone rai s es di g oxi n l eve l s. Li d ocaine : 10ml of 1% sol uti on contai ns 100mg. No effec t on SVT. Loadi ng achi ev ed by 1mg/kg sl ow IV b ol us fol l owe d b y i nfusi on. Contraind i c ated i n 2° and 3° heart b l ock. May cause brady cardi a and C NS si d e-e ffec ts , e. g. drowsi nes s, sei zures. Verapami l : s houl d not be gi ven wi t h β -bl ock ers as profound hy pot ens i on and brad yarrhy thm i as may resul t. Pret re atm ent wi t h 3–5m l 10% cal ci um g l uconate by sl ow IV b ol us p re vent s t he hyp ote nsi ve effect s of ve rap ami l wi t hout affec ti ng i ts anti a rrhythmi c prop ert i es . P.205

Modes of action (Vaughan-Williams classification) Class I

Action

Examples

Reduces rate of rise of action potential: •Ia: increases action potential duration

•Ia: disopyramide

•Ib: shortens duration

•Ib: lidocaine

•Ic: little effect

•Ic: flecainide

II

Reduces rate of pacemaker discharge

β-blockers

III

Prolongs duration of action potential and hence length of refractory period

Amiodarone Sotalol

IV

Antagonises transport of calcium across cell membrane

Verapamil Diltiazem

Drug dosages

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Adenosine

3mg rapid IV bolus. If no response after 1min give 6mg. If no response after 1min give 12mg.

Amiodarone

5mg/kg over 20min (or 150–300mg over 3min in emergency) then IV infusion of 15mg/kg/24h in 5% glucose via central vein. Reduce thereafter to 10mg/kg/24h (approx. 600mg/day) for 3–7 days then maintain at 5mg/kg/24h (300–400mg/day)

β-blockers

Esmolol: a titrated loading dose regimen is commenced followed by an infusion rate of 50–200µg/kg/min. Propranolol: Initially given as slow IV boluses of 1mg repeated at 2min intervals until effect is seen to a maximum of 5mg. Labetalol: 0.25–2mg/min

Bretylium

In emergency 5mg/kg by rapid IV bolus. If no response after 5min, repeat or increase to 10mg/kg.

Digoxin

0.5mg given IV over 10–20min. Repeat at 4–8h intervals until loading achieved (assessed by clinical response). Maintenance dose thereafter is 0.0625–0.25mg/day depending on plasma levels and clinical response.

Lidocaine

1mg/kg slow IV bolus for loading then 2–4mg/min infusion. Should be weaned slowly over 24h.

MgSO 4

10–20mmol over 1–2h. Can be given over 5min in emergency.

Verapamil

2.5mg slow IV. If no response repeat to a maximum of 20mg. An IV infusion of 1–10mg/h may be tried. 10% calcium gluconate solution should be readily available.

See also: Defi bri l l at i on, p 52; ECG moni t ori ng, p108; Bas i c res us ci t ati on, p270; C ard i ac arres t, p272; T achyarrhythmi a s P.206

Chronotropes Types Ant i chol i nergi c: e.g . at ropi ne, gl y cop yrrol a te

Modes of action The ant i c hol i ne rgi c d rugs act by com pet i t i ve ant agoni s m of acet yl c hol i ne at pe ri pheral muscari ni c re cep tors and decreas e atri ov ent ri c ul a r c ond uc ti on t i me .

Uses Al l ty pes of brady cardi a i ncl udi ng 3° heart bl ock. Hi g h d ose atropi ne i s us ed i n cardi opul monary re sus ci tat i on protocol s for tre atm ent of as yst ol e .

Side-effects/complications Ant i chol i nergi c d rug s p rod uce dry m out h, red uct i on and t hi c keni ng of bronc hi al sec ret i ons, and i nhi b i t i on of sweati ng. Uri nary ret ent i on may oc cur b ut parent eral admi ni s trati on does not l ead to gl auc oma.

Notes The anti c hol i nerg i c age nts are usually gi ven by IV bol us , repe ate d as nece ssary. The y are fre que ntl y used as a b ri dge to tem porary paci ng b ut shoul d not b e c ons i de red a sub sti tute. Ex ternal or i nt ernal paci ng s houl d be readi l y acce ssi bl e. At rop i ne ne bul i se rs hav e b een us ed s uc ces sful l y i n pati e nts de vel opi ng sym ptomat i c bradyc ard i a duri ng e ndotrache al suc ti on.

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Neurol ogi cal e ffec ts may be se en w i t h at ropi ne b ut not gl ycopyrrol ate . P.207

Drug dosages Atropine

0.3–0.6mg IV bolus. 3mg is needed for complete vagal blockade.

Glycopyrrolate

0.2–0.4mg IV bolus.

See also: Tem porary paci ng (1), p54; Temp orary pac i ng (2), p56; ECG moni tori ng, p108; Bas i c res usc i t ati on, p270; Cardi ac arres t, p272; Brad yarrhy thm i as , p 318 P.208

Antianginal agents Types Vas odi l at ors : e .g. ni trates , c al c i um antag oni st s β-bl ock ers Potassi um channe l openers : e .g. ni corand i l Asp i ri n, hep ari n, cl opi dog rel

Modes of action Cal c i um c hannel bl ock ers cause compet i t i ve bl ock ade of cel l m emb rane and sl ow c al c i um channel s l e adi ng to decreas ed i nfl ux of calci um i ons i nt o c el l s. Thi s l ead s t o i nhi bi ti on of c ont rac ti on and rel axati on of c ard i ac and smooth mus cl e fi bres res ul t i ng i n c oronary and s yst emi c v asodi l at ati on. Ni t rat es may cause effl ux of calci um i ons from sm oot h musc l e and cardi ac cel l s and al so i nc re ase cGMP s ynt hes i s res ul t i ng i n coronary and s yst emi c v asodi l at ati on. β-bl ock ers i nhi bi t β-adrenorec ept or sti mul at i on, reduci ng m yoc ard i al work and oxy gen consumpt i on. T hi s effec t i s som ewhat offs et by c omp ens atory peri p heral vas oconst ri c ti on. Potassi um channe l openers cause vasod i l atat i on by re l ax ati on of vas cul ar smooth muscl e. The potas si um c hannel openi ng ac ti on w ork s on t he art eri al ci rcul at i on whi l e a ni t rate act i on provi des ad di t i onal vas odi l at ati on. Though asp i ri n, he pari n and cl opi dog rel have no di rect anti a ngi nal effec t, pat i ents wi t h unst abl e angi na benefi t from the reducti on i n pl ate l et ag gre gat i on and t hrombus form ati on.

Uses Ang i na pe ctori s

Side-effects/complications See Di l at ors , Hypotensi v e agents. Ni c orandi l i s c ont raind i cated i n hy pot ens i on and c ard i og eni c s hoc k. It shoul d be av oi d ed i n hyp ovol aem i a. Head ache and fl ushi ng are the m ajor reporte d s i de -effect s. Rap i d and se vere hyperkal aem i a has be en rep ort ed afte r c ardi a c s urg ery .

Notes Com bi nati on the rap y i nvol vi ng i nt ravenous ni t rates , c al c i um antag oni sts , β -bl ock ade and hepari ni sati on has bee n shown to be b ene fi c i a l i n unst abl e angi na; throm bol yti c t herapy confe rs no add ed advantage. Pot ass i um channel ope ners b el ong to a new c l as s of d rug ye t t o b e ex tensi vel y ev al uate d i n c ri ti c al l y i l l pati e nts and shoul d be thus use d w i th cauti on, es pec i al l y whe n hype rkalae mi a i s a concern. Ang i na may occasi onal l y be worsened by a ‘c oronary s teal’ phenom enon w here bl ood fl ow i s di v ert ed away from ste nos ed coronary ves sel s. Thi s d oes not, how ever, occ ur wi t h ni corandi l .

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P.209

Drug dosages Glyceryl trinitrate

0.3mg sublingually, 0.4–0.8mg by buccal spray, 2–40mg/h by IV infusion.

Isosorbide dinitrate

10-20mg tds orally, 2–40mg/h by IV infusion.

Nifedipine

5–20mg PO. The capsule fluid can be aspirated then injected down nasogastric tube or given sublingually.

Propranolol

Given either orally at doses of 10–100mg tds or IV as slow boluses of 1mg repeated at 2min intervals to a maximum of 5mg until effect is seen. This can be repeated every 2–4h as necessary.

Nicorandil

10–20mg PO bd.

Clopidogrel

75mg PO od.

Aspirin

75–150mg PO od.

See also: Ac ute coronary syndorme (1), p 146; Ac ut e c oronary s yndrome (2), p322

Ovid: Oxford Handbook of Critical Care

Ed itors: Si nge r, M ervyn; We bb, An dre w R. Ti tle : O xf ord Ha ndbook of Cr itic al Car e, 2nd Ed ition Cop yri ght © 1997,2005 M. Si nge r and A. R. W ebb , 1997, 2005. Publ i shed i n the Uni te d Stat es by Oxford Uni ve rsi ty Press Inc > Tab le of Co n te n ts > Ren al Dr u gs

Renal Drugs Diuretics Types Loop di ureti cs: e. g. furose mi d e, bume tani d e Osm oti c d i ureti cs : e. g. manni t ol Thi azi des : e. g. met ol a zone Potassi um sp ari ng di uret i c s: e .g. am i l ori de, sp i ronol act one , p otassi um canrenoat e

Uses To i nc rease uri ne vol ume Cont rol of chroni c oed ema (t hi a zi d es, l oop di uret i c s) Cont rol of hy pertensi on (thi azi des ) To p rom ote re nal ex cre ti on (e.g . forc ed di ures i s, hy percal caemi a)

Routes IV (manni t ol , furosemi de , bumet ani de, potas si um c anrenoate ) PO (met ol a zone, furose mi d e, bume tani d e, ami l ori de , s pi ronol ac tone)

Modes of action Osm oti c d i ureti cs —re duc e d i st al tub ul ar wate r reab sorpt i on

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Thi azi des —i nhi b i t di stal t ubul ar N a + l os s and carboni c anhydrase and i ncreas e N a + and K + ex change . T hi s red uce s t he s up pl y of H + i ons for exc hange wi t h N a + i ons p rod uc i ng and al kal i ne natri uresi s wi t h p otas si um l os s Loop di ureti cs— inhi b i t Na + and Cl - re abs orp ti on i n t he asc end i ng l oop of Henlé Potassi um sp ari ng di uret i c s—i nhi bi t d i st al tub ul a r N a + and K + exc hange

Side-effects Hypovol aem i a Hyponat rae mi a or hy pernat rae mi a Hypokal aem i a Oede ma format i on (manni tol ) Reduced catec hol ami ne effect (thi a zi d es) Hype rgl yc aemi a (thi azi de s) Metabol i c al kal osi s (l oop d i ureti cs ) Hypomag nes aem i a (l oop d i uret i cs ) Panc reati ti s (furosem i de )

Notes It i s i m portant t o c orrect pre-renal c aus es of ol i guri a before re sorti ng to di uret i c use . Di ure ti c s d o not pre vent renal fai l ure but m ay convert ol i g uri c t o p ol y uri c renal fai l ure. If the re i s i nadeq uat e g l om erul ar fi l t rat i on, m anni tol i s ret ai ned and pas ses t o the e xtrace l l ul a r fl ui d t o p rom ote oed ema format i on. Bum etani d e m ay be used i n porp hyri a where t hi azi des and ot her l oop di ure ti c s are contrai ndi c ate d. Pot ass i um sp ari ng di ure ti c s s houl d be avoi de d w i th AC E i nhi bi tors as t here i s an i ncreas ed ri s k of hype rkalae mi a . P.213

Drug dosages Oral Mannitol

IV

Infusion

100g over 20min 6-hrly

Metolazone

5–10mg od

Furosemide

20–40mg 6–24-hrly

5–80mg 6–24-hrly

1–10mg/h

Bumetanide

0.5–1mg 6–24-hrly

0.5–2mg 6–24-hrly

1–5mg/h

Amiloride

5–10mg 12–24-hrly

Spironolactone

100–400mg od

K + canrenoate

200–400mg od

P.214

Dopamine The effec ts of d opami ne are dep end ent on the dose i nfuse d. Dop ami ne was use d w i de l y at l ow dos es i n an att emp t t o sec ure prefe renti al DA 1 sti mul ati on and i ncreas e renal pe rfusi on; how eve r, a l arg e mul t i ce ntre rand omi sed control l ed study com pari ng ‘renal dos e’ d opami ne and di uret i c s s howe d no d i ffere nce i n the i nci dence of renal fai l ure. The wi d esp read use of l ow dos e d opami ne (< 3µg /kg /mi n) has thus d i m i ni she d c ons i de rab l y i n re cent ye ars . Hig her doses i nc re ase cardi ac contracti l i ty vi a β 1 st i m ul a ti on and produc e vasoc ons tri ct i on vi a α st i mul a ti on. Whe re vas oconst ri cti on i s i nappropri a te thi s w i l l reduce renal perfus i on. T here i s, howe ver, e vi d enc e of natri uresi s and di ure si s by enhanc ed Na + trans port i n t he asc end i ng l oop of Henlé. Thi s effe ct i s si mi l ar to that of a l oop di uret i c. In add i ti on to the re nal effec ts of DA 1 sti mul ati on the re may be preferenti a l p erfusi on of the sp l anchni c bed , t hough any benefi ts to pat i ents hav e y et to b e s how n. P.215

Key trial

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Bel l omo R , for the Austral i an and Ne w Zeal and Intensi v e C are Soci e ty (AN ZIC S) Cl i ni c al Tri al s Group. Low -dose dop ami ne i n pat i ents wi t h e arl y renal d ysfunc ti on: a p l ac ebo-control l ed random i se d t ri al . Lance t 2000; 356:2139–43

See also: Di l ureti cs , p212; Ol i guri a , p 330; Ac ute re nal fai l ure—managem ent , p 334

Ovid: Oxford Handbook of Critical Care

Ed itors: Si nge r, M ervyn; We bb, An dre w R. Ti tle : O xf ord Ha ndbook of Cr itic al Car e, 2nd Ed ition Cop yri ght © 1997,2005 M. Si nge r and A. R. W ebb , 1997, 2005. Publ i shed i n the Uni te d Stat es by Oxford Uni ve rsi ty Press Inc > Tab le of Co n te n ts > Gas tr oi n te sti n al Dr u g s

Gastrointestinal Drugs H 2 blockers and proton pump inhibitors Types H 2 antagoni st s: e.g . rani ti di ne, ci m eti di ne Prot on pum p i nhi bi tors: e.g . om eprazol e

Modes of action The se age nts i nhi b i t se cre ti on of g ast ri c ac i d, reduc i ng b oth vol ume and aci d conte nt, ei the r b y antagoni sm of the hi s tami ne H 2 re cep tor or by i nhi b i t i ng H + K + -AT Pas e whi c h fuel s t he p ari et al cel l p rot on pum p on whi c h ac i d se cre ti on dep end s.

Uses Pept i c ul cerati on, gastri t i s, duode ni t i s Refl ux oes ophagi ti s Prop hyl axi s agai ns t s tre ss ul c erati on Uppe r g ast roi nt est i nal haem orrhag e of p ept i c/stress ul cer ori g i n Wi t h non-s teroi dal anti -i nfl am mat ory ag ent s i n p ati ent s w i th dy spe psi a Gas tri c t onomet ry measureme nt

Side-effects/complications The maj or concern v oi c ed agains t t hes e agents i s the i ncre ase d ri s k of nosoc omi al pne umoni a by re moval of t he aci d b arri er. Howe ver, a mul ti centre RCT compari ng rani ti di ne w i th sucral fate showed no di ffe rence i n pneumoni a rat e and a l ower i nci dence of GI bl e edi ng. H 2 antagoni st s: rare b ut i ncl ude arrhyt hmi as, al tered l i ver funct i on te sts , c onfusi on (i n the e l de rl y ). Prot on pum p i nhi bi tors: al t ere d l i ve r func ti on t es ts.

Notes Al though l i censed and freq uentl y us ed for st res s ul ce r p rop hyl axi s, ove rwhel m i ng support i ve evi dence i s sc ant y. Ent eral nut ri t i on has b een shown to be as effe ct i ve . No ad equate l y powe red st ud y of proton p ump i nhi b i t ors has ye t bee n p erform ed i n ICU pat i ents . Som e s tud i es have shown e ffi cac y i n uppe r g ast roi nt est i nal haem orrhag e s econdary to stress ul cerat i on or pe pti c ul c erati on. Dos age s s houl d be mod i fi ed i n renal fai l ure. Ci m eti di ne c an affect me tab ol i sm of othe r d rugs, i n parti cul ar warfari n, p henytoi n, theophyl l i ne and l i d ocaine (rel a ted to hep ati c c ytochrome P450-l i nked enzym e sy st ems). T hi s does not oc cur wi th rani t i di ne. Ome prazol e c an del ay el i mi nati on of di a zep am, phenyt oi n and w arfari n. P.219

Drug dosages

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Ranitidine

50mg tds by slow IV bolus, 150mg bd PO

Cimetidine

200–400mg qds by slow IV bolus, 400mg bd PO

Omeprazole

40mg IV od (over 20–30min), 20–40mg PO

Key trial Cook D , G uyat t G , M ars hal l J, e t al. A c omp ari son of sucral fate and rani ti d i ne for t he pre venti on of up per gas troi ntes ti nal bl e edi ng i n pat i e nts re qui ri ng m echani cal ve nti l a ti on. Canadi an C ri ti c al Care T ri a l s Group . N Eng l J Med 1998; 338:791–7

See also: Upp er gas troi ntes ti nal end osc opy , p 74; Sucral fat e, p 220; Antaci d s, p222; Uppe r g ast roi nt est i nal haem orrhag e, p344; Bl eedi ng vari c es, p346; Bowe l p erforati on and obs truct i on, p 348 P.220

Sucralfate Modes of action Suc ral fat e i s a basi c al umi ni um s al t of sucrose oct as ul p hat e and i s probab l y not abs orbed from t he gast roi nt est i nal t ract. Exerts a c ytoprotec ti ve effe ct by pre venti ng m ucosal i njury. A p rot ec ti v e b arri er i s forme d b oth ov er normal mucosa and any ul ce r l esi on provi d i ng p rot ect i on ag ai nst penetrati on of gas tri c aci d, bi l e and peps i n as wel l as i rri t ant s s uch as as pi ri n and al cohol . Di rect l y i nhi b i ts pe psi n acti vi ty and abs orb s b i l e s al t s. Weak antac i d act i vi ty .

Uses Pept i c ul cerati on, gastri t i s, duode ni t i s Refl ux oes ophagi ti s Prop hyl axi s agai ns t s tre ss ul c erati on

Side-effects/complications Cons ti pat i on Reduced bi oav ai l abi l i ty of s ome drugs gi ven oral l y, e.g . d i goxi n, p henytoi n. Can b e ov erc ome by gi vi ng agents at l eas t 2h apart. Use wi t h c aut i on i n renal fail ure due t o ri sk of i ncre ase d alum i ni um abs orp ti on.

Notes Al though l i censed and freq uentl y us ed for st res s ul ce r p rop hyl axi s, ove rwhel m i ng support i ve evi dence i s sc ant y. Ent eral nut ri t i on and g ast ri c ac i d bl ock ers have b een shown to be as effect i ve . Evi dence for a red uce d i nci dence of nos ocomi a l p neumoni a c omp are d t o H 2 bl ock er the rap y i s als o c onfl i c ti ng. Si gni fi c ant re duc ti on i n nos ocom i al p neum oni a has bee n s hown compared to a com bi nati on of H 2 bl ock er pl us antaci d but not agai nst H 2 bl ock er al one. Indee d, a l arg e mul t i ce ntre R CT comp ari ng rani t i di ne wi t h s uc ral fat e s howe d no di fferenc e i n p neumoni a rat e and a l ower i nci dence of GI b l ee di ng w i t h rani ti d i ne . Ant ac i ds shoul d not be gi v en for 30m i n before or after sucralfate. P.221

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1g six times a day PO or via ng tube.

Key trial Cook D , G uyat t G , M ars hal l J, e t al. A c omp ari son of sucral fate and rani ti d i ne for t he pre venti on of up per gas troi ntes ti nal bl e edi ng i n pat i e nts re qui ri ng m echani cal ve nti l a ti on. Canadi an C ri ti c al Care T ri a l s Group . N Eng l J Med 1998; 338:791–7

See also: Upp er gas troi ntes ti nal end osc opy , p 74; H 2 b l oc kers and proton pump i nhi bi tors, p218; Antaci d s, p222; Uppe r gas troi ntes ti nal hae morrhage, p344; Bl e edi ng vari ce s, p346; Bowel pe rforat i on and obst ruc ti on, p348 P.222

Antacids Types Sod i um bi carbonate Magnesi um-bas ed ant aci ds: e. g. magnesi um tri si l i cat e Al umi ni um -based antac i ds : e .g. al umi ni um hydroxi de (Al udrox) Prop ri etary com bi nati ons : e .g. Gavi s con

Modes of action Neut ralis es gas tri c aci d Prov i d es p rotec ti v e c oat i ng on up per gas troi ntes ti nal muc os a

Uses Symp tom ati c rel i ef of gas tri ti s, duodeni t i s, oe sop hagi ti s Stress ul cer prop hyl axi s (c ont ent i ous)

Side-effects/complications Poss i b l e i nc reased ri sk of nos ocomi a l p neumoni a Al umi ni um toxi c i t y (i f alum i ni um -contai ni ng ant aci ds are us ed l ong-t erm i n pati e nts wi th renal dys functi on) Di a rrhoea (magne si um-b ase d antaci d s) Cons ti pat i on (al umi ni um-b ase d antaci d s) Metabol i c al kal osi s i f l arg e amounts are admi ni s tered Mi l k-al kal i syndrome res ul t i ng i n hy percal caemi a, m etabol i c al kal osi s and renal fai l ure i s v ery rare

Notes As thei r main use i s for s ymp tomati c rel i ef, antac i ds are rare l y nee ded i n me chani c al l y v ent i l ated pati ent s. Conti nual nasog ast ri c i nfusi on of a weak s odi um bi c arb onate sol uti on has be en use d s ucc ess ful l y i n treati ng st res s ul c er-re l at ed haem orrhag e. P.223

Drug dosages

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Magnesium trisilicate

10–30ml qds

Aluminium hydroxide

10–30ml qds

Gaviscon

10–30ml qds

See also: Upp er gas troi ntes ti nal end osc opy , p 74; H 2 b l oc kers and proton pump i nhi bi tors, p218; Sucral fate , p 220; Up per gas troi ntes ti nal hae morrhage, p344; Bl e edi ng vari ce s, p346; Bowel pe rforat i on and obst ruc ti on, p348 P.224

Anti-emetics Types Phenothi az ines: e.g . p roc hl orp erazi ne, chl orp rom azi ne Benzami de s: e .g. me toc l op ram i de Ant i hi st ami nes : e. g. cyc l i zi ne 5HT 3 rece ptor antagoni st s: e.g. ondanset ron, g rani s etron

Modes of action Phenothi az ines i nc rease the thres hol d for vom i ti ng at the chemorec ept or tri gge r z one vi a c ent ral DA 2 -dop ami nergi c bl ock ade ; at hi gher dos es the re may al s o b e s ome effect on the v omi ti ng c ent re. Metocl oprami de act s c ent ral l y and by i ncre asi ng gas tri c mot i l i ty. The exact mec hani sm of cyc l i zi ne acti on i s unknow n. It i nc re ases l ower oe sop hag eal sp hi ncte r t one and m ay i nhi bi t t he mi d brain eme ti c c ent re. Ond ans etron i s a hi ghl y sel ect i ve 5HT 3 re cep tor antag oni st ; i t s pre ci s e m ode of act i on i s unknown but may ac t both ce ntral l y and peri p heral l y.

Uses Naus ea Vomi ti ng

Side-effects/complications Dys toni c or dys ki neti c reac ti ons , oc ul ogy ri c cri s es (prochl orperazi ne, me toc l op ram i de ) Arrhyt hmi as (me toc l op ram i de , p roc hl orp erazi ne) Head aches, fl ushi ng (ondanse tron) Urt i cari a , d row si ness , d ry mouth, bl urred vi si on, uri nary ret ent i on (cy cl i zi ne) Post ural hyp otensi on (prochl orperazi ne, cy cl i zi ne) Rare l y, ne urol ep ti c m al i gnant syndrome (prochl orperazi ne, me toc l op ram i de )

Notes The i ni t i al choi c e s houl d fal l b etw een prochl orperazi ne, me toc l op ram i d e or cy cl i zi ne. Prochl orperaz i ne and c ycl i zi ne are prefe rab l e whe n vomi t i ng i s rel a ted to drugs and m etabol i c di s turbance s acti ng at the chemorec ept or tri gge r z one whi l e met ocl oprami de shoul d be tri e d fi rs t i f a gastroi ntes ti nal cause i s i m pl i cat ed. Met ocl oprami de and prochl orperazine dosag e shoul d b e reduced i n renal and hepati c fail ure . Ond ans etron dos age shoul d b e reduced i n he pat i c fai l ure. P.225

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Prochlorperazine

5–10mg tds PO, 12.5mg qds IM or by slow IV bolus (note: not licensed for IV use)

Metoclopramide

10mg tds by slow IV bolus, IM or PO

Cyclizine

50mg tds slow IV bolus, IM or PO

Ondansetron

4–8mg tds by slow IV bolus, IM or PO

Granisetron

1–3mg by slow IV bolus up to max 9mg/24h

See also: Ent eral nut ri t i on, p 80; Vom i ti ng/gas tri c stasi s , p 338 P.226

Gut motility agents Types Metocl oprami de Ery thromy ci n

Modes of action Metocl oprami de p robabl y act s b y bl oc ki ng p eri phe ral DA 2 -dop ami nergi c rece ptors Ery thromy ci n i s a mot i l i n agoni st ac ti ng on antral enteri c neurones

Uses Il e us, l a rge nasog ast ri c as pi rat es Vomi ti ng

Side-effects/complications Dys toni c or dys ki neti c reac ti ons , oc ul ogy ri c cri s es (met ocl oprami de ) Arrhyt hmi as (me toc l op ram i de and e ryt hromyc i n) Chol est ati c jaundi ce (ery thromy ci n)

Notes Met ocl oprami de dos i ng shoul d b e reduced i n renal fail ure and he pat i c fai l ure, whi l e erythrom yci n d osi ng shoul d be red uce d i n hepati c fail ure . P.227

Drug dosages Metoclopramide

10mg tds by slow IV bolus, IM or PO

Erythromycin

250mg qds PO or IV

See also: Ent eral nut ri t i on, p 80; Vom i ti ng/gas tri c stasi s , p 338; Bow el perforati on and obs truct i on, p 348 P.228

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Antidiarrhoeals Types Lop erami d e Code i ne phosp hat e

Modes of action Lop erami d e and cod ei ne p hos phate bi nd t o g ut wal l op i ate rec ept ors , reduci ng p rop ul si v e p eri stalsi s and i ncre asi ng anal s phi nc ter tone

Side-effects/complications Abd omi nal cramp s, bl oati ng Cons ti pat i on (i f ex ces si ve amounts gi ven)

Notes Shoul d not b e used when abdomi nal di ste nsi on dev el ops, parti cul arl y wi t h ul ce rat i ve col i t i s or ps eud omem branous col i t i s, or as sol e the rap y i n i nfe cti ve di a rrhoea. Cauti on w i th l operami de i n l i ver fai l ure, and c odei ne i n re nal fai l ure. P.229

Drug dosages Loperamide

2 capsules (20ml) initially, then 1 capsule (10ml) after every loose stool for up to 5 days

Codeine phosphate

30–60mg 4–6hrly PO, IM or by slow IV bolus

See also: Ent eral nut ri t i on, p 80; Di a rrhoea, p 340 P.230

Anticonstipation agents Types Laxati ves : e. g. l ac tul os e, p rop ant hel i ne, mebe veri ne , c ast or oi l Bul ki ng agents: e.g . d i et ary fi bre (b ran), hem i ce l l ul oses (me thy l c el l ul ose, i s pag hul a husk ) Sup pos i tori e s: e.g . g l yc eri ne Enem ata: e .g. warmed normal s al i ne, ol i ve oi l or arac hi s oi l ret ent i on enemata

Modes of action Laxati ves i ncl ude i. anti spasmodi c ag ent s s uch as anti c hol i nerg i cs (e .g. propanthel i ne) and me bev eri ne (a phenyl ethyl a mi ne d eri vat i ve of re serpi ne) ii. non-absorbabl e di sacchari des (e .g. l a ctul os e) whi ch soften the st ool by an os mot i c effect and by l a ct i c aci d p rod uct i on from a b act eri al fermenti ng e ffe ct iii. i rri tants , s uch as castor oi l , whi ch i s hydrol y sed i n the s mal l i nte sti ne rel eas i ng ri ci nol ei c aci d Bul ki ng agents are hy drophi l i c and t hus i ncreas e t he w ate r c ont ent of the s tool .

Side-effects/complications Bl oati ng and ab domi nal d i st ens i on

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Di a rrhoea i f exc es si v e am ounts gi ven

Notes Surgi cal cause s p res ent i ng as const i p ati on suc h as b owel ob st ruc ti on m ust be ex cl uded . Othe r m eas ure s s houl d be tak en i f pos si b l e to i mp rov e b owel func ti on, e.g . reduci ng c onc urrent op i at e d osage, st art i ng enteral nutri ti on. The ag ent of choi c e i s l act ul ose. Larger d oses of l a ctul ose are use d i n hepati c fail ure as the pH of the c ol oni c conte nts i s reduced ; thi s l owers format i on and absorpt i on of amm oni um i ons and other ni t rogenous produc ts i nto the portal c i rcul ati on. Prove n b enefi t i n pat i ents has not b een shown. Ant hraqui none gl y cos i de s (e.g . s enna) and l i q ui d paraffi n are no l ong er rec omm end ed for routi ne use . P.231

Drug dosages Lactulose

15–50ml tds PO

P.232

See also: Ent eral nut ri t i on, p 80; Fai l ure t o op en bow el s , p 342

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Ed itors: Si nge r, M ervyn; We bb, An dre w R. Ti tle : O xf ord Ha ndbook of Cr itic al Car e, 2nd Ed ition Cop yri ght © 1997,2005 M. Si nge r and A. R. W ebb , 1997, 2005. Publ i shed i n the Uni te d Stat es by Oxford Uni ve rsi ty Press Inc > Tab le of Co n te n ts > Neu r ol ogi cal Dr u gs

Neurological Drugs Opioid analgesics Types Natural opi a tes : e. g. morphi ne, codei ne Semi sy ntheti c: e.g . d i am orp hi ne, di hydrocodei ne Synthe ti c : e .g. pet hi di ne, fent any l , al fent ani l , re mi fent ani l

Uses Analge si a . Strong analge si c s are ext rac ts from opi um or s ynt het i c subst anc es wi t h s i mi l a r p rop ert i es . T hey are useful for conti nuous pai n rat her than sharp, i ntermi t te nt pai n. Sed ati on Mi l d v asod i l atati on i n heart fai l ure (d i am orp hi ne, morphi ne) Ant i di arrhoeal (codei ne)

Routes IV (morphi ne , di amorp hi ne, papaveretum, pet hi d i ne, fent any l , al fent ani l , rem i fe ntani l ) IM/SC (morphi ne, codei ne, di amorphi ne , d i hy drocod ei ne, pet hi d i ne ) PO (morphi ne, codei ne, di amorphi ne , d i hy drocod ei ne, pet hi d i ne)

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Epi dural (morphi ne , d i am orp hi ne, fentanyl , al fent ani l )

Side-effects Resp i ratory depres si on Cent ral ne rvous sys tem de pre ssi on Add i ct i on (rare i n the c ri ti c al l y i l l ) Wi t hdrawal s ynd rom e (w i thdraw s l ow l y) Sti mul ati on of the vom i t i ng ce ntre App eti te l os s Dry mouth Dec reased gas tri c emp tyi ng and gut m oti l i t y Hi s tam i ne re l ease and i t chi ng Inc reased mus cul ar tone

Notes Morphi ne i s poorl y ab sorbed from the gastroi ntes ti nal tract and i s t herefore usual l y admi ni ste red parenteral l y. It i s met abol i s ed to morphi ne-6-g l uc uroni d e i n t he l i ver whi ch i s si x t i me s m ore potent t han morphi ne and ac cum ul ates i n renal fai l ure. Cod ei ne i s a weak anal ges i c but i s favoured by some i n head i njury s i nce i t i s l es s s edati v e t han morphi ne . Pet hi d i ne has l ocal anae stheti c properti e s associ a ted wi th cardi ac depres si on and vasodi l at ati on. It i s me tab ol i sed to norpet hi di ne whi c h may l ead to se i zures on ac cum ul a ti on. Res pi rat ory dep res si on occ urs de spi te mai nte nance of res pi rat ory rate. Fentanyl and al fent ani l are good, short -act i ng anal ges i cs wi th poor s edati v e q ual i ty . T hey cause se vere resp i ratory dep res si on and mus cul ar ri gi d i t y. R emi fentani l i s ul tra-short -ac ti ng and the pati e nt may suffer from reb ound p ai n i f the i nfus i on i s s top ped tem porari l y . P.235

Drug dosages Intravenous Bolus

Infusion

Morphine

0.1–0.2mg/kg

0.05–0.07mg/kg/h

Diamorphine

0.05–0.1mg/kg

0.03–0.06mg/kg/h

Pethidine

0.5mg/kg

0.1–0.3mg/kg/h

Fentanyl

5–7.5µg/kg

5–20µg/kg/h

Alfentanil

15–30µg/kg

20–120µg/kg/h

Remifentanil

1µg/kg

0.05–2µg/kg/min

Other routes

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Morphine

10mg IM/SC 4-hrly

5–20mg PO 4-hrly

Codeine

30–60mg IM 4-hrly

30–60mg PO 4-hrly

Diamorphine

5mg IM/SC 4-hrly

5–10mg PO 4-hrly

Dihydrocodeine

50mg IM/SC 4–6-hrly

30mg PO 4–6-hrly

Pethidine

25–100mg IM/SC 4-hrly

50–150mg PO 4-hrly

Note that the above doses are a guide only and may need to be altered widely according to individual circumstances. The correct dose of an opiate analgesic is generally enough to ablate pain.

See also: IPPV—fai l ure t o t ol e rat e ve nti l a ti on, p12; Non-op i oi d anal ges i cs , p 236; Sedat i v es, p238; Pai n, p532; Pos t-op erati ve i nt ens i v e c are , p534 P.236

Non-opioid analgesics Types Non-ste roi dal anti -i nfl a mmat ory drug s: e .g. as pi ri n, i ndomet hac i n, di cl ofenac Paracet amol Ketami ne Ni t rous oxi d e Loc al anae st het i cs : e .g. l i doc ai ne, bup i vacai ne

Uses Pai n as soc i a ted wi t h i nfl am matory condi ti ons (as pi ri n, i ndom ethaci n, di cl ofenac) Post -op erati v e p ai n and m usc ul oske l et al pai n (asp i ri n, i ndom ethaci n, di c l ofenac, parace tam ol , ket ami ne, ni trous oxi d e, l i doc ai ne, bup i vacai ne) Opi ate sp ari ng effect (as pi ri n, i ndomet hac i n, di cl ofenac use d w i th st rong anal ges i c s) Ant i py ret i c (as pi ri n, p aracet amol )

Routes IV (ket ami ne) IM (di c l ofenac) PO (asp i ri n, i ndom ethaci n, di c l ofenac, parace tam ol ) PR (asp i ri n, di cl ofenac, parac etam ol ) Loc al /re gi onal (l i docai ne, bupi v acaine ) Inhal e d (ni t rous oxi d e)

Side-effects Gas troi nt est i nal bl e edi ng (asp i ri n, i ndom ethaci n, di c l ofenac) Renal d ysfunc ti on (i nd ome thaci n, d i cl ofe nac i f any hypovol aemi a) Reduced pl ate l et ag gre gat i on (aspi ri n, i nd omet hac i n, d i cl ofe nac ) Reduced prothrom bi n formati on (asp i ri n, i ndom ethaci n, di c l ofenac) Myoc ard i al d epress i on (l i docai ne, bupi v acaine ) Hype rt ens i on and tachy cardi a (k etami ne) Sei zures (l i doc ai ne, bup i vacai ne)

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Hal l uc i nati ons and ps ychoti c t end enc i e s (k etami ne—p rev ent ed by concurrent use of benz odi az epi nes or droperi dol )

Notes Parace tam ol ove rdose can cause sev ere he pat i c fai l ure d ue to the effec ts of alky l at i ng me tab ol i te s. Though normal l y rem ove d b y c onjugat i on wi th gl utathi one , s tores are rapi d l y dep l et ed i n ove rdose. Non-st eroi dal anti -i nfl ammatory agents shoul d be ge neral l y avoi ded i n pati e nts wi th renal dys functi on, GI bl eed i ng or coagul opathy . Ket ami ne i s a d eri vat i ve of phe ncy cl i di ne use d as an i ntrave nous anaes the ti c agent . In s ub anae stheti c dos es i t i s a pow erful analge si c . It has sev eral advantages ove r opi ates i n t hat i t i s as soc i at ed wi t h g ood ai rway maintenanc e, al l ows sp ont ane ous re spi rati on and p rovi d es cardi ovas cul ar sti mul at i on. It i s also a bronchodi l at or. Ni t rous oxi de i s a powerful , s hort act i ng anal g esi c used to cover short , p ai nful proce dures. It may b e useful when del i ve red vi a an i nte rmi tt ent posi t i ve press ure breat hi ng sys tem as an adj unc t t o c hes t p hys i ot herapy . N i trous ox i de shoul d not b e used i n cases of undraine d p neumothorax s i nce i t may di ffus e i nto the p neumot horax res ul t i ng i n tensi on. P.237

Drug dosages Aspirin

600mg PO/PR 4-hrly

Indomethacin

50–100mg PO/PR 12-hrly

Diclofenac

25–50mg PO 8-hrly, 100mg PR 12–24-hrly, 75mg IM 12-hrly

Ketorolac

10mg PO 4–6-hrly, 10–30mg IV, IM 4–6-hrly

Sulindac

200mg PO 12-hrly

Paracetamol

0.5–1g PO/PR 4–6-hrly

Ketamine

5–25µg/kg/min IV

Lidocaine

Maximum 200mg

Bupivicaine

Maximum 150mg*

*Local anaesthetic doses vary according to the area to be anaesthetised. Maximum doses may be increased if epinephrine is used locally.

See also: Opi oi d anal ges i cs , p 234; Sal i c yl a te poi soni ng , p 454; Rhe umati c di sorde rs, p492; Pyrexi a (1), p518; Pyrexi a (2), p520; Pai n, p532; Post -op erati v e i nte nsi ve care, p534 P.238

Sedatives Types Benzod i az epi nes : e. g. di azep am, mi dazol a m, l oraze pam Major t ranqui l l i se rs : e. g. chl orpromazine , hal operi dol Anaest het i c age nts : e. g. propofol , i s ofl urane α 2 agoni st s e.g. cl oni di ne, de xmed etomi d i ne

Uses Sed ati on and anx i ol ysi s

Routes

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IV (di aze pam, mi daz ol a m, l oraze pam , c hl orpromazi ne, hal ope ri dol , p rop ofol , cl oni d i ne , d exm ede tomi di ne) IM (di a zep am, chl orpromaz ine, hal operi d ol ) PO (di a zep am, l oraz epam, chl orp rom azi ne, halop eri dol , cl oni d i ne ) Inhal e d (i sofl urane)

Side-effects Hypotensi on (di a zep am, mi dazol a m, chl orp rom azi ne, halop eri dol , propofol , cl oni di ne, dex mede tom i di ne ) Resp i ratory depres si on (di a zep am, mi d azol am , c hl orp rom azi ne, halop eri dol , p rop ofol ) Arrhyt hmi as (chl orpromaz i ne, hal operi d ol ) Dry mouth (cl oni di ne, dex med etomi d i ne ) Extrap yrami d al di s ord er (chl orpromazine, hal operi d ol ) Fl uori de toxi ci ty (i s ofl urane)

Notes Sed ati on i s nec es sary for m ost IC U p ati ent s. Whi l e the ap propri at e use of s edati v e d rug s c an provi d e c omfort , m ost hav e c ard i ov asc ul a r and res pi rat ory si de-effe cts . Obje ct i ve ass es sment of t he dep th of s edati on i s nec ess ary to ens ure that com fort d oes not g i ve way to ex ces si v el y and d ange rousl y d eep l ev el s of se dat i on. Al l se dat i ve s are pot ent i al l y cumul ati ve so dos es m ust be ke pt to a mi ni mum . Benzod i az epi ne s have the ad vantag e of be i ng am nes i c. Di aze pam i s mainl y admi ni s tered as an emul si on i n i ntralip i d as org ani c s ol vent s are ext rem el y i rri tant t o v ei ns. Mi d azol am i s short er act i ng t han di aze pam al t hough 10% of pat i ents are sl ow met abol i s ers. Al l be nzodi a zep i ne s accumul at e i n renal fail ure ; c are mus t be t ake n t o avoi d exc ess i ve dosag e b y regul ar re ass ess ment of need. Some pat i ents suffer unpre di c tabl e se vere resp i ratory d epress i on wi t h hypotensi on. Propofol use d i n s ubanae stheti c d ose s i s s hort-act i ng thoug h effec ts are cumul ati ve whe n i nfusi ons are prol onge d or wi t h c oex i st i ng hepat i c or re nal failure. It i s gi ven as an em ul s i on i n 10% i ntral i pi d s o l arg e v ol umes may contri b ute si gni fi c ant l y to cal ori e i nt ake. As chl orpromaz ine and hal operi dol antagoni se catec hol ami nes , t hey may cause vasod i l atat i on and hypotensi on. Dys toni c re act i ons and arrhyt hmi as are al so occ asi onall y se en. α 2 ant agoni s ts al s o p rov i d e anal g esi a and are sy nergi s ti c w i th op i at es. De xmed etomi d i ne c aus es m i ni mal resp i ratory dep res si on and the pati e nt i s eas i l y rous abl e. Bradyc ard i a and hy pot ens i on may oc cur, esp eci al l y w i th the l oad i ng dos e. Isofl urane i s l argel y e xhal ed unc hanged and i s t herefore short act i ng. Cumul at i v e effec ts hav e b een rec orded wi t h prol onged us e, carryi ng the t heoret i cal ri s k of fl uori de toxi c i t y. Exhaled i sofl urane shoul d b e s cave nge d. P.239

Drug dosages Bolus

Infusion

Diazepam

0.05–0.15mg/kg

Excessive half-life

Midazolam

50µg/kg

10–50µg/kg/h

Lorazepam

1mg PRN

Propofol

0.5–2mg/kg

1–3mg/kg/h

Chlorpromazine

12.5–100mg

Excessive half-life

Clonidine

100–150µg/min

Dexmedetomidine

Loading infusion of 6.0µg/kg/h over 10min, followed by maintenance infusion of 0.2–0.7µg/kg/h.

Note that the above doses are a guide only and may need to be altered widely according to individual circumstances.

Monitoring sedation

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Fre que nt, ob jec ti v e reas ses sme nt of s edati on d ept h w i th corresp ond i ng ad jus tme nt of i nfusi on d ose s i s nec ess ary to avoi d sev ere cardi ovascul ar and resp i ratory dep res si on. Si m pl e se dat i on sc ores are avail abl e t o ai d asse ss ment .

UCL Hospitals Sedation Score Agitated and restless

+3

Awake and uncomfortable

+2

Aware but calm

+1

Roused by voice, remains calm

0

Roused by movement

-1

Roused by painful or noxious stimuli

-2

Unrousable

-3

Natural sleep

A

Sed ati on dos es are ad jus ted to ac hi e ve a sc ore as cl os e as possi bl e t o 0. Posi t i v e s cores req ui re i ncreas ed sed ati on dos es and ne gat i ve sc ore s requi re re duc ed sed ati on dos es.

See also: IPPV—fai l ure t o t ol e rat e ve nti l a ti on, p12; Opi oi d anal ges i cs , p 234; Ag i tati on/c onfusi on, p370; Sed ati ve poi soni ng , p458; Pos t-op erati ve i nt ens i ve care, p534 P.240

Muscle relaxants Types Depol ari s i ng : e .g. suxame thoni um Non-dep ol a ri s i ng: e .g. pancuroni um, atracuri um, vec uroni um

Mode of action Sux amet honi um i s s tructural l y re l at ed to acet yl chol i ne and causes i ni ti al st i mul at i on of muscul ar contrac ti on seen cl i ni call y as fasci cul at i on. D uri ng thi s proces s, the conti nue d s ti m ul ati on l eads to d ese nsi ti sat i on of the post -sy nap ti c me mbrane of the neuromus cul ar junct i on wi th effl ux of pot ass i um i ons . Subs equent fl acc i d paral y si s i s short ac ti ng (2–3mi n) and cannot be re versed (i s ac tual l y p ote nti ate d) by anti chol i nes terase drugs . Prol onged effect s are see n where there i s c ong eni tal or ac qui red ps eud ochol i nes teras e de fi c i e ncy . Non-dep ol a ri s i ng m usc l e rel axants preve nt ace tyl chol i ne from de pol ari si ng the pos t-s ynapti c memb rane of t he neuromusc ul a r j unc ti on b y c omp eti ti v e b l oc kad e. Reve rsal of p aralys i s i s ac hi e ved by ant i c hol i ne ste ras e d rug s suc h as ne ost i g mi ne. They have a s l owe r onse t and l onger durat i on of ac ti on t han the d epol ari si ng age nts .

Uses To faci l i tat e e ndot rache al i nt ubati on. To faci l i tat e m echani cal ve nti l at i on where op ti m al sed ati on doe s not pre vent pati ent i nterferenc e w i th the func ti on of t he venti l ator.

Routes IV

Side-effects Hype rt ens i on (suxam ethoni um, pancuroni um ) Bradyc ard i a (suxame thoni um)

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Tachycard i a (pancuroni um ) Hype rkalae mi a (s uxamet honi um )

Notes Mod ern i ntensi ve c are pract i c e and d eve l op ments i n venti l at or tec hnol og y have rendered the us e of muscl e rel axants l es s c omm on. Furtherm ore , i t i s rarel y ne ces sary t o ful l y p aralys e m usc l es to faci l i t ate mec hani cal v ent i l ati on. Req ui reme nt for muscl e rel a xants shoul d be re ass ess ed fre que ntl y. Ide al l y, rel axants shoul d b e s top ped i nt ermi t tentl y to al l ow de pth of sed ati on to be ass ess ed. If me chani c al venti l ati on procee ds smoothl y whe n rel a xants hav e b een st oppe d t hey probabl y shoul d not be res tarted . Sux ame thoni um i s c ont rai nd i cated i n sp i nal neurol ogi cal di sease, he pat i c di s eas e and for 5–50 d ays after burns . At rac uri um i s non-cumul ati ve and popul ar for i nfus i on. N on-enzymat i c (Hoffm an) deg rad ati on al l ows c l earance i nd epe nde nt of renal or hep ati c func ti on, al t hough effect s are prol onged i n hy pot hermi a . P.241

Drug dosages Bolus

Infusion

Suxamethonium

50–100mg

2–5mg/min

Pancuronium

4mg

1–4mg/h

Atracurium

25–50mg

25–50mg/h

Vecuronium

5–7mg

Excessive half-life

See also: IPPV—fai l ure t o t ol e rat e ve nti l a ti on, p12; End otrac heal i ntubat i on, p 36; Sed ati ves , p 238; Post -ope rat i ve i ntensi ve care, p534 P.242

Anticonvulsants Types Benzod i az epi nes : e. g. l orazepam , d i azepam, cl onazepam Phenytoi n Carb amazep i ne Sod i um val proat e Magnesi um sul phate Thi opental

Uses Cont rol of st atus e pi l ep ti c us Int erm i tt ent se i zure control Myoc l oni c se i zures (c l onaze pam , s odi um val proate )

Routes IV (l oraz epam, d i az epam, cl onazepam, phe nyt oi n, s odi um val proate , magne si um s ul phate, thi op ent al ) PO (di a zep am, cl onazep am, phenyt oi n, c arbamazap i ne, s odi um val proate ) PR (di a zep am)

Side-effects Sed ati on (benzod i az epi nes , t hi ope ntone) Resp i ratory depres si on (benzodi azepi nes , t hi opentone)

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Naus ea and vomi t i ng (p henytoi n, sodi um valp roate) Ataxi a (pheny toi n, carbam azapi ne) Vi s ual di st urb anc e (p henytoi n, carbamazapi ne) Hypotensi on (di a zep am, thi op ent one ) Arrhyt hmi as (pheny toi n, carbam azapi ne) Panc reati ti s (t hi opentone) Hepati c fail ure (s odi um val proate )

Notes Com mon i nsul ts causi ng s ei zures i nc l ud e c ere bral i sc hae mi c damag e, s pac e occupyi ng l es i ons, drugs or drug/al c ohol wi t hdrawal, met abol i c encep hal o-p athy (i nc l ud i ng hy pog l yc aem i a), and neurosurg ery . Anti convul sants provi de c ont rol of sei zures but do not repl ace re mov al of t he cause whe re thi s i s p oss i b l e. Ons et of sei zure c ont rol m ay b e d el a yed by up to 24h wi th phe nyt oi n but a l oadi ng dos e i s usually gi ven duri ng t he acute phase of s ei zures. Mag nes i um sul phate i s es pec i al l y us eful i n e cl a mpt i c sei zures (and i n t hei r pre venti on). Phe nyt oi n has a narrow t herapeuti c rang e and a non-l i ne ar rel at i onshi p b etw een dos e and pl a sma l e vel s. It i s the refore es senti a l t o m oni tor pl as ma l eve l s freque ntl y. Ent eral feed i ng s houl d be s top ped te mporari l y whi l e oral phe nyt oi n i s ad mi ni s tered. Intravenous us e s houl d onl y oc cur i f t he ECG i s moni t ore d c ont i nuous l y. Carbam aze pi ne has a wi der therapeuti c rang e t han phe nyt oi n and t here i s a l i near rel ati ons hi p be twe en dos e and pl a sma l e vel s. It i s not , t herefore, cri t i cal t o m oni tor pl as ma l eve l s freque ntl y. Pl a sma conce ntrati ons of sodi um v al p roate are not rel a ted to effect s s o m oni tori ng of pl as ma l eve l s i s not us eful . P.243

Intravenous drug dosages Bolus

Infusion

Lorazepam

4mg

Diazepam

2.5mg repeated to 20mg

Phenytoin

18mg/kg at <50mg/min

100mg 8hrly

Magnesium sulphate

20mmol over 10–20min

5–10mmol/h

Sodium valproate

400–800mg

Clonazepam

1mg

1–2mg/h

Thiopental

1–3mg/kg

Lowest possible dose

Key trial T re i man VA for the Ve terans Affai rs Status Ep i l ept i cus C oop erati v e Stud y G roup. A c omp ari son of four tre atm ent s for generali zed convul si ve status ep i l e pti cus. N Engl J M ed 1998; 339:792–8

M agp i e Tri al Col l a borati on Group. Do wom en wi t h p re-ecl amp si a , and the i r bab i es , b ene fi t from magnesi um s ul phate? The Magpi e T ri al : a rand omi sed pl ace bo-control l ed t ri al . Lance t 2002; 359:1877–90

W hi ch ant i convul sant for wom en wi t h e cl a mps i a? Ev i d enc e from the Col l a borati ve Ecl amp si a Tri a l . Lancet 1995; 345:1455–63

P.244

Neuroprotective agents Types Di uret i cs : e .g. manni tol , furosem i de (frus emi de)

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Ste roi ds: e. g. dexamet has one Cal c i um antag oni st s: e .g. ni mod i pi ne Barbi t urates : e .g. thi op ent al

Uses Reducti on of cerebral oed ema (manni tol , furosem i d e, d examet has one ) Prev ent i on of ce reb ral vasos pas m (ni m odi pi ne) Reducti on of cerebral met abol i c rate (thi op ent al )

Routes IV

Notes Cerebral protec ti on req ui res generalis ed sed ati on and ab ol i ti on of s ei z ures to red uce cereb ral me tab ol i c rate , c ere bral oed ema and ne uronal damag e d uri ng i sc hae mi a and repe rfusi on. Manni t ol red uc es c erebral i nt ers ti ti a l w ate r b y t he osmoti c l oad . T he e ffe ct i s trans i ent and at i ts be st where t he bl ood–brain barri er i s i ntac t. Int ers ti ti a l w ate r i s m ai nl y red uce d i n norm al are as of brain and thi s may acc ent uat e cerebral shi ft . R epeated doses ac cum ul a te i n the i nterst i ti um and may ev ent ual l y i nc re ase oed ema format i on; manni t ol shoul d onl y be gi v en 4–5 ti mes i n 48h. In add i ti on to i ts os mot i c effect , t here i s s ome ev i de nce of cereb ral vas oconst ri cti on due to a reduct i on i n bl ood vi scosi t y and fre e radi cal sc ave ngi ng. The l oop di uret i c effect of furos emi de enc ourage s s al t and water l oss . T here may also be a red uct i on of CSF chl ori d e trans port reduci ng t he format i on of CSF . Dex ame thasone reduces oed ema around s pac e oc cupyi ng l es i ons s uch as tumours. St eroi d s are not curre ntl y consi dered useful i n head i njury or aft er a c ere brovas cul ar acc i d ent but b enefi t has be en shown i f gi v en earl y afte r spi nal i njury. St eroi ds encourag e s al t and w ate r rete nti on and must be wi t hdrawn sl owl y t o av oi d re bound oed ema. Ni m odi pi ne i s use d t o preve nt cerebral vas os pas m duri ng rec ove ry from ce reb rovasc ul ar i ns ul t s. As a cal ci um c hannel bl ocke r i t al s o p rev ent s c al c i um i ngre ss duri ng neuronal i njury. Thi s cal ci um i ng res s i s associ ate d wi th cel l death. It i s com monl y use d i n t he managem ent of subarachnoi d haem orrhag e for 5–14 days. Thi ope ntal reduces c ere bral m etabol i sm thus prol ongi ng t he ti me t hat the b rai n m ay sus tai n an i schaem i c i nsul t. How ever, i t al s o reduces ce reb ral bl ood fl ow, al though bl ood fl ow i s red i st ri but ed pre ferent i al l y to i sc hae mi c areas . Thi ope ntal acut el y reduc es i ntracrani a l p re ssure and thi s i s probab l y the main cerebroprote ct i ve effect . Sei z ure control i s a furt her be nefi t. De spi te the se effe ct s, barbi t urate com a has not bee n s how n t o i mprove out com e i n cerebral i nsul ts of vari ous c aus es. P.245

Drug dosages Bolus Mannitol

20–40g 6-hrly

Furosemide Dexamethasone

1–5mg/h 4mg 6-hrly

Nimodipine Thiopental

Infusion

0.5–2.0mg/h 1–3mg/kg

Lowest possible dose

Key trials Al l en GS et al . C ere bral arte ri a l s pas m—a control l ed tri al of ni mod i pi ne i n pat i ents wi th sub arachnoi d he morrhage. N Eng l J Me d 1983; 308:619–24 Brack en M B, et al . Ad mi ni s trati on of m ethyl p red ni s ol one for 24 or 48 hours or ti ri l az ad mes yl a te for 48 hours i n the treatm ent of ac ute sp i nal c ord i njury. Res ul t s of t he Thi rd Nat i onal Ac ute Sp i nal C ord Injury R and omi zed Control l ed Tri al . N ati onal Acut e Spi nal Cord Injury St udy . JAMA 1997; 277:1597–604

See also: Int racrani a l p res sure m oni tori ng, p134; Jug ul a r v enous bul b s aturat i on, p 136; EEG/C FM m oni tori ng, p138; Othe r

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neurol ogi cal m oni tori ng , p 140; Basi c re sus ci tat i on, p 270; Generalis ed sei zures , p372; Int rac rani a l haemorrhag e, p376; Sub arachnoi d haemorrhage , p 378; Rai se d i ntracrani al press ure , p 382; Head i njury (1), p504; He ad i nj ury (2), p506

Ovid: Oxford Handbook of Critical Care

Ed itors:

Si nge r, M ervyn; We bb, An dre w R.

Ti tle : O xf ord Ha ndbook of Cr itic al Car e, 2nd Ed ition Cop yri ght © 1997,2005 M. Si nge r and A. R. W ebb , 1997, 2005. Publ i shed i n the Uni te d Stat es by Oxford Uni ve rsi ty Press Inc > Tab le of Co n te n ts > H ae mato log ica l D r u gs

Haematological Drugs Anticoagulants Types Hepari n Low mol ecul ar we i ght (LMW ) hepari n: e .g. dal te pari n, enoxi pari n Ant i coagul ant p ros tanoi d s: e.g . e pop ros tenol , al prostadi l Sod i um ci trate Warfari n Act i vated Prote i n C

Modes of action Hepari n p otenti ate s natural l y occ urri ng AT-III, re duc es the ad hes i onof pl a tel ets to i njured art eri al wal l s , b i nd s t o pl a tel ets and p rom otes in vi tro ag gre gat i on. LMW hep ari n appe ars t o sp eci fi cal l y i nfl ue nce factor Xa acti vi ty; i t s s i mp l er pharm acoki neti cs al l ow for a smalle r (two thi rd s) dos e t o b e ad mi ni s tered to the same e ffe ct. The effect s of t he p rostanoi ds dep end on the balance bet weenTXA 2 and PGI 2 . Sod i um ci trate che l at es i oni s ed c al ci um. Warfari n produc es a c ont rol l ed de fi c i ency of vi t ami n K dep end ent coagul at i on factors (II, VII, IX and X). Act i vated Prote i n C i s t he act i vated form of t he end oge nous anti coagul ant , Prot ei n C

Uses Mai ntenanc e of an ex tracorporeal c i rc ul ati on Prev ent i on or treat ment of t hromboemb ol i sm Seve re sep si s (act i vated Protei n C)

Routes IV (hep ari ns , anti coagul ant prost anoi ds , s odi um ci trate, ac ti v ate d Prot ei n C, AT -III) SC (hep ari ns) PO (warfari n)

Side-effects Bl e edi ng Hypotensi on (ant i coagul ant p ros tanoi ds) Hepari n i nduced throm boc ytopeni a Hypocal cae mi a and hype rnatraemi a (sod i um ci trate)

Notes Al prostadi l has s i mi l a r e ffec ts to epoprost ani l b ut i s l es s p ote nt. As i t i s m etabol i se d i n t he l ungs, sy st emi c vas odi l at ati on effect s are usual l y m i ni mal . Thi s m ay b e an i mportant adv ant age i n the s hoc ked pat i ent. Maj or use s i n

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i nt ens i v e c are are for anti coagul at i on of fi l te r c i rc ui ts, di gi t al vas cul i t i s/i s chaemi a and p ul m onary hyp ert ens i on. For ex tracorporeal us e c i t rat e has advantages ov er hep ari n i n t hat i t has no k nown anti p l a tel et act i vi ty, i s readi l y fi l te red by a haem ofi l te r (red uci ng sys tem i c ant i c oag ul a ti on), and i s ov erw hel med and neut ral i se d w hen re turned to central venous bl ood. Warfari n i s gi ven oral l y and need s 48–72h to dev el op i ts effect . It c an be reve rs ed b y fres h froz en pl a sma or l ow dos es (1m g) of v i tami n K. Ac ti v ate d Prot ei n C has ant i -i nfl amm atory and pro-fi bri nol yt i c prope rti es i n add i t i on to i t s anti coagul ant ac ti ons. P.249

Drug dosages Heparin Dos e requi rement i s vari ab l e to produc e an APTT of 1.5–3 ti m es control . Thi s usual l y requi re s 500–2000IU/h wi t h an ini ti al l oadi ng d ose of 3000–5000IU.

Low molecular weight heparin For de ep vei n t hrombos i s prophyl a xi s gi ve 2500IU SC 12-hrl y. For anti coagul ati on of an e xtracorporeal c i rcui t a bol us of 35IU/kg i s g i ve n IV fol l owed by an i nfus i on of 13IU/k g. The dose i s adj ust ed to mai ntain ant i -fact or Xa act i vi ty at 0.5–1IU/m l (or 0.2–0. 4IU/ml i f there i s a hi g h ri sk of hae morrhage). For pul monary e mbol i s m g i ve 200IU/kg SC dai l y (or 100IU/kg bd i f at ri sk of b l ee di ng)

Anticoagulant prostaglandins Usual range of 2.5–10ng/k g/m i n. If us ed for an ext rac orporeal ci rcul a ti on t he i nfusi on shoul d be st art ed 30m i n pri or to com mencem ent .

Sodium citrate Infuse d at 5mmol p er l i t re of ext rac orp ore al bl ood fl ow.

Warfarin St art at 10mg/d ay orally for 2 days the n 1–6mg /day accordi ng to INR . For D VT prophyl a xi s , p ul m onary emb ol us, mi t ral s tenosi s, atri al fi bri l l at i on and t i ss ue val ve rep l ac ements the INR s houl d be mai ntaine d b etw een2 and 3. F or rec urrent D VT or pul monary em bol us and mec hani c al val ve repl ac ements the IN R s houl d be kep t b etwe en 3 and 4.5.

Activated Protein C (Drotrecogin α activated) For se psi s, an i nfusi on of 24 µg/kg/h i s gi ven for 96h.

See also: Ext rac orporeal re spi rat ory support , p34; Haemo(di a)fi l t rat i on (2), p 64; Pl as ma e xchang e, p68; C oag ul a ti on moni tori ng, p156; Thromb ol y ti c s, p250; Pul m onary emb ol us, p308; Acute coronary syndrome (1), p320; Ac ute coronary syndrome (2), p322; Cl ot ti ng d i sorde rs , p398; Hyp erosmol ar di abe ti c em erg enc i es , p 444; Se psi s and sep ti c shock— treatm ent , p 248; Post -ope rat i v e i nte nsi ve care, p534 P.250

Thrombolytics Types Al t epl ase (rt-PA) Strept oki nas e Urok i nase

Modes of action Ac ti v ate pl asm i nogen to form p l as mi n whi c h de grades fi bri n

Uses Li fe t hre ate ni ng v enous t hromb osi s Li fe t hre ate ni ng p ul m onary embol us Acute myoc ardi a l i nfarct i on To unbl ock i ndwe l l i ng vas cul ar ac ces s c athete rs

Routes

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IV

Side-effects Bl e edi ng, parti cul arl y from i nvasi v e p roc edures Hypotensi on and arrhyt hmi as Embol i sat i on from pre -exi st i ng cl ot as i t i s broken down Anaphyl ac toi d reac ti ons (ani st rep l ase, st rep tok i nase, uroki nas e)

Contraindications (absolute) Cere brovas cul ar ac ci d ent i n l a st 2 m ont hs Act i ve bl eed i ng i n l a st 10 day s Preg nancy Rece nt pep ti c ul ce rat i on Rece nt surgery

Contraindications (relative) Sys tol i c BP >200mm Hg Aorti c di ss ect i on Prol i ferati v e d i ab eti c reti nopat hy

Notes In acute myocardi a l i nfarc ti on t hey are of most val ue when us ed wi t hi n 12h of t he ons et. The y m ay req ui re adjuvant the rap y (e.g . as pi ri n wi th strep toki nase or hepari n wi th rt -PA) t o maxi m i se the e ffe ct i n acute myoc ardi a l i nfarct i on. rt -PA i s said to be c l ot s el e cti ve and i s there fore useful where a ne ed for i nvas i ve proce dures has be en i denti fi e d. Anaphy l ac toi d reacti ons to st rep tok i nase are not uncommon, p art i c ul a rl y i n t hos e who have had st rep toc oc cal i nfect i ons, and pati ent s s houl d not be exp ose d t wi c e b etw een 5 d ays and 1 year of rece i vi ng the l a st dos e. P.251

Drug dosages Alteplase (rt-PA)

The dose schedule for acute myocardial infarction is 10mgin 1–2min, 50mg in 1h and 40mg over 2h intravenously.

Anistreplase

Single intravenous injection of 30U over 4–5min.

Streptokinase

In acute myocardial infarction (1.5mu over 60min).In severe venous thrombosis (250,000U over 30min followed by 100,000U/h for 24–72h).

Urokinase

For unblocking indwelling vascular catheters 5000–37,500IU are instilled. For thromboembolic disease 4400IU/kg is given over 10min followed by 4400IU/kg/h for 12–24h.

See also: Coagul ati on moni tori ng, p156; C oag ul a nts and anti fi b ri nol yti cs, p254; Pul monary emb ol us, p308; Acute coronary syndrome (1), p320 P.252

Blood products Types Pl as ma: e. g. fre sh frozen pl asm a Pl at el ets Conc ent rat es of coagul ati on fac tors: e.g . c ryopre ci p i t ate , factor VIII c onc ent rat e, fac tor IX compl ex

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Uses Vi t ami n K defi c i ency (fresh frozen pl as ma, fac tor IX c ompl ex) Haem ophi l i a (cryoprec i pi tat e) von Wi l l e brand' s d i se ase (c ryopre ci p i t ate ) Fi bri noge n d efi ci e ncy (c ryopre ci p i tate) Chri st mas di sease (fac tor IX c omp l ex )

Routes IV

Notes A uni t (150m l ) of fre sh frozen pl asm a i s usually col l e ct ed from one d onor and c ont ai ns al l coagul at i on factors i nc l udi ng 200 uni ts fac tor VIII, 200 uni ts fac tor IX and 400m g fi bri nogen. F res h froz en pl a sma i s st ore d at -30° C and shoul d be i nfus ed wi t hi n 2h once defros ted . Pl a tel et concentrate s are v i ab l e for 3 day s w hen st ore d at room tem perature. If they are re fri gerate d v i ab i l i ty dec reases . T hey must be i nfuse d q ui c kl y vi a a short gi vi ng s et wi t h no fi l t er. Indi cat i ons for pl a tel et concentrates i nc l ude pl a tel et count <10 × 10 9 , or <50 × 10 9 wi t h s pontaneous b l ee di ng, or to cove r i nv asi ve p roced ure s and spontaneous bl e edi ng wi t h p l at el e t d ysfunc ti on. The y are l es s useful i n condi ti ons ass oci ate d w i th i m mune p l at el e t des truct i on (e. g. ITP). A 15ml vi al of cry opreci pi tat e c ont ai ns 100 uni ts fac tor VIII, 250m g fi bri nogen, fact or XIII and von Wi l l e brand fac tor and i s st ored at -30° . In haem ophi l i a, cry opreci pi tat e i s g i ve n t o achi eve a fact or VIII l ev el >30% of normal. Fac tor VIII conce ntrate contains 300 uni t s fact or VIII per vi al . In se vere haemorrhage due t o haemophi l i a 10–15 uni ts /kg are gi ven 12-hrl y. Fac tor IX compl ex i s ri ch i n fac tors II, IX and X. It i s form ed from pool e d p l as ma so fre sh frozen pl asm a i s p referred. P.253

See also: Coagul ati on moni tori ng, p156; Bl ood t ransfusi on, p182; Ant i c oagul ants , p 248; Bl eed i ng di sorders, p396; C l ot ti ng di s orders, p398; Post -op erati v e i nte nsi ve care, p534; Post -partum haemorrhage , p 542 P.254

Coagulants and antifibrinolytics Types Vi t ami n K Prot ami ne Tranexami c ac i d Act i vated factor VII (F VIIa)

Uses To reve rse a prol onged prothrom bi n ti me, e. g. mal abs orp ti on, oral anti coagul ant t herapy , β l a ctam anti bi oti c s or cri ti c al i l l ne ss (vi tam i n K) To reve rse the e ffe cts of hep ari n (protam i ne) Bl e edi ng from raw s urfac es, e.g . p ros tat ec tomy , d ent al ext rac ti on (tranex ami c aci d ) Bl e edi ng from t hrombol yt i cs (t ranexami c ac i d) Bl e edi ng from major traum a or haem ophi l i a (F VIIa)

Routes IV (vi tami n K, p rot ami ne, trane xam i c aci d, F VIIa) PO (vi t ami n K , t ranexami c ac i d)

Notes The effec ts of v i t ami n K are prol onge d s o i t s houl d be avoi de d where pati e nts are d epe nde nt on oral anti coagul ant the rap y. A d ose of 10mg i s gi v en oral l y or by sl ow i nt rav enous i nj ect i on daily . In l i fe threateni ng haemorrhage

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5–10mg i s gi ven by sl ow i nt rav enous i nj ect i on wi th other coagul ati on fac tor conce ntrat es. If INR >7 or i n l e ss sev ere hae morrhage 0.5–2m g may b e g i ve n b y s l ow i ntravenous i njec ti on wi th mi ni m um l as ti ng e ffe ct on oral anti coagul ant the rap y. Protam i ne has an anti coagul ant effec t of i t s own i n hi g h d ose s. Protam i ne 1m g neut ral i s es 100IU unfract i onat ed hep ari n i f g i ve n w i thi n 15m i n. Less i s re qui red i f gi ven l a ter s i nc e hepari n i s ex cre ted rapi d l y. Protami ne s houl d be gi v en by sl ow i ntrave nous i nje cti on acc ord i ng t o the APTT . T otal d ose shoul d not exc eed 50m g. Protam i ne i njec ti on may cause se vere hy pot ens i on Tranex ami c aci d has an anti fi b ri nol yti c e ffe ct by antagoni s i ng pl asm i nogen. T he usual dos e i s 1–1. 5g 6–12-hrl y oral l y or by sl ow i ntrave nous i nje cti on. Rec omb i nant fac tor VIIa i s l i censed for use i n haem ophi l i a but a numb er of cas e s eri es i n maj or trauma, orthopaedi c and cardi ac surge ry rep ort be nefi t i n sev ere , i ntract abl e b l ee di ng t hat had not res ponded to st and ard me asures . T he dos e i s 4500IU/kg over 2–5mi n, fol l owed by 3000–6000IU/kg d epe ndi ng on the se veri ty of bl eed i ng . P.255

See also: Coagul ati on moni tori ng, p156; Ant i coagul ants, p248; Thromb ol y ti c s, p250; Aproti ni n, p 256; Bl eed i ng di sorde rs, p396; Cl otti ng di sorders, p398; Post-ope rat i ve i ntensi ve c are, p 534;Pos t-p art um hae morrhage, p542 P.256

Aprotinin The rol e of seri ne prote ase i nhi b i t ors i n coagul at i on and anti coagul ati on i s com pl i cated due t o thei r e ffec ts at vari ous poi nts i n t he c oag ul ati on pat hway . Aproti ni n i s a nat urally oc curri ng, non-s pec i fi c s eri ne protease i nhi b i tor w i th an el i mi nat i on half-l i fe of ab out 2h. Prev ent i on of sys tem i c bl eed i ng wi th aproti ni n does not promote coag ul ati on wi t hi n the ex tracorporeal ci rc ul a ti on and may eve n c ont ri but e t o t he m ai ntenanc e of e xtracorporeal anti coagul ati on.

Modes of action The effec ts of aproti ni n on the c oagul at i on c asc ade are de pendent on t he ci rcul at i ng pl asm a c onc ent rat i ons (ex pre sse d as k al l i krei n i nac ti v ati on uni ts—kIU/ml ) s i nc e t he affi ni ty of aproti ni n for p l as mi n i s si gni fi cantl y great er than t hat for p l as ma kal l i k rei n. At a p l asma l ev el of 125kIU/ml aprot i ni n i nhi bi ts fi b ri nol ysi s and com pl e ment act i vati on. Inhi b i ti on of pl a sma kal l i kre i n req ui res hi ghe r d ose s t o p rov i de pl asm a l eve l s of 250–500kIU/ml . Pl as ma kal l i kre i n i nhi bi ti on—red uce s b l ood c oag ul a ti on m edi ate d v i a contac t wi th ani oni c surfac es and , i n t he cri ti c al l y i l l pati ent , i mproves c i rc ul a tory s tab i l i ty vi a reduced ki ni n ac ti vati on. Prev ent i on of i napp rop ri ate pl ate l et ac ti v ati on—neutrophi l act i vati on (comp l e ment or kall i krei n me di a ted ) c aus es a se condary acti vat i on of pl ate l et s. Imp ort ant i n t hi s pl ate l et –ne utrophi l i nteract i on i s t he rel eas e of Cathe psi n G by ne utrophi l de granul ati on. It has b een dem ons trate d rece ntl y t hat ap rot i ni n c an si g ni fi c ant l y i nhi bi t the pl a tel et act i vati on d ue to puri fi ed Cat hep si n G, thi s mec hani sm formi ng a d i re ct i nhi b i ti on of i nappropri at e neut rophi l m edi ate d p l at el e t acti vat i on.

Uses The mai n rol e of ap rot i ni n i n t he manage ment of the e xtracorporeal c i rcul ati on has be en to pre vent b l ee di ng ass oci ate d wi th hep ari ni sat i on. High dose aproti ni n g i ve n duri ng cardi opul monary by pas s p roc edures has b een show n t o reduce pos t-operati ve bl ood l os s d ram ati cal l y. P.257

Drug dosages Aprotinin—loading dose of 2 × 10 6 kIU followed by 500,000kIU/h

See also: Ext rac orporeal re spi rat ory support , p34; Haemo(di a)fi l t rat i on (2), p 64; Anti coagul ant s, p248; Post -op erati v e i nt ens i v e c are , p534

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Ed itors:

file:///C:/Documents%20and%20Settings/MVP/Application%20Data/Mozilla/Firefox/Profiles/2...

Si nge r, M ervyn; We bb, An dre w R.

Ti tle : O xf ord Ha ndbook of Cr itic al Car e, 2nd Ed ition Cop yri ght © 1997,2005 M. Si nge r and A. R. W ebb , 1997, 2005. Publ i shed i n the Uni te d Stat es by Oxford Uni ve rsi ty Press Inc > Tab le of Co n te n ts > Misc ell an e ou s Dr u g s

Miscellaneous Drugs Antimicrobials Types Peni ci l l i ns : e. g. benzyl peni ci l l i n, fl uc l ox aci l l i n, pi peraci l l i n, amp i c i l l i n Cephal ospori ns: e.g . c efotax i me , c eft azi di m e, cefuroxi m e Carb ape nem s: e.g. i mi p enem , m eropenem Ami nog l yc osi des : e .g. gentam i c i n, am i kaci n, t obramy ci n Qui nol one s: e .g. ci profl oxac i n Gl y cop ept i de s: e.g. te i c opl ani n, vancomy ci n Macrol i de s: e.g. erythromyci n, cl ari thromy ci n Other ant i bacte ri a l s :. e .g. cl i ndamy ci n, metroni dazol e, l i nezol i d, c o-t ri moxazol e, ri famp i c i n Ant i fungals: e. g. amphote ri ci n, fl uc ytosi ne, fl uconazol e, caspofungi n, v ori conazol e, i traconazol e Ant i vi ral s: e.g . aci c l ovi r, g anc i cl ovi r

Uses Tre atme nt of i nfect i on. Prop hyl axi s agai ns t i nfe cti on, e. g. peri -operati vel y Loc al choi ce of ant i m i crobi al vari es . Howe ver, as a gui de , t he fol l owi ng choi c es are com mon: Pneumoni a (hospi tal -ac qui red Gram neg ati ve)—ce ftazi d i me , c i profl oxaci n, m eropenem or pi p eraci l l i n/t azobac tam (pi p taz obact am) Pneumoni a (communi t y-ac qui re d)—cefuroxi m e + cl a ri thromy ci n Sys tem i c sep si s —ce furoxi me ± g ent ami ci n (+ met roni d azol e i f anae rob es l i kel y)

Routes Generall y IV i n c ri t i c al l y i l l pati e nts .

Side-effects Hype rs ens i ti vi t y reac ti ons (al l ) Sei zures (hi gh dos e p eni ci l l i ns, hi gh dos e m etroni dazol e , c i profl oxaci n) Gas troi nt est i nal di s turbance (ce phalos pori ns , e ryt hromyc i n, c l i ndam yci n, tei cop l ani n, vancomyc i n, co-t ri moxazol e, ri famp i c i n, me troni d azol e, ci profl oxac i n, am photeri c i n, fl ucy tos i ne ) Ves ti b ul a r d amage (ami nog l yc os i de s) Renal fai l ure (ami nogl ycosi d es, te i c opl ani n, vancomy ci n, ci p rofl ox aci n, ri famp i c i n, amp hot eri ci n, aci cl ovi r) Ery the ma m ul t i form e (c o-t ri m oxazol e) Leucop eni a (c o-t ri moxazol e, met roni dazol e, tei cop l ani n, c i profl oxaci n, fl uc ytosi ne, aci cl ovi r) Thrombocyt ope ni a (l i ne zol i d ) Peri pheral neuropathy (me troni dazol e )

Notes Ant i m i crobi al s s houl d be c hos en acc ordi ng t o mi crobi al sensi ti v i ti es, us ual l y bas ed on adv i ce from the mi crobi ol og y l ab oratory. App ropri ate em pi ri c the rap y for seri ous i nfect i ons s houl d be det erm i ne d b y l i ke l y org ani sms , t aki ng i nt o account known comm uni ty and hospi tal i nfe cti on and re si s tance pat terns. Up to 10% of peni ci l l i n-al l ergi c pati e nts are also ce phalos pori n-al l ergi c .

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P.261

Drug dosages (intravenous)

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Benzylpenicillin

1.2g 6-hrly (2-hrly for pneumococcal pneumonia)

Flucloxacillin

500mg–2g 6-hrly

Ampicillin

500mg–1g 6-hrly

Piptazobactam

4.5g 6–8-hrly

Cefotaxime

1–4g 8-hrly

Ceftazidime

2g 8-hrly

Ceftriaxone

1–4g daily

Cefuroxime

750mg–1.5g 8-hrly

Gentamicin

1.5mg/kg stat then by levels (usually 80mg 8-hrly)

Amikacin

7.5mg/kg stat then by levels (usually 500mg 12-hrly)

Tobramycin

5mg/kg stat then by levels (usually 100mg 8-hrly)

Erythromycin

500mg–1g 6–12-hrly

Metronidazole

500mg 8-hrly or 1g 12-hrly PR

Clindamycin

300–600mg 6-hrly

Ciprofloxacin

200–400mg 12-hrly

Co-trimoxazole

960mg 12-hrly in Pneumocystis carinii pneumonia

Imipenem

1–2g 6–8-hrly

Meropenem

500mg–1g 8-hrly

Rifampicin

600mg daily

Teicoplanin

400mg 12-hrly for 3 doses then 400mg daily

Vancomycin

500mg 6-hrly (monitor levels)

Linezolid

600mg 12-hrly

Chloramphenicol

1–2g 6-hrly

Amphotericin

250µg–1mg/kg daily

Flucytosine

25–50mg/kg 6-hrly

Fluconazole

200–400mg daily

Caspofungin

70mg stat then 50–70mg daily

Voriconazole

400mg 12-hrly on first day then 200–300mg 12-hrly

Itraconazole

200mg 12-hrly for 2 days then 200mg daily

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Common choices for specific organisms Staph. aureus

flucloxacillin

Methicillin-resistant Staph. aureus

teicoplanin, vancomycin, linezolid

Strep. pneumoniae

cefuroxime, benzylpenicillin

N. meningitidis

ceftriaxone, cefotaxime, benzylpenicillin

H. influenzae

cefuroxime, cefotaxime

E. coli

ampicillin, ceftazidime, ciprofloxacin, gentamicin, ciprofloxacin, gentamicin, imipenem, meropenem

Klebsiella spp.

ceftazidime, ciprofloxacin, gentamicin, imipenem, meropenem

Ps. aeruginosa

ceftazidime, ciprofloxacin, gentamicin, imipenem, meropenem, piptazobactam

P.262

Steroids Uses Ant i -i nfl amm atory— ste roi ds are often gi ven i n hi gh dos e for the i r ant i -i nfl amm atory effe ct , e. g. ast hma, alle rgi c and anaphy l ac toi d reac ti ons , vasc ul i ti c di sorde rs, rheum atoi d art hri ti s, i nfl am mat ory bowel di sease, neop l as m-rel a ted ce reb ral oe dem a, the fi bro-prol i ferati ve phase of ARD S, pne umoc oc cal meni ngi t i s, pneumoc yst i s pneumoni a , l arynge al oed ema (e. g. aft er rep eat ed i nt ubati on) and aft er sp i nal c ord i njury. Benefi t i s unp rov ed as y et i n cerebral oed ema fol l owi ng head i njury or c ard i oresp i ratory arrest , and may be harmful i n cerebral mal ari a and sep si s (at hi gh dose). A mul t i ce ntre t ri al has shown i mp roved out com es wi t h ‘ l ow dose’ hy drocorti s one (50mg qd s for one wee k) i n sept i c shock pati e nts wi th dep res sed ad renal functi on (subnormal p l as ma corti s ol re sponse to ACT H, oft en desp i t e ‘ normal ’ or rai s ed pl a sma l e vel s). Some pat i ents wi t h hypotensi on not res pondi ng t o c ate chol am i ne s w i l l i mp rov e wi th corti cos teroi d therapy. Repl ace ment t herapy i s ne ede d for p ati ents wi t h Addi son's di seas e and aft er adrenalec tom y or p i tui tary surge ry. In t he l onger t erm , fl ud roc ort i sone i s usual l y req ui red i n add i ti on for i t s mi neraloc ort i c oi d sodi um-retaini ng effe ct. Hi ghe r repl ac ement d ose s are nee ded i n chroni c ste roi d take rs (i .e. >2 week s w i thi n the l ast year) unde rg oi ng a st res s, e.g . s urg ery , i nfe cti on. Immunos upp res si ve— aft er org an t ransp l antat i on

Side-effects/complications Sod i um and water re tenti on (esp eci al l y w i t h mi neral ocorti coi ds ) Hypoadrenal c ri si s i f st opp ed abrupt l y aft er prol onged treat ment Immunos upp res si ve— pos si b l y i nc re ased i nfec ti on ri s k (q.v .) Neut rophi l i a Impaired gl ucos e t ol e rance/di a bet es mel l i t us Hypokal aem i c al k al osi s Ost eop orosi s , p rox i mal m yop athy (l ong -te rm use ) Inc reased susce pti bi l i t y t o p ept i c ul c er di seas e and GI bl e edi ng

Notes The pe rce i ve d hei g hte ned ri sk of sys tem i c i nfect i on ap pears exagge rat ed. Chroni c ste roi d users g ene ral l y app ear no more affec te d t han the ge neral pop ul a ti on; studi es i n ARD S and sep si s re vealed no great er i nc i de nce of i nfec ti on pos t-s teroi d ad mi ni s trati on. Oral fung al i nfec ti on i s rel a ti vel y common w i th i nhal ed ste roi ds but s yst emi c and pul monary fungal i nfe cti on i s predom i nant l y seen i n t he s eve rel y i mmunoc omp rom i se d (e.g . AIDS, pos t-c hem otherapy) and not t hos e t aki ng hi g h-d ose st eroi ds al one .

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The choi c e of c ort i cost eroi d for short -te rm ant i -i nfl amm atory effe ct i s probab l y i rrel evant provi d ed the dose i s suffi c i e nt. Chroni c hyd roc ort i sone shoul d be av oi d ed for ant i -i nfl am matory use be cause of i ts mi neral ocorti coi d e ffec t but i s ap propri at e for adrenal repl ace ment. Pre dni sone and corti sone are i nac ti ve unt i l met abol i s ed by the l i ver to predni sol one and hyd roc ort i s one res pec ti vel y. Gl ucocorti c oi d s antagoni s e the e ffe cts of ant i c hol i ne ste ras e d rugs. St eroi ds are p rob abl y not l i k el y to cause cri ti cal i l l ness my opathy thoug h t hi s re mai ns a c ont ent i ous i ss ue. P.263

Relative potency and activity Drug

Glucocorticoid activity

Mineralocorticoid activity

Equivalent anti-inflammatory dose (mg)

Cortisone

++

++

25

Dexamethasone

++++

—

0.75

Hydrocortisone

++

++

20

Methylprednisolone

+++

+

4

Prednisolone

+++

+

5

Prednisone

+++

+

5

Fludrocortisone

+

++++

—

Drug dosages Drug

Replacement dose

Anti-inflammatory dose

Dexamethasone

—

4–20mg tds IV

Hydrocortisone

20–30mg daily

100–200mg qds IV

Methylprednisolone

—

500mg–1g IV daily

Prednisolone

2.5–15mg mane

40–60mg od PO

Fludrocortisone

0.05–0.3mg daily

—

Weaning Acute use (<3–4 days)

can stop immediately

Short-term use ≥3–4 days)

wean over 2–5 days

Medium-term use (weeks)

wean over 1–2 weeks

Long-term use (months/years)

wean slowly (months to years)

Key papers Annane D, Seb i l l e V, Charpe nti er C e t al . Effe ct of tre atm ent wi th l ow doses of hyd roc ort i s one and fl udroc ort i sone on m ort al i ty i n pati e nts wi th sep ti c shock . JAMA 2002; 288:862–71

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Bracke n MB, et al. Ad mi ni st rat i on of me thy l predni s ol one for 24 or 48 hours or ti ri l azad m esy l at e for 48 hours i n t he treat ment of ac ute sp i nal c ord i njury. Res ul t s of t he Thi rd Nat i onal Ac ute Sp i nal C ord Injury R and omi zed C ont rol l e d T ri a l . Nat i onal Acute Sp i nal C ord Injury Stud y. JAM A 1997; 277:1597–604

Pras ad K, Garner P. St eroi ds for t re ati ng cerebral mal ari a. Coc hrane Dat abase Sys t R ev 2000; (2):C D000972. R evi ew.

d e G ans J, van de Be ek D; Europe an D examet has one i n Ad ul t hood Bact eri al Meni ngi t i s St udy Invest i g ators. D examet has one i n ad ul t s w i th bacte ri a l m eni ngi ti s. N Engl J Med 2002; 347:1549–56

v an de Bee k D , et al . C ort i c ost eroi ds i n ac ute bacte ri al meni ng i ti s. Coc hrane Dat abase Sys t R ev 2003; (3):CD004305. Rev i ew .

P.264

Prostaglandins Types Epop ros te nol (pros tac ycl i n, PGI 2 ) Al p ros tad i l (PGE 1 )

Modes of action Sti mul ate ad eny l c ycl ase thus i nc reasi ng pl a tel et cAM P c onc ent rat i on; t hi s i nhi bi t s p hos phol i pas e and cyc l ox ygenase and t hus re duc es pl a tel et agg reg ati on (ep oprost enol i s t he mos t p ote nt i nhi bi tor k nown) Reduces pl ate l et proc oagul ant act i vi ty and re l ease of hepari n ne utral i si ng fac tor May hav e a fi b ri nol yti c e ffe ct Pul monary and sy ste mi c vasod i l ator by re l ax ati on of vas cul ar smooth muscl e

Uses Ant i coagul at i on, p art i c ul a rl y for e xtracorporeal c i rcui ts , ei ther as a subs ti t ute or i n ad di t i on to he pari n Pul monary hyp ert ens i on Mi c rov asc ul a r hypoperfus i on (i ncl udi ng di gi t al vas cul i t i s) Haem ol y ti c uraem i c sy ndrome Acute res pi ratory fai l ure (by i nhal a ti on)

Side-effects/complications Hypotensi on Bl e edi ng (parti cul arl y at c annul a s i te s) Fl us hi ng, he adac he

Notes Epoproste nol i s ac ti ve on b oth pul monary and sys tem i c ci rcul at i ons. Al though al prostadi l i s c l ai med to be met abol i s ed i n the l ung and have onl y p ul m onary v asodi l at i ng effect s, fal l s i n sys tem i c bl ood press ure are not unc ommonl y se en, es pec i al l y i f met abol i s m i s i nc omp l et e. Avoi d ext rav asati on i nt o pe ri phe ral ti ssues as sol ut i on has hi gh pH. Effect s l ast up to 30mi n fol l owi ng d i sc ont i nuat i on of the drug . Prostagl andi ns may potenti a te the effec t of he pari n. Rec ent st udi es hav e s hown i mprovem ent i n gas e xchang e b y se l ec ti ve pul monary vas odi l a tat i on fol l owi ng i nhalat i on of epoproste nol at doses of 10–15ng/k g/mi n. The effi c acy ap pears si m i l ar to that of ni tri c oxi de i nhal a ti on b ut i s not as rap i d. P.265

Drug dosages

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Epoprostenol

2–20ng/kg/min

Alprostadil

2–20ng/kg/min

See also: Hae mo(d i a)fi l trati on (2), p64; Pl asm a ex change , p 68; Vasod i l ators, p198; Ni t ri c oxi d e, p190; Anti coag ul ant s, p248; Ac ute re spi rat ory di st res s s ynd rom e (1), p292; Acut e resp i ratory d i s tre ss syndrome (2), p294; Cl ot ti ng di s ord ers , p398; Vas cul i t i de s P.266

Novel therapies in sepsis Greate r unde rs tandi ng of t he p athophysi ol ogy of sep si s has s ti mul ate d t he d eve l op ment and i nv est i gati on of agent s that m odul at e d i ffere nt com ponent s of the i nfl amm atory res ponse. These drugs have been targe ted at tri g gers (e.g. end otoxi n), cyt oki nes (e. g. tum our ne crosi s fact or, i nterl euki n (IL)-1), and effec tor ce l l s and t hei r produc ts (e. g. neutrophi l s , free oxy gen radi c al s, ni t ri c ox i de ) or aim to boos t a ge neral ant i -i nfl amm atory res ponse (e. g. ste roi ds). An i ncre asi ng are a of researc h i s i n repl ace ment or augm ent ati on of e ndogenous anti -i nfl am mat ory sy ste ms, e. g. act i vated Prote i n C, ant i throm bi n-III, IL-10, as t here i s an i ncreas i ng re al i sati on of the d egree of di s rup ti on and i mb al a nce be twe en pro- and anti -i nfl a mmatory s ubs tances . Unfort unatel y, due to de fi c i enci e s i n t ri al des i gn and s i ze , c hoi ce of app rop ri a te pat i ent, ti mi ng of drug adm i ni st rat i on, d osage, and l ack of standardi sat i on of concurrent therapi e s, onl y t wo agents (‘l ow dos e’ hyd roc ort i s one and ac ti vat ed Prot ei n C) have b een shown to produce outc ome be nefi t i n reasonabl y s i ze d m ul t i c ent re tri al s. For many othe r p rod uct s, promi si ng resul t s from p ost -hoc subgroup anal y si s and from ti ghtl y control l ed small pat i ent s tudi e s have not be en rep rod uce d. Conc ern ov er cos t has hi ghl i ghted the p ote nti al bud get ary i m pl i cati ons of any succe ssful the rap y t hough, i n te rms of l i fe years, the c ost –be nefi t wi l l b e rel a ti vel y c heap .

Uses Sep si s Mul ti p l e-org an dys functi on

Activated Protein C Ac ti v ate d Prot ei n C has ant i -i nfl amm atory, anti c oag ul a nt and pro-fi bri nol y ti c prope rti es . Its benefi ci a l e ffec ts i n sep si s are m ost l i ke l y to b e rel ated to i t s ant i -i nfl amm atory p roperti e s. A l arg e p ros pec ti ve randomi se d c ont rol l ed tri al de mons trate d outc ome benefi t for pat i ents wi t h s eve re sep si s t reated wi t hi n 48h of p res ent ati on wi t h a 96h i nfusi on of 24µ g/k g/h aPC . M ost be nefi t was see n i n t hos e w i th ≥2 organ dys funct i ons. The maj or si d e e ffe ct was bl e edi ng so cauti on s houl d be exe rci sed i n t hos e at hi gh ri sk of p ote nti al l y cat ast rop hi c bl eed i ng, e .g. concurrent coagul opathy , or a re cent hi st ory of surge ry, major traum a, head i njury and/or pep ti c ul cer d i se ase .

Corticosteroids Large random i s ed m ul t i c ent re studi e s of hi gh dose met hyl predni sol one s how ed e i t her no benefi t or a trend to harm. How ever, sub seq uent s tud i es wi th l ow er dos es of c orti c ost eroi ds (e .g. 50mg qds hy drocorti s one ) reve al e d earl i er res ol uti on of s hoc k and i mp rov ed survi v al i n those pat i ents wi t h an i mpaired (<250nm ol /l [9µg /dl ]) ri s e i n p l as ma corti sol to a synthe ti c AC TH challe nge . P.267

Examples of drugs investigated in multicentre studies Cort i c ost eroi ds (m ethyl p red ni s ol one, hy drocorti sone) Pol y cl onal i mmunogl ob ul i n Ant i -e ndotoxi n ant i body (HA-1A, E5) Ant i tumour necrosi s fact or ant i b ody Tumour nec ros i s factor s ol ubl e re cep tor anti body Int erl euk i n-1 rece ptor antagoni st Pl at el et act i vati ng fact or ant agoni s ts, PAF-ase Bradyk i ni n antagoni st s Nal oxone

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Ibuprofen N-ac ety l c yst ei ne, procys tei ne L-N -mono-me thy l -argi ni ne (L-NMM A) Ant i throm bi n III Ti s sue fac tor p athway i nhi b i tor Act i vated Prote i n C

Key trials Bernard GR, for the PROW ESS st udy group . Effi cac y and safety of rec omb i nant hum an act i vated prote i n C for seve re sep si s. N Engl J M ed 344:699–709 Annane D, et al . Effe ct of t re atme nt wi t h l ow dos es of hydroc ort i sone and fl udrocorti sone on m ort al i ty i n pat i e nts wi t h s ept i c shock . JAMA 2002; 288:862–71

See also: Sep si s and s ept i c shock —treat ment, p486

Ovid: Oxford Handbook of Critical Care

Ed itors:

Si nge r, M ervyn; We bb, An dre w R.

Ti tle : O xf ord Ha ndbook of Cr itic al Car e, 2nd Ed ition Cop yri ght © 1997,2005 M. Si nge r and A. R. W ebb , 1997, 2005. Publ i shed i n the Uni te d Stat es by Oxford Uni ve rsi ty Press Inc > Tab le of Co n te n ts > Resu sci tati on

Resuscitation Basic resuscitation In any se vere c ard i oresp i ratory di s turbance the order of pri ori t y s houl d be t o s ecure the ai rway, mai ntain res pi rat i on (i . e. manual venti l at i on i f ne ces sary), re store the ci rc ul a ti on (wi t h e xternal c ard i ac massage i f nec ess ary ) and consi der mec hani c al vent i l ati on. Ini t i al as ses sme nt of t he pat i ent s houl d i ncl ude pat enc y of the airway, palpati on of the pul se s, measureme nt of bl ood p re ssure, presumpt i ve di agnosi s and consi d erati on of t reatme nt of the cause .

Airway protection The ai rway s houl d be opened by l i fti ng t he jaw forward and ti l ti ng the forehead . The m out h and pharynx s houl d be cl eared b y s uct i on and l oos e fi tt i ng d ent ure s removed. If ne ces sary an orop haryng eal (Guede l ) ai rway may be i ns erted .

Manual ventilation Onc e t he ai rway i s prote cte d t he pat i ent w ho i s not breat hi ng requi res manual venti l at i on wi th a s el f-i nfl a ti ng b ag and mask (Amb u b ag). Oxyg en s houl d be del i v ere d i n maxi m um concentrati on (FIO 2 1.0 for manual v ent i l ati on, FIO 2 0.6–1. 0 for spontaneousl y b reathi ng pat i ents). If t he pat i ent b reathe s i nad equate l y (poor art eri al sat urati on, hyp erc apni a, rapi d s hal l ow breat hi ng) v ent i l atory sup port s houl d conti nue.

Circulation If pul ses are not pal pab l e or are we ak or i f t he pat i ent has a s eve re bradyc ard i a ext ernal cardi a c m ass age i s re qui re d and treat ment s houl d conti nue as for a cardi a c arre st . Hy pot ens i on shoul d b e t reated i ni t i al l y wi t h a fl ui d chal l enge al t hough l i fe-t hreate ni ng hypotensi on m ay req ui re b l i nd tre atm ent wi th epi nep hri ne 0.05–0.2m g i ncreme nts at 1–2mi n i nterval s i nt rav enousl y unti l a sati sfac tory bl ood p re ssure i s res tored. Such treat ment s houl d not be prol onged wi thout ci rcul at ory moni t ori ng to ens ure ad equacy of cardi ac out put as wel l as correc ti on of hypotensi on.

Venous access Venous ac ces s m ust be se cured earl y duri ng b asi c resusci tati on. Large-bore c annul a e are nece ssary, e. g. 14G. In cas es of hae morrhage t wo cannul ae are re qui red . Smal l peri pheral v ei ns s houl d be avoi de d; fore arm fl exure vei ns are app rop ri ate i f now here e l se i s av ai l abl e. In very d i ffi cul t pat i e nts a Sel di nger ap proach to the femoral vei n or a central vei n may b e appropri at e. The l a tte r has the ad vant age of provi di ng c ent ral ve nous m oni tori ng. P.271

See also: Oxy gen therapy, p2; Vent i l a tory s upp ort —i ndi cat i ons, p4; Endotrache al i nt ubati on, p36; Ce ntral venous cat het er—inserti on, p116; Col l oi d s, p180; Inot rop es, p196; Vasop res sors, p200; F l ui d c hal l e nge, p274; Hy pot ens i on, p312 P.272

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Cardiac arrest As wi t h b asi c res usc i t ati on the order of pri ori ty i s ai rway, bre athi ng and c i rcul ati on fol l ow ed by d rug t reatment. If the cardi ac arrest i s wi tne sse d a precordi al thump may re vert v ent ri c ul ar tac hyc ard i a or ventri cul ar fi bri l l ati on. Ini ti al manage ment of the airw ay and re spi rat i on i s as for b asi c res usc i tati on. Whe n i ntubat i on i s atte mpt ed i t shoul d be effect ed aft er adeq uat e p re- ox ygenati on and qui ck l y to avoi d hyp oxae mi a . If i ntubat i on i s d i ffi cul t mai ntain manual venti l at i on wi th an Ambu bag, mas k and 100% ox yge n.

Cardiac massage Ext ernal cardi ac mas sag e provi des mi ni mal ci rcul a tory s upp ort duri ng c ard i ac arre st. A com pre ssi on rat e of 80–100/mi n i s l i k el y to provi de t he opt i mum b l ood fl ow duri ng c ard i ac massage wi t h a manual breat h from an ass i s tant for every 5 compress i ons. Av oi d mas sag e d uri ng manual i nsp i rati on i f t he pat i ent i s not i ntub ate d (t o avoi d gas tri c di l atati on); ot herwi s e c ard i ac massage i s more e ffec ti ve i f not synchroni se d t o resp i rati on.

Defibrillation Defi bri l l at i on shoul d b e p erform ed urg ent l y i f VT or VF cannot be ex cl uded . It i s i mportant to res tart cardi a c m ass age i mm edi ate l y aft er defi bri l l at i on wi thout wai ti ng for the EC G t o recover. Ce reb ral d amag e c ont i nues whi l e the re i s no bl ood fl ow.

Drugs Few drugs are neces sary for fi rst l i ne cardi ac arrest manag ement. Drugs shoul d b e gi ven vi a a l a rge ve i n si nce vas oconst ri cti on and poor fl ow creat e d el a y i n i nje cti ons gi ven vi a s mal l p eri pheral v ei ns reac hi ng t he central ci rcul at i on. Acc ess shoul d b e s ecured earl y duri ng t he res usc i t ati on; i f venous ac ces s c annot be sec ure d d oub l e or tri pl e d ose s of drug s may b e g i ve n v i a the end otrac heal t ube.

Epinephrine The α constri c tor effect s pre domi nate d uri ng cardi ac arres t, hel pi ng t o m ai ntai n d i as tol i c bl ood press ure and t hus coronary and ce reb ral pe rfusi on. Epi ne phri ne shoul d b e g i ve n i rre spe cti ve of rhy thm at 1m g (10ml of 1:10, 000 sol ut i on) ev ery 10 CPR se que nce s.

Vasopressin A rec ent random i z ed c ont rol l e d t ri al comp ari ng vas opres si n and e pi nephri ne s how ed i mp rov ed outc ome s w i th vas opress i n for pati ent s i n asys tol e.

Atropine A s i ngl e 3m g dose i s gi ven earl y i n asy st ol e .

Calcium chloride Use d i n e l ec tromec hani c al di s soc i at i on i f there i s hyperkal aem i a, hy poc al c aem i a or cal ci um antagoni st us e. A d ose of 10m l of a 10% sol ut i on i s usual. The mai n di s adv ant age of cal ci um i s the re duc ti on of reperfusi on of i schaemi c brain and promoti on of c ytosol i c cal ci um acc umul at i on duri ng c el l de ath.

Bicarbonate Onl y used i f re sus ci tat i on i s prol ong ed t o c orrec t t emp orari l y a potenti a l l y l e thal p H. A d ose of 50ml of 8.4% sol ut i on i s gi ven. The m ai n di sad vantag e i s t hat i ntracel l ul ar and resp i ratory aci dos i s are ex ace rbated unl es s v ent i l a ti on i s i nc re ase d and t he cause of the met abol i c ac i d osi s i s not corre cte d. P.273

Key trial W enzel V for the Europ ean Re sus ci t ati on Counci l Vas opress or duri ng CPR s tud y. A c omp ari son of vas opress i n and e pi nephri ne for out -of- hosp i tal c ard i op ul monary res us ci t ati on. N Eng l J Med 2004; 350:105–13

P.274

Fluid challenge Hyp ovol ae mi a mus t be t re ated urgentl y t o av oi d the s eri ous c ompl i c ati on of org an fai l ure. An ade quat e c i rcul ati ng vol ume must be provi d ed before consi deri ng ot her me thods of c i rcul atory sup port. Cl i ni cal si gns of hy pov ol a emi a (re duc ed ski n t urg or, l ow C VP, ol i guri a, tac hyc ard i a and hyp ote nsi on) are l ate i ndi cat ors . Li ft i ng t he l egs of a sup i ne pat i ent and wat chi ng for an i m provem ent i n the c i rc ul a ti on i s a us eful i nd i cator of hy povol ae mi a . A hi gh i ndex of sus pi ci on m ust be mai nt ai ned; a norm al heart rat e, bl ood pre ssure and CVP d o not e xcl ud e hy pov ol a emi a and t he CVP i s parti cul arl y unrel i abl e i n p ul m onary vas cul ar di s eas e, ri ght ventri cul ar di se ase , i sol ate d l eft ventri cul ar fail ure and val vul ar heart di seas e. The ab sol ute CVP or PAWP are al so di ffi cul t t o i nte rp ret si nce pe ri p heral venoconst ri cti on may mai ntain the se fi l l i ng pre ssures de spi te hyp ovol ae mi a ; i nde ed, they m ay fal l i n resp ons e t o fl ui d. The re sponse to a fl ui d chal l eng e i s t he safest met hod of as ses sme nt.

Choice of fluid The ai m of a fl ui d chal l eng e i s t o p rod uce a s i g ni fi cant (200ml ) and rap i d i nc rease i n pl a sma vol um e. Col l oi d fl ui ds

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are i d eal ; a ge l at i n sol uti on i s re com mend ed for short te rm pl a sma vol um e e xpansi on i n si m pl e hy povol ae mi a , and hyd rox yet hyl st arc h w here t here i s a probabi l i t y of capi l l a ry l eak. Pack ed red ce l l s have a hi gh haemat oc ri t and d o not ad equate l y expand the pl asm a v ol ume. Cryst al l oi d fl ui d s are rap i d l y l os t from the c i rc ul ati on and do not gi ve a rel i a bl e i ncre ase i n pl asm a v ol ume.

Assessing the response to a fluid challenge Ide al l y, the re sponse of CVP, or stroke vol ume and PAWP, s houl d be moni tored duri ng a fl ui d chal l eng e. Fl ui d chall eng es s houl d be rep eat ed whi l e the re sponse sugge sts conti nui ng hy povol ae mi a . Howe ver, i f s uch moni t ori ng i s not av ai l abl e i t i s reasonabl e t o as ses s t he cl i ni cal resp ons e to up to tw o fl ui d c hal l enges (200m l e ach).

CVP response The chang e i n C VP afte r a 200ml fl ui d c hal l enge depe nds on the s tarti ng bl ood v ol ume (se e fi gure). A 3mm Hg ri se i n CVP re pre sents a s i gni fi cant i nc rease and i s probabl y i ndi cat i ve of an ade quate c i rcul ati ng vol ume . Howe ver, a pos i t i ve re sponse may somet i me s occur i n t he vas oconst ri cte d p ati ent wi th a l ower bl ood vol um e. It i s i mp ort ant t o ass ess the c l i ni c al res ponse i n add i t i on; i f i nade quate, i t i s ap propri at e t o m oni tor st rok e v ol ume and PAW P b efore furthe r fl ui d challe nge s or c ons i de ri ng furthe r c i rc ul atory sup port.

Stroke volume and PAWP response In the i nade quatel y fi l l ed l eft v ent ri cl e a fl ui d challe nge wi l l i ncre ase the s troke v ol ume. Failure to i nc re ase the stroke vol um e w i th a fl ui d challe nge may represe nt an i nadequate chal l enge, parti cul arl y i f t he PAW P fai l s t o ri s e si gni fi c ant l y (3m mHg ). T hi s i ndi cat es that c ard i ac fi l l i ng was i nad equate and the fl ui d c hal l e nge shoul d b e repeated . Suc h a re sponse may also be see n i n ri g ht heart fai l ure, peri c ard i al tamponad e and m i tral st enosi s . It i s i mport ant to moni tor s troke vol ume rathe r t han cardi ac out put duri ng a fl ui d c hal l enge. If the heart rate fal l s ap propri ate l y i n res ponse to a fl ui d c hal l enge the cardi ac out put may not i nc rease des pi t e an i ncreas e i n s troke vol ume . P.275

CVP and stroke volume response to fluid challenge

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Figure. No Caption Available.

See also: Central v enous cat het er— use , p 114; Pul m onary art ery cat het er—us e, p118; C ard i ac output—t hermod i l uti on, p122; Cardi a c outp ut— other i nvasi ve, p124; Cardi ac out put —non-i nvasi v e (1), p126; Cardi a c outp ut—non-i nvas i ve (2), p128; Lac tat e, p170; Col l oi ds, p180; Hyp ote nsi on, p312; Ol i guri a , p 330; Met abol i c aci d osi s, p434; D i ab eti c ket oac i dosi s , p 442; Syst emi c i nfl amm ati on/mul ti organ fai l ure, p 484; Sep si s and s ept i c shock —treat ment, p486; Burns —fl ui d manag ement, p510; Post -op erati v e i nte nsi ve care, p534

Ovid: Oxford Handbook of Critical Care

Ed itors:

Si nge r, M ervyn; We bb, An dre w R.

Ti tle : O xf ord Ha ndbook of Cr itic al Car e, 2nd Ed ition Cop yri ght © 1997,2005 M. Si nge r and A. R. W ebb , 1997, 2005. Publ i shed i n the Uni te d Stat es by Oxford Uni ve rsi ty Press Inc > Tab le of Co n te n ts > Resp ir a tor y D iso r de r s

Respiratory Disorders Dyspnoea Defi ne d as d i ffi cul t y i n b reathi ng. The resp i ratory rate may b e i ncreas ed or dec reased , t hough t he res pi rat ory effort i s us ual l y i nc reased wi th the us e of ac ces sory m usc l e s. The pat i e nt may show s i gns of p rog res si v e fati gue and

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i mp ai red gas ex change .

Commoner ICU causes Respiratory

respiratory failure

Circulatory

heart failure, hypoperfusion, pulmonary embolus, severe anaemia

Metabolic

acidosis

Central

stimulants, e.g. aspirin

Anaphylactic

upper airway obstruction, bronchospasm

Psychiatric

hysterical

Principles of management 1. O 2 the rap y t o maint ai n SaO 2 (i d eal l y >90–95%) 2. Correc t ab normal i t y where possi bl e 3. Sup port t herapy unti l re cov ery m echani cal , e .g. pos i t i ve press ure ve nti l at i on, CPAP p harmac ol ogi c al tre atm ent , e .g. bronc hod i l ators, vas odi l a tors 4. Rel i eve anxi e ty A p syc hi atri c cause of dys pnoea i s onl y made aft er exc l us i on of ot her treat abl e c aus es. Dual c o-e xi s ti ng p athol ogi es shoul d be consi dered, e. g. c hes t i nfect i on and hypov ol a emi a. P.279

See also: Oxy gen therapy, p2; Vent i l a tory s upp ort —i ndi cat i ons, p4; Ai rway obs truct i on, p 280; Res pi rat ory fai l ure, p282; At el e ctasi s and p ul m onary col l ap se, p284; Chroni c ai rfl ow l i m i t ati on, p286; Acute che st i nfect i on (1), p288; Acut e che st i nfect i on (2), p290; Acute res pi rat ory di stress sy ndrome (1), p 292; Ac ute re spi ratory d i st res s s ynd rom e (2), p294; Ast hma—ge neral manage ment , p 296; Pneumot horax, p300; Pul monary em bol us, p308; He art fai l ure—ass ess ment, p324; Heart fail ure —manag ement, p326; Acute weaknes s, p368; Sal i c yl a te poi soni ng , p 454; Anaemi a, p400; Pos t-op erati ve i nt ens i ve care, p534 P.280

Airway obstruction Causes In t he l umen, e. g. forei g n b ody , b l ood c l ot , v omi tus , s put um pl ug In t he wal l , e.g . e pi g l ot ti ti s , l arynge al oed ema, anaphyl a xi s , neop l as m Out si d e t he wal l , e.g . t rauma (fac i al , neck ), thy roi d m ass , haematom a

Presentation In s pontaneousl y breat hi ng pat i ent: s tri dor, dys pnoea, fat i g ue, cy anos i s In v ent i l ate d p ati ent (due t o i ntral umi nal ob struct i on): rai sed ai rway p res sures , d ecreas ed t i d al vol ume , hypoxae mi a , hypercapni a

Diagnosis Ches t and l at eral neck X-ray Fi breop ti c l ary ngoscopy/bronchosc opy CT s can

Management

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Presentation outside ICU/operating theatre: 1. Hi g h FIO 2 2. If c ol l ap sed or i n ext re mi s : i mmed i ate orot rache al i nt ubati on. If i mp oss i bl e, eme rge ncy cri c othyroi dotom y or trache ost omy. 3. If s ymp tom ati c b ut not in ex tre mis : c ons i de r c aus e and tre at as app rop ri a te, e. g. fi b reopti c or ri g i d bronchosc opy for remov al of forei g n b ody, surg ery for t hyroi d mas s. El ect i ve orotracheal i ntub ati on or trache ost omy may be re qui red . 4. Wi t h acut e ep i g l ot ti t i s , t he use of a t ong ue depres sor or nasendos cop y may p rec i pi tate comp l e te obst ructi on so shoul d be und ert ake n i n an operati ng the atre read y t o p erform eme rge ncy trac heos tom y. The re sponsi bl e org ani sm i s usual l y Haemop hil us influenzae and earl y tre atm ent wi th chl orampheni col s houl d be b egun. Ac ute epi gl otti ti s i s recogni sed i n ad ul t s, eve n t hos e of ad vanced ag e. 5. Cons i de r Hel i ox (79%He /21%O 2 ) alone or as a suppl eme nt to oxyg en to red uce vi scosi t y and i mp rov e airfl ow .

Presentation within ICU/operating theatre: 1. If i nt ubated : High FIO 2 Pass sucti on cat het er dow n t he e ndotracheal tube, ass ess ease of pas sag e and t he contents suc ti one d. If t he t ube i s patent, att emp t repe ated suct i on i nterspe rs ed w i th 5m l b ol uses of 0. 9% sal i ne . Urge nt fi b reopti c b ronchoscopy may be nec ess ary for d i ag nos i s and , i f p oss i bl e, rem oval of a forei gn b ody . If t hi s cannot b e removed by fi b reopti c b ronchosc opy , urge nt ri g i d bronchosc opy shoul d b e p erform ed by an e xpe ri e nce d operator. If the end otrac heal t ube i s obs truct ed, re mov e t he t ube , oxyg enate b y face mask t hen rei ntub ate . 2. If not i nt ub ated : As for out -of-ICU prese ntati on. If rece ntl y e xtubat ed, consi der l a ryngeal oede ma. Pos t-e xtubat i on l a ryngeal oede ma i s unpred i ct abl e t hough occ urs more com monl y afte r p rol ong ed or rep eat ed i nt ubati on; the i nci denc e m ay be red uce d b y p rop er tet heri ng of the e ndot rache al tub e and p rev ent i on of ex ces si v e c oug hi ng. If di a gnosed (by nase ndos copy), de xam ethasone 4mg × 3 dos es ove r 24h may re duc e t he s wel l i ng though re -i ntub ati on i s often ne ces sary i n t he i nteri m. P.281

See also: Oxy gen therapy, p2; Vent i l a tory s upp ort —i ndi cat i ons, p4; Endotrache al i nt ubati on, p36; Trac heot omy , p 38; Mi ni t rac heotom y, p 40; Fi bre opt i c bronc hos cop y, p 46; Bronc hod i l ators, p186; Steroi d s, p262; Ate l ec tas i s and pul monary col l aps e, p 284; Chroni c ai rfl ow l i m i tati on, p286; Ast hma—general m anagem ent , p 296; Haemopty si s , p 304 P.282

Respiratory failure Defi ne d as i mpaire d p ul m onary gas ex change l e adi ng to hypoxae mi a and/or hy percap ni a.

Commoner ICU causes

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Central

Cerebrovascular accident, drugs (e.g. opiates, sedatives), raised intracranial pressure, trauma

Brainstem/spinal cord

Trauma (at or above phrenic level), tetanus, Pickwickian syndrome, motor neurone disease

Neuropathy

Guillain–Barré, critical illness polyneuropathy

Neuromuscular

Muscle relaxants, organophosphorus poisoning, myasthenia gravis

Chest wall/muscular

Flail chest, heart failure, myopathy (including critical illness and disuse myopathy)

Airways

Upper airways obstruction, airway disruption, asthma, anaphylaxis

Parenchymal

Pneumonia, ARDS, fibrosis, pulmonary oedema

Extrapulmonary

Pneumothorax, pleural effusion, haemothorax

Circulatory

Pulmonary embolus, heart failure, Eisenmenger intracardiac shunt

Types of respiratory failure Typ e I: Hypox aem i c— oft en parenc hym al i n ori gi n Typ e II: Hyp oxae mi c , hype rcapni c—ofte n m echani cal i n ori g i n

Principles of management 1. Ens ure SaO 2 com pat i bl e w i th survi val (i .e. us ual l y >80%, pre ferabl y >90–95%) 2. Correc t ab normal i t y where possi bl e, e.g . drai n p neumothorax, rel i e ve/b ypass obs truct i on. 3. Sup port t herapy unti l re cov ery Posi ti v e p res sure v ent i l ati on N on-i nvasi ve res pi ratory sup port Pharmac ol ogi c al tre atm ent , e .g. bronc hod i l ators, ant i b i ot i cs , opi a te ant agoni s ts , resp i ratory s ti mul ant G ene ral me asures , e .g. hyd rat i on, ai rway hum i di fi cat i on, removal of sec re ti ons, physi otherapy, b ronchoscopy 4. Unl ess the pati ent i s sy mpt omat i c (e. g. drowsy , d ysp noe i c) whi l e be i ng me chani c al l y v ent i l a ted , t he PaCO 2 may be l eft el evated to mi ni m i se ve nti l at or traum a (p erm i ss i v e hy percap ni a).Hig her PaCO 2 v al ues may al so be tol erated i f the pati ent i s chroni call y hypercapni c (Type II resp i ratory fai l ure ). P.283

See also: Oxy gen therapy, p2; Vent i l a tory s upp ort —i ndi cat i ons, p4; C ont i nuous posi t i ve ai rway p res sure, p26; Non-i nvas i ve res pi rat ory support, p32; Endot rache al i nt ubati on, p36; Pul se ox i me try , p 90; Bl ood gas anal y si s, p100; Re spi ratory sti mul ants, p188; Opi oi d anal g esi cs , p 234; Sed ati ves , p 238; Basi c resusc i tati on, p270; Dy spnoea, p278; Ai rw ay obs truct i on, p 280; At el e ctasi s and p ul monary col l a pse , p 284; C hroni c ai rfl ow l i mi t ati on, p286; Ac ute chest i nfec ti on (1), p 288; Acut e c hes t i nfe ct i on (2), p 290; Ac ute re spi ratory d i st res s s ynd rome (1), p292; Acut e resp i ratory di s tress syndrome (2), p294; Asthma— general m anag eme nt, p296; Pneumothorax , p 300; Pul m onary emb ol us, p308; Acute weaknes s, p368; Gui l l ai n–Barré s ynd rom e, p384; My ast heni a gravi s , p 386; IC U neuromuscul ar di sorde rs, p388; Poi soni ng —ge neral pri nc i pl es , p452; Sedati ve p oi s oni ng , p458; Organophosp hat e poi s oni ng, p472; Sys tem i c i nfl am mat i on/mul ti organ fai l ure, p484; HIV rel at ed d i s eas e, p 488; Mul t i pl e t rauma (1), p500; Mul ti pl e trauma (2), p502; Head i njury (1), p504; He ad i nj ury (2), p 506; Spi nal cord i nj ury, p 508; Ne ar drowni ng, p526; Pain, p532; Pos t-operati ve i nt ens i ve care, p534 P.284

Atelectasis and pulmonary collapse A c ol l ap sed l obe or s egm ent i s us ual l y vi si b l e on a CXR. Mac roatel ect as i s i s al s o e vi d ent as vol um e l oss . In mi c roatel ec tas i s the CXR may b e norm al but A-aDO 2 wi l l be hi gh. At el e ctasi s reduc es l ung comp l i anc e and PaO 2 , and i nc re ase s work of bre athi ng . T hi s may resul t i n poor g as exc hange, i ncre ase d airw ay pre ssures , reduced ti dal vol ume and , i f s eve re, ci rcul a tory c ol l aps e.

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Causes Col l aps ed l ob e/s egm ent —bronc hi a l obst ructi on (e. g. sputum re tenti on, forei g n b ody , bl ood cl ot , vomi t us , mi s pl a ced endot rac heal t ube ) Macroat el ect asi s—air space com pre ssi on by heavy, oed ematous l ung ti ss ue, ext ernal com press i on (e. g. pl e ural effusi on, hae mot horax), sp ut um ret ent i on Mi c roatel ect asi s—i nadequate de pth of re spi rat i on, ni t rog en washout by 100% oxyg en wi t h s ubs equent ab sorpti on of oxyg en occ urri ng at a rat e g reater than rep l eni shment.

Sputum retention Exc ess mucous (sputum ) norm al l y s ti m ul a tes coughi ng . If c i l i ary c l earance i s red uc ed (e.g . s mok i ng , s edati v es) or muc ous vol um e i s e xce ssi ve (e.g . asthma, bronc hi ect asi s, cys ti c fi brosi s, chroni c bronchi ti s) sputum re tenti on m ay occ ur. Sput um ret ent i on may al so be the re sul t of i nad equate coughi ng (e .g. chroni c obs truct i ve l ung di s eas e, pai n, neurom usc ul ar di s eas e) or i nc reased muc ous vi sc osi ty (e. g. hypovol aem i a, i nade quate humi di fi c ati on of i ns pi red gas ).

Preventive measures Sputum hyd rati on—m ai ntenanc e of sy ste mi c hy drati on and hum i di fi cat i on of i nspi red gases (e .g. neb ul i ze d sal i ne /bronc hod i l ators, heated water bath, heat m oi s ture exchang i ng fi l t er). Coug h—requi res i ns pi rati on to near t otal l ung c apac i t y, gl otti c c l os ure, contracti on of abd omi nal mus cl es and rap i d openi ng of the g l ot ti s. Dynami c c omp res si on of t he airways and hi gh ve l oc i t y ex pi rat i on exp el s s ecreti ons . The proces s i s l i m i te d i f t otal l ung c apac i t y i s reduced , abdomi nal mus cl e s are weak , p ai n l i mi ts contracti on or smal l ai rway s c ol l aps e on ex pi rat i on. It i s usual t o fl ex the abdomen on coughi ng and thi s shoul d be si mul at ed i n sup i ne pat i e nts by drawi ng the kne es up. Thi s al s o l i m i ts pain i n pat i ents wi t h an uppe r abdomi nal wound. Phys i ot herap y—post ural d rai nag e, percus si on and vi b rat i on hy peri nfl a ti on, i nt erm i t tent p osi ti v e p res sure bre athi ng , i nce nti ve spi rom etry or m anual hyp eri nfl ati on. Mai ntenanc e of l ung vol um es—inc reased V T CPAP, PEEP, pos i t i oni ng to re duc e c omp res si on of l ung ti ss ue b y oede ma.

Management Spe ci fi c manage ment d epe nds on the c aus e and s houl d be correc ti ve. Al l m eas ure s t ake n for p re vent i on s houl d conti nue. If there i s l obar or s egme ntal c ol l ap se wi t h obst ruc ti on of p rox i mal airw ays , b ronchoscopy may be use ful to al l ow di rec ted sucti on, forei gn bod y remov al and saline i ns ti l l at i on. Pati ent s wi t h hi gh FIO 2 m ay det eri orate due to the effec ts of e xce ssi ve l av age or sucti on red uc i ng mi nut e v ent i l a ti on. P.285

See also: Oxy gen therapy, p2; Vent i l a tory s upp ort —i ndi cat i ons, p4; IPPV—compl i cati ons of venti l at i on, p 14; Posi ti v e e nd exp i ratory p res sure (1), p22; Pos i ti ve end exp i ratory pre ssure (2), p24; Conti nuous p osi ti ve airway pre ssure, p26; Non-i nvas i ve re spi rat ory s upp ort , p 32; Lung re crui t ment, p28; Endot rac heal i ntubat i on, p 36; Mi ni t rac heotom y, p 40; Fi b reopti c bronchosc opy , p 46; Ches t p hys i ot herap y, p 48; Bl ood gas anal ysi s, p100; Bronchodi l at ors , p 186; Chroni c ai rfl ow l i m i tati on, p286; Acut e c hes t i nfe ct i on (1), p 288; Ac ute chest i nfec ti on (2), p290; Pos t-operati ve i nt ens i ve care, p534 P.286

Chronic airflow limitation Many p ati ent s requi ri ng IC U ad mi s si on for a c omm uni ty acq ui red pne umoni a have c hroni c resp i ratory fai l ure. An acute exacerbat i on (whi c h m ay or m ay not be i nfect i on-rel a ted ) resul ts i n de com pensat i on and s ympt omati c det eri orati on. Infec ti ons res ul t i ng i n acut e e xace rb ati ons i ncl ude vi rus es, Hae mop hil us influe nzae, Kle bsi ell a and St aph. aureus i n addi ti on t o Strep. pneumoniae, Myc opl asm a pneum oni ae and Legi one lla pneum ophi la. Othe rwi se, pat i ents wi t h c oi nci dental chroni c ai rfl ow l i m i tati on (CAL) are adm i tt ed for ot her re asons or as a prophyl act i c measure i n v i ew of the i r l i mi t ed res pi rat ory funct i on, e .g. for el ec ti v e p ost -ope rat i v e ve nti l a ti on.

Problems in managing CAL patients on the ICU Di s abi l i ty d ue to chroni c i l l he al t h Fati gue , m usc l e weakne ss and dec re ased physi ol ogi cal re serve l eadi ng t o e arl i er ne ed for ve nti l at ory support , i nc reased di ffi cul ty i n weani ng, and great er phy si c al dep end enc y on s upp ort therapi e s Psyc hol ogi cal d epe ndency on sup port t herapi es More prone to pneum othoraces Usuall y have gre ate r l eve l s of sputum producti on Ri ght v ent ri cul ar dys functi on (cor p ul m onale)

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Notes Dec i si ons on whether or not to i ntub ate shoul d b e made i n consul tat i on wi th the pati ent (i f possi bl e), the fami l y, and a resp i ratory phys i c i an wi th knowl e dge of the pati e nt. The p ati ent shoul d b e g i ve n t he b ene fi t of the d oub t and i nt ub ated i n an ac ute si tuati on where a preci se hi story and quali ty of l i fe i s not know n. Tri al s of non-i nvas i v e ve nti l a tory s upp ort ± res pi ratory sti mul ants suc h as d oxep ram have shown c ons i d erabl e suc ces s i n avoi di ng i ntubat i on and m echani cal ve nti l at i on. Acc ept l ower targe t l eve l s of PaO 2 Acc ept hi ghe r t arg et l ev el s of PaCO 2 i f pat i ent i s k now n or s usp ect ed to have chroni c CO 2 retenti on on t he bas i s of e l ev ate d p l as ma bi c arb onate l ev el s on adm i s si on t o hosp i tal.

Weaning the patient with CAL An earl y tri al of ext ubati on m ay b e w ort hwhi l e be fore t he p ati ent b ecom es venti l at or-d epe nde nt. Weani ng may b e a l engt hy p roc edure . D ai l y t ri a l s of spontaneous bre athi ng may reveal fast er-than-anti ci pat ed progre ss. Prov i d e pl ent i ful enc ourage ment and p syc hol ogi cal s upp ort . Sett i ng dail y t arg ets and earl y mobi l i s ati on may be advantageous. Do not ti re by p rol onged spontaneous bre athi ng . C ons i de r g rad ual l y i ncre asi ng peri od s of s pontaneous b reathi ng i nt ers persed by pe ri ods of res t. Ens ure a good ni ght's sl eep . Use pat i ent appe arance and l ack of sym ptoms (e. g. tac hyp noea, fati gue ) rather than s pec i fi c b l ood g as val ues to judg e t he durati on of spontaneous bre athi ng . Earl y trache ost omy may be nefi t when di ffi cul ty i n we ani ng i s exp ect ed. The pat i ent m ay cop e b ett er wi t h a tracheos tom y mask than C PAP. Add i ti on of ext ri nsi c PEEP or CPAP m ay p rev ent earl y ai rways cl osure and thus reduce the work of b reathi ng . Howe ver, t hi s shoul d b e d one wi th cauti on b ecause of the ri sk of i nc re ased ai r trappi ng. Cons i de r heart fai l ure as a cause of di ffi c ul t y i n w eani ng . P.287

Key trials Brochard L, et al . Noni nvas i ve venti l at i on for acut e e xac erb ati ons of chroni c obs truct i ve pul monary di se ase. N Engl J Med 1995; 333:817–22

Ant one l l i M, et al . A compari s on of noni nv asi ve p osi ti ve-pre ssure venti l ati on and conve nti onal m echani cal v ent i l ati on i n pat i ents wi t h acut e resp i ratory fai l ure. N Engl J M ed 1998; 339:429–35

Eps tei n SK, Ci ubotaru RL. Indep end ent effec ts of e ti ol ogy of fai l ure and t i me to re i nt ubati on on outc ome for p ati ents fai l i ng e xtubat i on. Am J Res pi r Cri t Care M ed 1998; 158:489–93

P.288

Acute chest infection (1) Pat i ents may prese nt to i nt ens i ve care as a resul t of an acute c hes t i nfect i on or may de vel op i nfect i on as a com pl i cati on of i nte nsi ve care manag eme nt. Ty pi c al features i nc l ude feve r, cough, purul ent sp utum p rod uct i on, bre athl es sness , p l euri t i c pain and bronc hi a l b reathi ng. Urgent i nve sti gati on i ncl ude s arte ri al gas es, CXR, b l ood c ount and cul ture s of bl ood and s put um. In communi t y acqui re d p neumoni a, ac ute phase ant i body ti t re s s houl d be take n.

Diagnosis and initial antimicrobial treatment Bas i c re sus ci t at i on i s re qui red i f there i s c ard i oresp i ratory c omp rom i s e. App rop ri a te tre atm ent of the i nfe cti on dep end s on CXR and cul ture fi ndi ngs, al though em pi ri c ‘b est guess ’ anti bi oti c t reatment m ay be starte d b efore cul ture res ul ts are avail abl e. Tre atm ent i ncl udes physi otherapy and me thods to aid sp utum c l earance.

Clear CXR Ac ute bronc hi t i s i s as soc i at ed wi t h c oug h, muc oi d sp utum and w hee ze. In previ ous l y healthy p ati ent s a vi ral ae ti ol og y i s mos t l i k el y and there i s often an up per re spi ratory p rod rom e. Symp tom ati c rel i ef i s us ual l y al l t hat i s re qui red . Li kel y organi s ms i n acute on c hroni c b ronchi ti s i ncl ude St rep . p neumoni ae, H. in. uenz ae or Staph. aureus. App ropri ate anti b i ot i c s i ncl ude ce furoxi me or amp i ci l l i n and .ucl oxac i l l i n. Vi ral p neumoni a may be confus ed by the pre sence of bac teri a i n the sp utum b ut sec ond ary bacte ri a l i nfect i on i s common.

Pulmonary cavitation on CXR Cav i tati on s houl d al e rt to the possi bi l i t y of anaerob i c i nfect i on (s put um i s oft en foul s mel l i ng). Staph. aureus, K.

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pne umoniae or t ube rc ul osi s are also as soc i at ed wi t h c avi tat i on. App rop ri a te ant i bi oti cs i ncl ude met roni dazol e or cl i nd amyc i n for anaerobi c i nfect i on, fl uc l ox aci l l i n for Stap h. aureus and ce ftazi d i m e and g ent ami ci n for K. pne umoniae. A fore i gn body or pul monary i nfarct shoul d al so be consi d ered w here t here i s a si ngl e absc ess .

Consolidation on CXR The re cent hi st ory i s i mportant for de ci d i ng the c aus e of a pne umoni a : Hosp i t al acq ui red pne umoni a —enteri c (Gram neg ati ve) organi sm s t reated wi th ceftaz i di me and gentam i c i n, Staph. aureus t reated wi th ceftazidi me and gentam i c i n, St aph. aure us tre ate d w i th fl ucl oxaci l l i n (or tei cop l ani n/vancomy ci n i f mul t i re si stant). Rece nt asp i rati on— anae rob i c or Gram neg ati ve i nfect i on treat ed wi t h c l i ndam yci n or c efurox i me and metroni dazol e. Comm uni ty acq ui red pne umoni a i n a pre vi ousl y heal thy i ndi v i dual —Strep. pneumoniae (oft en l ob ar, ac ute ons et) or atyp i c al pne umoni a (i nsi di ous ons et, known com muni ty outbreak s, renal fai l ure and el e ctrol yte di sturbance i n Leg i onnai re' s d i se ase ). App rop ri ate ant i b i ot i c the rap y i s c efurox i me and c l ari t hromyc i n. Pneumoni a com pl i cat i ng i nfl uenza—Staph. aureus t reated wi th fl ucl oxac i l l i n. Both Staph. aureus and H. infl uenzae are c omm on i n those deb i l i tat ed by chroni c d i s eas e (e .g. al cohol i sm, di abe tes , c hroni c airfl ow l i m i tati on or t he el d erl y). Immunos upp res se d—op portuni s ti c i nfec ti ons (e. g. tub ercul osi s, Pneumocys ti s c ari nii Herpes vi ruses , C MV or fung i ). P.289

Antimicrobial treatment

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Drug

Dose

Organism

Acyclovir

10mg/kg 8-hrly IV

Herpes viruses

Amphotericin B

250mg–1g 6-hrly IV

Fungi

Ampicillin

500mg–1g 6-hrly IV

H. influenzae Gram negative spp.

Benzylpenicillin

1.2g 2–6-hrly IV

Strep. pneumoniae

Ceftazidime

2g 8-hrly IV

K. pneumoniae Ps. aeruginosa Gram negative spp.

Cefuroxime

750mg–1.5g 8-hrly IV

Strep. pneumoniae H. influenzae Gram negative spp.

Clarithromycin

500mg 12-hrly IV (250–500mg 12-hrly PO if less severe)

Atypical pneumonia Strep. pneumoniae

Erythromycin

1g 6–12-hrly (500mg 6-hrly PO if less severe)

Atypical pneumonia Strep. pneumoniae

Clindamycin

300–600mg 6-hrly IV

Anaerobes Gram negative spp.

Cotrimoxazole

120mg/kg/day IV

Pneumocystis carinii

Flucloxacillin

2g 6-hrly IV (500mg–1g 6-hrly PO if less severe)

Staph. aureus

Ganciclovir

5mg/kg 12-hrly IV (over 1h)

CMV

Gentamicin

1.5mg/kg stat IV(thereafter by levels—usually 80mg 8-hrly)

K. pneumoniae, Ps. aeruginosa Gram negative spp.

Metronidazole

500mg 8-hrly IV or 1g 12-hrly PR

Anaerobes

Teicoplanin

400mg 12-hrly for 3 doses then 400mg daily

Methicillin-resistant Staph. aureus

Vancomycin

500mg 6-hrly (monitor levels)

Methicillin-resistant Staph. aureus

Linezolid

600mg 12-hrly IV or PO

Methicillin-resistant Staph. aureus

Key trial Ire gui M et al. Cl i ni cal i m portance of del ays i n the i ni t i at i on of ap propri at e anti bi oti c treat ment for v ent i l ator-associ a ted pneumoni a. C hes t 2002; 122: 262–8

P.290

Acute chest infection (2) Laboratory diagnosis The fol l owi ng s amp l es are requi re d for l ab oratory d i ag nos i s : Sputum (e. g. cough spe ci m en, endot rac heal t ube as pi rate , p rot ect ed brush sp eci men, bronchoal v eol ar l av age spec i m en) Bl ood cul tures Serol ogy (i n com muni t y ac qui re d p neum oni a)

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Uri ne for ant i g en t es ts (i f Leg ionell a, Cand id a or p neumoc occ us sus pec ted ) In sev ere pneum oni a, bl i nd ant i bi oti c the rap y s houl d not be wi t hhe l d whi l e awaiti ng re sul ts. Sp eci mens s houl d , how ever, be t ake n b efore starti ng ant i bi ot i cs . Mi c robi ol og i cal y i el d i s usual l y v ery l ow, e spe ci al l y i f anti bi oti c t herapy has st arted before sampl i ng . Whe re cul tures are p osi ti v e t here i s ofte n m ul t i pl e g row th. Se parati ng pat hog eni c org ani sms from c ol oni si ng org ani sms may b e d i ffi cul t. In hos pi t al ac qui red pneum oni a, k now n nosocom i al pathogens are t he l i kel y s ource, e. g l ocal Gram ne gat i ve fl ora, MRSA.

Continuing treatment Ant i b i ot i cs s houl d be adjuste d accordi ng to sensi ti v i ti es onc e avai l ab l e. Failure to res pond t o t reatme nt i n 72h shoul d prompt consi derat i on of i nfect i ons more c ommon i n t he i mm unocom promi s ed or other di a gnoses . Hos pi t al -acq ui red pneumoni a requi re s t reatme nt wi t h appropri at e anti bi oti cs for 24h after s ympt oms subs i de (us ual l y 3–5 days). Afte r t hi s pe ri od c ul tures shoul d be re peated (off anti bi oti cs i f the re has bee n i mprove ment). Some ICUs wi l l use l onger c ourses —a rec ent mul ti centre s tud y s howe d no d i ffere nce i n outcome b etw een 8 and 15 day s' treatm ent . In aty pi c al or pne umococ cal pneum oni a, 10–14 day s of anti b i oti c treat ment i s usual (though no evi de nce bas e e xi s ts to i nd i c ate the op ti mal durat i on of the rap y). P.291

Key trial C has tre J, for t he PneumA Tri al Group . C ompari son of 8 v s 15 d ays of ant i b i ot i c the rap y for venti l ator-associ a ted p neumoni a i n adul ts : a randomi z ed tri al . JAMA 2003; 290:2588–98

P.292

Acute respiratory distress syndrome (1) ARD S i s the re spi rat ory component of mul t i pl e organ d ysfunc ti on. It may be predom i nant i n the cl i ni cal p i c ture or b e of l es ser cl i ni cal i mport anc e i n rel a ti on t o d ysfunc ti on of ot her organ sy st ems.

Aetiology As part of t he exagge rat ed i nfl am mat ory re sponse fol l owi ng a maj or exog enous i ns ul t w hi c h m ay b e e i ther di rec t (e. g. che st trauma, i nhalat i on i njury) or di s tant (e.g . p eri toni t i s, major hae morrhage, burns ). Hi s tol og y reveals agg reg ati on and ac ti v ati on of neutrophi l s and pl ate l et s, pat chy endot hel i a l and alve ol a r d i s rup ti on, i nt ersti ti al oed ema and fi brosi s. Cl a ssi cal l y , t he acut e p has e i s c haract eri se d b y i ncreas ed cap i l l ary pe rme abi l i ty and the fi b rop rol i ferati v e p has e (afte r 7 days) by a p red omi nant fi brot i c reacti on. Howeve r, more rece nt dat a w oul d s ugg est suc h d i s ti ncti ons are not so cl e ar-cut ; t here m ay be e vi d enc e of m ark ers of fi b rosi s as earl y as day 1.

Definitions Acute lung injury (ALI) PaO 2 /FIO 2 ≤ 300mmHg (40kPa) Regardl ess of l e vel of PEEP Wi t h b i l ateral i nfi l trates on CXR Wi t h p ul m onary art ery wed ge pre ssure <18mmHg

Acute respiratory distress syndrome (ARDS) As above but PaO 2 /FIO2≤200mm Hg (26.7kPa)

Prognosis Prognosi s de pends i n part on t he und erl yi ng i ns ul t , t he pre sence of other org an d ysfunc ti ons and t he age and chroni c health of the p ati ent . Pred omi nant s i ng l e-org an ARD S c arri e s a mortal i t y of 30–50%; the re doe s ap pear t o have be en som e i mprove ment ov er the l a st dec ade . Som e d ete ri orat i on on l ung functi on tes ti ng i s usual l y d ete ctabl e i n s urv i vors of ARD S, even i n t hos e who are rel at i ve l y asym ptomat i c . Re cent s tud i es i ndi cat e t hat a si g ni fi cant proporti on of s urvi v ors of ARD S have physi cal and /or ps ychol ogi c al seq uel ae at 1 y ear. P.293

Key trials Bernard GR for the The Ameri can–European C ons ens us Confere nce on AR DS. De fi ni t i ons, mec hani sm s, rel evant out com es, and c l i ni c al tri al coordi nati on. Am J Re spi r C ri t Care Med . 1994; 149:818–24

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Herri dge MS, Cheung AM for the Canadi an Cri ti cal Care Tri al s Group. One-year outc ome s i n s urv i vors of the ac ute res pi rat ory di stres s s ynd rom e. N Engl J M ed 2003; 348:683–93 Marshall RP, et al . Fibroprol i ferat i on oc curs e arl y i n t he acute res pi rat ory di stress sy ndrome and i mpacts on outcome. Am J R esp i r Cri t C are Me d 2000; 162:1783–8

See also: Oxy gen therapy, p2; Vent i l a tory s upp ort —i ndi cat i ons, p4; IPPV—compl i cati ons of venti l at i on, p 14; Posi ti v e e nd exp i ratory p res sure (1) Pos i ti ve end ex pi ratory pre ssure (2), p 24; Conti nuous p osi ti ve ai rway press ure , p 26; Lung rec rui tm ent , p 28; Prone pos i ti oni ng, p30; Extracorp ore al res pi ratory sup port, p34; End otracheal i ntubat i on, p 36; Bl ood gas anal y si s , p 100; Bact eri ol ogy, p158; Vi rol ogy, se rol ogy and as says, p160; Col l oi d osmoti c pres sure, p172; Col l oi ds , p180; Bronc hod i l ators, p186; N i tri c oxi de , p190; Surfac tant, p192; Ant i mi crobi a l s , p 260; Ste roi ds , p 262; Prostagl andi ns , p 264; Basi c re sus ci tat i on, p 270; Acute che st i nfect i on (1), p288; Acut e c hes t i nfe cti on (2), p 290; Ac ute re spi rat ory di st res s s ynd rom e (2), p294; Inhal at i on i njury, p306; Infe cti on—di a gnosi s , p 480; Infect i on—t reatment, p482; Sys tem i c i nfl am mat i on/mul ti org an fai l ure, p484; Se psi s and sep ti c s hoc k—t reatme nt, p486; Mul ti p l e trauma (1), p500; M ul t i p l e trauma (2), p 502; Py rex i a (1), p 518; Pyre xi a (2), p 520 P.294

Acute respiratory distress syndrome (2) General management 1. Remove t he cause whe nev er pos si b l e, e. g. drain pus , anti bi oti c t herapy , fi x l ong bone fracture. 2. Sed ate wi t h an opi a te–benzod i azepi ne com bi nati on as mec hani cal v ent i l ati on i s l i k el y to be prol onge d. Dos es shoul d be kep t t o t he l ow est possi bl e but c ons i s tent wi th ade quate sed ati on. 3. Musc l e re l ax ati on i s i nd i c ated i n s evere ARDS t o i mprove che st wal l c omp l i anc e and g as exc hange. 4. Haem ody nam i c mani pul at i on wi th ei t her fl ui d, di l ators, press ors, di uret i c s and/or i not ropes may i m prove oxyg enati on. Thi s m ay be achi eve d b y e i ther i nc re asi ng cardi a c outp ut, and t hus mi xed ve nous s aturat i on i n l ow outp ut st ate s, or by d ecreas i ng c ard i ac output t hereby l e ngt heni ng pul monary t ransi t t i me s i n hi gh output states . Care shoul d be taken not t o c ompromi se the ci rc ul a ti on.

Respiratory management 1. Mai ntai n adeq uat e g as exc hange w i t h i ncreas ed FIO 2 and, de pendi ng on s everi t y, ei t her non-i nvasi v e resp i ratory sup port (e .g. CPAP, Bi PAP) or p osi ti ve p res sure vent i l ati on. Sp eci fi c modes may b e ut i l i se d, suc h as p res sure cont rol l e d i nve rse rati o ve nti l a ti on. Whi l e general agre eme nt exi sts for m i ni mi s i ng VT (6-7m l /k g) and pl a teau ins pi ratory pre ss ure s (≤ 30c mH 2 O) i f p oss i b l e, there i s no conse nsus regardi ng the up per de si red l ev el of FIO 2 and PEEP. Gre ate r e mphasi s i s c urrentl y pl ace d on hi gher l ev el s of PEEP (up to 20c m H 2 O) Whi l e the c urrent European v i ew favours the us e of hi ghe r F IO 2 (up to 1. 0), a c omm on US app roach i s to keep the F IO 2 ≤0.60 but to m ai ntai n SaO 2 wi th hi ghe r l eve l s of PEEP. A rece nt s tudy ass ess i ng hi ghe r l eve l s of PEEP s howe d no outc ome bene fi t . 2. Non-venti l atory res pi rat ory support tec hni ques s uc h as ECCO 2 R can be us ed i n sev ere AR DS but have yet to show conv i nci ng b ene fi t ove r c onv ent i onal venti l at ory te chni ques. 3. Bl ood gas val ues shoul d b e aime d at m ai ntai ni ng s urvi v al wi t hout s tri vi ng t o achi eve normalit y. Permi s si ve hype rc apni a, whe re PaC O 2 val ues are allowed to ri se, somet i me s above 10kPa, has been as soc i at ed wi t h outc ome be nefi t. Ac cep tab l e l ev el s of SaO 2 are controversi al ; i n ge neral , value s ≥ 90–95% are targe ted but i n seve re ARD S t hi s m ay b e rel a xed to 80–85% or ev en l ow er provi d ed org an functi on rem ai ns adeq uat e. 4. Pati ent posi ti oni ng m ay provi d e i mprove ment s i n gas exc hange. Thi s i nc l udes ki net i c the rap y usi ng s pec i al rot ati onal b eds , and p rone p osi ti oni ng wi t h t he pat i ent b ei ng t urned fre que ntl y t hrough 180°. Care has to be take n d uri ng prone pos i t i oni ng to preve nt tub e d i sp l ac eme nt and shoul der i njuri es . 5. Inhal e d ni tri c oxi de or epoproste nol i m proves gas e xchang e i n s ome 50% of pat i e nts , t hough no outc ome be nefi t has bee n s how n. 6. Hi g h d ose st eroi ds commenced at 7–10 day s are benefi ci a l i n 50–60% of p ati ent s, at l e ast i n te rms of i m provi ng gas exc hange. 7. Surfac tant t herapy i s current l y not i ndi c ate d for ARD S. 8. Venti l ator t rauma i s ubi qui tous. Mul ti pl e pneum othoraces are c omm on and may re qui re mul ti pl e chest drai ns. They may b e di ffi cul t to di a gnose by X-ray and, de spi te the at tendant ri s ks, CT scanni ng may re veal undi ag nos ed p neumot horace s and ai d corre ct si ti ng of c hes t d rai ns. P.295

Key trials Ac ute Res pi rat ory Di stress Synd rom e Ne twork. Ve nti l a ti on wi th l ower ti dal vol um es com pared w i t h t rad i ti onal t i d al vol ume s for acute l ung i njury and the ac ut e resp i ratory d i st re ss syndrome. N Engl J Med 2000; 342:1301–8 Hi c kl i ng KG , et al . Low mortal i t y rate i n ad ul t re spi rat ory di st res s s ynd rom e usi ng l ow-vol ume , pres sure-l i mi ted venti l at i on wi th permi s si v e hype rcapni a: a pros pec ti v e s tud y. Cri t C are Med 1994; 22:1568–78

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Med uri GU, e t al. Effect of prol onge d me thy l pred ni s ol one the rap y i n unre sol vi ng acut e resp i ratory di s tre ss syndrome: a rand omi zed control l ed tri al . JAMA 1998; 280:159–65 Gat ti noni L, e t al for the Prone-Sup i ne Stud y Group. Effe ct of prone pos i ti oni ng on the survi val of pati e nts wi th acute res pi rat ory failure. N Eng l J Med 2001; 345:568–73

See also: Oxy gen therapy, p2; Vent i l a tory s upp ort —i ndi cat i ons, p4; IPPV—compl i cati ons of venti l at i on, p 14; Posi ti v e e nd exp i ratory p res sure (1) Pos i ti ve end ex pi ratory pre ssure (2), p 24; Conti nuous p osi ti ve ai rway press ure , p 26; Lung rec rui tm ent , p 28; Prone pos i ti oni ng, p30; Extracorp ore al res pi ratory sup port, p34; End otracheal i ntubat i on, p 36; Bl ood gas anal y si s , p 100; Bact eri ol ogy, p158; Vi rol ogy, se rol ogy and as says, p160; Col l oi d osmoti c pres sure, p172; Col l oi ds , p180; Bronc hod i l ators, p186; N i tri c oxi de , p190; Surfac tant, p192; Ant i mi crobi a l s , p 260; Ste roi ds , p 262; Bas i c re sus ci t at i on, p 270; Acute che st i nfect i on (1), p 288; Acut e c hes t i nfe cti on (2), p290; Ac ute re spi rat ory di st res s syndrome (2), p294; Inhalat i on i njury, p306; Infe cti on—di a gnosi s, p480; Infec ti on—tre atm ent , p 482; Sy ste mi c i nfl am mat i on/mul ti organ fai l ure, p484; Seps i s and se pti c shock—tre atm ent , p 486; Mul ti pl e traum a (1), p500; Mul ti p l e trauma (2), p 502; Pyrexi a (1), p518; Pyrexi a (2), p520 P.296

Asthma—general management Pathophysiology Ac ute bronc hos pas m and m ucus p l ug gi ng, oft en sec ond ary to an i nsul t s uc h as i nfec ti on. The pati ent may progress to fat i gue, res pi rat ory fai l ure and col l a pse . T he ons et may dev el op s l ow l y over days, or oc cur rapi dl y wi thi n m i nutes to hours.

Clinical features Dys pnoe a, whe eze (ex pi ratory ± i nsp i ratory), di ffi cul ty i n talki ng, us e of acce ssory res pi rat ory mus cl es, fati g ue, agi tat i on, c yanosi s, com a, c ol l ap se. Pul sus parad oxus i s a poor i nd i cati on of s everi t y; a fati g ui ng p ati ent c annot g ene rat e s i g ni fi cant res pi rat ory swi ngs i n i ntrathorac i c press ure . A ‘ si l ent ’ c hes t i s al s o a l a te s i g n s ugg est i ng se verel y l i mi ted ai rfl ow. Pneumot horax and l ung/l ob ar col l ap se.

Management of asthma As thm ati cs mus t b e m anag ed i n a w el l -moni t ore d area. If c l i ni cal feat ure s are sev ere , t hey shoul d b e ad mi tte d t o an i nt ens i v e c are uni t where rapi d i ns ti t ut i on of mec hani cal v ent i l ati on i s availabl e . M oni tori ng shoul d c omp ri se, as a mi ni mum, pul se oxi met ry, conti nuous ECG, regul ar b l ood pres sure m eas ure ment and b l ood g as analys i s. If se vere, an i nt ra-arteri al cannul a ± c ent ral ve nous acce ss shoul d be i nserted . 1. Hi g h FIO 2 (≥0.60) t o maintai n SpO 2 ≥95%. 2. Nebul i sed β 2 -agoni s t (e.g . s al b utamol )—may b e repe ate d ev ery 2–4h or, i n se vere attacks , admi ni s tered cont i nuousl y 3. IV ste roi ds for 24h t hen oral pre dni sol one . N ebul i sed i p rat rop i um bromi de may gi ve addi ti onal b ene fi t . 4. IV bronchodi l at ors , e .g. salbutam ol , magne si um s ul p hat e. 5. Excl ud e pneum othorax and l ung/l obar c ol l aps e. 6. Ens ure ade quate hyd rat i on and fl ui d repl ac ement. 7. Comm enc e anti bi oti c s (e.g . c efurox i me ± c l a ri t hromyc i n) i f st rong e vi d enc e of b act eri al che st i nfect i on. Gre en sputum doe s not nec ess ari l y i ndi c ate a bac teri al i nfec ti on. 8. If no resp ons e t o abov e me asures or i n e xtremi s c ons i de r: IV s al b utamol i nfus i on Epi nephri ne SC or b y nebul i s er M echani cal ve nti l at i on Anec dot al suc ces s has bee n reporte d w i th subanaes the ti c doses of a v ol a ti l e anae st het i c age nt suc h as i sofl urane whi ch both cal ms/sed ate s and b ronchodi l at es.

Indications for mechanical ventilation Inc reasi ng fati gue and ob tundat i on Resp i ratory fai l ure—ri s i ng PaCO 2 fal l i ng PaO 2 Card i ov asc ul ar col l ap se

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Facilitating endotracheal intubation Sum mon se ni or assi st anc e. Pre -oxy genate wi th 100% O 2 . Pe rform rap i d se quence i nduc ti on w i th suxam ethoni um and etomi d ate or ke tam i ne . ‘ Bre athi ng down’ wi th an i nhal a ti onal anaes the ti c (e .g. i s ofl urane) pre- i nt ubati on s houl d onl y be att emp ted by an exp eri enc ed cl i ni ci a n. To mi ni ms e b arotrauma, c are shoul d b e t aken to av oi d ex ces s air trappi ng , hi g h airway pre ssure s and hi g h t i dal v ol umes . P.297

Drug dosage Epinephrine

0.5ml 1:1000 solution SC or 2ml 1:10,000 solution by nebuliser

Hydrocortisone

100–200mg qds

Ipratropium bromide

250–500µg qds by nebuliser

Prednisolone

40–60mg od initially

Salbutamol

2.5–5mg by nebuliser 5–20µg/min by IV infusion

Magnesium sulphate

1.2–2.0g IV over 20min

See also: Oxy gen therapy, p2; Vent i l a tory s upp ort —i ndi cat i ons, p4; Endotrache al i nt ubati on, p36; Pul s e ox i me try , p 90; Bl ood gas anal y si s , p 100; Bact eri ol ogy, p158; Bronchodi l a tors, p186; Se dat i ve s, p238; Ste roi ds , p 262; Dy spnoea, p278; As thm a—ve nti l a tory m anag eme nt, p298; Anaphyl a ctoi d reacti ons , p 496 P.298

Asthma—ventilatory management Early period 1. Ini ti a l l y gi ve l ow V T (5ml /kg ) b reaths at l ow rate (5–10/mi n) t o asse ss deg ree of bronc hos pas m and air trapp i ng . Sl owl y i ncre ase V T (to 7-8ml /kg) ± i nc rease rat e, tak i ng care to avoi d si g ni fi cant ai r t rap pi ng and hi g h i ns pi ratory pre ss ure s. Low rates wi th prol onged I:E rati o (e .g. 1:1) m ay be advantageous. Av oi d ve ry short expi ratory t i me s.D o not stri ve to ac hi e ve normoc apni a. 2. Adm i ni ste r m usc l e re l ax ant s for a mi ni mum 2–4h, unt i l se vere bronc hos pas m has abated and g as e xchang e i mp rov ed. Al though at rac uri um may cause hi stami ne rel e ase , i t d oes not appear c l i ni c al l y to w ors en bronchosp asm . 3. Sed ate wi t h e i t her st and ard med i c ati on or wi t h agents suc h as k etam i ne or i sofl urane that have bronc hod i l ati ng properti e s. Ket ami ne g i v en alone m ay cause hal l uc i nati ons whi l e i s ofl urane carri e s a theoreti cal ri sk of fl uori de toxi ci ty. 4. If s i g ni fi cant ai r trap pi ng remains , c ons i de r v ent i l ator d i sc onnect i on and forc ed manual chest compress i ons e very 10–15mi n 5. If s eve re bronchosp asm pe rsi st s, consi d er i nj ect i ng 1–2ml of 1:10, 000 ep i ne phri ne down endotracheal tube. Repe at at 5mi n i nte rvals as nec ess ary .

Maintenance 1. Ens ure ade quate rehydrati on. 2. Gene rous humi di fi c ati on shoul d be gi ven to l oose n mucus p l ug s. Use a heat –moi st ure ex change r p l us ei ther hourl y 0. 9% s al i ne neb ul i se rs or i ns ti l l a ti on of 5ml 0.9% s al i ne down the e ndotrache al tub e. 3. Phys i ot herap y as si sts mobi l i s ati on of s ecret i ons and removal of mucus pl ugs . Hype rve nti l at i on s houl d be avoi ded . 4. Wi t h i mprove ment , g radual l y normalis e v ent i l a tor se tt i ng s (V T , rate, I:E rati o) t o achi eve normocap ni a be fore al l owi ng pat i ent t o waken and b reathe sp ont aneousl y 5. Cons i de r p neumot horax or l ung/l obar c ol l aps e i f acut e d ete ri orati on occurs. 6. If m ucus p l uggi ng consti tut es a m ajor p rob l em , i nst i l l at i on of a m ucol yt i c (N-ace tyl cy ste i ne ) m ay b e c ons i d ere d though thi s may i nd uc e furt her bronc hos pas m. Bronchosc opi c removal of pl ugs shoul d onl y be pe rforme d by an expe ri enc ed operator.

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Assessment of air trapping (intrinsic PEEP, PEEPi) Meas ure PEEPi by press i ng end-e xpi rat ory hol d but ton of venti l at or. No p aus e b etw een exp i ratory and i ns pi rat ory sound s. Di s connec ti on of v ent i l a tor and t i mi ng of aud i bl e e xpi rat ory wheeze. An i nc reasi ng PaCO 2 m ay resp ond to re duc ti ons i n mi nut e v ol ume w hi c h w i l l l ower t he l eve l of i ntri nsi c PEEP.

Weaning Bronchosp asm may i ncreas e on l i ghteni ng se dat i on due t o aw are nes s of e ndot rache al tub e and i nc reased coug hi ng. May nee d t ri a l of e xtubat i on whi l e st i l l on hi gh FIO 2 Cons i de r e xtubat i on under i nhal at i onal or short-act i ng IV s edat i on. space out i nterval s b etw een β 2 ag oni st neb ul i sers. Convert othe r anti ast hmati c d rug s t o oral me di c ati on. Theop hyl l i ne dos es shoul d be ad jus ted to ens ure t herape uti c l eve l s. P.299

See also: Oxy gen therapy, p2; Vent i l a tory s upp ort —i ndi cat i ons, p4; Endotrache al i nt ubati on, p36; Pul s e ox i me try , p 90; Bl ood gas anal y si s , p 100; Bact eri ol ogy, p158; Bronchodi l a tors, p186; Se dat i ve s, p238; Ste roi ds , p 262; Dy spnoea, p278; As thm a—ge neral manage ment, p296; Anap hyl ac toi d reac ti ons, p496 P.300

Pneumothorax Si gni fi c ant col l ect i on of ai r i n t he pl e ural s pac e t hat may oc cur s pontaneous l y , fol l owi ng t rauma (i ncl udi ng i at rogeni c), as thma, chroni c l ung d i se ase , and i s a c ommon s equel of vent i l ator t rauma.

Clinical features May be asy mpt omat i c . Dys pnoe a, pai n. Dec reased breat h s ound s, hyp er-res onant, as ymm etri c che st exp ans i on—may b e d i ffi cul t to ass ess i n a vent i l ate d p ati ent . Resp i ratory fai l ure and det eri orati on i n g as exc hange. Inc reasi ng airw ay pre ssures and d i ffi cul t y t o ve nti l a te. Card i ov asc ul ar det eri orati on w i th me di a sti nal s hi ft (tensi on).

Diagnosis CXR— mos t e asi l y see n on e rec t v i ew s where ab sent l ung marki ngs are s een l a teral to a w el l -de fi ned l ung b ord er. Howe ver, v ent i l a ted pati e nts are ofte n i mag ed i n a supi ne p osi ti on; pneumothorax may b e easi l y m i s sed as i t may be l yi ng ant eri or to normal l ung gi vi ng t he m i s l eadi ng appe arance of l ung m ark i ng s on t he rad i og rap h. Sup i ne pneumothorax shoul d b e c ons i de red i f the fol l owi ng are se en: Hyperl ucent l ung fi el d compared to the c ont ral ate ral si de Loss of cl ari ty of the di aphrag m outl i ne ‘ Dee p s ul c us’ si gn, gi vi ng the app earanc e of an i nve rte d d i ap hragm A parti cul ar cl ear part of the cardi ac contour A l a teral fi l m m ay hel p. Tensi on p neumot horax res ul t s i n m ark ed medi as ti nal shi ft away from the affec ted s i de . Ul trasound —may b e he l pful but i s hi ghl y ope rat or dep end ent CT sc an— very s ens i t i ve and may b e useful i n di ffi c ul t si tuati ons , e .g. AR DS, and t o d i re ct drainage of l ocalis ed pne umothorax Pne umothorax mus t be d i s ti ngui she d from bul l a e, esp eci al l y w i t h l ong -st andi ng emp hys ema; i nad vertent d rai nag e of a b ul l a m ay cause a bronc hop l e ural fi st ul a . Ass i st anc e s houl d be sought from a radi ol ogi s t.

Management 1. Inc rease FIO 2 i f hy pox aem i c. 2. If l i fe-thre ateni ng wi th ci rcul at ory c ol l aps e, need l e asp i rate pl eura on affec ted si de, fol l owed by formal c hes t

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drain i ns ert i on. 3. Repe ate d needl e aspi rati on m ay b e s uffi ci ent i n s pontaneous l y breat hi ng p ati ent s w i thout re spi ratory fai l ure ; howe ver, t hi s i s not rec omme nde d i f t he pat i ent i s v ent i l a ted . 4. Ches t d rai n i ns ert i on. T hi s may b e d one und er ul t rasound or CT g ui d anc e, esp eci al l y i f l oc al i sed due t o surroundi ng l ung fi bros i s. A s mal l pneumot horax (<10% hemi thorax ) m ay b e l eft undraine d b ut prompt ac ti on s houl d be i ns ti tut ed i f cardi ore spi rat ory de teri orat i on oc curs. Pat i ents shoul d not b e t ransfe rred b etw een hospi tal s, parti cul arl y b y p l ane, wi t h an undrai ned pne umothorax . D rai ns may be rem ove d i f not swi ngi ng/bub bl i ng for se veral day s.

Bronchopleural fistula Denote d b y c ont i nual drainage of ai r. Usually re sponds to conse rvati v e t reatme nt wi t h c ont i nual app l i cat i on of 5kPa neg ati ve pre ssure; thi s may take week s t o resol ve . F or seve re l eak and/or com promi s ed vent i l ati on, hi gh fre que ncy jet ve nti l at i on and/or a doubl e l ume n endob ronchi al tube may be consi d ere d. Surgi cal i nterventi on i s rarel y nec ess ary . P.301

Chest X-ray appearance

Figure. No Caption Available.

See also: IPPV—c omp l i cat i ons of ve nti l a ti on, p14; Hi gh freq uency venti l at i on, p 20; Ches t d rai n i ns ert i on, p 42; Cent ral ve nous cat het er— inserti on, p116; Basi c resusci tati on, p270; Res pi rat ory fai l ure, p282; Acute res pi rat ory di stres s s ynd rom e (1), p 292; Acut e resp i ratory di s tress sy ndrome (2), p 294; Mul ti p l e traum a (1), p500; M ul t i p l e trauma (2), p 502 P.302

Haemothorax Usual l y s econdary to che st trauma or fol l owi ng a proce dure, e.g . c ard i ac surge ry, chest drai n i nse rti on, ce ntral venous cathe ter i nserti on. Sp ont ane ous hae mot horax i s very rare , e ven i n pat i e nts wi th cl otti ng di sorders.

Clinical features Stony d ul l ne ss. Dec reased breat h s ound s. Hypovol aem i a and det eri orati on i n gas ex change (i f l arg e).

Diagnosis Ere ct CXR— bl unt i ng of hem i d i ap hragm and progress i ve l oss of bas al l ung fi el d Sup i ne CXR—i ncreas ed opac i t y of affec ted he mi t horax pl us d ecreas ed cl a ri ty of c ard i ac c ont our on that s i d e. Large bore ne edl e aspi rati on t o c onfi rm prese nce of bl ood. A small bore need l e may be unabl e to as pi rat e a haem othorax i f i t has cl otte d.

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Management 1. If s mal l , obs erve w i th se ri al X-rays and moni tor for s i gns of c ard i oresp i ratory det eri orati on. 2. Ens ure any coagul op athy i s c orrec ted by adm i ni st rat i on of fresh froze n p l as ma and/or pl a tel ets as i ndi cat ed. 3. Ens ure that cross-mat che d b l ood i s avai l ab l e for urgent t ransfusi on i f nece ssary. 4. If s i g ni fi cant i n si ze or p ati ent b ecom es sym ptomat i c, i nsert l arge bore c hes t d rai n, e.g . s i ze 28 Fr. T he drain shoul d be di rec ted poste ro-i nferi orl y t oward the de pendent area of l ung and pl a ced on 5kPa s uct i on. 5. If d rai nage e xce eds 1000m l or > 200ml /h for 3–4h de spi te corre cti ng any coagul op athy, c ont ac t t horaci c s urg eon. 6. Fact or VIIa may be consi d ere d for i nt rac tabl e bl eed i ng , t hough onl y anecd otal report s of be nefi t exi st. 7. Drains i nserted for a haemot horax may be re move d afte r 1–2 day s i f no furt her bl eed i ng oc curs. Perforati on of an i nt erc ost al ves sel duri ng che st drain i ns erti on m ay c aus e c ons i de rab l e bl eedi ng i nto the pl eura. If dee p t ens i on sutures around the c hes t d rai n fai l t o s tem bl ood l os s, re move the c hes t d rai n and i ns ert a Fol ey ure thral cathe ter through the hol e. Infl a te the bal l oon and app l y tract i on on the cathe ter t o tamponad e t he bl e edi ng ves sel . If t hes e m eas ure s fai l , c ont act a thorac i c surge on. P.303

See also: Che st drain i ns erti on, p42; Central v enous cat het er—ins erti on, p116; Bl ood trans fus i on, p182; Bl ood p rod uct s, p252; Coagul ant s and ant i fi bri nol yt i cs , p 254; Ap rot i ni n, p256; Pneum othorax, p300; Bl eed i ng di sorders, p396 P.304

Haemoptysis May range from a few sp eck s of bl ood i n ex pec torate d s put um to mas si v e p ul m onary haem orrhage. More l i kel y t o d i s rup t g as exc hange b efore l i fe-t hre ate ni ng hypovol aem i a ens ues . May be a pres ent i ng fe ature of a pati e nt adm i tt ed to i nt ens i ve care or may re sul t from cri t i cal i l l nes s and i ts tre atm ent .

Causes Massive haemoptysis Di s rup ti on of a bronc hi a l arte ry by acute i nfl am mat i on or i nvas i on (e .g. pul monary ne opl asm , t rauma, cavi t ati ng TB, bronc hi e ctasi s , l ung ab sc ess and as pergi l l oma). Rupt ure of arteri ov enous mal format i ons and bronchovascul ar fi st ul a e. Pul monary i nfarc ti on sec ond ary to prol onge d pul m onary art ery cat het er wed gi ng or p ul monary art ery rupt ure .

Minor haemoptysis Int rap ul m onary i nfl am mat i on or i nfarcti on (e. g. pul monary emb ol us) Endotracheal tube t rauma (e. g. muc osal e ros i on, b al l oon ne crosi s , t rauma from t he tub e t i p, traum a t o a trache ost omy st oma, traum a from sucti on cat het ers ). Ti s sue break down i n cri t i call y i l l pat i ents (e. g. ti s sue hy pop erfusi on, coagul op athy, poor nutri ti onal state, se psi s and hyp oxaemi a.)

Investigation and assessment Urg ent as ses sme nt of cardi ores pi rat ory funct i on and c ard i oresp i ratory moni tori ng are req ui red. Massi ve hae mop tys i s may re qui re res usc i t ati on and urgent i ntubat i on. T he di a gnosi s may b e s ugg est ed by t he hi s tory and a C XR may i de nti fy a c avi tat i ng l esi on. Lower l obe s had owi ng on a CXR m ay be the re sul t of ov ers pi l l of bl ood from el se where i n the bronc hi al tre e. Earl y surgi c al i nterventi on s houl d be prompt ed by a chang i ng ai r-fl ui d l ev el , persi ste nt opaci fi c ati on of a previ ous cavi t y or a mobi l e m ass . Earl y b ronchoscopy may i d ent i fy the source of haem opt ysi s, al t hough onl y w hi l e b l ee di ng i s act i ve . Bl ood i n m ul t i pl e b ronchi al ori fi ces may b e c onfusi ng but saline l avage m ay l eave the sourc e v i si bl e. R i gi d b ronchosc opy i s us eful i n m ass i ve haemop tys i s al l ow i ng oxy genati on and wi de bore suc ti on.

Management Bas i c res usc i t ati on (hi gh FIO 2 , endot rac heal i ntubat i on and b l oodtrans fus i on) i s need ed for cardi ore spi ratory comp rom i s e. Correc ti on of coagul op athy i s a pri ori t y. Bronchosc opy al l ow s d i re ct i ns ti l l a ti on of 1 i n 200,000 epi nep hri ne i f the sourc e of haemorrhag e c an b e found or,

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al t ernati vel y, end obronc hi a l t amp onade w i t h a bal l oon c athete r. In c as es of s eve re hae morrhage from one l ung a doubl e l umen end otrac heal t ube may preve nt som e ov ers pi l l to the other l ung w hi l e d efi ni ti v e t reatme nt i s org ani sed . Defi ni ti v e t reatme nt may i ncl ude rad i ol ogi cal bronchi al art ery em bol i sati on, or surgi cal re sec ti on. Ind uce d hy pot ens i on may b e useful i n bronchi al artery haem orrhag e. In c as es of p ul m onary art ery haemorrhage , PEEP may be us ed w i t h me chani c al venti l at i on to re duc e p ul m onary bl e edi ng. P.305

See also: Oxy gen therapy, p2; Vent i l a tory s upp ort —i ndi cat i ons, p4; Posi ti v e e nd expi ratory p res sure (1), p22; Posi ti ve e nd exp i ratory p res sure (2), p24; Cont i nuous p osi ti v e airw ay pre ssure, p26; Endot rac heal i nt ubati on, p36; Fi bre opt i c bronchosc opy , p 46; Bl ood trans fus i on, p 182; Bl ood prod uct s, p252; C oagul ants and anti fi b ri nol y ti cs, p254; Basi c res us ci t ati on, p270; Acute che st i nfect i on (1), p 288; Acut e c hes t i nfe cti on (2), p290; Pul monary em bol us, p308; Bl eedi ng di sorders, p396; Amni oti c fl ui d e mbol us , p 544 P.306

Inhalation injury Causes i ncl ude smoke, st eam , noxi ous gas es and as pi rati on of gas tri c contents.

Clinical features Dys pnoe a, coughi ng Stri dor (i f upp er ai rway ob struct i on) Bronchosp asm Si g ns of l ung/l obar c ol l aps e (esp eci al l y w i th as pi rat i on) Si g ns of res pi ratory fai l ure Cherry-red sk i n col our (c arbon monoxi de) Agi tat i on, c oma ARD S (l at e)

General principles of management 1. 100% O 2 2. Earl y i nt ubati on i f uppe r airw ay com promi s ed or threat ene d. 3. Earl y bronchosc opy i f i nhal ati on of soot , d ebri s , v omi t s usp ect ed.

Specific conditions Smoke inhalation Smok e rare l y causes thermal i njury b eyond t he l ev el of bronchi as i t has a l ow s pec i fi c heat c ont ent . Howev er, soot i s a maj or i rri t ant to the uppe r airw ays and can p rod uce ve ry rap i d and marke d i nfl amm ati on. Urg ent l a ryngos cop y s houl d be p erform ed i f soot i s p res ent i n t he nare s, mouth or pharynx. If s oot i s s een or the l a rynx appe ars i nfl a med , p erform earl y endot rac heal i ntubat i on. As t he upp er ai rway can obst ruct wi t hi n mi nut es i t i s ad vi s abl e t o i ntubat e as a prophyl a cti c m eas ure rathe r t han as an eme rge ncy where i t may prove i mp oss i bl e. Aft er i nt ubati on, perform urge nt bronchosc opy wi th bronchi al t oi l et usi ng warmed 0. 9% s al i ne to re move as much soot as pos si b l e . Comm enc e b enz yl p eni ci l l i n 1.2g qd s IV. Spe ci fi c tre atm ent for p oi s ons containe d w i thi n smoke (e.g . c arbon monoxi de, cy ani de)

Steam inhalation Cons i de r e arl y/p rop hyl ac ti c i ntub ati on Ste am has a m uch hi ghe r heat conte nt than s moke and c an cause i nj ury to the whol e re spi ratory t rac t. Cons i de r e arl y b ronchosc opy and l a vag e w i th cool 0.9% s al i ne.

Aspiration of gastric contents

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Earl y bronchosc opy and physi ot herapy to rem ove as muc h p arti c ul a te and l i qui d m att er as pos si bl e . Ei t her ce furoxi me pl us m etroni dazol e , or c l i ndam yci n for 3–5 days. Ste roi d t herapy has no prove n b ene fi t . P.307

See also: Oxy gen therapy, p2; Vent i l a tory s upp ort —i ndi cat i ons, p4; Endotrache al i nt ubati on, p36; Fi breopt i c bronc hos cop y, p46; Bl ood g as analys i s, p100; Ant i m i crobi al s , p 260; Ai rway obst ruc ti on, p280; Inhal e d p oi s ons , p 466; Burns—fl ui d manage ment , p 510; Burns— general m anagem ent , p 512 P.308

Pulmonary embolus Aetiology Usuall y ari s es from a dee p v ei n throm bos i s i n fem oral or p el v i c vei ns . The ri s k i ncreas es aft er prol onged i mmobi l i s ati on and wi th pol ycy thaemi a or hypervi scosi t y d i s ord ers . Amni ot i c fl ui d emb ol us. Fat emb ol us afte r p el v i c or l ong b one traum a. Ri ght heart s ource , e. g. mural throm bus .

Clinical features Pl euri ti c -ty pe che st pai n, dys pnoea, ± haem opt ysi s. The pat i ent w i th a maj or embol us often prefe rs to l i e fl at . D ysp noea i m proves due t o i ncreas ed venous re turn and ri ght he art l oadi ng. Det eri orati on i n g as exc hange—may fi nd a l ow PaO 2 l ow or hi gh PaC O 2 and a met abol i c ac i dosi s. Howe ver, t hes e .ndi ng s are i nc ons i st ent and non-di a gnosti c. Card i ov asc ul ar feat ures, e.g . t achycard i a, l ow/hi gh BP and col l aps e. CXR: may be normal b ut a m ass i ve emb ol us may produc e fewer vasc ul a r m ark i ng s (pul monary ol i gaemi a) i n a hemi thorax ± a b ul g i ng pul monary hi l um. A w edg e-s hap ed p eri pheral p ul m onary i nfarc t m ay be s een after a few days fol l owi ng a sm al l er emb ol us. ECG: ac ute ri ght ve ntri c ul a r s trai n, i .e. S 1 Q 3 T 3 , t ac hyc ard i a, ri ght ax i s dev i at i on, ri g ht bundl e branc h b l oc k, P pul monale. Echocardi ogram: may re veal e vi d enc e of pul monary hype rte nsi on and ac ute ri ght ve ntri c ul a r s trai n. D-di mers— though a rai sed l e vel i s non-di ag nos ti c , a normal v al ue c arri es a hi g h p rob abi l i ty of e xcl usi on of a pul monary emb ol us.

Definitive diagnosis CT s can wi th contrast —the i nves ti gat i on of choi c e for major e mbol us . Pul monary ang i og rap hy Venti l ati on–perfus i on s can—deg re e of ce rtaint y i s red uce d i f area of non-perfused l ung corres ponds to any CXR abnormali ty. Fat gl obul es or foe tal ce l l s i n p ul m onary art ery bl ood may be found i n fat and amni oti c fl ui d embol us , res pec ti v el y .

General management 1. FIO 2 0. 6–1.0 to mai ntain SaO2 ≥ 90–95% 2. Li e pati e nt fl a t; i mp rov ement ofte n fol l ows i ncre ase d v enous ret urn. 3. Fl ui d challe nge to opt i m i se ri ght he art fi l l i ng . 4. Epi nep hri ne i nfusi on i f ci rcul at i on st i l l c omp rom i se d. 5. Mechani cal ve nti l a ti on m ay b e need ed i f the pat i e nt ti res or cannot maint ai n ad equate oxy genati on. Gas exchang e m ay w ors en due to l oss of pre ferent i al shunt i ng and d ecreas es i n cardi ac out put .

Management of blood clot embolus St art anti c oag ul a ti on w i th l ow m ol e cul ar wei ght he pari n adj ust ed for wei ght. Cons i d er thromb ol y si s i f there i s a maj or emb ol us and cardi ovas cul ar com promi se, and em bol ect omy i f the p ati ent re mai ns mori bund. Ot herwi s e, at 24–48h

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com mence warfari n but conti nue he pari n for further 2–3 days aft er adeq uat e oral dosi ng.

Management of fat embolus Other than g ene ral me asures i ncl udi ng oxy genati on, fl ui d re sus ci t at i on and ri ght heart l oad i ng , t reatme nt rem ai ns controversi al . Vari ous aut hori t i es ad voc ate st eroi ds , hepari ni s ati on or no s pec i fi c the rap y. P.309

Low molecular weight heparin regimen Sub cutaneous l ow m ol e cul ar wei ght he pari n i s gi ven unt i l oral ant i coagul ant t herapy i s ful l y es tabl i she d.

Dalteparin 200 uni ts /kg (m ax. 18, 000uni ts ) ev ery 24h (or 100uni ts/kg twi ce dai l y i f i nc reased ri sk of hae morrhage)

Enoxaparin 1.5mg/kg (150uni ts /kg) ev ery 24h

Tinzaparin 175uni ts /kg onc e d ai l y

Thrombolytic regimens rt -PA (100mg ov er 90mi n) shoul d be gi ven fol l owed by a hepari n i nfus i on (24,000–36, 000uni ts /day ) t o m ai ntai n t he parti al thromb opl ast i n ti me at 2–3 × norm al . Thi s i s the treat ment of c hoi ce i f surgery or angi ography i s contem pl a ted . St rep tok i nase (500,000uni t s as a l oadi ng d ose ov er 30m i n fol l ow ed by 100, 000uni ts /h for 24h). NB: Ce ntral venous cathe ters s houl d i de al l y b e i nse rt ed p re thromb ol y si s by an exp eri enced ope rat or to mi ni m i se the ri sk of b l ee di ng/haem atoma.

Key trials K ons tanti ni d es S, for the Manag eme nt Strate gi e s and Prognosi s of Pul monary Embol i s m-3 Tri al Inves ti g ators . Hepari n p l us al tep l as e c omp are d wi th hep ari n al one i n pat i ents wi t h s ubm ass i ve pul monary e mbol i s m. N Engl J M ed 2002; 347:1143–50

Ovid: Oxford Handbook of Critical Care

Ed itors:

Si nge r, M ervyn; We bb, An dre w R.

Ti tle : O xf ord Ha ndbook of Cr itic al Car e, 2nd Ed ition Cop yri ght © 1997,2005 M. Si nge r and A. R. W ebb , 1997, 2005. Publ i shed i n the Uni te d Stat es by Oxford Uni ve rsi ty Press Inc > Tab le of Co n te n ts > Car dio vasc u la r Diso r d er s

Cardiovascular Disorders Hypotension The ov erall pri nc i pl e i n t he managem ent of hy pot ens i on i s to maint ai n the m i ni mum me an art eri al pre ssure that w i l l ens ure ad equate ti ssue p erfusi on. A normal bl ood press ure d oes not guarante e an adequate cardi ac out put and ci rcul at ory support shoul d ai m t o achi eve ad equate bl ood fl ow as w el l . In ext re mis , t he . rs t l i ne treat ment opti ons shoul d i ncl ude ext ernal cardi ac mas sag e and e pi nephri ne 0.05–0.2m g i ntrave nous b ol uses (1m g i n c ardi a c arre st).

Assessment of hypotension Hyp ote nsi on req ui res treat ment i f t he m ean BP <60mmHg (hi g her i f the p ati ent was p rev i ousl y hy pertensi ve) wi t h si gns of poor t i s sue perfus i on (e .g. ol i guri a, confus i on, alte red consc i ousne ss, cool peri p heri es , m etabol i c aci dos i s ). Spe ci fi c treat ment s houl d be consi d ere d for hae morrhage, acute myocardi a l i nfarc ti on, arrhyt hmi as, pul monary emb ol us, cardi ac t amp onade, pneum othorax, anap hyl axi s, di a rrhoe a and v omi ti ng, ket oac i dosi s , hypoadrenali sm, hyp opi tui tari s m and poi soni ng .

Initial treatment of hypotension Mos t c ase s of hypot ens i on requi re fl ui d as fi rs t-l i ne manage ment t o c onfi rm an ad equate ci rcul at i ng vol um e. Exc ept i ons m ay i nc l ud e acut e heart fai l ure, arrhyt hmi as, cardi ac tam ponade and pneum othorax. In cas es of l i fe-t hreate ni ng haem orrhag e g roup s pec i fi c or O negat i v e bl ood shoul d b e used urgentl y .

Pharmacological treatment If hyp ote nsi on persi s ts aft er an ade quate ci rcul at i ng vol um e, rat e and rhyt hm has be en res tored, the appropri at e choi c e of drug tre atm ent de pends on whet her there i s my ocardi al fai l ure (si gns of l ow output or m eas ure d l ow stroke

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vol ume ) or p eri phe ral vascul ar fail ure (warm, vasod i l ated pe ri p hery or m eas ure d norm al stroke vol um e). A l ow stroke vol ume shoul d b e t reated wi th an i notrope (e.g . e pi nephri ne, dob utami ne) and peri p heral vas cul ar fai l ure wi t h a vas opress or (e. g. norepi nep hri ne).

Inotropic support Epi nep hri ne (st arted at 0.2µg /kg/mi n), dop ami ne or d obutam i ne (s tarted at 5µ g/k g/mi n) shoul d be ti trate d ag ai nst stroke vol um e (i f moni tored ). M ost hy pot ens i ve pati e nts re qui ri ng i notropes shoul d have a pul monary artery c athete r i ns erted . T he alt ernati ve i s to ti t rat e agai nst bl ood press ure, but there i s a dang er of produc i ng i nap propri ate vas oconst ri cti on. Dobut ami ne i s safer i n thi s res pec t b ut has the di sadvantag e of p rod uci ng exc ess i ve vasod i l atat i on i n som e p ati ent s.

Vasopressors Onc e s troke vol ume has b een opt i mi se d, norepi nep hri ne (st art ed at 0.05µg /kg /mi n) s houl d be ti t rated agains t mean BP. In most pat i ents, wi th previ ous l y normal bl ood press ure , 60mm Hg i s an adeq uat e t arg et but may need to be hi g her t o ensure organ p erfusi on i n the el derl y and those wi th pre vi ous hyp ert ens i on. N orepi nep hri ne may red uc e cardi ac out put . T hi s effect s houl d be m oni tored and correct ed b y adjustm ent of dos e. Vas opres si n (or i ts synthe ti c analog ue, te rl i press i n) i s i ncreas i ng l y use d for hi g h outp ut, catec hol ami ne-res i st ant , v asodi l atory shock. Care shoul d be tak en to avoi d e xce ssi ve peri pheral constri ct i on or i mpairm ent of organ perfus i on. P.313

See also: Int ra-aorti c b al l oon count erp ul s ati on, p58; Bl ood p res sure m oni tori ng, p110; Arteri a l c annul a ti on, p112; Pul monary art ery cathe ter—use, p118; Pul monary artery c athete r—i ns ert i on, p 120; Cardi a c outp ut—the rmodi l ut i on, p 122; Cardi a c outp ut— other i nvasi ve, p124; Cardi ac out put —non-i nvasi v e (1), p126; Cardi a c outp ut—non-i nvas i ve (2), p128; Col l oi ds, p180; Bl ood trans fus i on, p 182; Inotrope s, p196; Vas opress ors , p 200; Basi c resusci tat i on, p 270; Cardi a c arrest , p 272; Fl ui d chal l eng e, p274; Pneumot horax, p300; Haemothorax , p302; Pul m onary e mbol us , p 308; Tac hyarrhythmi as, p316; Bradyarrhythmi a s, p318; Acut e c oronary s ynd rom e (1), p320; Acute coronary syndrome (2), p322; Heart fai l ure—asse ssm ent , p 324; He art failure —manage ment, p326; Uppe r g ast roi nt est i nal haem orrhag e, p344; Bl eedi ng vari c es, p346; Abdomi nal sep si s, p350; Pancreat i t i s, p354; Ol i guri a , p 330; Met abol i c ac i dosi s, p434; Di abet i c ket oac i d osi s, p442; Hy poadre nal cri s i s, p448; Poi s oni ng —ge neral pri nci pl es, p452; Syst emi c i nfl am mat i on/mul ti organ fai l ure, p484; Seps i s and se pti c shock—tre atm ent , p 486; Mul ti pl e traum a (1), p500; Mul ti p l e trauma (2), p 502; Spi nal cord i njury, p 508; Burns—fl ui d m anagem ent , p 510; Burns —ge neral manage ment , p 512; Pyrexi a (1), p518; Pyrexi a (2), p520; Hy perthe rmi a, p522; Pos t-op erati ve i nt ens i ve care, p534; Post -part um hae morrhage, p542; Care of t he pot ent i al organ donor, p 552 P.314

Hypertension Oft en defi ne d i n adul t p ati ent s as a di ast ol i c pre ssure >95mmHg and a sy stol i c p res sure > 180mmHg .

Common causes in intensive care Idi opathi c/e sse nti al Agi tat i on/pain, es pec i al l y whe re mus cl e re l ax ant s are use d Exce ss i ve vas oconst ri cti on, e. g. col d, vas opress or drugs Head i njury, cerebrovascul a r acci dents Drug-rel a ted Di s sec ti ng aneurys m, aorti c c oarctati on Vas cul i ti s, throm bot i c thromb ocy top eni c p urp ura (Pre -)e cl a mps i a Aorti c coarc tat i on (m ay pre sent acut el y i n ad ul t hood) Endocri ne , e .g. phaeoc hromoc ytoma (rare) Renal fai l ure, renal art ery st enosi s (rare ) Spuri ous— und erd amp ed transd uce r s yst em

Indications for acute treatment Hyp ert ens i ve encep hal opathy , heart fai l ure , e cl a mps i a and ac ute di sse cti ng ane urysm are the p ri me i ndi cati ons for rap i d and ag gre ssi ve, al bei t control l e d, red uct i on of bl ood press ure. In other condi t i ons, es pec i al l y chroni c hype rt ens i on and fol l owi ng acut e neurol ogi cal ev ent s, e.g. he ad i nj ury , cerebrovascul a r acci dents, a pre ci p i t ate re duc ti on i n b l ood p res sure m ay adve rs el y affect pe rfusi on l ead i ng t o furt her det eri orati on. Hy pertensi on p ost -ce reb ral ev ent i s not usually treat ed unl ess ve ry hi g h, e.g . m ean BP >140–150m mHg , s yst ol i c BP > 220–230mm Hg. In thi s i ns tance, control l ed and part i al re duc ti on i s mand atory, e. g. usi ng sod i um ni tropruss i d e i nfusi on wi th conti nuous i nv asi ve moni tori ng. In the prese nce of a rai sed IC P, a ce reb ral perfus i on pres sure ≥60–70mm Hg i s usual l y target ed.

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Hypertensive crisis Thi s occ urs when t he pat i ent b ecomes sy mpt omati c (i ncreas i ng drows i ness , s ei z ure s, pap i l l oed ema, reti nop athy) i n the prese nce of el evat ed sys tem i c press ure s. The di ast ol i c BP usual l y e xce eds 120–130mm Hg and the m ean BP >140–150m mHg , al thoug h encep hal opathy can occur at l owe r p res sures .

Principles of management 1. Ade quat e m oni tori ng (i nv asi ve BP, ECG, C VP, CO, uri ne outp ut) 2. Cons i de r p ai n, hypovol aem i a, hy pot hermi a and ag i t ati on, es pec i al l y i f paral y sed . 3. Cons i de r s pec i fi c tre atm ent for, e.g . p haeochromocyt oma, t hyroi d cri s i s, aorti c d i s sec ti on, i nfl am mat ory vasc ul i ti s 4. Sl ow i ntrave nous i nfusi on of ni trate or ni tropruss i de . GTN i s usual l y g i ve n fi rst before consi deri ng sodi um ni t rop rus si de. Ot her op ti ons i nc l ud e l abe tal ol or esm ol ol i nfusi ons , and hydral azi ne (IV or IM ). Sub l i ngual ni fedi pi ne or IV hydral a zi ne m ay som eti mes produce pre ci p i tate fal l s i n BP. Us e c aut i ousl y and s tart wi t h l ow dose s. 5. Ai m to re duc e t o mi l d l y hyp ert ens i ve l e vel s unl e ss a d i ss ect i ng aneurys m i s p res ent where sys tol i c BP shoul d b e l owe red <100–110mmHg. Aft er certai n t ype s of s urg ery (e .g. cardi ac, aorti c), control of sys tol i c bl ood press ure <100–120mm Hg may be req ues ted to re duc e ri s k of bl eed i ng . 6. Longer te rm tre atm ent , e. g. an oral ACE i nhi b i tor, shoul d be i nsti tuted wi th cauti on, starti ng at l ow doses . P.315

Drug doses Drug

Dose

GTN

0.5–20mg/h

Sodium nitroprusside

0.5–1.5µg/kg/min, increased slowly to 0.5–8.0g/kg/min

Labetolol

50mg IV over 1min repeated every 5min to maximum 200mg

Esmolol

50–200µg/min

Hydralazine

5–10mg slow IV followed by 50–150µg/min

See also: IPPV—fai l ure t o t ol e rat e ve nti l a ti on, p12; Bl ood press ure moni t ori ng, p110; Int rac rani al pres sure m oni tori ng , p 134; Vas odi l a tors, p198; Hypotensi v e agent s, p202; Opi oi d anal ges i cs , p 234; Non-op i oi d anal ges i cs , p 236; Sedat i v es, p238; Int rac rani a l haemorrhag e, p 376; Subarachnoi d haem orrhag e, p378; Rais ed i nt rac rani al pres sure, p382; Pai n, p532; Pre -ec l am psi a and e cl amps i a , p 538; HELLP s yndrome , p 540 P.316

Tachyarrhythmias If pul ses are not pal pab l e or the re i s sev ere hy pot ens i on, a tachy arrhyt hmi a requi res c ardi a c m ass age and urgent D C cardi oversi on. Ot herwi s e, the i ni ti al treat ment p ri or t o d i ag nos i s i ncl udes corre ct i on of hyp oxaemi a, p otass i um (to ens ure a pl a sma K + >4. 5mm ol /l ) and mag nes i um (ofte n t o l evel s of 1.5–2mm ol /l ).

Causes of tachyarrhythmias Whe re pos si b l e the cause of a tac hyarrhythmi a shoul d b e t reated . Common c aus es for whi ch sp eci fi c treat ment m ay be req ui red i ncl ude hyp ovol aem i a, hy pot ens i on (m ay also be due t o t he arrhyt hmi a), acute myocardi a l i nfarc ti on, pai n, anaemi a, hyp erc apni a, fev er, anxi e ty, thyrotox i cosi s and d i g oxi n t oxi ci t y.

Diagnosis of tachyarrhythmias Broad complex tachycardia Reg ul a r c omp l ex es wi t h AV d i s soc i at i on (fusi on beat s, capture beat s, QRS>140ms , axi s <-30°, concordance ) s ugg est ventri cul ar tachy cardi a . If t here i s no AV d i s soc i at i on the arrhythmi a i s p rob abl y s uprave ntri cul ar wi th abe rrant conduc ti on; ade nos i ne may be us ed as a d i ag nos ti c te st si nce SVT m ay res pond and VT w i l l not. Irreg ul a r b road com pl e xes are p rob abl y atri al fi b ri l l a ti on w i t h ab errat i on. T ors ade s d e poi ntes i s a form of ve ntri cul a r t achycardi a wi t h a vari a bl e ax i s.

Narrow complex tachycardia

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The ab sence of P waves sugges ts at ri a l fi bri l l at i on. A P wav e rate >150 i s s ugg est i v e of SVT w hereas sl owe r P wav e rat es may re pre sent a si nus tachy cardi a or at ri al fl utte r w i th bl oc k. T he P w aves are abnormal (fl utte r w aves ) i n atri a l fl ut ter and QRS com pl e xes may be i rreg ul ar i f the bl ock i s vari a bl e . Extreme l y fas t SVT may be due to a re-ent ry pat hway wi th re trograde conduc ti on and pre mat ure ec top i c atri al ex ci tat i on. In W ol ff–Parki ns on–Whi te syndrome the re -entry pathway i nse rt s b el ow the His bundl e al l owi ng rapi d AV c ond uct i on and re-e ntry tac hyarrhyt hmi as. Thi s may be di a gnosed by a s hort PR i nt erv al and a d el t a w ave.

Treatment of tachyarrhythmias Ventricular tachycardia Li doc ai ne, ami odarone or magne si um form the mainstay of drug treatm ent . Overdri ve pac i ng may b e used i f a p aci ng wi re i s i n s itu, c apt uri ng the ve ntri cl e at a paci ng rate hi ghe r t han the arrhythmi a and g rad ual l y red uc i ng the p aci ng rat e. Torsad es de poi nte s m ay be e xac erb ate d b y anti arrhyt hmi cs so mag nes i um or ov erd ri ve p aci ng are safes t.

Supraventricular tachycardia and atrial flutter Caroti d s i nus mass age may b e us ed i n pat i e nts wi th no ri s k of c al c i fi ed atheromat ous carot i d dep osi ts. Ami odarone, ade nos i ne or magne si um are usual l y t he mos t useful drugs i n the cri t i cally i l l . Ve rap ami l m ay be used i f compl exe s are narrow (no ri s k of mi sd i ag nos ed vent ri cul ar tac hyc ardi a ) al though i t and othe r AV nod e bl oc kers s houl d be avoi de d i n re-e ntry t achycardi as.

Atrial fibrillation Ac ute or paroxy smal atri al fi bri l l ati on shoul d be treat ed as for supravent ri cul ar tac hyc ardi a . D i goxi n i s more use ful for chroni c at ri a l fi bri l l at i on and d oes not p rev ent paroxy smal e pi s ode s. P.317

Drug doses and cautions Adenosine

3mg IV as a rapid bolus. If no response in 1min give 6mg followed by 12mg.

Verapamil

2.5mg IV slowly. If no response repeat to a maximum of 20mg. An intravenous infusion of 1–10mg may be used. 10ml CaCl 10% should be available to treat hypotension associated with verapamil. Verapamil should be avoided in re-entry tachyarrhythmias since ventricular response may increase. Life threatening hypotension may occur in misdiagnosed ventricular tachycardia and life threatening bradycardia may occur if the patient has been β-blocked.

Lidocaine

1mg/kg intravenously as a bolus followed by an infusion of 2–4mg/min.

Amiodarone

5mg/kg over 20min then infused at up to 15mg/kg/24h in 5% glucose via a central vein. Avoid with other class III agents (e.g. sotalol) since QT interval may be severely prolonged.

Magnesium

20mmol MgSO 4 over 2–3h. In an emergency it may be given over 5min

See also: Defi bri l l at i on, p 52; ECG moni t ori ng, p108; Ant i arrhythmi c s, p204; Basi c resusci tati on, p270; Cardi ac arrest , p 272; Fl ui d chall eng e, p 274; Hypotensi on, p312; Acute coronary syndrome (1), p320; Hyp erkal aemi a, p420; Hyp okal aem i a, p422; Thy roi d e mergenci e s, p446; Tri cyc l i c anti dep res sant p oi s oni ng, p460; Anaem i a, p400; Py rex i a (1), p518; Pyrexi a (2), p520; Pai n, p532 P.318

Bradyarrhythmias If peri pheral pul ses are not pal pab l e a brady arrhy thm i a req ui res ext ernal cardi ac m ass age and t reatme nt as for asy stol e. For asym ptomat i c bradyc ard i a tre atm ent may not b e requi red other than c l os e moni tori ng and c orrect i on of the cause . T he exc ept i on to thi s i s hi g her de gre es of heart bl ock occ urri ng after an ac ute anteri or my ocardi al i nfarc ti on where p aci ng may be re qui red prophyl a cti cally .

Causes of bradyarrhythmias Whe re pos si b l e the cause of a bradyarrhythmi a shoul d b e t reated . Common c aus es for whi ch sp eci fi c treat ment m ay be req ui red i ncl ude hyp ovol aem i a, hy pot ens i on (m ay also be due t o t he arrhyt hmi a), acute myocardi a l i nfarc ti on, di g oxi n t oxi ci ty, β-b l ocker t oxi ci t y, hyp erk al a emi a, hypothy roi di sm, hy pop i tui tari sm and rai se d i ntracrani al press ure . Di goxi n t oxi ci ty may req ui re tre atm ent wi th ant i di gox i n ant i bodi e s.

Diagnosis of bradyarrhythmias Sinus bradycardia

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Sl ow v ent ri cul ar rat e w i th normal P wav es, normal PR i nte rval and 1:1 AV conducti on.

Heart block Normal P wave s, a p rol ong ed PR i nt erv al and 1:1 AV c ond uct i on sugge st 1° heart bl ock. In 2° he art bl oc k the ventri cl es fai l t o resp ond to at ri a l c ont rac ti on i nt erm i tt ent l y . T hi s may be as soc i at ed wi t h regul ar P wav es and an i nc re asi ng PR i nt erv al unt i l ventri cul ar de pol ari sat i on fail s (M obi tz I or Wenk ebach) or a normal PR i nt erval wi t h reg ul ar fai l ed ventri cul ar de pol ari sati on (Mobi tz II). In the l a tte r c ase the AV c ond uct i on rati o may b e 2:1 t o 5:1. In 3° heart bl ock the re i s compl ete AV di ssoci ati on wi t h a sl ow, i di ove ntri c ul a r rat e.

Absent P wave bradycardia Abs ent P wav es may rep res ent sl ow atri a l fi bri l l at i on or si no-atri al dy sfunct i on. In t he l at te r c ase there wi l l be a sl ow, i di ove ntri c ul a r rate .

Treatment of bradyarrhythmias Hyp oxaemi a must be corre cte d i n all sym ptomat i c bradyc ard i as . F irst l i ne d rug treat ment i s usuall y at ropi ne 0.3m g or gl y cop yrrol ate 200µg i ntravenous l y. If the arrhythmi a fails to re spond, 0. 6mg fol l owed by 1.0mg atropi ne may be gi v en. Failure to res pond t o d rug s requi res tem porary pac i ng. Thi s m ay b e accompl i s hed rapi d l y wi t h an ex ternal sys tem i f there i s haemodynami c c omp rom i se or trans venous l y. Ot her i ndi cat i ons for tem porary pac i ng are shown opp osi te. Hi ghe r d egrees of he art bl ock after an ant eri or my ocardi al i nfarc ti on wi l l usually re qui re permanent paci ng.

Indications for temporary pacing Persi ste nt sym ptomati c bradyc ard i a Bl ack out s as soci a ted wi th 3° heart bl ock 2° heart bl ock RBBB and l eft p ost eri or hem i bl ock Card i ov asc ul ar col l ap se Infe ri or myoc ardi a l i nfarct i on wi th sym ptomat i c 3° heart bl ock Ant eri or myocardi a l i nfarc ti on w i th 3° heart bl ock RBBB and l eft p ost eri or hem i bl ock Al t ernati ng RBBB and LBBB P.319

See also: Tem porary paci ng (1), p54; Temp orary pac i ng (2), p56; ECG moni tori ng, p108; C hronot rop es, p206; Basi c res us ci t ati on, p270; Card i ac arre st, p272; Acute coronary syndrome (1), p320; Thyroi d eme rge nci es, p446; Hyp otherm i a, p516 P.320

Acute coronary syndrome (1) Principles of management of the uncomplicated myocardial infarct Oxyg en— to mai ntain SaO 2 ≥98% Good ve nous acce ss Cont i nuous EC G m oni tori ng Ade quat e p ai n rel i ef Earl y thromb ol y si s pl us asp i ri n (he pari n i f usi ng rt-PA) Earl y β bl oc kade Gradual m obi l i s ati on

Complications of myocardial infarction Card i op ul monary arres t Cont i nui ng c hes t p ai n—may be i s chaemi c or p eri cardi ti c i n ori g i n Pump failure Hypotensi on—apart from cardi og eni c s hoc k c ons i de r hypovol aemi a (e.g . p ost -di ure ti c s) and a thromb ol y si s reac ti on

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Tachyarrhythmi a s/b rad yarrhy thm i as Val ve d ysfunc ti on— pre dom i nantl y m i tral Peri cardi al tam ponade (rare ) Ventri cul ar se ptal d efec t (unusual, oft en pre sents 2–5 days pos t-i nfarct ) Comp l i c at i ons of thrombol yt i c the rap y—arrhythmi a s, bl e edi ng, anaphyl a ctoi d react i on

Management of the complicated myocardial infarct General Oxyg en to mai ntain SaO 2 ≥98% App rop ri a te and promp t m oni tori ng and i nve sti gat i ons as i nd i cated , e .g. ec hoc ard i og ram , p ul m onary art ery cat het er, ang i ography , EC G Earl y thromb ol y si s shoul d s ti l l be gi v en. rt -PA fol l owed by hep ari n s houl d be gi v en i n pre ferenc e t o s tre ptoki nase i f i nv asi ve p roced ure s and/or s urgery are c ont emp l at ed. Art eri al or central venous cannul at i on shoul d not be d el ayed i f cl i ni cally i ndi cat ed. These proced ures shoul d be performed by an expe ri enc ed operat or to m i ni mi se the ri sk of bl e edi ng. The s ubc l av i an route shoul d b e avoi ded. Ang i op l as ty or rev asc ul a ri sat i on surge ry i s benefi ci al i f performed earl y. The c ard i ol og i st shoul d b e i nforme d prompt l y i f a pati ent i s ad mi t ted i n pump fai l ure, conti nui ng p ai n, or v al v ul a r d ysfunc ti on.

Specific Card i op ul monary arres t—c ard i op ul m onary res usc i t ati on Cont i nui ng c hes t p ai n: If i sc hae mi c —IV ni trate and he pari n i nfus i ons, asp i ri n, cl opi dog rel , c al c i um antag oni st and β-bl ocke r (unl ess cont raind i cated ); consi d er urg ent angi ography . If p eri cardi ti c—c ons i de r non-ste roi dal anti -i nfl am mat ory ag ent Managem ent of heart fai l ure—al s o c ons i de r IABP Tachyarrhythmi a —anti a rrhythmi c s, sy nchroni se d D C c ard i ov ers i on Bradyc ard i as —chronotrop e, c ons i d er tem porary pac i ng Val ve d ysfunc ti on— heart fai l ure m anageme nt; consi der surg ery Peri cardi al tam ponade —pe ri c ard i al as pi rat i on Ventri cul ar se ptal d efec t—heart fai l ure m anag eme nt, consi der s urg ery Thrombol ys i s compl i cati ons P.321

Drug dosage

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Diamorphine

2.5mg IV. Repeat prn + anti-emetic

Streptokinase

1.5 million units in 100ml 0.9% saline IV over 1h

rt-PA (alteplase)

100mg IV over 90min (15mg bolus, then 50mg over 30min, then 35mg over 60min

Reteplase

10units IV + further 10units IV 30min later

Aspirin

150mg PO od

Clopidogrel

75mg

Atenolol

50mg PO od (increase to 100mg od if not hypotensive and heart rate exceeds 70bpm) or 5mg slow IV bolus

Propranolol

10–40mg PO qds (titrate to heart rate of 60bpm)

Isosorbide dinitrate

2–40mg/h IV

GTN

10–200µg/min IV or 0.5–1mg SL

Diltiazem

60mg PO tds

Nifedipine

5–10mg sublingual or PO tds

Atropine

0.3mg IV. Repeat to maximum of 2mg

Lidocaine

1mg/kg slow IV bolus then 2–4mg/min

Amiodarone

5mg/kg over 20min then infused up to 15mg/kg/day in 5% glucose via central vein (in emergency give 150–300mg in 10–20ml 5% glucose over 3min)

Key papers Tas k forc e or M anag eme nt of acute myoc ard i al i nfarct i on of the European Soci ety of Cardi ol og y. Manage ment of ac ute myocardi a l i nfarc ti on i n p ati ent s p res ent i ng wi th ST se gment e l ev ati on. Eur Heart J 2003; 24:28–66

See also: Defi bri l l at i on, p 52; Temp orary pac i ng (1), p54; T emp orary pac i ng (2), p 56; Intra-aort i c bal l oon c ounterpul sati on, p58; ECG moni tori ng, p108; Bl ood p res sure m oni tori ng, p110; Ce ntral venous cathe ter—us e, p114; Cent ral ve nous cat het er—inserti on, p116; Pul monary arte ry cat het er—us e, p 118; Pul m onary art ery cathe ter—i nserti on, p120; C ard i ac out put —thermodi l uti on, p122; C ard i ac output—othe r i nvasi v e, p124; Cardi a c outp ut—non-i nvas i ve (1), p 126; C ard i ac out put —non-i nvasi v e (2), p128; Inotrope s, p196; Vas odi l at ors , p 198; Vasop res sors, p200; Ant i arrhythmi c s, p204; Chronotropes , p 206; Anti coagul ant s, p248; Thrombol yt i c s, p250; Basi c res usc i tati on, p270; Cardi ac arrest , p 272; Fl ui d chall eng e, p 274; Hypotensi on, p312; Tac hyarrhythmi a s, p316; Brad yarrhy thm i as , p 318; Acut e c oronary syndrome (2), p322; Heart fail ure —as ses sme nt, p324; Heart fai l ure—m anagem ent , p 326; Pain, p532 P.322

Acute coronary syndrome (2) Angina Isc hae mi c or, rarel y , s pas mod i c constri c ti on of c oronary arte ri e s resul t i ng i n pain, us ual l y pre cordi al , press i ng or crushi ng , and wi t h or wi thout radi a ti on t o j aw, nec k or arms . T he sed ate d, v ent i l ate d p ati ent wi l l not us ual l y com pl a i n of pai n b ut si g ns of di s com fort m ay be apparent, e.g . s weati ng, hyp ert ens i on, t achycardi a. The EC G s houl d be reg ul a rl y s cruti ni s ed for ST seg ment and/or T wave change s. Uns tab l e ang i na encom pas ses a spe ctrum of s ynd romes bet wee n s tab l e ang i na and my ocardi al i nfarcti on. Angi nal att ack s m ay be i nc reased i n frequenc y and/or s eve ri t y, persi st l onger, resp ond l e ss to ni t rates , and occ ur at res t or aft er mi ni mal e xerti on.

Pathophysiology

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Myoc ard i al ox yge n s upp l y–dem and i m bal anc e usually due t o c oronary arte ry atheroma ± di srupt i on of pl aque or new non-oc cl usi v e t hrombus form ati on. Sp asm (Pri nzme tal angi na) i s unc omm on. Vas opress or drugs may compromi se myoc ardi a l p erfusi on by furthe r c ons tri ct i ng an al ready ste nos ed vess el . Vas odi l at or drugs may al so com promi s e m yoc ard i al pe rfusi on b y a ‘c oronary s teal’ phe nom enon where bl ood fl ow i s red i st ri but ed away from ste nos ed vess el s.

Diagnosis Symp tom s, esp eci al l y che st pai n b ut al s o non-s pec i fi c, e. g. sweati ng ECG change s—ST s egm ent el evati on/d epress i on, T wave i nve rs i on No ri s e i n c ard i ac enzym es or troponi n above t he myocardi a l i nfarc ti on t hre shol d Dys ki neti c areas of my ocardi um may be se en on e chocardi ography or angi ography

Treatment Ens ure ade quate oxy genati on Correc t hypot ens i on and t i s sue hyp ope rfusi on Cons i de r d rug c aus es, e.g . v asopre ssors Gl y ceryl tri ni trate 0.5mg SL, or ni trol i ngual spray (0. 4–0.8m g) repe ate d as nece ssary If s ymp tom s are sev ere and/or pe rs i st i ng , m ai ntai n b ed res t Asp i ri n 75mg od PO (unl e ss contraind i c ate d).

For continuing angina: IV Ni t rat e i nfusi on, e.g . g l yc ery l t ri ni t rate, i s osorbi de tri ni trate Cons i de r c al ci um antagoni st , e .g. di l ti azem t hough not al one Cons i de r β -bl ock er (unl es s c ont raind i cated ), e.g . prop ranol ol , ate nol ol LMW hep ari n and cl opi dog rel (unl e ss contraind i c ate d) Cons i de r G P2b 3a i nhi b i tor (IV ept i fi bat i d e or t i rofi b an) i n ad di t i on to as pi ri n and cl opi dogre l i f c ons i de red at hi gh ri s k of MI or de ath If s ymp tom s or ST-s egm ent chang es persi s t d esp i t e op ti mal pharm acol og i cal i nte rve nti on, i nform c ardi ol og i st wi t h a vi e w t o angi ography and p oss i b l e ang i op l as ty or surgery. P.323

Key trial Y us uf S for t he Cl opi d ogrel i n Uns tab l e Angi na t o Preve nt Rec urrent Ev ent s T ri al Inv est i gators. Effect s of c l opi d ogrel i n add i ti on to asp i ri n i n pat i ents wi t h acut e c oronary s ynd rom es wi t hout ST-s egm ent el evat i on. N Engl J Me d. 2001; 345:494–502

P.324

Heart failure—assessment Imp ai red abi l i ty of t he heart to sup pl y ad equate ox ygen and nutri ents to mee t t he dem and s of the b ody 's met abol i s i ng t i ss ues .

Major causes Myoc ard i al i nfarct i on/i s chaemi a Drugs e.g . β -bl ocke rs , c ytotoxi cs Tachy- or bradyarrhythmi a s Val ve d ysfunc ti on Sep si s Sep tal de fect Card i om yop athy/m yocard i ti s Peri cardi al tam ponade

Clinical features

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Decreased forward flow leading to poor tissue perfusion Musc l e fat i g ue l ead i ng ul ti mat el y to hy percap ni a and c ol l aps e Confusi on, ag i tati on, drowsi nes s, coma Ol i guri a Inc reasi ng m etabol i c aci dos i s , arte ri a l hypoxae mi a and dy spnoea

Increased venous congestion secondary to right heart failure Peri pheral oedem a Hepati c c ong est i on Spl anc hni c i sc haem i a Rai s ed i nt racrani a l p res sure

Increased pulmonary hydrostatic pressure secondary to left heart failure Pul monary oed ema, dy spnoea Hypoxae mi a

Investigations Test

Diagnosis

ECG

Myocardial ischaemia/infarction, arrhythmias

CXR

With left heart failure: pulmonary oedema (interstitial perihilar (‘bat's wing’) shadowing, upper lobe blood diversion, Kerley B lines, pleural effusion) ± cardiomegaly

Pulmonary artery catheter

Low cardiac output and stroke volume, low mixed venous oxygen saturation (<60%), raised PAWP (with left heart failure), raised RAP (with right heart failure). V waves with mitral or tricuspid regurgitation

Blood tests

Low SaO 2 , variable PaCO 2 , base deficit >2mmol/l, hyperlactataemia, low venous O 2 (mixed or central venous), raised cardiac enzymes, troponin, BNP, thyroid function (if indicated)

Echocardiogram

Poor myocardial contractility, pericardial effusion, valve stenosis/incompetence

Notes Peri pheral oede ma i mp l i e s t otal b ody salt and water re tenti on b ut not ne ces sari l y i ntravascul ar fl ui d ov erl oad . P.325

See also: ECG moni t ori ng, p108; Bl ood press ure moni t ori ng, p110; Cent ral ve nous c athete r—use, p114; Ce ntral venous cat het er—inserti on, p116; Pul monary arte ry cat het er—us e, p 118; Pul m onary art ery cathe ter—i nserti on, p120; C ard i ac out put —thermodi l uti on, p122; C ard i ac output—othe r i nvasi v e, p124; Cardi a c outp ut—non-i nvas i ve (1), p 126; C ard i ac out put —non-i nvasi v e (2), p128; Hyp ote nsi on, p312; Tachy arrhyt hmi as, p316; Brady arrhyt hmi as, p318; Acute coronary syndrome (1), p320; Heart fail ure —manag ement, p326 P.326

Heart failure—management Basic measures 1. Det erm i ne l i kel y c aus e and t re at as appropri a te, e. g. anti arrhy thm i c 2. Oxyg en— to mai ntain SaO 2 ≥98% 3. GTN sp ray SL then com menc e IV ni t rat e i nfusi on t i t rat ed rap i dl y unti l g ood cl i ni cal e ffe ct. Be ware hy pot ens i on whi c h, at l ow dosag e, i s sug ges ti v e of l eft ventri cul ar underfi l l i ng, e. g. hyp ovol ae mi a , t amponad e, mi t ral ste nos i s, pul monary e mbol us

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4. If p ati ent i s agi t ate d or i n p ai n, g i ve di amorphi ne IV. 5. Cons i de r e arl y C PAP, Bi PAP and/or IPPV t o reduce work of breat hi ng and provi d e g ood ox ygenati on. Cardi ac outp ut wi l l oft en i mp rov e. D o not del ay unt i l the pati e nt i s i n e xtremi s. 6. Furosem i de i s rare l y need ed as fi rst l i ne the rap y unl e ss i nt rav asc ul ar fl ui d ove rl oad i s causat i ve . Ini t i a l symp tom ati c rel i ef i s provi ded by i t s p rom pt vas odi l at i ng ac ti on; how eve r, sub seq uent d i uresi s m ay res ul t i n mark ed hyp ovol ae mi a l e adi ng to c omp ens atory vas oconst ri cti on, i ncrease d c ard i ac work and worse ni ng myoc ard i al func ti on. Di uret i c s m ay b e i ndi cat ed for ac ute -on-chroni c fai l ure, esp eci al l y i f the pat i e nt i s on l ong term di ureti c t herapy but s houl d not be us ed i f hyp ovol aem i c. If furos emi de i s req ui red , s tart at l ow dos es the n reas se ss.

Directed management 1. Ade quat e m oni tori ng (e .g. pul monary arte ry cat het eri sati on) and i nvest i g ati on (ec hoc ard i og rap hy). 2. If e vi d enc e e xi s ts for hy pov ol a emi a, gi v e 100–200m l c ol l oi d fl ui d c hal l e nges t o ac hi eve opt i mal s troke vol ume . 3. If v asoconstri c ti on p ers i s ts (SVR >1400dyn/s/cm 5 ), t i trat e ni trate i nfus i on further to opt i mi se st rok e vol um e and, i d eal l y , reduce SVR <1300d yn/s/c m 5 . If hyp ovol ae mi a i s suspe ct ed (i .e . s troke vol ume fal l s ), fl ui d chal l e nge s s houl d be gi v en t o re-opti mi se t he st rok e vol um e. Wi t hi n 24h of ni trat e i nfus i on, comm enc e ACE i nhi bi ti on, i ni ti al l y at l ow dos e b ut rap i dl y i ncreas ed to app rop ri ate l ong-t erm doses . 4. Inot ropes are i ndi cat ed i f evi dence of t i s sue hyp ope rfusi on, hyp ote nsi on or vas oconst ri cti on persi sts de spi te opti mal fl ui d l oad i ng and ni trate dosi ng. Consi d er epi nep hri ne , dobut ami ne or mi l ri none; w hi l e e pi nephri ne may some ti mes cause exc ess i ve const ri cti on, dobut ami ne and mi l ri none m ay exce ss i ve l y vasodi l at e. Lev osi mendan i nc reases cardi ac out put thoug h not at the exp ens e of i ncreas ed cardi ac w ork . 5. Int ra-aorti c balloon counte rpul s ati on augm ent s c ardi a c outp ut, re duc es cardi a c w ork and i mprove s c oronary art ery perfusi on. 6. Ang i op l as ty or surgi cal re vas cul ari zat i on are b ene fi c i a l i f p erform ed e arl y afte r m yoc ard i al i nfarct . Surg ery may al s o be ne ces sary for mec hani cal d efe cts , e .g. ac ute mi tral regurg i tati on.

Treatment end-points 1. BP and cardi ac out put ade quate to mai ntain org an perfus i on (e .g. no ol i guri a , c onfusi on, dy spnoea nor me tab ol i c aci dos i s). A me an BP of 60mm Hg i s usual l y s uffi ci ent but m ay nee d t o be hi ghe r, esp eci al l y i f pre morbi d bl ood pre ssures are hi gh. 2. A mi xed ve nous oxyg en s aturati on ≥60%. Ex ces si v e i not rop es shoul d be av oi d ed as myoc ardi a l oxyge n d emand i s i nc reased . 3. Symp tom ati c rel i ef. P.327

Drug dosage

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GTN

2–40mg/h IV or 0.4–0.8mg by SL spray

Isosorbide dinitrate

2–40mg/h IV

Nesiritide

2µg/kg bolus followed by infusion of 0.01–0.03µg/kg/min.

Sodium nitroprusside

20–400µg/min IV

Captopril

6.25mg PO test dose increasing to 25mg tds

Enalapril

2.5mg PO test dose increasing to 40mg od

Lisinopril

2.5mg PO test dose increasing to 40mg od

Epinephrine

Infusion starting from 0.05µg/kg/min

Dobutamine

2.5–25µg/kg/min IV

Dopamine

2.5–25µg/kg/min IV

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Milrinone

Loading dose of 50µg/kg IV over 10min followed by infusion from 0.375–0.75µg/kg/min.

Enoximone

Loading dose of 0.5–1mg/kg IV over 10min followed by infusion from 5–20µg/kg/min.

Levosimendan

12–24µg/kg over 10min followed by 0.1µg/kg/min for 24h

Diamorphine

2.5mg IV. Repeat every 5min as necessary

Furosemide

10–20mg IV bolus. Repeat or increase as necessary

Key trials Cot ter G, et al . R and omi sed tri al of hi gh-dos e i sos orb i de di ni t rate pl us l ow-d ose furos emi de versus hi gh-dos e furose mi d e p l us l ow-d ose i s osorbi de di ni t rat e i n s eve re pul monary oed ema. Lanc et 1998; 351:389–93 Cuffe M S, et al . Rati onal e and des i gn of the OPTIME C HF tri al : outcomes of a p ros pec ti ve t ri al of i nt rav enous mi l ri none for exac erb ati ons of chroni c he art fai l ure. Am He art J 2000; 139:15–22 Fol l at h F , e t al. Effi cacy and safety of i ntravenous l e vos i me ndan c ompared wi th dob utami ne i n s eve re l ow -out put heart fai l ure (the LIDO st udy ): a randomi s ed doubl e -bl i nd tri al . Lancet 2002; 360:196–202

See also: Oxy gen therapy, p2; Vent i l a tory s upp ort —i ndi cat i ons, p4; Posi ti v e e nd expi ratory p res sure (1), p22; Posi ti ve e nd exp i ratory p res sure (2), p24; Cont i nuous p osi ti v e airw ay pre ssure, p26; Inotrop es, p196; Vas odi l a tors, p198; Vas opres sors, p200; Anti arrhy thm i cs , p 204; Chronotropes , p 206; Basi c res usc i tati on, p270; Fl ui d chal l enge, p274; Heart fai l ure— ass ess ment, p324

Ovid: Oxford Handbook of Critical Care

Ed itors: Si nge r, M ervyn; We bb, An dre w R. Ti tle : O xf ord Ha ndbook of Cr itic al Car e, 2nd Ed ition Cop yri ght © 1997,2005 M. Si nge r and A. R. W ebb , 1997, 2005. Publ i shed i n the Uni te d Stat es by Oxford Uni ve rsi ty Press Inc > Tab le of Co n te n ts > Ren al Dis or d er s

Renal Disorders Oliguria Defi ne d as a uri ne output < 0.5ml /kg/h and c aus ed by: Post -re nal —uri nary tract ob struc ti on, e.g . b l oc ked cat het er, uret eri c t rauma, prost ati sm , rai s ed i nt ra-abd omi nal pre ssure, bl ood cl ot, bl add er tum our. Renal—e stabl i shed acute renal fai l ure, acute tub ul a r necrosi s, gl omerul one phri ti s. Pre-renal — hyp ovol ae mi a , l ow cardi a c outp ut, hy pot ens i on, i nad equate re nal bl ood fl ow. Obs truct i on and p re-renal causes of ol i guri a must be exc l ud ed before res orti ng t o d i ureti cs .

Urinary tract obstruction A ful l b l ad der shoul d b e ex cl ude d by palpati on. Ens ure a pat ent cathe ter i s pres ent . If ob st ruc ti on i s d ue to bl ood cl ot the bl add er shoul d be i rri gat ed. If ob struct i on i s s usp ect ed hi g her i n the renal t rac t an ul t ras ound s can i s re qui red for di a gnosi s and p oss i b l e urol og i cal i nt erv ent i on (e. g. nep hrostomi e s). Raise d i ntra-abdomi nal pre ssure may cause ol i guri a by i m ped i ng re nal ve nous drai nag e (p art i c ul a rl y i f >20mm Hg). Re l i e f of t he hi g h p res sure ofte n p rom ote s a di ure si s .

Hypovolaemia Onc e renal t ract obs tructi on i s exc l uded , i t i s m and atory to c orrec t hypovol aemi a b y fl ui d c hal l e nge . Ol i g uri a i n hyp ovol ae mi c pati e nts may b e a phy si ol og i c al res ponse or due to a reduced re nal bl ood fl ow.

Inadequate renal blood flow and/or pressure If cardi ac outp ut re mai ns l ow des pi te c orrec ti on of hypov ol a emi a, correc ti on wi t h v asod i l ators and /or i notrope s w i l l be nec ess ary . If t he bl ood pre ssure rem ai ns l ow aft er i mp rov i ng the c ard i ac output, vas opress ors may b e neede d t o achi ev e a mean b l ood p res sure of at l eas t 60mm Hg. In el derl y pat i ents and ot hers w i th pre-e xi s ti ng hype rte nsi on, a

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hi g her me an bl ood pre ssure may be nec ess ary t o maint ai n uri ne outp ut.

Persistent oliguria At temp ts to i ncre ase uri ne output w i th di ure ti cs may fol l ow the abov e me asures i f ol i g uri a p ers i st s. Furos emi de i s gi v en i n a d ose of 5–10mg i ntravenous l y wi t h hi g her i ncre ments at 30m i n i nt erv al s to a max i mum of 250mg . Higher dos es may be nee ded i f the p ati ent has p rev i ousl y re cei ved di ure ti c t herapy . A l ow dose i nfusi on may be st art ed (1–5mg /h IV). Manni tol (20g i nt ravenousl y) may be consi dered al t hough fai l ure t o p rom ote a d i ures i s may i ncre ase oed ema format i on. Fai l ure t o re-es tab l i sh uri ne out put may requi re re nal support i n the form of di a l ys i s or hae mofi l t rat i on. T here i s no p oi nt i n conti nui ng d i uret i c the rap y i f i t i s not effect i ve ; l oop di ure ti c s i n p art i c ul a r m ay be nep hrotox i c. Indi c at i ons for renal sup port i ncl ud e fl ui d ov erl oad , hype rkalae mi a , m etabol i c aci dos i s , c reati on of space for nutri ti on or drugs, pe rsi st ent re nal fai l ure wi t h ri s i ng urea and creat i ni ne, and s ympt omati c urae mi a . P.331

Biochemical assessment Pre-renal cause

Renal cause

Urine osmolality (mOsmol/kg)

>500

<400

Urine Na (mmol/l)

<20

>40

Urine:Plasma creatinine

>40

<20

Fractional Na excretion*

<1

>2

*

See also: Hae mo(d i a)fi l trati on (1), p62; Haemo(di a )fi l trat i on (2), p 64; Pe ri t one al di al y si s , p 66; Bl ood pre ssure moni t ori ng, p110; Ure a & creat i ni ne, p144; Uri nal ysi s, p166; Col l oi d osmot i c press ure , p 172; Cryst al l oi ds, p176; Col l oi ds, p180; Di ure ti c s, p212; D opam i ne, p 214; Basi c res usc i tati on, p270; Fl ui d chal l enge, p274; Hyp ote nsi on, p312; Ac ute re nal fai l ure—di a gnosi s , p 332; Ac ute re nal fail ure —manage ment, p334; Bowe l p erforati on and obs tructi on, p348; Abd omi nal s eps i s, p350; Panc reati t i s , p 354; Ac ute l i ver fail ure , p 360; Hype rkalae mi a , p 420; Seps i s and se pti c shock— treatm ent , p 486; M al a ri a , p 490; Mul t i pl e t rauma (1), p500; Mul ti pl e t rauma (2), p502; Burns —fl ui d manage ment , p 510; Rhab dom yol ysi s, p528; Pos t-operati ve i nt ens i ve care, p534 P.332

Acute renal failure—diagnosis Renal fai l ure i s d efi ned as re nal funct i on i nade quate to cl e ar the waste products of met abol i sm des pi t e t he abs enc e of or corre cti on of haem ody nam i c or mec hani cal c aus es. Re nal fai l ure i s sug ges ted by : Urae mi c s ympt oms (d row si ness , naus ea, hi ccough, t wi t chi ng ) Rai s ed pl a sma creat i ni ne (>200µ mol /l ) Hype rkalae mi a Hyponat rae mi a Metabol i c ac i dosi s Persi ste nt ol i guri a may be a feat ure of ac ute re nal fai l ure but non-ol i g uri c renal fai l ure i s not unc omm on; 2–3l of p oor quali ty uri ne per day may occur d esp i te an i nade quate gl omerul a r fi l t rati on rate . T he prognosi s i s be tte r i f uri ne out put i s maint ai ned . Cl i ni cal feat ure s m ay s ug ges t t he c aus e of renal fai l ure and d i ct at e furt her i nves ti g ati on. Ac ut e tub ul ar nec ros i s i s a c omm on aeti ol ogy i n the c ri t i c al l y i l l (e. g. fol l ow i ng hy povol ae mi a , e xte nsi ve burns) but othe r causes must be borne i n mi nd. In sep si s , t he ki d ney often has a normal hi st ol ogi c al app earanc e. Anaemi a i mpl i es chroni c renal fai l ure.

Post-operative renal failure Ri s k fact ors i ncl ude hyp ovol ae mi a , haem odynami c i ns tab i l i ty (parti cul arl y hyp ote nsi on), m ajor ab dom i nal s urgery i n those >50 years , major surg ery i n jaundi ce d pati ent s and b i l i ary and other sep si s . Surgi c al proced ure s (parti cul arl y gynaec ol ogi c al ) may b e compl i c ate d b y damag e t o t he l owe r uri nary t rac t w i th an ob struct i v e ne phropathy . Abd omi nal aort i c ane ury sm surgery m ay b e associ a ted wi th renal art eri al di srupt i on and s houl d be i nve st i gated urg ent l y wi t h renography and p oss i bl e art eri ography or re-e xpl orati on.

Other causes

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Nephrot oxi ns —may cause re nal failure vi a ac ute tubul ar nec rosi s , i nte rs ti t i al ne phri t i s or renal tub ul ar obst ructi on. Al l pot ent i al ne phrotoxi ns s houl d be wi t hdrawn. Rhab dom yol ysi s—s ugg est ed by myogl obi nuri a and rai sed CPK i n p ati ent s w ho have suffe red a c rush i nj ury , c oma or s ei zures. Gl omerul a r d i se ase —re d c el l c ast s, haem aturi a, protei nuri a and sy ste mi c fe atures (e .g. hyp ertensi on, purpura, art hralgi a, vas cul i t i s) are al l sug ges ti v e of g l om erul ar di sease. Re nal bi ops y or s pec i fi c b l ood t est s (e.g . Good pas ture' s s ynd rom e, v asc ul i ti s) are re qui red to confi rm di agnosi s and appropri a te tre atm ent . Haem ol y ti c uraem i c sy ndrome—sugges te d by haemol ys i s, uraem i a, throm boc ytopeni a and ne urol og i cal abnormali ti e s. Crys tal nephrop athy—s ugg est ed b y t he pre sence of cry stals i n the uri nary se di m ent . M i crosc opi c e xam i nati on of the cryst al s confi rms the d i ag nos i s (e. g. urate, ox al a te). Re l ease of p uri ne s and urate are re sponsi bl e for acut e renal fai l ure i n t he tum our l y si s sy ndrome . Renovas cul ar di s orders—l oss of vascul ar suppl y m ay be d i agnos ed by renography. Comp l e te l os s of arteri a l sup pl y may oc cur i n ab dom i nal t rauma or aorti c d i se ase (part i cul arl y di sse cti on). M ore com monl y, the arte ri al sup pl y i s parti al l y c omp rom i s ed (e.g . renal arte ry ste nos i s ) and b l ood fl ow i s further red uce d b y haemodynami c i ns tab i l i ty or l ocal l y vi a drug the rap y (e .g. NSAIDs, AC E i nhi bi tors). Renal vei n obst ruc ti on may be due to thromb osi s or e xte rnal c omp res si on (e.g . rai s ed i nt ra-abd omi nal press ure). P.333

Nephrotoxins The fol l owi ng are som e c ommon nephrot oxi ns:

Allopurinol

Aminoglycosides

Amphotericin

Cephalosporins

Dextran 40

Furosemide

Heavy metals

Herbal medicines

Narcotics

NSAIDs

Organic solvents

Paraquat

Penicillins

Pentamidine

Phenytoin

Radiographic contrast

Sulphonamides

Tetracyclines

Thiazides

Vancomycin

See also: Uri nal ys i s, p166; Fl ui d chall eng e, p 274; Hypotensi on, p312; Ol i guri a, p330; Acute renal fai l ure—m anagem ent , p 334; Bow el perforati on and ob struct i on, p348; Abdomi nal sep si s , p 350; Pancreat i ti s, p354; Acute l i v er fai l ure, p360; Hae mol ysi s, p404; Pl a tel et di s ord ers, p406; Seps i s and se pti c s hoc k—t reatme nt, p486; Mal ari a, p490; R heumat i c di s orders, p492; Vasc ul i ti des , p 494; Mul ti pl e traum a (1), p500; Mul ti p l e trauma (2), p 502; Burns—fl ui d managem ent , p510; Burns— general m anagem ent , p 512; Post-ope rat i ve i ntensi ve c are , p 534 P.334

Acute renal failure—management Ide nti fi cat i on and c orrect i on of re versi b l e causes of re nal failure i s cruci al . Al l cas es req ui re c areful at tenti on to fl ui d manage ment and nutri t i onal sup port. Di al y si s and/or fi l t rat i on t echni q ues wi l l mak e s pac e for adeq uat e fl ui d and nut ri ti onal i ntak e.

Urinary tract obstruction Low er tract obs truct i on re qui re s t he i ns ert i on of a c at het er (sup rapub i c i f the re i s ure thral di srupti on) to al l ow tract dec omp res si on. Ure teri c ob struct i on requi re s uri nary trac t d ecompress i on by nep hrost omy or st ent . A mas si ve di ure si s i s common after d ecom press i on so i t i s i m portant t o e nsure ade quate ci rcul at i ng vol um e t o preve nt sec ond ary pre-renal fai l ure.

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Haemodynamic management Pre -re nal failure i s re versi b l e before i t be com es est abl i shed. Careful fl ui d managem ent to ensure an adeq uat e ci rcul at i ng vol um e and any nec ess ary i not rop e or vasop res sor s upp ort may es tab l i sh a d i uresi s. If ol i guri a pe rsi st s aft er pre -re nal factors hav e b een corre cte d, the us e of di ureti cs (furos emi de, manni tol ) may e stabl i sh a d i ures i s.

Metabolic management Hyp erk al a emi a m ay b e l i fe -threateni ng (> 6.5mmol /l or ECG chang es) and m ay b e p rev ent ed by p otass i um re stri c ti on, earl y di a l ys i s or haemo(di a )fi l trat i on. Hypoc al cae mi a and hy ponatraem i a are be st tre ate d wi th di al y si s and/or hae mo(d i a)fi l trati on, al though calci um suppl ementat i on may b e used . Hyponatraem i a i s us ual l y due to wat er exc ess al t hough sal t-l os i ng ne phropathi es (ac ute tubul ar nec ros i s, ot her renal t ubul ar di sorders) may re qui re sod i um chl ori de suppl eme nts . Hype rphosp hat aemi a m ay be tre ate d wi th di al y si s , fi l trati on or alum i ni um hyd rox i de oral l y. Met abol i c ac i d osi s (not due to ti ss ue hypoperfus i on) m ay be c orrec ted wi th di a l ys i s, fi l t rat i on or 1. 26% sodi um bi c arbonate i nfus i on.

Nephrotoxins and crystal nephropathies Al l nephrot oxi c agents shoul d be wi thhel d i f possi bl e . Al l ne ces sary d rug s s houl d hav e t hei r d osage modi fi ed acc ord i ng t o t he G FR. In some c as es uri nary e xcreti on of nephrotoxi ns and c rys tal s m ay be e ncouraged by uri nary al k al i ni sat i on to maint ai n thei r sol ubi l i ty wi th an i nd uce d d i ures i s (rhabd omyol ys i s , aci d i c cryst al s ). Di a l ys i s may al s o b e useful .

Glomerular disease Imm unosup pre ssi ve the rap y m ay be useful aft er di agnosi s has been confi rme d. Di al y si s i s often re qui red for t he more sev ere forms of gl omerul one phri ti s d esp i t e s teroi d re sponsi veness .

Urgent treatment of hyperkalaemia 10–20ml c al c i um chl ori d e 10% b y s l ow i ntravenous i njec ti on. 100m l 8.4% sodi um b i carb onat e i nt rav enousl y. Gl ucos e (50g) and i nsul i n (10–20IU) i ntrave nousl y wi th careful b l ood g l uc os e moni t ori ng and urge nt haem odi al y si s.

Renal replacement therapy Conti nuous haem ofi l trati on forms the mains tay of re pl a cem ent therapy i n cri ti cal l y i l l pati ent s who ofte n c annot tol erate hae mod i al ysi s d ue to hae mod ynam i c i nstabi l i t y. Peri toneal d i al ysi s i s not com monl y use d t oday. Acute renal fai l ure i n the cri ti cal l y i l l usuall y recovers wi thi n 1–6 wee ks; pe rmanent renal fai l ure i s rare . P.335

General indications for dialysis or haemo(dia)filtration Fl ui d exce ss (e. g. pul monary oe dema) Hype rkalae mi a (> 6.0mmol /l ) Metabol i c ac i dosi s (p H <7.2) due t o renal fai l ure Cl earance of di a l ys abl e nephrot oxi ns and ot her drugs Creati ni ne ri si ng >100µm ol /l /d ay Creati ni ne >300–600µmol /l Urea ri si ng >16–20mmol /l /day To c reate space for nutri ti on or drugs

See also: Hae mo(d i a)fi l trati on (1), p62; Haemo(di a )fi l trat i on (2), p 64; Pe ri t one al di al y si s , p 66; Cry stalloi d s, p176; Col l oi d s, p180; Di uret i c s, p212; Dopam i ne , p 214; Basi c resusc i tati on, p270; Fl ui d chal l eng e, p274; Ol i guri a , p330; Acute renal fai l ure—di a gnosi s , p 332; Hy perkal aem i a, p420; Hyp onatraemi a, p418; Hypocal cae mi a , p 428; M etabol i c aci dos i s , p434

Ovid: Oxford Handbook of Critical Care

Ed itors:

Si nge r, M ervyn; We bb, An dre w R.

Ti tle : O xf ord Ha ndbook of Cr itic al Car e, 2nd Ed ition Cop yri ght © 1997,2005 M. Si nge r and A. R. W ebb , 1997, 2005. Publ i shed i n the Uni te d Stat es by Oxford Uni ve rsi ty Press Inc > Tab le of Co n te n ts > Gas tr oi n te sti n al Di sor der s

Gastrointestinal Disorders

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Vomiting/gastric stasis Whi l e vom i ti ng per se i s re l at i v el y rare i n the ICU pati e nt, l arg e vol um e g ast ri c aspi rat es are commonpl ace and probab l y rep res ent t he m ajor reas on for fai l ure of ent eral nutri ti on.

Ileus Il eus affect s t he stomac h m ore frequent l y than t he res t of the g ast roi nt est i nal t rac t. Ab dom i nal s urg ery , d rug s (parti cul arl y opi ate s), gut d ysfunc ti on as a com ponent of mul ti -organ dy sfunct i on, hypoperfus i on and p rol ong ed starvati on m ay al l contri b ute to gas tri c i l eus . Earl y and c ont i nued us e of the b owel for feed i ng ap pears to mai ntain forward p rop ul s i v e ac ti on. Manage ment c ons i st s of t reati ng t he cause whe re pos si b l e, the use of m oti l i ty sti mul ant s suc h as m etocl oprami d e or e ryt hromyc i n and , i n res i st ant cases , b ypassi ng the st omach wi t h a nas oduode nal /nasoje junal tub e or a je junost omy.

Upper bowel obstruction Rel ati vel y unus ual ; apart from pri mary surgi cal cause s s uch as ne opl asm or adhesi ons , t he predom i nant cause i n the ICU i s gastri c outl e t obst ruc ti on. Thi s may be rel ate d t o l ong -st and i ng pe pti c ul c er di s eas e or m ay occur i n the short term from py l ori c and /or duode nal sw el l i ng conse que nt to gas tri ti s or d uod eni ti s . T hi s c an b e d i ag nos ed end osc opi cal l y and treat ed by bow el res t p l us an H 2 antagoni st , p rot on pum p i nhi bi tor or sucralfate.

Gastric irritation Drugs or chemi cal s—e i ther acc i d ent al or adve rs e reac ti on (e .g. st eroi d s, asp i ri n), i ntenti onal (e .g. al cohol , bl eac h) or the rap eut i c (e. g. i pe cac uanaha sy rup ) m ay i nduce vom i ti ng . Treat ment, whe re app rop ri a te, may c omp ri s e (i ) rem oval of the cause , (i i ) di l ut i on wi th cop i ous amounts of fl ui d (i i i ) ne utral i sati on wi th al kal i and/or H 2 ant agoni s t or p rot on pum p i nhi bi tor and (i v) adm i ni st rat i on of ant i -e met i c (e. g. met ocl oprami de).

Neurological St i mul at i on of the em eti c c ent re may fol l ow any neurol ogi cal ev ent (e. g. trauma, C VA), d rug therapy (e.g . che mot herapy ), pai n and m etabol i c di sturbance s. Manage ment i s b y treat i ng t he cause w here p oss i bl e and by jud i ci ous use of anti -em eti cs, i ni t i al l y met ocl oprami de or prochl orperazi ne. Consi der ondanset ron or grani set ron i f the se are unsuc ces sful . P.339

See also: Ent eral nut ri t i on, p 80; El e ctrol y tes , p 146; Opi oi d analge si c s, p234; Anti -em eti cs, p224; Gut moti l i t y agents, p226; Bow el perforati on and obs truct i on, p348; El e ctrol yte manage ment, p414; Poi s oni ng—general p ri nci pl es P.340

Diarrhoea The de fi ni ti on of di a rrhoea i n the ICU pat i ent i s p rob l em ati c as t he amount of st ool pas se d dail y i s d i ffi cul t to measure. Fre que ncy and consi st enc y m ay also vary si g ni fi c ant l y. Loose /wat ery and freq uent ( ≥ 4 × d ay) stool wi l l oft en req ui re i nve sti gati on and/or t re atme nt.

Commoner ICU causes Infe ct i on—Cl ost rid ium di ffi cil e, g ast roent eri ti s (e .g. Sal monell a, Shi gel la), rare r t rop i c al causes (e. g. chol era, dyse ntry, gi ard i as i s, trop i cal s prue). Drugs, e. g. ant i bi oti cs , l axat i v es. Gas troi nt est i nal — feed (e .g. l a ctose i nt ol e rance), c oel i ac di sease, ot her malab sorpti on syndromes , i nfl amm atory bowe l d i se ase , d i ve rti cul i t i s , p el v i c abs ces s, bow el obs tructi on wi t h overfl ow. Ent eral feed i s often i m pl i cat ed but rarel y c aus ati ve. For bl oody di arrhoe a c ons i de r i nfect i on, i schaem i c or i nfl am mat ory bowel di sease.

Diagnosis Rect al exami nati on to rul e out i mp act i on wi th ove rfl ow. Consi der si gmoi doscopy i f col i t i s or C. di ffi cil e s usp ect ed (pse udomem brane seen). Stool sent t o l aborat ory for MC & S, C. diffic ile toxi n. Fat est i mati on (mal abs orp ti on) i s rarel y neces sary i n the ICU pati e nt If i sc hae mi c or i nfl a mmatory b owel di sease sus pec ted , p erform a sup i ne ab dom i nal X-ray and i ns pec t for di l ate d l oop s of b owe l (N B toxi c megacol on), t hi c kened wal l s (i ncrease d s eparat i on be twe en l oops) and ‘t hum bpri nti ng’ (sug ges ti ve of m ucosal oe dema). Fl ui d l ev el s se en on ere ct or l at eral abdomi nal X-ray may be see n i n d i arrhoea or p aral y ti c i l eus and d o not nec ess ari l y i nd i c ate obs truct i on. D i arrhoea i s oft en but not always bl oody . If absc ess s usp ect ed, perform ul t ras onography or CT sc an

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Management 1. Tre at c aus e w here p oss i bl e e .g. for C. di ffi cil e, met roni dazol e p l us c hol esy trami ne (b i nds the toxi n). 2. Cons i de r t emp orary (12–24h) ces sat i on of ent eral feed i f ve ry sev ere . Consi de r c hange i n feed i f ap propri at e, e.g. coel i ac di sease, l a ctose i nt ol e rance. 3. Cons i de r s toppi ng ant i bi oti cs . 4. Gi v e anti di a rrhoeal i f i nfe cti on exc l ud ed. 5. Care ful at tenti on t o fl ui d and el e ctrol yte bal ance (i n parti cul ar Na + , K + , Mg 2 + ). 6. Request surgi cal opi ni on i f i nfarcte d or i nfl ame d b owe l or absc ess suspe cte d. P.341

See also: Ent eral nut ri t i on, p 80; Ant i di arrhoeal s, p228; Anti mi c rob i al s, p260; Abdomi nal sep si s , p 350; Infec ti on—d i ag nos i s , p480 P.342

Failure to open bowels Commoner ICU causes Prol onged i l eus /dec re ase d gut m oti l i ty (e. g. opi ates , p ost -surg ery ) Lac k of enteral nut ri ti on Bowe l obst ructi on— thi s i s a rel a ti v el y uncom mon sec ond ary ev ent and i s m ai nl y see n p ost -ope rat i v el y , ei ther afte r a curat i v e proc edure or w i t h de vel opm ent of adhesi ons

Management 1. Cl i ni c al l y e xcl ude ob struc ti on and c onfi rm p res enc e of st ool pe r rec tum . 2. Ens ure ade quate hyd rat i on. 3. Ant i const i p ati on the rap y may b e g i ve n, usual l y s tarti ng w i t h l axat i v es (e.g . l act ul ose or, for m ore urgent res ponse, mag nes i um sul p hat e), the n p roc eed i ng to gl yce ri ne s upp osi tori e s and, fi nal l y, enemata i f g ent l e r meas ure s p rov e unsucce ss ful . 4. Cons i de r red uci ng/stoppi ng dos e of op i at e i f p oss i b l e. P.343

See also: Ant i c ons ti p ati on age nts , p 230; Op i oi d anal ges i cs , p 234; Bowel perforat i ons and obs tructi on, p348; Abd omi nal se psi s, p350 P.344

Upper gastrointestinal haemorrhage Causes Pept i c ul cerati on Oes ophagi ti s /gastri t i s/duodeni ti s Vari ce s Mal l ory–W ei s s l owe r oesophag eal te ar Neop l as ms

Pathophysiology Pep ti c ul ce rat i on i s re l at ed to protec ti ve b arri e r l oss l e adi ng to aci d or b i l i ary d amage of t he und erl yi ng m ucosa and sub muc osa. Barri e r l oss oc curs sec ond ary to cri ti cal i l l ness , alcohol , d rugs, e.g . non-ste roi dal s, poi sons i nc l ud i ng corrosi v es. Di rec t d amage, es pec i al l y at the l ower oes ophagus, may oc cur from feed i ng t ube s. Muc osal d amag e (‘s tress ul cers’) may al so occ ur as a c ons equenc e of t i ss ue hyp ope rfusi on. Gas tri c hyp ers ecreti on i s unc omm on i n cri ti cal l y i l l p ati ent s; i nd eed , g ast ri c ac i d conte nt and sec re ti on i s ofte n reduced .

Prophylaxis Smal l -bore fe edi ng tub es Nasogas tri c ent eral nutri t i on (nasoj ejunal and p are nte ral fe edi ng has al so been shown to re duc e t he i nc i de nce of

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stress ul cer bl eed i ng) Ade quat e t i s sue pe rfusi on (fl ow and p res sure) The rol e of p rop hyl act i c drug the rap y i ncl udi ng H 2 antagoni st s, proton pump i nhi bi tors and sucralfate i s cont roversi a l . Evi dence sug ges ts that e nte ral nutri ti on al one i s as effect i ve and there are c l ai ms that l os s of t he aci d envi ronment i n t he s tomach predi sp ose s t he pat i ent t o nosoc omi al i nfec ti on. Pat i ents at hi g hes t ri s k are thos e requi ri ng prol onge d m echani cal ve nti l at i on or wi th a c onc urrent c oag ul opat hy.

Treatment of major haemorrhage Fl ui d res usc i tati on w i t h c ol l oi d and b l ood wi th bl ood products as ap propri ate to corre ct any coagul op athy. Mai ntai n haem ogl obi n b etw een 7–10g /dl and have ade quat e c ross-matc hed bl ood av ai l abl e s houl d further l arge haem orrhag es occ ur. If p oss i b l e, di sconti nue any on-goi ng anti coagul ati on, e. g. hepari n. Urg ent di agnost i c fi b reopti c e ndoscopy. Local i njec ti on of e pi nephri ne or a sc l e ros ant i nto (or therm al sealing of) a bl eed i ng pe pti c ul c er bas e m ay hal t furt her bl eed i ng . Li ke wi s e, bandi ng or s cl e ros ant i njec ti on may arrest bl e edi ng vari ce s. If oesophageal v ari ces are k nown or hi ghl y sus pec ted , c ons i de r v asopre ssi n or t erl i p res si n ± a Seng staken-ty pe tub e for s eve re hae morrhage, ei the r as a bri dg e t o endos cop y or i f b and i ng /i njec ti on i s uns ucc ess ful . R emem ber that s ources of bl eedi ng other than v ari ce s may b e p res ent , e .g. pe pti c ul ce r. For pep ti c ul ce rat i on and g eneral i se d i nfl amm ati on com mence an H 2 antag oni st or proton pump i nhi bi tor. Gi v e i nt rav enousl y t o ensure effe ct. Enteral ant aci d may al s o b e b ene fi c i al . Surgery i s rare l y nec ess ary but s houl d be consi dered i f b l e edi ng conti nues , e .g. >6–10 uni t t ransfusi on req ui reme nt. Inform a surge on p rom ptl y of any pat i ent w i th major bl eedi ng . P.345

See also: End otracheal i ntubat i on, p 36; Sengst ake n-t ype tub e, p72; Uppe r g ast roi nt est i nal e ndoscopy, p74; Coagul at i on moni tori ng, p156; Col l oi ds, p180; Bl ood transfusi on, p182; H 2 bl ocke rs and proton p ump i nhi b i t ors , p 218; Suc ral fat e, p220; Ant aci ds , p222; Coagul ant s and ant i fi bri nol yt i cs , p 254; Basi c re sus ci tat i on, p 270; Fl ui d challe nge , p 274; Vom i t i ng /gas tri c stasi s, p338; Bl eed i ng vari c es, p346; Bl e edi ng di s ord ers , p 396; Sy ste mi c i nfl ammati on/m ul t i organ fai l ure, p484 P.346

Bleeding varices Vari c es dev el op fol l owi ng a prol onge d p eri od of portal hy pertensi on, usual l y rel ate d t o l i ve r c i rrhosi s . Approxi mat el y one thi rd wi l l bl eed . T hey are commonl y found i n the l ower oe sop hag us but , occasi onal l y, i n the s tom ach or duodenum. Torre nti al hae morrhage may occ ur. Approxi mat el y 50% of pati e nts di e w i t hi n 6 week s of p res ent ati on of the i r fi rst bl eed ; e ach subse quent b l e ed c arri e s a 30% mortali ty.

Management 1. If airway and /or breat hi ng are com promi s ed, pe rform end otracheal i ntub ati on and i nsti tute mechani cal vent i l ati on. Thi s fac i l i tates Se ngs tak en-t ype tube pl a cem ent and e ndos copy b ut may be as soc i at ed wi t h s evere hypotensi on s econdary to cov ert hy pov ol a emi a. If p oss i b l e, ensure adequate i ntravas cul ar fi l l i ng be fore i nt ubati on. 2. Fl ui d res usc i tati on w i t h c ol l oi d and b l ood wi th bl ood products as ap propri ate to corre ct any coagul op athy. Ens ure good ve nous acce ss (at l e ast two 14G c annul a e). Group -sp eci fi c or O-neg ati ve bl ood may be nee ded for emergency use . M ai ntai n haem ogl obi n > 10g /dl and have at l east 4 uni t s of c ros s-m atc hed bl ood avail abl e for urg ent trans fus i on. T here i s a theoreti cal ri sk that over-transfusi on m ay p rec i p i tate furthe r b l ee di ng b y rai s i ng portal venous pres sure. Cardi a c outp ut moni tori ng s houl d be consi d ere d i f t he pat i ent remains haemodynami cal l y uns tab l e or the re i s a hi st ory of heart di sease. 3. If b l ee di ng i s torrenti a l , i nsert a Se ngs tak en-t ype tube and commence adm i ni st rat i on of IV vasopre ss i n/terl i p res si n (q. v.). 4. Gent l e pl ace ment of a l arge-bore nasogas tri c t ube i s a reasonabl y s afe proce dure t hat fac i l i tates drai nag e of bl ood, l es se ns the ri sk of aspi rati on and can be use d t o asse ss conti nui ng bl ood l os s. 5. Perform urgent fi breop ti c e ndoscopy t o e xcl ude ot her sourc es of bl e edi ng. Thi s al so p ermi t s v ari ceal b and i ng or l oc al i nj ect i on of a s cl erosi ng agent. Bl e edi ng i s arres ted i n up to 90% of cases . Endoscopy may be i mp oss i bl e i n the short te rm i f bl e edi ng i s too se vere. It may hav e t o be de l ay ed for 6–24h unti l a peri od of tamponade by the Sengst aken-ty pe tub e ± vas opress i n has enabl ed som e c ont rol of the b l ee di ng. 6. Ei t her oc tre oti de, vasop res si n or te rl i press i n can be ad mi ni s tered for sev ere bl eed i ng , or p rop hyl axi s agai ns t fres h b l e edi ng. Vasop res si n control s b l ee di ng i n approxi mat el y 60% of cases and i ts effi cacy and safet y ap pears to b e e nhance d b y c onc urrent GT N. The si de-effe ct profi l e of t erl i p res si n i s l ower as i t d oes not ap pear t o pre ci p i tate as muc h m ese nte ri c , c ard i ac or di gi tal i s chaemi a, Oct re oti de i s a s omat os tat i n analog ue b ut l onger-act i ng t han i t s p are nt com pound; l i ke s omatos tat i n, i t i s p rob abl y as e ffec ti ve as v asopre ss i n but wi thout

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the si de-e ffe cts . 7. If b l ee di ng c ont i nues aft er prol onge d b al l oon tamponade (2–3 days ) and rep eat ed endosc opy, consi der transj ugul ar i ntrahep ati c portos yst emi c s tented shunt (T IPSS). Thi s can be pe rforme d q ui c kl y and c arri es a rel ati vel y l ow mortal i ty compared to surge ry al t hough the ri sk of enc ephal opat hy i s i nc reased . 8. The tradi ti onal al ternat i ve to TIPSS i s oesop hag eal trans ec ti on (now performed wi th a s tap l e gun) wi th or wi t hout de vas cul ari sati on. Mortal i t y i n t he acut e s i t uat i on i s of the orde r of 30%. P.347

Drug dosages Octreotide

50µg bolus then 50µg/h infusion

Vasopressin

20 units over 20min then 0.4 units/min infusion Also give glyceryl trinitrate 2–20mg/h to counteract myocardial and mesenteric ischaemia

Terlipressin

2mg IV followed by 1–2mg IV 4–6-hrly until bleeding controlled for up to 72h

See also: End otracheal i ntubat i on, p 36; Sengst ake n-t ype tub e, p72; Uppe r g ast roi nt est i nal e ndoscopy, p74; Coagul at i on moni tori ng, p156; Col l oi ds, p180; Bl ood transfusi on, p182; Bas i c re sus ci tat i on, p 270; Fl ui d challe nge , p 274; Up per gas troi ntes ti nal hae morrhage, p344; Acute l i v er fai l ure, p360; Chroni c l i v er fai l ure, p364 P.348

Bowel perforation and obstruction Pat i ents wi t h b owe l p erforati on or obst ruc ti on may be adm i tt ed to the IC U after surg ery , for p re-ope rat i ve res us ci t ati on and cardi ore spi ratory opti mi s ati on, or for c ons erv ati ve manage ment . Al t hough rarel y oc curri ng de novo i n the IC U p ati ent , t hes e c ond i ti ons may b e d i ffi cul t to di a gnose bec aus e of se dat i on ± mus cl e re l ax ati on. Consi der whe n t here i s: Abd omi nal pain, te nde rne ss, pe ri t oni sm Abd omi nal di ste nsi on Agi tat i on Inc reased nas ogast ri c as pi rat es, vom i ti ng Inc reasi ng m etabol i c aci dos i s Si g ns of hypovol aem i a or sep si s A fi rm di ag nos i s i s oft en not mad e unti l l ap arotom y al though supi ne and ei t her erec t or l ate ral ab dom i nal X-ray m ay rev eal ei the r free gas i n t he peri toneum (perforati on) or di l at ed bowe l l oop s w i t h mul t i pl e fl ui d l eve l s (ob struc ti on). Ul t rasound i s usual l y unhe l pful though faecal fl ui d m ay occ asi onally be as pi rate d from the pe ri toneum fol l owi ng perforati on. It may be di ffi cul t t o d i st i ngui sh bow el obs tructi on from a paral yti c i l e us as (i ) bow el sounds may be prese nt or abs ent i n ei the r and (i i ) X-ray appe arance s m ay b e s i mi l a r.

Management 1. Correc t fl ui d and el e ctrol y te abnorm al i ti es. Res usc i t ati on shoul d be promp t and aggres si v e and usuall y c ons i st s of c ol l oi d repl ace ment p l us bl ood to mai nt ai n Hb >7g /dl . Inot rop es or vas opress ors may b e requi re d t o rest ore an adeq uat e c i rc ul ati on, parti cul arl y fol l ow i ng pe rforat i on. Earl y c ard i ac output m oni tori ng s houl d be consi d ere d i f t he ci rcul at ory st atus remains unst abl e or v asoact i ve drugs are requi re d. 2. The surgeon s houl d be i nform ed earl y. A conservat i ve ap proach may be ad opt ed, e. g. wi t h upper s mal l b owel perforati on; how eve r, surgery i s usuall y requi re d for l arge bowe l p erforati on. Sm al l or l a rge bowel ob struct i on may som eti mes be manage d c ons erv ati vel y as s pontaneous resol ut i on may occur, e.g . adhes i ons. Promp t expl orati on shoul d be enc ourage d i f t he pat i ent s how s s i gns of s yst emi c t oxi ci ty. 3. Bot h c ons erv ati ve and pos t-operati ve manage ment of pe rforat i on and obst ruc ti on usual l y requi re conti nuous nasogas tri c drainage to dec omp res s t he stomac h, ni l by mouth and parenteral nut ri ti on. 4. Pai n rel i ef shoul d not b e wi thhel d. 5. Broad spe ctrum ant i bi oti c the rap y s houl d be c omm enc ed for bowel perforati on aft er app rop ri ate sp eci mens have been taken for l aborat ory anal y si s . T herapy us ual l y com pri ses ae rob i c and anaerobi c Gram ne gat i ve cover (e. g. 2nd or 3rd ge nerati on cep hal os pori n, qui nol one or c arb ape nem , pl us met roni d azol e ± am i nogl ycos i d e).

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6. Post -op erati v e m anageme nt of bow el perforati on may i nv ol v e repe ate d l aparot omi es to exc l ud e c ol l ect i ons of p us and bow el i sc hae mi a /i nfarcti on; surge ry shoul d be ex ped i te d i f t he pat i ent's condi ti on det eri orates . Al t ernati vel y, reg ul ar i magi ng ± drai nage of col l ec ti ons may be ne ede d. P.349

See also: Parent eral nutri t i on, p 82; Fai l ure t o open bowel s , p 342; Abdomi nal sep si s, p350; Pancreat i ti s, p354; Met abol i c aci dos i s , p 434; Sy ste mi c i nfl a mmati on/m ul t i organ fail ure , p 484; Post -op erati v e i nte nsi ve care, p534 P.350

Lower intestinal bleeding and colitis Causes of lower gastrointestinal bleeding Bowe l i sc hae mi a /i nfarcti on Infl amm atory bow el di s eas e (ul c erati v e c ol i ti s, Crohn' s d i se ase ) Infe ct i on, e. g. Shige lla, Campy lob act er, am oeb i c dys ent ry Uppe r g ast roi nt est i nal s ource , e. g. pep ti c ul ce rat i on Ang i od ysp l as i a Neop l as m Al though re l at i ve l y rare, mas si v e l owe r g ast roi nte st i nal haemorrhag e c an b e l i fe -threateni ng .

Ischaemic/infarcted bowel Can oc cur fol l owi ng p rol ong ed hyp ope rfusi on or, occ asi onally , s econdary to a m esenteri c em bol us. It us ual l y pre sents wi t h s eve re abd omi nal pain, bl ood y d i arrhoea and si gns of sys te mi c toxi c i ty i ncl udi ng a rapi dl y i ncreasi ng met abol i c aci dos i s . Pl as ma p hos phate l ev el s may also be el evat ed. X-ray ap pearances of thi ck ene d, oede mat ous bowel l oops (‘t hum b p ri nti ng’ ) wi th an i ncre ase d d i st anc e b etw een bow el l oops are sugge sti ve. Treat ment i s b y rest orati on of ti ssue p erfusi on, bl ood trans fus i on to maint ai n haemog l obi n >7g /dl and, i f cl i ni cal fe atures fail to set tl e promp tl y, l ap arotom y w i th a vi e w to bowel ex ci s i on.

Inflammatory bowel disease Pre sents wi t h w ei g ht l os s, abd omi nal pain and di arrhoea w hi c h usuall y c ont ai ns b l ood. Comp l i cat i ons of ul ce rat i ve col i t i s i nc l ude p erforati on and tox i c meg acol on whi l e compl i c ati ons of Crohn' s d i s eas e i ncl ude fi stul ae , absc ess es and perforati ons . Manage ment i nvol ves : 1. Fl ui d and el e ct rol yte re pl a cem ent . 2. Bl ood transfusi on to mai ntain hae mogl ob i n >7g/dl . 3. Hi g h d ose st eroi ds IV and, i f di s tal bowel i nvol vem ent , b y enema. 4. Nut ri t i on (ofte n p are nte ral ). 5. Regul ar surg i cal revi ew. Surge ry may be i ndi c ate d i f s ymp tom s fail to se ttl e afte r 5–7 days , for tox i c meg acol on, perforati on, abs ce sse s or obst ruc ti on. 6. Ant i di arrhoeal drugs shoul d b e av oi d ed.

Angiodysplasia Usual l y p res ent s as fres h b l e edi ng per re ctum and t hi s m ay b e c ons i de rab l e . It i s d ue to an arte ri ovenous mal format i on and c omm oner i n t he e l d erl y. Loc al i sat i on and e mbol i s ati on by ang i og rap hy may be curat i ve duri ng act i ve bl eed i ng , Surgery m ay b e requi red i f b l ee di ng fai l s to set tl e on conse rvati v e manag eme nt and , oc casi onal l y, ‘bl i nd’ l ap aroscopi c em bol i s ati on of a me senteri c ves sel . Howe ver, l ocalis ati on of the l e si on m ay be d i ffi c ul t at l ap arotom y, nec ess i tati ng exte nsi ve bow el res ect i on. P.351

See also: Col l oi ds , p180; Bl ood trans fus i on, p 182; Coagul ants and ant i fi bri nol yt i c s, p254; Basi c resusci tat i on, p270; Fl ui d chall eng e, p 274; Bowe l p erforati on and obs tructi on, p348; Bl eed i ng di sorders, p396 P.352

Abdominal sepsis Thi s i s a c ommon b ut di ffi c ul t t o di ag nos e condi ti on i n i nt ens i ve care pat i ents. A proporti on of s uc h p ati ent s are adm i tt ed fol l ow i ng l a parotomy but ot hers m ay deve l op ab dom i nal s eps i s de nov o or as a se condary c omp l i c ati on fol l ow i ng ab dom i nal s urg ery, i n p arti c ul a r afte r b owe l rese cti on. Se psi s may ei t her be l ocal i s ed to an organ, e.g . chol ec yst i t i s, or the p eri toneal cavi t y (abs ces s); al ternat i ve l y, there may b e a generalis ed peri t oni ti s . N on-bow el

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i nfect i on or i nfl ammati on c an present i n a si mi l ar manne r, e.g . p anc reati t i s, chol ecys ti ti s , g ynaecol og i cal i nfect i on, pye l onephri t i s .

Clinical features Non-spe ci fi c si gns i ncl udi ng pyrexi a (e spe ci al l y s wi ngi ng), ne utrophi l i a, fal l i ng pl a tel et count, i ncreasi ng metabol i c ac i dosi s , c i rcul atory i ns tab i l i ty Abd omi nal di ste nsi on ± l ocalis ed di scomfort, peri t oni sm Abd omi nal mas s, e.g . g al l b l ad der, p seudoc yst , absc ess Fai l ure t o t ol e rat e enteral fee d/l arg e nasogas tri c asp i rates Pl eural e ffus i on (i f s ubd i ap hragmati c s eps i s) Di a rrhoea (i f pe l vi c sep si s )

Diagnosis Ul t ras ound CT s can Lap arotomy Gal l i um w hi t e c el l sc ans are occasi onal l y us eful for i de nti fi c ati on of abs ces ses . Sam pl e s s houl d be tak en for mi crobi ol og i c al anal ys i s from b l ood, uri ne, st ool , abdomi nal drain fl ui d and vagi nal di s charg e i f p res ent . A sampl e of pus i s pre ferred to a s wab . Hype ram yl a sae mi a may sugge st pancre ati ti s t hough amy l as e l eve l s can al so be el e vate d w i th ot her i ntra-ab dom i nal p athol ogi es.

Treatment Ant i bi oti c the rap y provi di ng Gram negati v e and anae rob i c cov er (e. g. 2nd or 3rd g enerat i on ce phalos pori n, qui nol one or carbapene m, pl us m etroni dazol e ± ami nog l yc osi de). T reatme nt can be ame nde d d epe ndi ng on cul ture resul t s and p ati ent resp ons e. Ul t ras oni c or C T-g ui d ed drainage of p us. Lap arotomy wi th rem oval of p us, peri t one al l av age , et c. A negati v e l aparot omy shoul d b e v i ewe d as a us eful m eans of ex cl udi ng i nt ra-abdomi nal sep si s rather than an unnece ssary proced ure. Laparot omy shoul d b e e ncouraged i f the p ati ent de teri orate s and a hi gh suspi ci on of abd omi nal pathol og y p ers i st s. Chol ec yst i t i s, wi th or wi t hout (acal cul ous) gal l st one s, may prese nt wi t h s i gns of i nfe cti on. There i s a charac teri s ti c ul t rasound appe arance of an enl arged organ wi t h a thi c kene d, oed ematous wall surround ed by fl ui d. Treat ment i s oft en conservat i ve wi th ant i bi oti cs (as ab ove ) and p erc ut aneous, ul trasound -gui de d drai nag e vi a a pi gtail cathe ter. Chol ec yst ect omy i s rarel y nece ssary i n the ac ute si tuati on unl ess the g al l bl add er has pe rforat ed, thoug h s ome aut hori t i es argue that thi s i s t he treatm ent of choi c e for acalcul ous c hol ecy st i ti s. P.353

See also: Parent eral nutri t i on, p 82; Bac teri ol og y, p158; Col l oi d s, p180; Inot rop es, p196; Vasop res sors, p200; Ant i mi crobi a l s , p260; Bas i c res us ci t ati on, p270; F lui d c hal l e nge, p274; Bowel pe rforat i on and ob st ruc ti on, p348; Panc reati t i s , p 354; Infect i on—di ag nos i s, p480; Infect i on—treat ment, p482; Syst emi c i nfl am mati on/mul ti org an fai l ure, p484; Sep si s and sep ti c s hoc k t reatment, p550; Pai n, p 532; Post -op erati v e i nte nsi ve care, p534 P.354

Pancreatitis Infl am mat i on of the p anc reas and s urroundi ng ret rop eri toneal t i ss ues . T he app earanc e of the p anc reas m ay range from m i l d l y oed ematous t o haemorrhagi c and nec roti s i ng . A ps eud ocy st may de vel op w hi c h c an bec ome i nfec ted and the bi l e duc t m ay be obs tructe d c aus i ng bi l i ary ob struct i on and j aundi c e. Though mortalit y i s quot ed at 5–10%, thi s i s muc h hi g her (ap prox. 40%) i n t hos e wi th sev ere pancreat i t i s req ui ri ng i nte nsi ve care.

Causes Al c ohol Gal l st one s Mi s cel l aneous, e.g . i schaem i a, traum a, vi ral , hy perl i p i d aemi a Part of the m ul t i pl e org an fai l ure s ynd rom e

Diagnosis

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Non-spe ci fi c features i ncl ude central, sev ere ab dom i nal p ai n, p yre xi a , haemodynami c i nst abi l i ty, vomi t i ng , i l e us. Di s col ourati on around the umbi l i cus (Cul l en' s s i gn) or fl anks (Grey T urner's si g n) i s rarel y s een. Pl as ma enz yme s—e l ev ate d l evel s of amyl ase (usually >1000IU/m l ) and pancreat i c l i pas e are s ug ges ti v e b ut non-spe ci fi c . Level s may be normal , e ven i n se vere pancreat i t i s. Ul t ras ound CT s can Lap arotomy

Complications Mul ti -org an dys func ti on syndrome Infe ct i on/abs ces s formati on Hypocal cae mi a Di a bet es mel l i t us Bl e edi ng

Management Gene ral me asures i ncl udi ng fl ui d re sus ci t ati on, maint ai ni ng Hb at 7–10g /dl , res pi ratory sup port, analge si a , and anti -em eti cs . Routi ne ant i b i ot i c the rap y i s of unprove d b enefi t . Ade quat e m oni tori ng s houl d be i ns ti t ut ed, i ncl udi ng c ard i ac output m oni tori ng i f c ard i oresp i ratory i ns tab i l i ty i s pre sent. The pat i ent i s convent i onal l y kept ni l by mout h w i th conti nuous NG drai nage , and nutri t i on and v i tami ns provi d ed IV. Howeve r, rec ent st udi es show s afe ty and effi c acy of di s tal nasoj ejunal —and e ven nasogas tri c— ent eral feed i ng . Gal l st one ob struct i on s houl d be rel i ev ed e i t her endos cop i cally or surgi cally . Hypocal cae mi a , i f s ymp tom ati c, shoul d be treat ed by i nt erm i t tent s l ow IV i njec ti on (or, oc cas i onal l y, i nfusi on) of 10% cal ci um c hl ori de. Hype rgl yc aemi a s houl d be control l ed by a conti nuous i nsul i n i nfusi on. No s pec i fi c tre atm ent i s routi nel y used . The rol e and ext ent of surge ry rem ai ns c ont rov ers i al ; Some ad voc ate percutaneous drai nag e of i nfec ted and/or necrot i c deb ri s whi l e surg ery frequent l y consi s ts of reg ul a r (oft en dai l y) l a parotomy w i th de bri dem ent of ne croti c ti s sue and p eri toneal l a vag e. Pseudoc yst s m ay res ol v e or requi re drai nag e ei ther percut ane ous l y or i nt o t he bowe l . P.355

Ranson's signs of severity in acute pancreatitis On hos pit al adm iss ion: Age >55 ye ars ol d Bl ood gl ucos e >11mm ol /l Serum l ac tat e d ehyd rogenase (LD H) >300U/l Serum asp art ate ami not ransferase (AST) > 250U/l Whi te bl ood c ount > 16× 10 9 /l At 48 h afte r admi ssi on: Haem atocri t fal l >10% Bl ood ure a ni troge n ri se >1mmol /l Serum cal ci um < 2mmol /l PaO 2 <8kPa Art eri al bas e d efi ci t >4mmol /l Est i mated fl ui d se que strati on >6000m l Pancre ati ti s s evere i f m ore than 2 c rit eri a m et wit hin 48h of ad mis si on

Imrie scoring system Whi te bl ood count >15 × 10 9 /l

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Bl ood gl ucose > 10m mol /l Bl ood urea ni t rog en > 16m mol /l LD H >600IU/l AST >200IU/l Al bum i n <32g /dl Pl a sma calci um <2m mol /l PaO 2 < 8kPa Pancre ati ti s s evere i f m ore than 2 c rit eri a m et wit hin 48h of ad mis si on

APACHE II scoring system Pancre ati ti s s evere i f APAC HE II score>8

See also: Venti l at ory support— ind i c ati ons , p 4; Enteral nut ri ti on, p80; Parent eral nutri t i on, p 82; Bas i c re sus ci t ati on, p270; F l ui d chall eng e, p 274; R esp i ratory fai l ure, p 282; Acut e resp i ratory d i s tre ss syndrome (1), p292; Acute res pi ratory di stress syndrome (2), p294; Hypot ens i on, p 312; Ol i guri a, p330; Abd omi nal se psi s, p350; Me tab ol i c aci dos i s, p434; Sys tem i c i nfl am mat i on/mul ti organ fai l ure, p484; Seps i s and se pti c shock—tre atm ent , p 486; Pai n, p532

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Ed itors: Si nge r, M ervyn; We bb, An dre w R. Ti tle : O xf ord Ha ndbook of Cr itic al Car e, 2nd Ed ition Cop yri ght © 1997,2005 M. Si nge r and A. R. W ebb , 1997, 2005. Publ i shed i n the Uni te d Stat es by Oxford Uni ve rsi ty Press Inc > Tab le of Co n te n ts > H ep ati c D isor de r s

Hepatic Disorders Jaundice Jaundi ce i s a c l i ni c al di a gnosi s of ye l l ow p i gm ent ati on of s cl era and s ki n re sul ti ng from a rai sed pl asm a b i l i rubi n. It i s usual l y v i s i bl e w hen the pl as ma b i l i rubi n ex cee ds 30–40µ mol /l .

Commoner causes seen in the ICU Pre-hep ati c—i nt rav asc ul a r haem ol y si s (e .g. drugs , m al a ri a , haem ol y ti c uraem i c syndrome), Gi l bert 's sy ndrome . Hepatoc el l ul ar— cri ti cal i l l ness , v i ral (hep ati ti s A, B, C , Ep st ei n–Barr), alcohol , d rug s (e.g . p aracet amol , hal othane), t oxopl a smosi s , l ept osp i rosi s. Chol est ati c— cri ti cal i l l ness , i ntrahe pat i c causes (e .g. drugs such as chl orpromaz i ne , eryt hromyc i n and i s oni azi d, pri mary b i l i ary ci rrhos i s ), e xtrahe pat i c causes (e .g. bi l i ary obs truct i on by galls tones, ne opl asm , p anc reati t i s ).

Diagnosis Uri nal ysi s—unconjugat ed bi l i rubi n d oes not appear i n the uri ne . Meas ure ment of c onj ugat ed and unconjug ate d b i l i rubi n—conjugat ed bi l i rubi n p red omi nat es i n chol es tat i c jaundi c e, unc onj ugated bi l i rub i n i n pre -he pat i c jaundi ce, and a mi xed pi cture i s oft en see n i n hepat oce l l ul a r jaundi c e. Pl as ma al k al i ne phosphatase i s usual l y markedl y e l ev ate d i n obst ruc ti ve jaundi ce w hi l e p rothromb i n ti m es, aspart ate trans ami nas e and alani ne am i notrans ferase are el evated i n he pat oce l l ul ar jaund i c e. Ul t ras ound or CT sc an wi l l di a gnose extrahepat i c bi l i a ry obs truct i on.

Management 1. Identi fy and treat cause. Where possi bl e, d i s conti nue any drug that c oul d b e i mpl i cated . If e xtrahe pat i c, cons i d er percut ane ous trans hep ati c d rai nage, bi l e duc t s tenti ng or, rarel y, s urgery. 2. Li v er bi opsy i s rarel y nece ssary i n a j aundi c ed ICU pati e nt unl ess the d i ag nos i s i s unknow n and the pos si bi l i t y exi s ts of l i ver i nvol vem ent i n the underl y i ng pathol og y, e.g. mali gnancy. 3. Non-obs truct i ve jaundi ce us ual l y set tl e s w i th conse rvati v e m anageme nt as the pati e nt rec ove rs. 4. An ant i hi stami ne and top i cal c al a mi ne l oti on may provi de sym ptomat i c rel i ef for p ruri t us i f troubl esome. Chol est yrami ne 4g t ds PO may be hel pful i n obs tructi ve jaundi ce.

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P.359

See also: Li ver funct i on te sts , p 152; Ac ute l i ver failure, p360; C hroni c l i ver fail ure , p 364; Hae mol ysi s, p404; Infect i on control — general p ri nci pl e s, p476; Infec ti on—d i ag nos i s, p480; Infect i on—treat ment, p482; Sys temi c i nfl am mat i on/mul ti organ fai l ure, p484; HELLP s ynd rom e, p540 P.360

Acute liver failure Thi s c ond i t i on re sul ts from m ass i ve ne crosi s of l i ver c el l s l ead i ng to se vere l i ve r d ysfunc ti on and enc ephal opat hy. Survi val rates for l i ve r fai l ure wi th Grade 3 or 4 he pat i c enc ephal opat hy vary from 10–40% on med i c al the rap y alone, to 60–80% wi th ort hot opi c l i ve r t ransp l antat i on.

Major causes Al c ohol Drugs, parti cul arl y parace tam ol overdos e Vi ral hep ati ti s, parti c ul arl y hepat i t i s B, hep ati ti s C Poi s ons , e .g. carbon t etrac hl ori d e Acute dec ompe nsati on of c hroni c d i se ase , e. g. fol l ow i ng i nfec ti on

Diagnosis Shoul d be consi dered i n any pat i e nt pre senti ng w i th jaund i ce , g ene ral i se d b l ee di ng, enc ephal opat hy or marked hypogl y cae mi a . Abnorm al l i v er functi on tes ts , i n p art i cul ar, p rol onged PT or INR and hyperbi l i rub i naemi a. In seve re l i ver fai l ure, pl a sma enz yme l e vel s m ay not be el e vat ed.

Management Gene ral me asures i ncl ude fl ui d re sus ci tat i on and b l ood t ransfusi on t o k eep Hb 7–10g/dl . The c i rc ul ati on i s usual l y hyperdy nami c and di l at ed; vas opress ors may b e need ed t o m ai ntai n an adeq uat e BP. Correc ti on of coagul op athy i s ofte n w i thhel d as t hi s provi des a good g ui d e t o recovery or t he need for transp l antat i on. Use of fres h frozen pl asma i s rest ri c ted to pati e nts who are bl e edi ng or are ab out to und ergo an inv asi ve p roced ure . Ade quat e m oni tori ng s houl d be i ns ti t ut ed i f c ardi ores pi ratory i nstabi l i t y i s p res ent . Mechani cal ve nti l a ti on m ay b e nece ssary i f the ai rway i s unprote cte d or resp i ratory fai l ure d eve l op s. Lung s hunts are fre que ntl y p res ent , c aus i ng hypox aem i a. Infe ct i on i s commonpl ace and i s frequent l y ei the r Gram posi t i ve or fungal. Cl i ni c al si gns are often ab sent. Samp l e s of bl ood , s put um, uri ne, w ound s i te s, drain fl ui d , i ntravascul ar c atheter s i te s and asc i te s s houl d be sent for reg ul ar mi c rob i ol ogi cal s urv ei l l ance. Syst emi c anti mi c rob i al t herapy , wi th or wi t hout s el ect i ve gut decontami nati on, has b een shown to re duc e t he i nfe ct i on rate. Fungal i nfec ti ons are al so wel l rec ogni se d. Som e Li v er Uni ts gi v e p rop hyl act i c ant i fung al the rap y. Hypogl y cae mi a i s a com mon oc currence. It shoul d b e freq uentl y moni t ore d and tre ate d wi th ei the r e nte ral (or parent eral) nut ri t i on, or a 10–20% g l uc ose i nfus i on to maint ai n normogl y cae mi a . Renal fai l ure oc curs i n 30–70% of cas es and may ne ces si tat e renal repl ace ment t herapy . T he i nc i de nce may be red uce d by careful mai nte nance of i nt rav asc ul a r v ol ume. Vasop res si n/t erl i pres si n has also be en used suc ces sful l y for hepatorenal s ynd rom e. Uppe r g ast roi nt est i nal b l ee di ng i s more c ommon d ue to the ass oc i at ed coag ul opat hy. Prophyl a ct i c H 2 bl ock ers or proton pum p i nhi bi tors m ay be of b ene fi t . N-ac ety l c yst ei ne and/or e pop ros tenol i mp rov es O 2 consum pti on. Thoug h t i ss ue hyp oxi a m ay b e reduced by these drugs, parti cul arl y when vasop res sor drug s are need ed, outcome bene fi t remai ns unproved. Cort i c ost eroi ds , p ros tag l andi n E and charcoal haemoperfus i on have not bee n s how n t o have any outcome b ene fi t . P.361

See also: Venti l at ory support— ind i c ati ons , p 4; Li ver funct i on te sts , p 152; Coagul at i on moni t ori ng, p156; Hep ati c enc ephal opat hy, p362; Parace tam ol poi soni ng, p 456 P.362

Hepatic encephalopathy Grading

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1. Confuse d, al t ere d m ood 2. Inap propri at e, drowsy 3. Stuporose but rous abl e, very c onfused , agi t at ed 4. Coma, unre sponsi ve to pai nful s ti m ul i The ri sk of cerebral oed ema i s far hi gher at Grades 3 and 4 (50–85%) and i s the l e adi ng cause of d eat h. Sug ges ti v e si gns i ncl ude sys tem i c hyp ert ens i on, p rog re ssi ve heart rat e s l ow i ng and i ncreas i ng muscl e ri g i di ty. These oc cur at i nt racrani a l p res sures >30mmHg.

Management Correc t/av oi d potenti a l aggravati ng fact ors, e.g. gut haem orrhag e, ove r-s edat i on, hypoxi a , hypogl y cae mi a , i nfect i on, e l ec trol yt e i mbalance. Cons i de r e arl y i nt rac rani al pres sure (ICP) moni t ori ng. CT and c l i ni c al feat ures correl ate poorl y w i th IC P t hough no c ont rol l e d s tud i es have yet bee n p erform ed to show outcome benefi t from ICP moni t ori ng whi ch carri es i ts own com pl i cat i on rate (bl eed i ng , i nfe ct i on). Mai ntai n pat i ent i n s l i g ht head-up p osi ti on (20–30° ). Regul ar l act ul ose, e. g. 20–30ml qd s PO, to achi ev e 2–3 bowe l m oti ons /day. Di e tary rest ri cti on of p rotei n i s now not enc ourage d as t hi s promotes endog enous protei n uti l i s ati on. Hype rve nti l a ti on t o achi eve a PaCO 2 of 3. 5–4kPa i s often at tem pte d b ut i s fre que ntl y unsucce ssful i n achi e vi ng i mp rov ement. It may al so com promi s e c ere bral b l ood fl ow . Manni t ol (0.5–1m g/k g over 20–30m i n) i f se rum os mol al i ty <320mOsmol /k g and ei t her a rai sed IC P or c l i ni cal si g ns of c erebral oed ema persi st. If se vere renal dy sfunct i on i s p res ent , use renal rep l ac eme nt the rap y i n conj unc ti on wi t h manni tol . Sod i um benzoate (2g td s PO) may be consi d ere d i f t he pat i ent i s s eve rel y hype ram monaemi c. If no resp ons e t o abov e, c ons i d er barbi t urate adm i ni st rat i on, e .g. thi op ent al i nfusi on at 1–5mg/kg/h, i deall y wi t h ICP m oni tori ng. If s ti l l no res ponse, consi der urgent l i v er transp l antat i on. Exerci se cauti on w i th concomi t ant drug usage.

Identification of patients unlikely to survive without transplantation Prot hromb i n ti m e >100s Or any three of the fol l owi ng: Age <10 or >40 y ears Aet i ol ogy i s he pat i ti s C , hal othane, or ot her drug reacti on Durati on of j aundi c e p re-enc ephal opat hy >2 d ays Prot hromb i n ti m e >50s Serum bi l i rubi n >225µ mol /l If p aracet amol -i nduced : pH < 7.3 or prothrom bi n ti me >100s and creat i ni ne >200µm ol /l p l us Grad e 3 or 4 e nce phalop athy. As onl y 50–85% of pat i ents i de nti fi e d as requi ri ng trans pl a ntati on w i l l s urv i ve l ong enough to re cei ve one, the Reg i onal Li v er Uni t s houl d be i nformed soon afte r d i ag nos i s of al l possi bl e c andi dates . P.363

See also: Venti l at ory support— ind i c ati ons , p 4; Intracrani al pre ssure moni tori ng, p134; Li ver funct i on te sts , p 152; Coagul ati on moni tori ng, p156; Sed ati ves , p 238; Jaund i ce , p 358; Chroni c l i ver failure , p364; Parace tam ol poi soni ng , p 456 P.364

Chronic liver failure Pat i ents adm i tt ed to i nt ens i v e c are wi t h c hroni c l i ve r fai l ure may d eve l op sp eci fi c as soc i at ed probl ems : Acute dec ompe nsati on— thi s m ay b e s econdary to i nfect i on, s edati on, hyp ovol ae mi a , hypot ens i on, d i uret i cs , gast roi nt est i nal haem orrhag e, exc ess di etary protei n and el e ctrol yte i m bal anc e. Infe ct i on—the p ati ent may trans mi t i nfe cti on, e. g. hep ati ti s A, B or C and, by bei ng i m munosuppress ed, i s al so more prone to ac qui ri ng i nfect i ons s uch as TB and fung i . Drug m etab ol i sm —as many d rug s are al l or p art -met abol i sed by the l i ver and/or e xcrete d i nto the b i l e, t he drug act i on may be prol onge d or s l ow ed depe ndi ng on whe the r t he met abol i t es are ac ti v e or not. Inparti c ul ar,

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sedati ves may have a great l y prol onged durat i on of ac ti on. Port al hyp ertensi on—resul ts i n as ci tes , v ari ces and s pl e nom egaly. As ci t es may produce di a phragm ati c s pl i nt i ng and i s at ri sk of b ecomi ng i nfe cte d. Drai nage may i ncur a consi d erabl e prot ei n l oss. Vari ces may bl eed whi l e spl enomegaly may re sul t i n t hrombocyt ope ni a . R enal fai l ure i s al so rec ogni s ed due to hi g h i nt ra-abdomi nal pre ssure. Bl e edi ng— an i nc reased ri sk i s prese nt due to dec reased product i on of cl ott i ng factors (II, VII, IX, X), vari c es and spl enomegaly rel at ed t hrombocyt ope ni a . Al c ohol —t he mos t freq uent c aus e of ci rrhos i s i n the we ste rn worl d; ac ute wi thd raw al may l ead t o d el i ri um tre mens wi th sev ere ag i tati on, hal l uci nati ons , s ei zures and cardi ovascul ar di st urb anc es. 2° hype ral doste roni sm —re sul ts i n ol i guri a, s al t and w ate r rete nti on. Inc reased te ndency to jaundi ce, es pec i al l y duri ng c ri t i c al i l l ne ss.

Management 1. Asc i te s T ake spe ci mens for m i crob i ol ogi cal anal y si s (i nc l ud i ng TB), protei n and cyt ol ogy. If WBC > 250 pe r hi gh p ower fi el d, g i v e Gram neg ati ve ant i bi ot i c cov er. If p res ent i n l a rge quant i ty , (i ) dec rease sod i um and water i ntak e, (i i ) c omm enc e sp i ronol ac tone PO (or p otassi um canrenoat e IV) ± furos emi de. Parac ent esi s ± col l oi d re pl a cem ent , or as ci ti c re i nfus i on (i f uni nfec ted /non-pancreat i t i c i n ori gi n) m ay be consi d ere d, parti c ul arl y i f d i ap hragmati c sp l i nti ng occ urs . 2. Coag ul opat hy: Vi tami n K 10m g/day s l ow IV bol us for 2–3 day s. Fres h froz en p l asma, pl at el e ts as nec ess ary . 3. Hypogl y cae mi a —shoul d b e p rev ent ed by adeq uat e nutri t i on or a 10% or 20% gl ucose i nfusi on. 4. Ade quat e nutri t i on and v i tami n suppl eme ntati on. 5. Acute dec ompe nsati on— avoi d any pre ci p i t ati ng causes , e .g. i nfec ti on, sed ati on, hy pov ol a emi a, e l ec trol y te i mb al a nce . 6. Drug admi ni s trati on— rev i ew typ e and dos e regul arl y. P.365

See also: Li ver funct i on te sts , p 152; Sed ati ves , p 238; Jaundi c e, p358; Acute l i v er fai l ure, p360

Ovid: Oxford Handbook of Critical Care

Ed itors:

Si nge r, M ervyn; We bb, An dre w R.

Ti tle : O xf ord Ha ndbook of Cr itic al Car e, 2nd Ed ition Cop yri ght © 1997,2005 M. Si nge r and A. R. W ebb , 1997, 2005. Publ i shed i n the Uni te d Stat es by Oxford Uni ve rsi ty Press Inc > Tab le of Co n te n ts > Neu r ol ogi cal Di sor der s

Neurological Disorders Acute weakness Sev ere ac ute we akne ss may re qui re urg ent i ntubat i on and me chani c al venti l at i on i f the F VC < 1l or gas ex change det eri orate s ac ut el y .

Investigation Metabol i c myopat hi e s—e xcl ud e and t reat hypophosphataemi a, hypokal aem i a, hy poc al c aem i a and hypomag nes aem i a. Prol onged effect s of m usc l e rel axants —a prol onged effect of suxam ethoni um wi l l usuall y be cl i ni cally ob vi ous and shoul d promp t as se ssm ent of pse udochol i nes terase l e vel s. Sux amet honi um effec ts wi l l al s o b e prol ong ed i n myas the ni c s. Prol onge d effec ts of non-dep ol a ri si ng m usc l e rel axants are s ugg est ed by a resp ons e t o an anti chol i nes terase (neos ti g mi ne 0.5 mg by s l ow IV b ol us wi th an ant i c hol i ne rgi c). Thi s shoul d not be atte mpt ed i f p aral y si s i s compl ete . Pati ent s w i th my ast heni a gravi s wi l l al so res pond. Gui l l a i n–Barré sy ndrome —a l um bar punct ure shoul d b e p erform ed t o c onfi rm rai s ed CSF protei n wi t h norm al cel l s. If these features are not found b ut sus pi c i on i s s trong, ne rve conducti on studi es m ay dem ons trate segm ent al dem yel i nati on w i th sl ow conduc ti on v el oci ti e s. Myas the ni a gravi s— fati gueabl e w eak nes s or p tos i s sug ges ts myastheni a g rav i s ; re sponse to IV ed rop honi um

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(Tensi l on tes t) and a strong l y pos i t i ve ace tyl chol i ne rec ept or ant i body ti t re confi rm thi s d i ag nos i s. A myastheni c synd rome associ ated wi th mal i g nanc y (Eat on–Lam bert s ynd rom e) i nv ol v es pel vi c and t hi g h m usc l es pre domi nantl y, tendi ng t o s pare t he ocul ar muscl es. Other di a gnoses are made l argel y on t he bas i s of cl i ni cal suspi ci on and spe ci fi c sp eci al i sed te st s.

General management FVC shoul d be moni t ore d 2–4-hrl y and i nt ubati on and mec hani cal v ent i l a ti on s houl d fol l ow i f FVC < 1l . Ot her i nd i ce s of resp i ratory func ti on are l es s s ens i t i ve . In p art i cul a r, art eri al bl ood gas es may be mai ntained up t o t he poi nt of resp i ratory arrest . Weak re spi ratory musc l es l e ad to progre ssi ve bas al ate l ec tas i s and sp utum rete nti on. Chest i nfec ti on i s a si g ni fi cant ri sk; reg ul ar che st phy si othe rap y w i th i ntermi t te nt pos i ti ve pre ssure bre athi ng are requi red for pre vent i on where me chani c al venti l at i on i s not nece ssary. Pati ent s who are i m mob i l e are at ri sk of ve nous s tas i s and de ep v enous thromb osi s. Prophy l ax i s wi t h sub cut ane ous hep ari n i s reasonabl e. Imm obi l e pat i ents al s o requi re at tenti on t o p ost ure t o preve nt pre ss ure sores and contract ure s. Weak bul bar m usc l es may c omp rom i se sw al l owi ng wi t h c ons equent malnutri ti on or pul monary asp i rati on. Enteral nut ri t i onal sup port vi a a nasogas tri c tub e i s nece ssary. In c as es w i t h c oexi st ent aut onomi c ne uropat hy ent eral nutri t i on may b e i mpos si bl e , nece ssi tat i ng parenteral nut ri t i onal sup port. These pat i ents may al so suffer arrhy thm i as and hypotensi on requi ri ng ap propri ate support. P.369

Causes of severe weakness Common in ICU Met abol i c my opathi es Prol onged effec ts of m usc l e re l ax ant s Cri ti cal i l l ness ne uropat hy or m yop athy Gui l l ai n–Barré s ynd rom e Myastheni a g rav i s Ponti ne C VA Sub st anc e ab use (e spe ci a l l y be nze ne ri ng c omp ounds)

Uncommon in ICU Chroni c rel aps i ng pol yneuri ti s End ocri ne my opathi es Sarcoi d neurop athy Pol i om yel i t i s Di pht heri a Carci nomatous neuropathy Porphy ri a Bot ul i sm Fam i l i al peri odi c paral ysi s Mul ti pl e sc l erosi s Lead p oi s oni ng Organophosphorus p oi soni ng

See also: Venti l at ory support— ind i c ati ons , p 4; IPPV—ass ess ment of we ani ng, p18; Ent eral nutri t i on, p 80; Pare nte ral nutri ti on, p82; Pul m onary func ti on tes ts, p94; El ec trol y tes , p 146; Calc i um , m agne si um and phosphate , p 148; Musc l e rel axants , p 240; Re spi ratory fail ure , p 282; Gui l l ai n–Barr é syndrome, p384; Myastheni a g rav i s , p 386; ICU ne uromus cul ar di sorders, p388 P.370

Agitation/confusion In the IC U, agi tat i on and/or c onfusi on are predom i nant l y rel ate d t o s eps i s, ce reb ral hy pop erfusi on drugs or drug wi t hdrawal. ‘IC U p syc hos i s’ , w i t h l oss of day –ni ght rhyt hm and i nabi l i t y t o s l ee p, i s a c ommon occurrenc e i n t he pat i ent rec overi ng from sev ere i l l ness .

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Commoner ICU causes Infe ct i on—i ncl udi ng g ene ral i s ed sep si s , c hes t, cannul a s i t es, uri nary tract. Ce reb ral i nfec ti on suc h as me ni ngi ti s , ence phali ti s and m al a ri a are rel a ti v el y rare but shoul d always be consi d ere d. Drug-rel a ted —(i ) ad verse reacti on (parti cul arl y affect i ng the e l de rl y ), e.g . s edati v es, anal g esi cs, di ureti cs; (i i ) wi t hdrawal , e .g. se dat i ve s, analge si c s, et hanol ; (i i i ) abuse, e. g. opi ate s, amp het ami nes , al cohol , hal l uci nog ens . Metabol i c —e. g. hypo- or hype rgl ycaemi a, hyp o- or hype rnatraemi a, hyp erc al c aem i a, uraem i a, he pat i c ence phalop athy, hyp o- or hype rt hermi a , d ehyd rat i on. Resp i ratory— infect i on, hypoxaem i a, hy percap ni a . Neurol ogi cal —i nfec ti on (meni ng o-e nce phal i t i s, malari a ), p ost -he ad i nj ury , s pac e-oc cupyi ng l es i on (i ncl udi ng haem atoma), post-i c tal , p ost -cardi ac arrest . Card i ac —l ow outp ut st ate, hy pot ens i on, e ndocardi t i s . Pai n—ful l bl add er (bl ock ed F ol e y c athete r), ab domi nal p ai n. Psyc hos i s —‘ICU psy chosi s ’, other psy chi atri c st ate s.

Principles of management 1. Exam i ne for s i gns of (i ) i nfect i on (e. g. pyrexi a, purul ent sp utum, cat het er si t es, ne utrophi l i a, fal l i ng pl a tel et count, CXR , m eni ngi sm), (i i ) cardi ovascul ar i nst abi l i ty (hyp ote nsi on, i ncreas i ng met abol i c aci d osi s, ol i guri a , arrhyt hmi as), (i i i ) c overt pai n, parti c ul arl y abdom i nal and l ow er l i mbs (e. g. com partme nt syndrome, DVT), (i v) focal neurol ogi cal si gns (e .g. meni ngi s m, une qual p upi l s, he mi p are si s), (v) re spi rat ory failure (arteri a l b l ood gase s), (v i ) metabol i c de rangeme nt (bi ochemi cal s cre en). If any of t he abov e are found, treat as app rop ri ate . Psyc hos i s shoul d not be ass umed unti l t reatab l e causes are e xcl ude d. 2. Reas sure and cal m t he pat i ent. Mai ntain qui et atm osp here and red uce noi se l e vel s. Att emp t t o rest ore day–ni ght rhy thm , e. g. by changi ng amb i ent l i ghti ng and us e of oral hyp not i c age nts . 3. Cons i de r s tarti ng, chang i ng or i ncreas i ng dose of s edati v e or m ajor t ranqui l l i se r t o c ont rol the p ati ent . If hi ghl y agi tat ed and l i kel y t o endanger thems el v es, rapi d short t erm control can be achi e ved by a s l ow IV bol us of sedati ve. Consi d er propofol , a benzod i azepi ne, halop eri dol or chl orpromazi ne i n t he smalle st pos si bl e dos e t o achi eve the d esi red effec t; obs erv e for hypotensi on, res pi rat ory de pre ssi on, arrhy thm i as and e xtra-p yrami d al effe cts . Opi ates may b e neede d, esp eci al l y i f pai n or wi thdrawal i s a fact or. An e thanol i nfus i on can b e cons i d ere d for del i ri um tremens resul t i ng from al c ohol w i thdrawal . 4. Sed ati on can be mai ntaine d b y c ont i nuous i nfus i on or i nte rmi tte nt i nj ect i on, e i t her re gul arl y or as requi red. The l es s agi t ate d p ati ent may resp ond to IM i nj ect i ons of a major tranq ui l l i ser, t hough the se shoul d be avoi de d w i th conc urrent c oag ul opat hy. P.371

Drug dosages for severe agitation •Chlorpromazine—12.5 mg by slow IV bolus. Repeat, doubling dose, every 10–15 until effect. May need up to 100 mg. For regular prescription, give qds. •Haloperidol—2.5 mg by slow iIV bolus. Repeat, doubling dose, every 10–15 minutes until effect. For regular prescription, give qds. •Midazolam/diazepam—2–5 mg by slow IV bolus. •Propofol—30–100 mg by slow IV bolus. •Morphine—2.5–5 mg by slow IV bolus. NB beware excessive central and respiratory depression with the above agents

See also: IPPV—fai l ure t o t ol e rat e ve nti l a ti on, p12; Tox i col og y, p162; Sed ati ves , p 238; Acut e l i ve r fai l ure, p 360; Chroni c l i v er fai l ure, p364; Thyroi d em erg enc i e s, p446; Poi s oni ng—general p ri nci pl es, p452; Am phe tam i ne s i nc l ud i ng Ec stasy, p462; Coc ai ne, p 464; Infe cti on—di agnosi s, p480; Syst emi c i nfl amm ati on/mul ti org an fai l ure, p484; Head i njury (1), p504; Head i njury (2), p506; Py rex i a (1), p518; Py rex i a (2), p 520; Pai n, p 532 P.372

Generalised seizures Control of s ei z ure s i s nec ess ary to prevent i sc hae mi c brai n damag e, t o reduce cerebral oxy gen re qui rem ent s and to red uce i ntracrani al pre ss ure . W here poss i bl e c orrect the c aus e and gi v e s pec i fi c t reatme nt. A CT scan m ay b e nec ess ary to i d ent i fy st ructural cause s. Com mon causes i ncl ude : Hypoxae mi a

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Hypogl y cae mi a Hypocal cae mi a Space-occupyi ng l e si ons Metabol i c and toxi c di sorde rs Drug wi thdrawal , e .g. al cohol , benzod i azep i ne s, ant i convul sants Infe ct i on, es pec i a l l y me ni ngoe nce phalit i s Trauma Idi opathi c e pi l eps y Mos t s ei z ures are sel f-l i m i ti ng, re qui ri ng no more t han protec ti on from i njury (com a p osi ti on, protec t head and d o not force any thi ng i nt o t he mouth).

Specific treatment Hypoxae mi a shoul d b e c orrect ed wi t h oxyg en (FIO 2 0.6–1. 0). Int ubati on and v ent i l ati on i f the ai rway i s unprote cte d or SpO 2 <90%. Bl ood gl ucos e s houl d be meas ured urg ent l y and hyp ogl ycaemi a c orrect ed wi t h IV 50 m l 50% gl ucos e. Ant i convul sant l ev el s shoul d b e c orrec ted i n known epi l ep ti cs. Cere bral oede ma shoul d be manage d w i th se dat i on, i nduced hy pot hermi a , c ont rol l e d hy perventi l at i on and osmoti c d i ureti cs . In p ati ents wi t h a known tum our, arte ri t i s or paras i ti c i nfect i on, hi gh dose dexamet has one may be gi ven. Thi ami ne 100 mg IV shoul d be gi ven to al cohol i cs . Cons i de r s urgery for space-occupyi ng l e si ons, e. g. bl ood c l ot, tum our.

Anticonvulsants Ant i c onv ul s ant s are nec ess ary where there are repeated se i z ure s, a s i ng l e sei zure l ast s >30 mi n or there i s c yanosi s. A b enz odi aze pi ne (e .g. l orazepam, di a zep am) i s the usual fi rs t l i ne t reatment. Phenytoi n— a l oad i ng dose shoul d be gi ven i ntravenous l y i f the pati e nt has not p rev i ousl y re cei ved pheny toi n. Phenytoi n may not p rov i de i m medi at e c ont rol of sei zures wi thi n t he fi rst 24 h. If sei zures conti nue ap propri ate anti c onv ul s ant s i nc l ud e: Magnesi um sul phate. Cl onaze pam , w hi c h i s p art i c ul a rl y us eful for myocl oni c se i zure s. Thi opental or p rop ofol i nfusi on i n s eve re i nt rac tab l e epi l ep sy. Wi t h all anti c onv ul s ant s c are shoul d b e t ake n t o av oi d hy pov ent i l a ti on and res pi rat ory failure. Howeve r, mec hani c al venti l at i on wi l l certai nl y be re qui re d i f t hi opental i s us ed, and p rob abl y t o maintai n oxyge nat i on i n cases of conti nue d sei zures .

Other supportive treatment Mus cl e rel a xant s p re vent muscul a r c ont rac ti on d uri ng se i zures but w i l l not p rev ent conti nued s ei zures. They m ay be nec ess ary to faci l i t ate mec hani c al vent i l ati on but conti nuous EEG moni t ori ng shoul d b e used to jud ge sei zure c ont rol . Correc ti on of c i rcul atory di s turbance i s re qui red to maint ai n op ti m al cerebral bl ood fl ow. P.373

Drug dosages

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Lorazepam

4 mg IV.

Diazepam

Initially 2.5–5 mg IV or PR. Further increments as necessary to a maximum of 20 mg.

Midazolam

Initially 2.5–5 mg IV or PR. Further increments as necessary to a maximum of 20 mg.

Phenytoin

Loading dose 18 mg/kg IV at a rate <50 mg/min with continuous ECG monitoring. Maintenance at 300–400 mg/day IV, IM or PO adjusted according to levels.

Magnesium sulphate

Initially 20 mmol over 3–5 min followed by 5–10 mmol/h by infusion as necessary.

Clonazepam

1 mg/h IV.

Thiopental

1–3 mg/kg IV followed by lowest dose to maintain control.

Propofol

0.5–2 mg/kg IV followed by 1–3 mg/kg/h.

Key trial T re i man VA for the Ve terans Affai rs Status Ep i l ept i cus C oop erati v e Stud y G roup. A c omp ari son of four tre atm ent s for generali zed convul si ve status ep i l e pti cus. N Engl J M ed. 1998; 339:792–8

P.374

Meningitis Thi s i s a l i fe -threateni ng condi ti on d emandi ng prompt treat ment. As the cl ass i c al pre sentat i on of meni ngi s m m ay b e abs ent , s usp ect i n t hos e pres ent i ng wi th obt und ati on, ag i tati on, sei zures or foc al neurol ogy . Si g ns may be sub tl e or pre sent i ns i di ous l y i n neutropeni c s and t he el d erl y. Meni ngoc occ aemi a p res ent s wi t h a promi nent rash i n 30% of cas es whi l e Li ste ria monoc ytog ene s m ay cause earl y sei zures and focal ne urol og i cal d efe cts .

Diagnosis Bac teri al me ni ngi t i s i s pri mari l y di a gnosed by CSF ex ami nat i on. T hi s i s unnec ess ary wi th a c l as si cal meni ngococ cal rash whe re the organi s m can b e ofte n c ul t ure d from the s ki n l e si ons. Lumbar p unc ture (LP) samp l es s houl d be s ent for urge nt mi c roscopy and cul ture, PCR , anti gen vi rol ogy , p rot ei n and g l uc os e es ti mat i on (wi t h c onc urrent p l as ma samp l e ). N orm al or l ym phocyt i c CSF may b e found i n earl y py oge ni c me ni ngi t i s , espe ci al l y L. monoc ytogenes . Rai s ed ICP i s common; unl ess confi dentl y exc l uded , d el a y l umbar p unc ture (LP) but not anti bi oti cs unt i l after CT scanni ng. A normal CT sc an d oes not c omp l et el y ex cl ude rai sed IC P. Empi ri c anti bi oti c t herapy wi th concurrent s teroi ds shoul d be commenced i m med i at el y after taki ng b l ood cul tures. The c hoi ce shoul d be based on the pati e nt' s age. CSF c ul t ures are pos i t i ve i n 50% i f anti bi oti c s are gi v en c omp are d t o 60–90% i n unt reated cases . CSF bac teri al anti gen te sti ng i s availabl e for m ost i nfec ti ng organi sms ; se nsi ti vi t y v ari es from 50–100% whi l e spec i fi ci ty i s hi gh.

Management 1. Ant i bi oti c the rap y, usual l y for ≥10 day s, though re cent s tud i es sugge st equal effi cacy wi t h s horter c ourses . 2. Dexamet has one 10 mg qds for 4 days shoul d be commenced wi th or jus t b efore the fi rst dose of ant i bi oti c, parti c ul a rl y for p neumoc occ al meni ng i t i s. 3. Gene ral me asures i ncl ude at tenti on t o fl ui d and el e ctrol y te rep l ac eme nt, ad equate gas ex change , nutri t i on, and ski n c are . 4. Managem ent of rai se d i ntracrani al press ure i f prese nt. 5. Gi v e oral ci profl oxac i n (ad ul t s onl y ) or ri fampi ci n to fami l y and cl ose soc i al contact s of me ni ngoc occ al and haem ophi l us m eni ngi ti s. The i ndex case shoul d al so rec ei v e t hi s treat ment b efore di s charge home.

Aseptic meningitis

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No org ani sms are i denti fi e d by routi ne CSF anal y si s de spi te a hi gh ne utrophi l and/or l ymphocy te count. Cause s i nc l ude vi ruse s (e.g . mumps , m eas l es ), Lym e d i se ase , fungi , l ep tos pi rosi s, l i ste ri osi s, brucel l osi s , atyp i cal T B, sarcoi dosi s , SLE.

Encephalitis Pre senti ng feat ure s i nc l ud e d row si ness , c oma, ag i t ati on, py rex i a, se i zures and focal s i gns; meni ng i sm ne ed not nec ess ari l y be prese nt.

Causes: Bac teri al (as for meni ng i ti s) Vi ruse s (i n parti cul ar, he rpe s s i mp l ex and p ost -measl es, chi ck en pox, mumps i nfec ti on). He rpe s s i mp l ex cl a ssi cal l y affect s t he tem poral l ob e and can be di agnosed by EEG. Gi v e aci c l ov i r 10 mg/kg tds IV for 10 d ays . Rarer causes i ncl ude l e ptospi ros i s and bruc el l osi s; the CSF reveals no org ani sms but a hi gh l ym phocyt e c ount i s pre sent. If i nd i c ate d, send CSF for aci d fast st ai n (T B) and Indi a Ink s tai n (Crypt ococcus). P.375

Typical CSF values in meningitis Pyogenic

Viral

Tuberculosis

Classical appearance

turbid

clear

fibrin web

Predominant cell type

polymorphs

lymphocytes

lymphocytes

Cell count/mm 3

>1000

<500

50–1500

Protein (g/l)

>1

0.5–1

1–5

CSF:blood glucose

<60%

>60%

<60%

Organisms and empiric starting antibiotic therapy Organism

Patients often affected

Antibiotic and dosage regimen (alternatives in brackets)

Neisseria meningitidis (Meningococcus)

young adults

ceftriaxone 2–4 g IV od (cefotaxime 50 mg/kg IV 8-hrly) (benzylpenicillin 1.2 g IV 2–4-hrly) (chloramphenicol 12.5 mg/kg IV 6-hrly)

Streptococcus pneumoniae (Pneumococcus)

older adults

ceftriaxone 2–4 g IV od (cefotaxime 50 mg/kg IV 8-hrly) (chloramphenicol 12.5 mg/kg IV 6-hrly)

Haemophilus influenzae

children

ceftriaxone 20–50 mg/kg IV od (cefotaxime 50 mg/kg IV 8-hrly) (chloramphenicol 12.5 mg/kg IV 6-hrly)

Listeria monocytogenes

elderly, immuno-compromised

ampicillin 1g IV 4–6-hrly plus gentamicin 120 mg IV stat, then 80 mg 8–12-hrly (adjust by plasma levels)

Mycobacterium tuberculosis Cryptococcus neoformans Staph. aureus

quadruple therapy (rifampicin/isoniazid/ ethambutol /pyrazinamide) immuno-compromised

amphotericin B starting at 250 µg/kg IV od + flucytosine 50 mg/kg IV 6-hrly flucloxacillin 2 g IV 6-hrly

Key papers

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de Gans J, et al . D examet has one i n ad ul t s w i th bacte ri al meni ng i ti s. N Engl J Med 2002; 347:1549–56. van de Be ek D , e t al. Corti c os teroi d s i n acut e b act eri al meni ng i t i s. Cochrane Datab ase Sy st Rev 2003; (3):CD004305. Rev i ew .

See also: Bac teri ol og y, p158; Vi rol og y, serol ogy and ass ays , p 160; Anti mi crobi a l s, p260; Ste roi ds, p262; Bas i c re sus ci t at i on, p270; Hyp ote nsi on, p312; General s ei zures, p372; Rai sed i ntracrani al pre ssure, p382; Infe cti on control —g ene ral pri nc i pl es, p476; Infect i on—di agnosi s, p480; Infe cti on—treat ment , p 482; Seps i s and se pti c s hoc k—t reatme nt, p486; Pyrexi a (1), p518; Pyrexi a (2), p520 P.376

Intracranial haemorrhage Extradural haemorrhage Usual l y p res ent s acutel y after he ad i nj ury . C haract eri se d by falli ng Gl asg ow C oma Sc ore progress i ng t o c oma, focal si gns (l ateral i si ng weakne ss or anae st hes i a, pupi l l ary s i g ns), vi sual di s turbances and s ei z ures. Treat ment by random burr hol es has bee n s upp l anted by di rec ted drai nag e fol l owi ng C T s can l ocal i s ati on. A c ons ervati ve app roach may be adopte d for small hae mat omat a b ut i ncre asi ng si z e (ass ess ed by reg ul a r C T s canni ng or cl i ni cal de teri orat i on) are i nd i cati ons for surgi cal d rai nag e.

Subdural haemorrhage Cl a ssi cally prese nts days to week s fol l owi ng head t rauma wi t h a fl uct uat i ng l e vel of consc i ousne ss (35%), agi tat i on, confus i on, s ei z ures and si gns of raise d i ntracrani al press ure , l ocali si ng s i gns, or a s l ow l y evol vi ng stroke . D i ag nos i s i s mad e b y CT sc an. Treat ment i s b y s urgi c al drainage.

Intracerebral haemorrhage Causes i ncl ude hyp ert ens i on, neop l as m, vas cul i t i s, coagul op athy and m ycoti c aneurys ms ass oci ate d wi th bac te ri a l end ocardi ti s. Cl i ni cal fe atures i ncl ude sud den onset coma, drowsi ne ss and /or neurol ogi cal d efi ci t . Head ache usually oc curs onl y wi t h c ort i c al and i ntraventri cul ar haemorrhage . T he rat e of ev ol uti on d epe nds on the si ze and si ze of the bl eed . T he are a affec te d i s t he put amen (55%), thal amus (10%), c ere bral c ort ex (15%), pons (10%) and c ere bel l um (10%).

Diagnosis CT scan i s t he defi ni ti ve t est . A c oagul at i on and v asc ul i ti s b l ood s creen may be i ndi c ate d. Ang i og rap hy i s i ndi c ate d i f surgi cal re pai r i s contemp l ated though not for drainage of bl ood cl ot.

Treatment Bed re st Sup porti v e (e.g. hy drati on, nut ri ti on, analge si a , v ent i l atory s up port) Phys i ot herap y Bl ood pre ssure control (mai ntain sys tol i c BP <220–230 mmHg) Correc t any c oag ul opat hy Cont rol rai s ed i nt rac rani a l p res sure Surgery—c ont act Re gi onal Centre, e.g. for e vac uat i on of hae mat oma, repair/cl i pp i ng of ane ury sm Ste roi d t herapy i s i neffect i ve P.377

See also: Venti l at ory support— ind i c ati ons , p 4; Bl ood press ure moni t ori ng , p 110; Int rac rani a l p res sure m oni tori ng, p134; Coagul ati on moni tori ng, p156; N europrot ect i ve age nts , p 244; Basi c resusci tati on, p270; Hyp ertensi on, p314; Generali sed se i zures , p 372; Subarachnoi d haemorrhag e, p 378; Raise d i nt rac rani al press ure, p382; Bl eed i ng di s orders, p396; Vasc ul i ti des , p 494; Head i njury (1), p504; Head i njury (2), p506; Brai n st em d eat h, p548; Wi t hd rawal and wi t hol di ng tre atm ent , p 550; Care of the p ote nti al org an donor, p552 P.378

Subarachnoid haemorrhage Pathology In 15% no cause i s found; of the re mai nde r, 80% are due t o a ruptured aneurysm , 5% t o arte ri ovenous mal form ati ons and 15% fol l ow traum a. The ant eri or part of t he Ci rcl e of Wi l l i s i s affect ed i n 85–90% of cas esw hi l e 10–15% affect the ve rt ebrobasi l ar sys tem.

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There i s a 30% ri s k of re bl e edi ng for whi ch the m ort al i ty i s 40%. T hos e s urv i vi ng a m ont h have a 90% chance of survi v i ng a year. Cere bral v asospasm occ urs i n 40–70% of p ati ent s at 4–12 days afte r t he bl eed. Thi s i s the most i m portant c aus e of m orb i di ty and mortali ty. Hydroc ephalus, sei zures, hy ponatraem i a and i napp rop ri a te ADH se creti on are re cog ni s ed com pl i cat i ons.

Clinical features SAH may be prece ded by a p rodrome of head ache, d i z zi ness and v ague ne urol ogi c al sym ptoms. Oft en t here i s rap i d ons et (mi nut es to hours) presentat i on i ncl udi ng col l a pse , s evere head ache ± meni ng i s m. Crani al nerv e pals i es , d row si ness and hemi pl e gi a may al so occ ur.

Diagnosis Di agnosi s i s usually made by C T s can; i f t here i s no e vi d enc e of rais ed i nt rac rani al pres sure, a l umb ar puncture may be performed re veal i ng b l ood-s tai ned CSF wi th xanthochromi a.

Management Bed re st. Mai ntai n adeq uat e hydrati on, nutri ti on, anal g esi a, sed ati on. Cere bral v asospasm i s prevented by ni mod i pi ne i nfusi on and maint enance of a ful l i ntravascul ar vol um e. Sys tem i c hyp ert ens i on shoul d onl y be treat ed i f sev ere (e. g. sys tol i c press ure >220–230 mmHg) and prol onge d. Surgery—t he ti m i ng i s c ont rov ers i al wi th ei t her earl y or de l ay ed (7–10 days ) i nte rve nti on bei ng adv ocated . T he Regi onal N eurosurg i cal C ent re shoul d be consul te d for l oc al pol i cy . Ant i fi bri nol yt i c the rap y (e.g . t ranexam i c aci d) red uc es t he i nci d enc e of rebl eedi ng but has no b ene fi c i al effec t on outc ome . P.379

Key trial Al l en GS, e t al. Cerebral art eri al sp asm—a c ont rol l e d t ri a l of ni modi p i ne i n pati ent s wi th subarachnoi d hemorrhage . N Eng l J Me d 1983; 308:619–24

See also: Venti l at ory support— ind i c ati ons , p 4; Bl ood press ure moni t ori ng , p 110; Int rac rani a l p res sure m oni tori ng, p134; Coagul ati on moni tori ng, p156; N europrot ect i ve age nts , p 244; Basi c resusci tati on, p270; Hyp ertensi on, p314; Generali sed se i zures , p 372; Intracrani a l haem orrhag e, p376; Raise d i ntrac rani al press ure, p 382; Bl eedi ng di sorders, p396; Brain st em d eat h, p548; W i thdrawal and w i thol d i ng treat ment, p550; Care of the potenti a l organ d onor, p552 P.380

Stroke Pathology Haem orrhag e, emb ol us or t hrombosi s . ‘Se condary’ stroke may oc cur wi th meni ng i t i s, bacte ri al endocardi ti s , s ubarac hnoi d hae morrhage and vascul i t i s . Di s sec ti on and cerebral venous throm bos i s nee d t o b e c ons i de red , as anti coagul ati on i s i ndi c ate d for bot h (unl ess a l arge i nfarct i s est abl i s hed, as there i s an i ncreas ed ri s k of bl eed i ng). Di sse cti on shoul d be suspe cte d i n younger pati ent s, ofte n p res ent i ng wi th se vere he adache or ne ck pai n ± Horner's sy ndrome ± s ei z ures afte r trauma or nec k m ani pul ati on. Ce reb ral ve nous t hrombosi s may m i mi c s troke, tumour, sub arachnoi d haemorrhage or m eni ngo-encep hal i ti s and may prese nt wi t h head ache, sei zures, focal si gns or ob tundat i on.

Urgent CT scan Ind i c ate d when the di agnosi s i s i n doub t, for conti nui ng de teri orati on, susp i ci on of sub arachnoi d haemorrhage , hyd roc ephal us or t rauma, or for p ati ent s w ho are anti c oag ul a ted or who have a b l ee di ng t end enc y.

Aims of treatment To p rot ect t he p enumbra w i th cl ose at tenti on t o oxyg enati on, hyd rat i on, g l yc aem i c control , and av oi d anc e of pyrexi a. Bl ood pre ssure control i s need ed for se vere hyperte nsi on (e.g . > 200/120 m mHg) and hypotensi on. Drug t herapy i ncl udi ng t hrombol ys i s and as pi ri n. T he evi dence for ant i c oag ul a ti on remains conte nti ous as there i s an i nc reased ri sk of bl e edi ng and no consi ste nt sub group benefi t has been shown. Earl y anti coagul ati on i s

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probabl y b ene fi c i a l for i nt rac rani al s tenosi s, a s troke-i n-evol ut i on, c ompl et e ve sse l occ l us i on wi th mi ni mal defi ci t and i n l ow ri sk pat i ents wi t h a hi gh probab i l i ty of rec urrence (sec ond ary preve nti on). For thromb ol y si s t he exte nt of rep erfusi on dep end s on t he aeti ol ogy wi t h b asi l a r > mi ddl e c ere bral arte ry > i nt ernal caroti d, and em bol i c > t hromboti c . Pool ed studi e s w i th rt -PA (0.9 mg/kg) gi v en wi t hi n 3 h of s troke onse t (and ti ght bl ood press ure c ont rol ) s howe d a favourabl e outc ome . Howe ver, t here was a 6-fol d i ncreas e i n haem orrhag e (to 5.9%), of whom 60% d i ed . T hi s was more com mon i n the e l de rl y , and wi t h m ore se vere st roke. Neuros urg i cal i nt erv ent i on may be consi dered for ce reb el l ar hae mat oma, c ere bel l ar i nfarct i on and the m al i gnant mi d dl e ce reb ral artery s ynd rom e (for mas si ve i nfarc ti on on t he non-dom i nant si d e). P.381

Key paper Hac ke W, et al . As soc i at i on of outcome wi t h earl y s troke tre atm ent : pool e d anal ysi s of ATLANT IS, EC ASS, and NIN DS rt -PA st rok e tri a l s. Lance t 2004; 363:768–74

See also: Venti l at ory support— ind i c ati ons , p 4; Bl ood press ure moni t ori ng , p 110; Neurop rot ect i ve ag ent s, p244; Basi c res us ci t ati on, p270; Hype rt ens i on, p 314; Ge neral i se d s ei z ure s, p372; Intracrani al hae morrhage, p376; Sub arachnoi d hae morrhage, p378; Rai sed i ntracrani al pre ss ure , p 382 P.382

Raised intracranial pressure Clinical features Head ache, vom i ti ng, di zz ine ss, vi sual d i st urbance Sei zures, focal ne urol og y, pap i l l oed ema Inc reasi ng b l ood p res sure, bradyc ard i a (l a te res ponses ) Agi tat i on, i ncreas i ng d row si ness , c oma Sl ow de ep bre aths, Che yne –St oke s b reathi ng, ap noea Ips i l a teral progress i ng to bi l at eral p upi l l ary di l at at i on Dec ort i cate progre ssi ng to dec erebrate pos turi ng

Diagnosis CT s can or MR I Int rac rani al pres sure (ICP) me asurem ent >20 mm Hg Lum bar punct ure s houl d be avoi ded be cause of t he ri sk of c oni ng . Nei the r C T s can nor abse nce of pap i l l oe dem a wi l l exc l ude a rai s ed ICP.

Causes Space-occupyi ng l e si on (e .g. ne opl asm , b l ood c l ot , absc ess ) Inc reased capi l l ary p erm eab i l i ty (e. g. trauma, i nfe cti on, encep hal opathy ) Cel l de ath (e .g. post-arrest hy pox i a) Obs tructi on (e. g. hyd roc ephal us)

Management 1. Bed re st, 20–308 head-up ti l t, se dat i on, q ui e t e nvi ronment, mi ni mal s uct i on and noi s e. Sed ati on i s oft en nece ss ary to ove rcome a hyperadrenerg i c state but se dat i ve -i nduc ed hyp ote nsi on shoul d be avoi de d. The tape tet heri ng the e ndot rache al tub e i n p l ac e s houl d not oc cl ude jug ul a r v enous drainage. 2. Venti l ate i f GC S ≤ 8, ai rway unp rot ec ted or exc ess i v el y agi tated . 3. Mai ntai n PaCO 2 at 4–4.5 kPa and av oi d rapi d ri ses . C SF bi c arb onate l ev el s re -eq ui l i b rat e wi thi n 4–6 h, neg ati ng any benefi t from hy pervent i l ati on. 4. If p oss i b l e, moni t or ICP. Ai m to mai ntain ICP <20 mm Hg and cerebral pe rfusi on p res sure (CPP= MAP-IC P) ≥ 70 mmHg . Vasopre ss ors may be ne ede d. D o not treat sys tem i c hyp ertensi on unl e ss very hi gh (e. g. sys tol i c >220–230 m mHg ). 5. Jugul ar bul b venous saturat i on (Sj O 2 ) and l act ate may be us eful m oni tori ng te chni ques though do not d ete ct reg i onal i sc hae mi a . 6. Gi v e manni tol 0.5 m g/k g over 15 mi n. R epe at 4-hrl y de pendi ng on CPP m eas ure ment s and/or cl i ni cal si gns of

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dete ri orati on. Stop w hen pl asm a os mol al i ty re aches 310–320 mOsm ol /k g. 7. Avoi d seve re al k al osi s as c ere bral v asc ul a r resi st anc e ri se s and cerebral i s chaemi a i ncreas es. 8. Cons i de r s pec i fi c tre atm ent , e .g. for me ni ngo-enc ephal i ti s, mal ari a, hep ati c e nce phalop athy, surgery. Som e neuros urg eons d ecom press the c rani um for g eneral i se d oedem a b y removi ng a skul l fl ap. Se ek l oc al advi ce . Dexamet has one 4–16 mg q ds IV i s be nefi ci al for oe dema surroundi ng a tumour or ab sc ess and for herp es si mpl ex ence phali ti s .

Acute deterioration/risk of imminent coning 1. Mechani cal l y venti l at e t o PaCO2 3. 0–3.5 kPa for 10–20 mi n. 2. Gi v e manni tol 0.5 g /kg IV ov er 15 mi n. R epeat 4-hrl y as nec ess ary whi l e pl asm a osmol al i ty <310–320 mOs mol /kg. Consi der furos emi de. 3. If no resp ons e i n ICP, CPP and/or c l i ni c al feat ures, gi ve thi ope ntal (suc ces sful i n 50% of res i st ant cases ). 4. Cons i de r rep eat CT scan and refer for urgent s urg ery i f a surgi c al l y amenabl e s pac e-occupyi ng l es i on i s di a gnos ed. P.383

See also: Venti l at ory support— ind i c ati ons , p 4; Bl ood press ure moni t ori ng , p 110; Int rac rani a l p res sure m oni tori ng, p134; Di ure ti c s, p212; N europrote cti ve age nts , p 244; Basi c re sus ci tat i on, p 270; Hyp ert ens i on, p 314; General i se d s ei z ures, p372; Int rac rani a l haemorrhag e, p 376; Subarachnoi d haem orrhag e, p378; Stroke, p380; Head i njury (1), p 504; Head i nj ury (2), p506; Brai n st em d eat h, p548; W i thdrawal and w i thol d i ng t reatment, p550; C are of the potenti a l organ donor, p552 P.384

Guillain–Barré syndrome Thi s i s an i mmunol ogi cally -me di a ted , ac ut e de mye l i nati ng pol yradi cul opathy . Vi ral i nfect i ons and i mm uni sat i ons are com mon antec edents . T he s ynd rom e i ncl ud es a progres si v e, are fl e xi c motor weakne ss (often sym met ri cal , asce ndi ng and i nvol vi ng c rani a l nerv es i nc l ud i ng faci a l , bul bar and e xtraoc ul ar) wi t h p rogre ssi on ove r d ays to wee ks. There are oft en mi nor sensory d i st urbances (e. g. paraes the si a e). Autonomi c d ysfunc ti on i s not unusual. The re i s no i ncre ase i n cel l count on C SF exami nati on but prote i n l ev el s us ual l y ri se progre ssi vel y (>0. 4 g /l ). Ne rve conducti on studi es show sl ow c ond uct i on ve l oc i t i es wi th prol onged F w ave s. Other features i nc l ude m usc l e tendernes s and bac k p ai n. T he maj or contri but ors t o morb i di ty and mortalit y are res pi rat ory mus cl e we akness and autonomi c dys functi on (hy pot ens i on, hype rte nsi on, arrhy thm i as , i l e us and uri nary ret ent i on).

Differential diagnosis Other causes of ac ute we akne ss mus t b e e xcl ude d b efore a di agnosi s of Gui l l a i n–Barré sy ndrome can be made.

Specific treatment Int rav enous g amm agl obul i n (0.4 g/k g/day for 5 d ays ) or pl as ma e xchang e (fi ve 50 ml /kg exc hanges ov er 8–13 days ) i s e ffe cti ve i f starte d w i thi n 14 day s of onset of sy mpt oms . Ste roi ds hav e not b een shown to be benefi ci al .

Supportive treatment Respiratory care Reg ul a r c hes t p hys i ot herapy and s pi rome try are requi red. Mec hani c al vent i l ati on i s nee ded i f FVC <1l or PaC O 2 i s rai se d. An earl y trache ost omy i s us eful s i nc e m echani cal ve nti l at i on i s l i ke l y to conti nue for se veral week s. Pat i ents wi t h b ul b ar i nvol veme nt or i nadeq uat e c oug h s houl d und erg o t rac heotom y, even i f sp ont ane ous breat hi ng c ont i nues.

Cardiovascular care Conti nuous c ard i ov asc ul ar moni tori ng i s requi red due to the effec ts of aut onom i c i nvol veme nt. Arrhythmi a s are parti cul arl y l i k el y wi t h anae sthesi a (esp eci al l y w i t h s uxam ethoni um). Hype rte nsi ve and hyp ote nsi ve res ponses are generall y ex agg erated wi th vas oac ti v e d rug s.

Nutritional support Parent eral nutri t i on wi l l be req ui red i n cases whe re the re i s i l eus . Ente ral nutri ti on i s pre ferred , i f p oss i b l e, eve n though energ y and fl ui d req ui reme nts are reduced i n Gui l l ai n–Barré syndrome.

Analgesia Analg esi a i s requi re d for mus cl e , abdomi nal and back pai n. Al t hough NSAID s m ay b e useful , op i at es are often req ui red .

Other support

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Parti cul ar att ent i on i s requi re d t o p res sure areas and deep ve i n thromb osi s p rophyl axi s. P.385

Key trials Pl a sma Ex change /Sandog l obul i n Gui l l ai n-Barre Sy ndrome Tri al Group. Rand omi sed tri a l of pl as ma e xchang e, i nt ravenous i mm unogl obul i n, and c omb i ned t re atme nts i n Gui l l ai n-Barré syndrome. Lance t 1997; 349:225–30 van Koni ngsv el d R, for the D utc h GBS st udy group . Effec t of m ethyl p red ni sol one whe n adde d t o s tandard t reatme nt wi t h i nt rav enous i mmunog l ob ul i n for Gui l l ai n–Barre s ynd rom e: randomi se d t ri a l . Lancet 2004; 363:192–6

See also: Venti l at ory support— ind i c ati ons , p 4; Bl ood press ure moni t ori ng , p 110; Neurop rot ect i ve ag ent s, p244; Basi c res us ci t ati on, p270; Hype rt ens i on, p 314; Ge neral i se d s ei z ure s, p372; Intracrani al hae morrhage, p376; Sub arachnoi d hae morrhage, p378; Rai sed i ntracrani al pre ss ure , p 382 P.386

Myasthenia gravis Myastheni a g rav i s i s ass oc i at ed wi t h p ai nl es s w eakness whi ch i s wors e after ex ert i on wi th det eri orati on duri ng st res s, i nfect i on or t rauma. Tendon re fl e xes are norm al . It i s an autoi mmune d i s eas e as soc i a ted wi t h acet yl chol i ne rece ptor and, rarel y, ant i -s tri at ed mus cl e anti b odi es. The re i s al s o an associ a ti on w i t h ot her autoi mmune di s eas es (e. g. thy roi d d i se ase , SLE, rheum atoi d art hri ti s). Younge r (<45 years), p red omi nantl y fe mal e p ati ent s m ay have a thy moma whi ch, i f rese cte d, may provi de rem i ss i on. Sev ere we akne ss may be the resul t of a my ast heni c or chol i nergi c (e .g. sw eat i ng , s al i vat i on, l acri m ati on, col i c , fas ci c ul ati on, confusi on, ataxi a , s mal l p upi l s, brady cardi a, hype rt ens i on, s ei z ure s) cri si s.

Diagnosis of myasthenia Edrophoni um i s a s hort act i ng anti c hol i ne st erase used i n t he d i ag nos i s of myastheni a i n p ati ent s w i t h no previ ous hi s tory of m yas the ni a gravi s. In myastheni c p ati ent s w i t h an ac ute de teri orat i on the t est may di st i ng ui s h a myastheni c from a chol i nerg i c cri si s. In chol i nergi c c ri s i s there i s a p oss i b i l i ty of furthe r d ete ri orati on and atropi ne and faci l i t i es for urge nt i nt ubati on and venti l ati on shoul d be av ai l abl e. An i ni ti al dos e of 2 mg IV i s gi ven. If t here are no chol i nergi c s i de -effect s a further 8 m g m ay be g i ve n. A p osi ti ve tes t i s j udg ed by i mprove ment of we akness wi t hi n 3 mi n of i njec ti on. The te st may be com bi ned wi t h obje cti ve ass ess ment of resp i ratory func ti on b y m eas uri ng the FVC resp ons e or b y as ses si ng the re sponse to re pet i ti ve sti mul at i on wi th an EMG.

Maintenance treatment Ant i c hol i ne ste ras e d rugs provi d e t he m ai nst ay of s ymp tom ati c t reatme nt but st eroi ds , i mmunos upp re ssi ves and pl a sma ex change may provi de pharmacol ogi cal remi ssi on.

Myasthenic crisis New myast heni cs may pres ent i n cri si s and treat ment shoul d b e s tarte d wi th st eroi ds , azat hi opri ne and pyri d ost i gm i ne . Pl as ma exchang e m ay be useful to red uce the anti bod y l oad . In k nown my ast heni cs an i ncreas ed d ose of pyri dosti gmi ne and st eroi d s wi l l be re qui red . If t he condi t i on de teri orat es drug t herapy shoul d b e s top ped ; pl asm a exc hange may be l i fe s avi ng. Anti chol i nest erases may p rod uce i m provem ent i n some m usc l e group s and c hol i nerg i c det eri orati on i n others due t o d i ffere nti al sensi t i v i ty . As w i th any c ase of acute weak nes s m echani cal ve nti l a tory sup port i s req ui red i f FVC <1l or t he PaC O 2 i s raise d.

Cholinergic crisis Chol i nerg i c sy mpt oms are us ual l y at thei r most sev ere 2 h after the l ast dose of ant i chol i nes teras e. It i s com mon to gi v e atropi ne p rop hyl act i c al l y i n t he tre atm ent of myast heni a w hi c h m ay mas k s ome of the chol i nergi c s ympt oms . If a det eri orati on of m yas the ni a fails to re spond to edrophoni um al l drugs s houl d be s top ped and atropi ne g i ve n (1 mg IV eve ry 30 mi n to a m axi mum of 8 m g). The ed rophoni um t est shoul d b e repeated ev ery 2 h and anti chol i nes terase s rei nt rod uce d when the te st i s pos i t i ve . M echani cal ve nti l at i on i s requi re d i f F VC < 1l or the PaCO 2 i s rai s ed. P.387

Drug dosages

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Prednisolone

80 mg/day orally

Azathioprine

2.5 mg/kg/day orally

Pyridostigmine

60–180 mg 6-hrly orally

Atropine

0.6 mg 6-hrly orally

Drugs causing a deterioration in myasthenia Ami nog l y cos i de s St rep tom yci n Tet rac ycl i nes Loc al anaest het i c s Mus cl e rel a xant s Opi at es

See also: Venti l at ory support— ind i c ati ons , p 4; Endot rac heal i ntubat i on, p 36; Spe ci al sup port s urface s, p86; Pl asma ex change , p68; Pul m onary func ti on tes ts, p94; Steroi ds, p262; Resp i ratory fai l ure, p282; Hypotensi on, p312; Tachyarrhythmi a s, p316; Bradyarrhythmi as, p318; Acute weak nes s, p368 P.388

ICU neuromuscular disorders Neurom usc ul ar di s ord ers i n the c ri ti c al l y i l l have l ong b een rec ogni s ed, parti cul arl y i n those b ei ng m echani cal l y venti l at ed. Fi rst suspi ci ons are often raise d w hen pati e nts fail to wean from mec hani cal v ent i l ati on or l i m b w eakness i s not ed on stoppi ng sed ati on. Di suse atrophy, c at abol i c st ate s and drug t herapy (e. g. hi g h d ose st eroi d s, mus cl e rel axants ) are probab l y res ponsi b l e for some cas es but do not ex pl ai n al l . A neuromy opat hi c c omp onent of mul ti -organ dys functi on syndrome may be i m pl i cat ed.

Critical illness neuropathy Neurop hys i ol ogi cal s tud i es have demonst rated an acute i di op athi c axonal deg ene rat i on i n pati ent s wi th a fl ac ci d weaknes s fol l owi ng a p rol onged peri od of i ntensi ve c are. N erv e c ond uct i on ve l oc i t i es are norm al i nd i cati ng no dem yel i nati on. CSF i s normal unl i ke Gui l l ai n–Barr é s ynd rom e. T he neurop athy i s s el f-l i mi ti ng b ut prol ongs the rec ove ry phase of c ri ti c al i l l ne ss. Re cov ery may take week s t o y ears. Pyri doxi ne (100–150 mg dail y PO) has bee n use d i n t he tre atm ent .

Critical illness myopathy Drug i nd uce d my opathy i s not uncommon i n c ri t i c al l y i l l pat i e nts . Steroi d i nduced myopat hy i s l es s c omm on as the i nd i c ati ons for hi gh dose ste roi ds hav e b een red uc ed. Mus cl e rel a xant s may hav e a prol onged effec t and may be pot ent i at ed by β 2 agoni s ts. Muscl e hi s tol ogi cal st udi es hav e d emonst rat ed abnorm al i ti e s (fi b re atrophy, mi t ochond ri al defect s, myopat hy and nec ros i s ) whi c h c oul d not b e associ ated wi th st eroi d or mus cl e re l ax ant therapy. Myopat hy may cause re nal damage vi a m yog l ob i nuri a . C ri t i c al i l l ne ss myop athy i s associ ate d wi th vari ous forms of m usc l e deg ene rat i on but i s usuall y s el f-l i mi t i ng . R ecovery m ay t ake wee ks to years. P.389

See also: Venti l at ory support— ind i c ati ons , p 4; IPPV—ass ess ment of we ani ng, p18; Spe ci a l s upp ort s urface s, p86; Pul monary functi on tes ts , p 94; Resp i ratory fai l ure, p282; Acut e w eak nes s, p368; Gui l l a i n–Barré sy ndrome, p384 P.390

Tetanus The cl i ni cal s ynd rom e i s c aus ed by the exotox i n tet anospasmi n from the anaerobe Clostridi um tet ani i n contam i nated or dev i tali sed wounds . T etanos pas mi n as cends i nt ra-axonal l y i n mot or and autonomi c nerv es, bl ock i ng re l ease of i nhi b i tory neurot ransmi tt ers . T he di s eas e may b e m odi fi e d b y previ ous i mmuni s ati on, thus mi l der or l ocalis ed sym ptoms occ ur wi t h heav i er toxi n l oads .

Clinical features Gradual onse t of st i ffnes s, dys phagi a, m usc l e pai n, hyp ert oni a, ri gi d i t y and m usc l e spasm. Laryng osp asm oft en fol l ow s d ysp hag i a. Musc l e sp asm i s oft en provok ed by mi nor di s turbance, e. g. l aryng osp asm may be provoked by swall owi ng.

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Ons et of s ymp tom s w i thi n 5 d ays of i njury i mpl i es a heavy t oxi n l oad and s eve re di s eas e. The di s eas e i s s el f-l i mi ti ng s o t reatme nt i s sup porti ve but may ne ed to conti nue for se veral week s.

Management of the wound If a c ont ami nat ed wound i s p re sent, i t shoul d be de bri ded surgi cal l y to re move the s ource of the toxi n. Benzyl peni c i l l i n 1. 2 g 6-hrl y and m etroni dazol e 500 m g 8-hrl y IV are ap propri at e anti bi oti c s.

Passive immunisation Hum an tet anus i mmunog l ob ul i n 1000–1500 uni ts IM may short en the cours e of t he d i s eas e by re mov i ng ci rc ul a ti ng tox i n. Rapi d fi xat i on of the t oxi n t o ti ss ues l i mi t s the us eful nes s of t hi s ap proac h.

Mild tetanus Pat i ents wi t h m i l d s ympt oms , no resp i ratory di s tre ss and a del aye d onset of sy mpt oms shoul d b e nurs ed i n a q ui t e env i ronme nt wi t h m i l d se dat i on to preve nt tet ani c s pas ms.

Severe tetanus Int ubate and venti l at e si nc e as phyxi a may occur d ue to prol onged re spi rat ory muscl e s pas m. Sed ati on may be achi ev ed wi t h d i azepam (20 m g 4–6-hrl y N G and 5 mg IV as ne ces sary). Musc l e ri gi d i t y i s b est treat ed wi t h m agne si um s ul phate 20 m mol /h IV ± c hl orpromazi ne 25–75 m g 4-hrl y IV or NG, wi t h m usc l e re l ax ant s i f nece ssary. Aut onomi c hy per-re act i vi ty i s a feat ure (arrhythmi a s, hyp ote nsi on, hy pertensi on and myoc ard i al i schaem i a). It i s mi ni mi sed by se dat i on, anaes the si a and t reated by at rop i ne 1–20 mg/h IV, propranol ol 10 mg 8-hrl y IV or NG, and mag nes i um sul phate 20 mm ol /h IV. P.391

Tetanus toxoid prophylaxis The di sease confers no i mmuni t y s o p ati ent s m ust be i m muni se d p ri or t o hosp i t al di s charge . Las t d ose of tet anus t oxoi d >5 years no furt her dose Las t d ose of tet anus t oxoi d <10 years 1 d ose No p rev i ous i mmuni sat i on 3 dos es

See also: Venti l at ory support— ind i c ati ons , p 4; Se dat i ve s, p238; Musc l e re l ax ant s, p240; Ant i mi crobi al s , p 260; Res pi ratory fai l ure, p282; Hypotensi on, p312; Hyp ert ens i on, p 314; T achyarrhy thm i as , p 316; Brady arrhyt hmi as , p 318 P.392

Botulism An unc omm on, l e thal d i se ase cause d b y t he exot oxi ns of the anaerobe Cl ost rid ium botul inum. Bot ul i sm i s mos t com monl y a food-borne di s eas e, esp eci al l y associ ated wi th canned foods . It m ay b e c ont rac ted by wound contam i nati on w i th aq uat i c soi l s . T he tox i n i s carri ed i n the bl ood to chol i nergi c ne uromus cul ar junct i ons where i t bi nds i rrev ers i bl y. Sy mpt oms beg i n bet wee n 6 h and 8 d ays after contami nati on and are more sev ere wi th earl i e r ons et. Botul i s m i s d i ag nos ed by i sol at i ng C los tridi um bot uli num from t he stool or by m ous e b i oassay (survi v al of i mm uni sed mi ce and de ath of non-i m muni se d m i ce when i nfect ed serum i s i nj ect ed).

Clinical features Symp tom s i nc l ud e g ast roi nte sti nal d i st urb anc e, sore t hroat, fati g ue, di zz i ne ss, parae sthesi ae, crani al i nv ol v ement and a p rog res si v e, des cendi ng fl ac ci d we akness . Parasym pat het i c sym ptoms are common. The di s eas e i s usual l y s el f-l i mi t i ng wi thi n sev eral we eks .

Respiratory care Reg ul a r s pi rome try and m echani cal ve nti l a ti on i f FVC < 1l . Pati e nts wi th bul bar p al s y need i nt ub ati on for ai rway protec ti on.

Toxin removal If the re i s no i l eus the us e of non-m agnesi um contai ni ng cat harti c s m ay rem ove the toxi n l oad. Magne si um m ay enhanc e t he effe ct of the toxi n.

Antitoxin

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May short en the cours e of t he d i s eas e i f gi ven earl y and t he tox i n typ e i s k nown (s eve n have bee n i denti fi ed ). The re i s a hi gh ri sk of anaphy l ac toi d reac ti ons .

Wound botulism Surgi cal de bri dem ent and p eni ci l l i n are the mai ns tay of treatm ent for c ont ami nat ed wounds . P.393

See also: Venti l at ory support— ind i c ati ons , p 4; Anti m i c rob i al s, p260; Re spi ratory fail ure , p 282; Brady arrhyt hmi as , p318

Ovid: Oxford Handbook of Critical Care

Ed itors: Si nge r, M ervyn; We bb, An dre w R. Ti tle : O xf ord Ha ndbook of Cr itic al Car e, 2nd Ed ition Cop yri ght © 1997,2005 M. Si nge r and A. R. W ebb , 1997, 2005. Publ i shed i n the Uni te d Stat es by Oxford Uni ve rsi ty Press Inc > Tab le of Co n te n ts > H ae mato log ica l D iso r de r s

Haematological Disorders Bleeding disorders A c omm on probl e m i n t he cri ti cal l y i l l , thi s m ay be d ue to (i ) l a rge ves se l b l ee di ng—usually ‘s urgi c al ’ or fol l owi ng a proced ure (e .g. chest drai n, t rac heost omy, ac ci d ent al arteri al punct ure, removal of i ntravenous or i ntra-arteri a l cat het er); p ept i c ul c er bl eedi ng i s now rel a ti v el y uncom mon due to i m proved at tenti on t o p erfusi on and nutri ti on; (i i ) around vascul ar cathe ter s i te s or from i ntub ate d/i nst rum ent ed l um ens and ori fi ce s—usuall y rel a ted to se vere mul ti sys tem i l l ne ss or exc ess anti c oag ul ant therapy, i ncl udi ng t hrombol yt i c s; (i i i ) smal l ves sel bl eed i ng , e .g. sk i n pet echi ae , g ast ri c e ros i ons—usuall y rel a ted to ant i c oagul a ti on or s evere g ene ral i s ed i l l nes s i nc l ud i ng di ss emi nat ed i nt ravas cul ar coagul ati on. A fal l i ng p l at el e t c ount i s ofte n an earl y s i gn of sep si s and cri ti cal i l l ne ss . Re cov ery of the count us ual l y coi nc i de s wi t h overal l pati ent re cove ry.

Common ICU causes Dec reased pl ate l et producti on, e. g. sep si s - or d rug -i nduc ed Dec reased producti on of c oag ul ati on fact ors, e.g . l i ve r fai l ure Inc reased consumpt i on, e .g. DIC, m ajor t rauma, bl eed i ng , hepari n-i nduc ed thromb ocy top eni a, ant i pl ate l et anti bodi e s, ext rac orp ore al ci rcui ts Impaired or derang ed p l at el et func ti on Drugs, e. g. hepari n, asp i ri n Dec reased prote ase i nhi b i tors, e. g. ant i thrombi n III, Prote i n S and Protei n C defi c i ency (fol l owi ng s eps i s)

Principles of management 1. An Int ernati onal N orm al i sed Rati o (INR) bet wee n 1.5–2.5 and /or pl ate l et c ount of (20–40) × 10 9 /l do not usually req ui re c orrect i on i f t he p ati ent i s not bl e edi ng or at hi g h ri sk e. g. act i ve pe pti c ul ce r, re cent c ere bral haem orrhag e, und erg oi ng an i nvasi v e p roc edure. 5–10 uni ts of pl a tel ets wi l l raise the c ount b y onl y 10–20 × 10 9 /l . The effec t i s ofte n t ransi e nt (<24 h) and t he i nc rem ent re duc es wi t h repe ti t i v e dosi ng. Treat ment of symp tom ati c t hromb ocyt ope ni a ai ms to i nc re ase the count >50 × 10 9 /l . A target IN R < 1.5 i s ac cep tab l e. Vi tam i n K i s gi ven for l i ve r fai l ure and c ons i d ere d for warfari n overdos age . 1 mg Vi tam i n K w i l l re verse warfari n effect s wi t hi n 12 h w hi l e 10 m g w i l l s aturat e l i ve r s tores, preve nti ng warfari n act i v i ty for s ome wee ks. Fresh frozen pl a sma (FFP) i s g i ve n for short term c ont rol . 2. If b l ee di ng and INR = 1.5–2, gi ve 2–3 uni ts FFP. If INR > 2, gi v e 4–6 uni ts FFP. If not b l ee di ng (or hi g h ri s k), gene ral l y onl y c orrec t i f INR >2.5–3. Re peat c l ot ti ng s creen 30–60 mi n after FF P i nfused . Gi ve more F FP i f bl e edi ng conti nues and/or INR > 3. 3. For bl e edi ng rel at ed t o t hrombol ys i s , (i ) s top t he d rug i nfusi on, (i i ) g i ve ei the r aproti ni n 500,000 uni t s over 10 mi n, t hen 200,000 uni t s over 4 h or t ranexami c ac i d 10 mg/kg rep eate d 6–8-hrl y (i i i ) g i ve 4 uni ts FFP. 4. Cryopre ci pi t ate i s rarel y need ed. Consi der when t he thromb i n ti me i s el e vat ed, e.g . w i th DIC. Si m i l arl y, fac tor VIII i s g ene ral l y use d for hae mop hi l i ac s onl y . 5. If aspi ri n has bee n t aken wi thi n t he pas t 1–2 wee ks, pl ate l et funct i on may be de ranged . Gi ve fresh pl ate l et s, even thoug h c ount m ay b e adeq uat e. 6. Fact or VIIa may be use ful for s evere, i ntractabl e bl eed i ng but m ore st udi es are ne ede d t o c onfi rm i t s e ffi cac y. P.397

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Management of major bleeding 1. If e xte rnal, di rec t occl usi on/dee p s uture. 2. Urg ent exp ert op i ni on—e.g . for surgery, end osc opy + i nj ect i on, e tc. 3. Correc t c oagul opat hy.

Management of vascular catheter or percutaneous drain site bleeding 1. Di rect press ure/oc cl usi ve dre ssi ng. 2. Correc t c oagul opat hy; consi d er us e of ap rot i ni n or t ranexami c ac i d . 3. Surgi c al i nterventi on i s rare l y nec ess ary al though pe rforat i on/l a cerat i on of l oc al artery/ve i n shoul d be cons i d ere d i f b l ee di ng fai l s t o s top or be com es si g ni fi cant.

See also: Coagul ati on moni tori ng, p156; Bl ood t ransfusi on, p182; Bl ood produc ts, p252; Coagul ant s and ant i fi bri nol yt i cs , p 254; Aprot i ni n, p256; Haemopty si s , p 304; Uppe r g ast roi nte st i nal haemorrhag e, p 344; Lower i ntes ti nal bl eedi ng and col i ti s , p348; Acute l i ver fai l ure, p360; Chroni c l i ver failure, p364; Pl a tel et di s ord ers , p 406; Syst emi c i nfl am mat i on/mul ti organ fai l ure, p484; Post -op erati v e i nte nsi ve care, p534 P.398

Clotting disorders Unc omm on as a se condary e vent i n c ri t i c al l y i l l pati e nts as they tend t o be auto-ant i coagul at ed. The ri sk of maj or venous throm bos i s i nc re ase s wi th l ong term i mmob i l i ty and p aralys i s, and i n s pec i fi c pro-throm bot i c condi t i ons s uc h as pre gnancy , t hromboti c thromboc ytopeni c purpura, SLE (l up us ant i coagul ant), si ckl e c el l c ri s i s , hype ros mol ar di a bet i c coma. Di sse mi nate d i ntravascul ar coagul at i on i s associ a ted wi th mi c rov asc ul a r c l otti ng, a consum pti on coagul opathy and i nc re ase d fi bri nol ys i s . Cl otti ng of ext rac orp ore al ci rcui ts , e .g. for renal repl ac ement t herapy , m ay be d ue to (i ) mec hani c al obs tructi on to fl ow, e.g . ki nk ed c athete r, (i i ) i nad equate anti c oag ul a ti on or (i i i ) i n sev ere i l l ne ss, a dec rease i n end oge nous ant i c oagul ants (e. g. ant i thrombi n III); thi s may re sul t i n ci rcui t bl ockage des pi t e a coe xi s ti ng thromb ocy top eni a and /or coagul op athy. Axi l l ary ve i n or sub cl a vi a n v ei n throm bos i s may re sul t from i ndwe l l i ng i ntravenous cathe ters.

Management If the pati e nt i s not auto-ant i coagul at ed, prophyl a cti c l ow mol ecul ar we i ght hepari n (5000 IU od SC ) s houl d be g i ve n for l ong term i mmobi l i t y/paral ys i s and to hi gh ri s k p ati ent s (e.g . p rev i ous D VT, fe moral fractures ). For pul monary e mbol i s m or d eep vei n t hrombosi s g i ve 200 IU/kg SC daily (or 100 IU/k g b d i f at ri sk of bl eed i ng ). Parti al thromb opl ast i n ti m es (PT T) s houl d be che cke d regul arl y i f gi vi ng unfract i onate d hepari n and m ai ntai ned at app rox i matel y 2–3 × norm al . Moni t ori ng i s not ne ces sary for LMW he pari n though anti -Fac tor Xa l e vel s c an be use d. Int ra-art eri al cl ot can be treat ed wi t h l ocal i nfusi on of t hrombol yt i c s, usual l y fol l owe d by he pari ni sati on. See k vas cul ar surgi cal ad vi c e. Axi l l ary ve i n or sub cl a vi a n v ei n throm bos i s shoul d be manag ed by e l ev ati on of the affect ed arm , e .g. i n a Bradford sl i ng , and hepari ni s ati on. Spe ci fi c condi ti ons may re qui re spe ci fi c therapi e s, e.g . p l as ma exchang e for SLE and T TP, whol e bl ood exc hange for si ckl e c el l cri s i s. Warfari ni sati on s houl d generally be av oi d ed unt i l shortl y b efore ICU di scharg e b ecause of the ri sk of conti nue d bl e edi ng fol l ow i ng rout i ne i nvas i ve proce dures suc h as c ent ral ve nous c athete ri s ati on. P.399

See also: Coagul ati on moni tori ng, p156; Ant i coagul ants, p248; Thromb ol y ti c s, p250; Bl ood produc ts, p252; Pul monary em bol us, p308 P.400

Anaemia Defi ne d as a l ow haemogl obi n due t o a dec re ase d red c el l m ass , i t m ay als o be ‘p hys i ol og i cal’ due to di l ut i on from an i nc re ase d pl as ma v ol ume, e. g. pre gnancy , vasod i l ate d s tat es.

Major causes in the ICU patient Bl ood l os s, e.g . haemorrhage , regul ar b l ood s ampl i ng Seve re i l l ne ss— analog ous to the ‘ anaemi a of chroni c di sease’ , t here i s d ecreas ed marrow producti on and ,

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poss i b l y, a dec reased l i fes pan

Rarer causes include: Mi c roc yti c anae mi a —predomi nant l y i ron d efi ci enc y Normocy ti c Chroni c d i se ase Bone marrow fai l ure (i di opat hi c, drugs, ne opl asm , radi ati on) Haem ol y si s Renal fai l ure Macroc yti c—v i tami n B 1 2 and fol a te defi ci enc y, al c ohol i sm, ci rrhosi s, si derobl ast i c anaemi a, hyp othyroi di sm Cong eni tal di se ases —s i ck l e cel l , thalas saemi a

Management 1. Tre atme nt of the cause whe re pos si bl e . 2. Bl ood transfusi on: T he i de al haem ogl obi n l eve l for opt i mal oxyg en carri a ge and vi scosi t y remains c ont ent i ous. A rece nt m ul t i ce ntre t ri al showed i m proved out com es i f a t ri g ger of 7 g/d l w as used . A hi gher transfusi on threshol d, e .g. 9–10 g /dl , m ay be need ed i n those wi t h c ard i ores pi ratory di s eas e. T ransfusi on i s usuall y gi ven as packe d c el l s w i th or wi thout a s mal l d ose of furos emi de to m ai ntai n fl ui d b al a nce . T hi s may ne ed to be gi v en rap i dl y d uri ng act i ve bl ood l oss, or sl owl y for corre cti on of a gradual l y fal l i ng haemogl obi n l e vel . Rarel y, pat i e nts ad mi t ted wi th a c hroni c al l y l ow hae mogl ob i n, e. g. < 4–5 g/dl , whi ch often fol l ows l ong t erm m al nutri ti on or vi tami n defi ci enc y, wi l l need a m uch sl owe r e l ev ati on i n hae mog l ob i n l ev el to avoi d p rec i pi tat i ng acut e heart fail ure . An i ni t i a l t arg et of 7–8 g/d l i s ofte n acce ptabl e . Obvi ous l y , t hi s may ne ed t o b e al tered i n the l i ght of any c onc urrent acut e i l l ness where el evati on of ox yge n d el i very i s d eem ed nece ssary. Eryt hropoe i ti n reduces t he need for b l ood t ransfusi on i n l ong -te rm ICU pati e nts and m ay b e useful i n those wi th mul ti pl e anti b odi es or dec l i ni ng t ransfusi on for rel i g i ous reas ons . P.401

Key trial Hebe rt PC, et al for t he T ransfusi on Requi rements i n Cri ti cal Care Inv est i gators, Canadi an Cri ti cal Care T ri al s G roup. A mul ti c ent er, randomi z ed, control l ed cl i ni cal t ri a l of t ransfusi on requi reme nts i n cri t i cal c are . N Engl J M ed 1999; 340:409–17

P.402

Sickle cell disease A c hroni c, heredi tary d i se ase al mos t e nti rel y c onfi ned t o t he bl a ck pop ul a ti on w here t he gene for Hb S i s i nhe ri t ed from e ach parent. The re d bl ood ce l l s l ack Hb A; whe n d epri ve d of oxyge n t hes e c el l s ass ume si ckl e and othe r b i z arre shapes re sul ti ng i n ery throst asi s, oc cl usi on of b l ood v ess el s , t hrombosi s and t i ss ue i nfarcti on. After st asi s, ce l l s rel eas ed bac k i nto the c i rcul ati on are more fragi l e and prone t o haem ol y si s . Occ asi onally , t here m ay b e b one marrow fai l ure.

Chronic features Pat i ents wi t h s i c kl e ce l l di s eas e are chroni cal l y anaemi c (7–8 g/dl ) wi th a hy perdynami c c i rcul ati on. Spl e nome gal y i s com mon i n youth but, wi t h p rog res si v e e pi s ode s of i nfarct i on, s pl e ni c at rophy occ urs l ead i ng to an i ncre ase d ri sk of i nfect i on, p arti c ul a rl y pneum ococcal. Chroni c feat ure s i nc l ud e s ki n ul cers, renal fai l ure, avascul a r b one nec ros i s (± sup erv eni ng ost eom yel i ti s, es pec i al l y Sal monell a), he pat omeg al y , j aundi c e and cardi omyopat hy. Sudde n c ard i ac de ath i s not uncommon, usuall y b efore t he age of 30.

Sickle cell crises Cri ses are p rec i p i tated by vari ous tri gge rs , e. g. hyp oxaemi a (air trave l , anae st hes i a, et c.), i nfec ti on, col d, dehydrati on and em oti onal s tre ss.

Thrombotic crisis Occ urs m ost frequent l y i n bones or joi nts but also affect s c hes t and abd ome n g i vi ng ri s e t o s eve re pai n. Neurol ogi cal sym ptoms (e. g. s ei zures, focal si gns ), hae mat uri a or p ri a pi s m m ay be pre sent. Pul monary cri se s are the commonest

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reason for ICU admi ss i on; s econdary c hes t i nfect i on or AR DS may supervene, w ors eni ng hyp oxaemi a and furt her exacerbat i ng the c ri si s .

Aplastic crisis Rel ate d t o p arv ovi rus i nfec ti on, i t i s sugge ste d b y worse ni ng anae mi a and a re duc ti on i n t he normal l y el e vat ed ret i c ul ocyt e c ount (10–20%).

Haemolytic crisis Int ravasc ul ar hae mol ysi s w i th haemog l ob i nuri a, jaundi ce and re nal fai l ure som eti mes oc curs.

Sequestration crisis Rap i d hep ati c and spl eni c e nl a rg ement d ue to red ce l l trappi ng wi th seve re anaemi a. Thi s c ond i ti on i s parti cul arl y seri ous.

Management Prophy l ax i s agains t c ri ses i ncl ude s av oi d anc e of hypoxaem i a and ot her known pre ci pi t ati ng fac tors, prophy l ac ti c peni ci l l i n and pneum ococcal v acc i ne , and exc hang e t ransfusi ons . 1. Pai nful c ri s es usual l y requi re p rom pt opi ate i nfus i ons. Al t hough psy chol og i c al dep end enc e i s hi gh, anal ges i a shoul d not be wi thhel d . 2. Gi v e ox yge n t o m ai ntai n SaO 2 at 100%. 3. Rehy drate wi t h i ntrave nous fl ui ds and ke ep warm. 4. If i nfe ct i on i s suspe cte d, ant i bi oti cs shoul d b e g i ve n as i ndi cat ed. 5. Transfuse bl ood i f hae mog l ob i n l ev el drops or central nervous s yst em or l ung c ompl i c ati ons prese nt. 6. Lowe r p rop orti on of si ck l e cel l s to <30% by ex change trans fus i on. 7. Mechani cal ve nti l a ti on m ay b e nece ssary for chest cri s es. P.403

See also: Oxy gen therapy, p2; Pul s e ox i me try , p 90; Ful l bl ood count, p154; Bacte ri ol og y, p158; Acut e c hes t i nfe ct i on (1), p288; Acute che st i nfect i on (2), p290; Acut e renal fai l ure—d i ag nos i s, p332; Acute renal fai l ure—m anageme nt, p334; Jaundi ce, p358; Anaemi a, p400; Hae mol ysi s, p404 P.404

Haemolysis Short eni ng of e ryt hrocy te l i fesp an bel ow t he exp ect ed 120 day s. Marked i ntravas cul ar haemol ysi s may l ead t o jaundi ce and haemog l ob i nuri a.

Causes Bl ood transfusi on reacti ons Haem ol y ti c uraem i c sy ndrome (mi croang i op athi c haemol yti c anae mi a ) Trauma (cardi ac val ve prosthesi s) Mal a ri a Si c kl e ce l l hae mol yti c c ri si s Drugs— e.g . hi gh-dose p eni ci l l i n, met hyl dopa Aut oi m mune (c ol d - or w arm anti b ody -med i at ed)—may b e i di opat hi c or se condary, e.g . l ymp homa, SLE, mycopl a sma Gl ucos e-6-phosphate de hyd rog enase defi ci enc y—oxi d ati ve cri ses oc cur fol l owi ng i ng est i on of fav a b eans, pri maq ui ne, sul phonam i de s l ead i ng to rapi d onset anaemi a and jaundi ce

Diagnosis Unconjugat ed hyp erb i l i rubi naem i a, i ncre ase d uri nary urob i l i nog en (i ncre ase d R BC bre akdown) Reti cul oc ytosi s (i ncreas ed RBC producti on) Spl eni c hype rtrophy (ext rav asc ul a r haem ol y si s ) Methaem ogl obi nae mi a , haemogl obi nuri a, free pl a sma hae mog l ob i n (i ntravas cul ar haemol ys i s), reduced se rum hapt ogl obi ns RBC fragme ntati on (mi c roangi opathi c haem ol y ti c anaem i a) Coom bs' te st (i m mune-me di a ted haemol ys i s)

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Other (i ncl udi ng haem ogl obi n e l ec trophores i s , b one marrow bi ops y)

Management 1. Identi fi c ati on and sp eci fi c treat ment of t he cause where p oss i b l e. 2. Bl ood transfusi on to mai ntain hae mogl ob i n >7g/dl 3. Mass i v e i ntravascul ar haemol ys i s may l e ad t o acut e renal fai l ure. Mai ntain a good di ures i s and haemo(di a)fi l t er i f nece ss ary . P.405

See also: Ful l b l ood c ount, p154; Bl ood transfusi on, p182; Ac ute re nal fai l ure—di a gnosi s , p 332; Ac ute re nal fai l ure—managem ent , p 334; Jaund i ce , p 358; Anae mi a , p 400; Si ck l e cel l d i s ease , p 402; Pl ate l et di sorders, p406; Mal ari a, p490; Vas cul i t i de s, p494; HELLP s ynd rom e, p 540 P.406

Platelet disorders Thrombocytopenia Rarel y sy mpt omati c unti l t he p l at el et count <50 × 10 9 /l ; sp ont ane ous bl eed i ng i s more l i kel y <20 × 10 9 /l . Al though bl e edi ng i s oft en mi nor, e. g. ski n p ete chi ae, oozi ng at i ntravascul a r c athete r s i te s, i t may be mas si ve or l i fe-t hreate ni ng, e.g . haem opt ysi s, i nt racrani a l haem orrhag e.

Causes Sep si s —i n the ICU thi s i s t he com monest cause of a l ow pl a tel et count; often provi des a g ood barom ete r of rec overy or d ete ri orati on Di s sem i nated i ntravas cul ar coagul at i on Drugs Rel a ted to anti p l at el et anti body p rod uc ti on, e.g . he pari n (he pari n-i nduc ed t hromb ocyt ope ni a sy ndrome , ‘ HIT S’ ), sul phonami de s, qui ni ne Resul t i ng i n bone m arrow sup press i on, e .g. chemot herapy ag ent s Others , e .g. as pi ri n, chl orpromazi ne, prochl orp erazi ne, di goxi n Fol l owi ng mas si ve b l ee di ng and mul ti pl e bl ood trans fus i ons Bone marrow fai l ure, e .g. tumour i nfi l t rat i on, d rug s Spl enomegaly Thromboti c t hrombocyt ope ni c purpura (TT P), hae mol yti c urae mi c s yndrome (HUS) Idi opathi c t hrombocyt ope ni c purpura (IT P) Spe ci fi c i nfect i ons, e.g . m eas l es , i nfe cti ous mononucl eos i s , t yphus Col l age n v asc ul a r d i s eas es, e.g . SLE

Management 1. Di rect ed at the cause , e. g. ant i b i ot i cs for s eps i s , s top pi ng offendi ng d rugs, pl asm a ex change for T TP, spl ene ctomy and ste roi ds for ITP. 2. Pl at el et sup port Gi ve n rout i ne l y (e. g. 6–10 uni t s/d ay) whe n c ounts <10–20 × 10 9 /l 6–10 uni ts gi ven i f <50 × 10 9 /l and ei t her sy mpt omati c or due t o unde rgo surge ry or anothe r i nvasi v e p roc edure 3. Unl ess ac ti v el y bl eed i ng , avoi d p l at el e t t ransfusi ons i n TTP or HUS.

Deranged platelet function Functi on may be derang ed, al bei t w i t h normal c ounts , e. g. fol l ow i ng as pi ri n wi thi n p ast 1–2 w eeks , e pop ros tenol , uraemi a. Fre sh pl a tel ets may b e requi re d i f t he pat i ent i s s ymp tom ati c. In uraemi a, one dose of v asopre ssi n (20µ g IV ove r 30 m i n) may be us eful b efore s urgery.

Thrombocythaemia Rare i n ICU pat i ents; pl ate l et count s ofte n ex cee d 800 × 10 9 /l .

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Causes Prol onged l ow-l eve l b l ee di ng, pos t-s pl e nec tom y, myel oprol i fe rat i ve di sorders. Es senti a l (i di opathi c) thromb ocy thaemi a i s unus ual .

Management As the major ri sk i s throm bos i s, manag ement i s b ase d upon mobi l i s i ng the p ati ent and ad mi ni s trati on of e i ther prophy l ac ti c aspi ri n (150 mg bd PO) or LMW he pari n (5000 IU od SC). Di py ri d amol e (300–600 m g t ds PO) i s occ asi onall y used . P.407

See also: Pl a sma ex change , p68; Ful l bl ood count, p154; Bl ood trans fus i on, p 182; Anti c oag ul ant s, p248; Bl ood p rod uct s, p252; Int racrani a l haem orrhag e, p376; Ab dom i nal s eps i s , p 350; Bl eedi ng di sorders, p396; Haemol ys i s , p404; Sy ste mi c i nfl am mat i on/mul ti organ fai l ure, p484; Vasc ul i ti des , p 494 P.408

Neutropenia Neutropeni a i s defi ne d as a ne utrophi l count <2 × 10 9 /l . Li fe threat eni ng i nfec ti ons may dev el op b el ow 1 ×10 9 /l and more c omm onl y b el ow 0. 5 × 10 9 /l . Absol ut e numb ers of neutrophi l s are m ore re l ev ant than percentag es as the tot al whi te cel l c ount m ay be ei t her de cre ase d, normal or i ncre ase d.

Clinical features Usuall y as ymp tom ati c unt i l i nfect i on supervenes

Causes Sys tem i c i nfl am mat i on re sul ts i n margi nat i on and ag gregat i on of ne utrophi l s i n v i tal organs, e. g. l ung, l i ver, gut . Predomi nant l y see n i n t he fi rst 24 h afte r s eve re i nfect i on or trauma, i t i s oft en a p rec ursor of mul ti pl e org an d ysfunc ti on Haem opoi et i c di seas es , e. g. l eukae mi a , l ymp hom a, m yel oma or as a c ons equenc e of c hem otherapy or radi at i on Nut ri t i onal defi ci enci e s, e.g . fol at e, vi t ami n B 1 2 , mal nut ri t i on Adv ers e d rug re act i on, e .g. carbi mazol e , s ul p honami des Part of ap l as ti c anaem i a, e. g. i di opathi c, drugs , i nfe cti on Spe ci fi c i nfect i ons, e.g . b ruc el l os i s, ty phoi d, vi ral , protozoal Hype rs pl e ni s m Ant i ne utrophi l ant i b odi es, e. g. sys tem i c l up us ery the mat osi s

Infections Ini ti a l i nfe cti ons are w i t h c ommon organi s ms suc h as p neumoc occ i , staphy l oc occ i and col i form s. Wi t h recurre nt i nfect i ons or aft er rep eat ed c ourse s of anti b i oti c s, more unus ual and/or anti bi oti c -re si stant org ani sms may be re sponsi bl e, e .g. ps eud omonas , fung i (p arti c ul a rl y Candi da and As pergil lusspp .), pneumoc yst i s , c ytomegalov i rus, TB.

Management 1. If no d i ag nos i s has be en mad e, urg ent i nves ti g ati ons i ncl udi ng a b one marrow as pi rat i on are i ndi cat ed. 2. Any i m pl i cat ed drugs shoul d be i m med i at el y di sc ont i nued. 3. If t he neutrophi l count fal l s bel ow 1 × 10 9 /l , the pat i e nt shoul d be prote cti vel y i sol ate d i n a cubi c l e wi th stri ct i nfect i on control proced ure s. Consi d er l am i nar fl ow ai r c ond i t i oni ng i f av ai l abl e. 4. Mi ni mi se i nv asi ve proced ure s. 5. Mai ntai n good oral hyg i ene. App l y top i c al tre atm ent as nec es sary, e.g. ny stati n mouthwas hes for oral fungal infect i on. 6. Cl ot ri maz ol e cream for fungal s ki n i nfec ti on. 7. Ant i bi oti c the rap y For s us pec ted i nfec ti on use agg res si v e, parent eral anti bi oti cs (broad sp ect rum i f no organi sm has b een i sol ate d). Have a hi gh i ndex of suspi ci on for aty pi c al i nfect i ons suc h as fung i . Al thoug h p rop hyl act i c broad -sp ect rum anti b i ot i c s are ofte n p res cri be d, thi s e ncourages anti b i ot i c

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resi stance . Anot her al te rnati v e i s t o m ai ntai n s tri ct i nfec ti on c ont rol wi th re gul ar survei l l anc e and t o t reat i nfe cti ons ag gre ssi vel y as i ndi cated by l i kel y s i te s and l ab re sul ts. Avoi d uncooked foods , e. g. sal ads (p seudom onas ri s k) and bot tl e d p epp er (as pergi l l us ). 8. Granul ocy te-col ony st i mul at i ng factor (G-C SF) i s freque ntl y g i v en t o s ti mul ate a b one marrow resp ons e. 9. Neut rophi l i nfusi ons are short -l i ve d, e xpe nsi ve and often i nduc e a pyrexi al re sponse . Thei r rol e re mai ns cont roversi a l . P.409

See also: Ful l b l ood c ount, p154; Bac teri ol og y, p 158; Anti mi c rob i al s, p260; Infe cti on control — general p ri nci pl e s, p476; Infect i on—di ag nos i s, p480; Infect i on—treat ment, p482 P.410

Leukaemia Suc h p ati ents may pre sent acut el y to an IC U wi th compl i cati ons ari si ng from ei ther the di sease or the therapy.

Complications arising from the disease Dec reased re si s tance to i nfect i on Hype rvi sc osi ty syndrome—drowsi nes s, com a, foc al neurol ogi cal de fec ts Cent ral ne rvous sys tem i nvol vem ent Anaemi a, t hrombocyt ope ni a , b l ee di ng t end enc y, DIC

Complications arising from the therapy Tumour l ys i s sy ndrome —hy perkal aemi a, hyp eruri cae mi a and ac ute re nal fail ure may fol l ow rapi d d est ruc ti on of a l arge whi te c el l m ass Neut ropeni a and i mm une compromi se wi t h an i ncreas ed ri s k of i nfe cti on Anaemi a Thrombocyt ope ni a l e adi ng to spontaneous bl e edi ng, us ual l y from i ntravasc ul a r c athete r s i te s, ski n, l ung, gut and brain Lung fi brosi s, e.g . fol l owi ng rad i ot herapy , b l eomyc i n Myoc ard i al fail ure , e .g. fol l owi ng mi tozantrone Graft versus host di s eas e (GVHD)—feat ures i nc l ud e m ucosi t i s , hepat i t i s, jaund i ce , d i arrhoea, ab dom i nal p ai n, ras h and p neumoni ti s

Management 1. Tumour l ys i s sy ndrome can be preve nte d b y adequate hy drati on, mai ntaini ng a g ood di uresi s and admi ni ste ri ng al l opuri nol . Once est abl i s hed , haemo(di a)fi l t rat i on and othe r m eas ure s t o l owe r s erum p otassi um l ev el s may b e nece ss ary . 2. The rai se d whi t e ce l l mas s may be red uce d b y l euc ophore si s . 3. Freq uent b l ood t ransfusi ons to mai nt ai n Hb l e vel s >7 g/dl 4. Pl at el et transfusi ons are requi red i f c ounts re mai n <10–20 × 10 9 /l , or i f <50 × 10 9 /l and rem ai ni ng s ympt omati c or unde rg oi ng an i nvas i v e proc edure. 5. Gi v e fres h froz en p l as ma and ot her bl ood products as ne ede d. 6. Neut ropeni a m anagem ent , i ncl udi ng prote cti ve i sol at i on, appropri a te anti bi oti c t herapy , ± granul oc yte col ony sti mul ati ng fac tor. 7. GVHD i s m anaged by sup porti ve t re atm ent and parenteral nut ri ti on. Prostagl andi n E 1 and i mm unosup pre ssi on may be hel pful . 8. Psyc hol ogi cal s upp ort for b oth pati e nt and fam i l y i s v i tal.

Respiratory failure 1. Mai ntenanc e of g as exc hang e. Mortal i t y i s hi gh (>60%) i f me chani c al venti l ati on i s nec es sary. Non-i nv asi ve tec hni que s i ncl udi ng CPAP and Bi PAP can prove hi ghl y e ffe cti ve i n avoi di ng the ne ed for i nt ub ati on. 2. Where p oss i b l e, treat the c aus e. Infect i on (i ncl udi ng aty pi c al organi sm s), fl ui d ove rl oad , ARDS and a pneumoni ti s/fi b ros i s sec ond ary to chemo- or radi otherapy s houl d be consi dered. P.411

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See also: Venti l at ory support— ind i c ati ons , p 4; Conti nuous pos i ti ve ai rway press ure , p 26; N on-i nv asi ve res pi rat ory support, p32; Acut e resp i ratory di s tre ss syndrome (1), p 292; Acute res pi rat ory di stres s s ynd rom e (2), p294; He art fai l ure— ass ess ment, p324; Heart fail ure —manag ement, p326; Acute renal fai l ure—di a gnosi s , p 332; Ac ute re nal fai l ure— managem ent , p 334; D i arrhoea, p340; Jaundi ce, p358; Anaemi a, p400; Pl a tel et di s ord ers , p 406; Ne utrope ni a, p408; Hyp erk al a emi a, p 420; Infe cti on—di agnosi s, p480; Infe cti on—tre atm ent , p 482

Ovid: Oxford Handbook of Critical Care

Ed itors:

Si nge r, M ervyn; We bb, An dre w R.

Ti tle : O xf ord Ha ndbook of Cr itic al Car e, 2nd Ed ition Cop yri ght © 1997,2005 M. Si nge r and A. R. W ebb , 1997, 2005. Publ i shed i n the Uni te d Stat es by Oxford Uni ve rsi ty Press Inc > Tab le of Co n te n ts > Meta bo lic Dis or d er s

Metabolic Disorders Electrolyte management A b al a nce must be achi ev ed bet ween el ect rol yt e i ntake and out put . C ons i de r: Al t ere d i ntake Impaired renal exc ret i on Inc reased bod y l oss es Bod y compartm ent re di stri buti on (e.g . i ncreas ed cap i l l ary l eak , s econdary hype ral dos te roni sm ) As wel l as N a + and K + , consi der Mg 2+ , Ca 2+ , Cl - and PO 4 3- b al anc e. Pl a sma el ect rol yt e value s are poorl y re fl e cti ve of whol e body st ores; how ever, exce ss i ve l y hi g h or l ow p l asma l ev el s may i nduc e s ymp tom s and d el e teri ous phy si ol og i cal and met abol i c se que l ae . Wat er bal anc e m ust al so be tak en i nt o ac count ; de pl e ti on or e xce ss rep l e ti on m ay resp ect i v el y conce ntrate or di l ut e el e ctrol yte l e vel s. The us ual daily re qui re ment s of N a + and K + are 60–80 mmol . Gravi tat i onal peri pheral oede ma i mp l i e s i ncreas ed tot al bod y N a + and w ater, though i ntravas cul ar sal t and wat er dep l et i on may c oex i st .

Electrolyte losses •Large nasogastric aspirate, vomiting

Na + , Cl -

•Sweating

Na + , Cl -

•Polyuria

Na + , Cl - , K + , Mg 2+

•Diarrhoea

Na + , Cl - , K + , Mg 2+

•Ascitic drainage

Na + , Cl - , K +

Principles of management 1. Est abl i sh sourc es and de gre e of fl ui d and e l ec trol y te l os ses . 2. Ass ess pati e nt for si gns of (i ) i ntravascul ar fl ui d d epl eti on—hyp ote nsi on (e.g . fol l owi ng change s i n p ost ure, PEEP, v asodi l ati ng drugs ) ol i g uri a, i nc re asi ng met abol i c ac i dosi s , t hi rst , (i i ) total body NaCl and w ate r overl oad—i .e. gravi tati onal oe dema. 3. Meas ure urea, creat i ni ne , os mol al i ty and el ec trol yt e c ont ent of pl asm a and uri ne. 4. As app rop ri a te, ei the r repl ac e es ti mat ed fl ui d and el e ct rol yte de fi c i t or i nc re ase exc ret i on (w i th di ureti cs, haem ofi l trat i on). For rat e of fl ui d and spe ci fi c el e ct rol yte re pl a cem ent se e i ndi vi d ual se cti ons . P.415

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See also: El e ct rol yte s , p 146; Uri nal y si s , p 166; Hy pernat raemi a, p 416; Hyponat rae mi a , p 418; Hy perkal aem i a, p420; Hyp okalae mi a , p 422; Hyp omagne saem i a, p424; Hypercalcaemi a, p426; Hypocal cae mi a , p 428; Hypop hos phatae mi a , p 430 P.416

Hypernatraemia Clinical features Thi rs t, l et hargy, coma, se i zures , m usc ul a r t re mor and ri gi di t y, and an i ncre ase d ri s k of i ntracrani al hae morrhage. Thi rs t usually oc curs w hen the p l as ma sod i um ri ses 3–4 m mol /l above norm al . Lack of thi rs t i s associ a ted wi th central nervous s yst em d i s eas e.

Treatment Dep end s upon the c aus e and w het her total body sod i um st ore s are normal , l ow or el e vat ed and bod y water i s norm al or l ow .

Rate of correction If hype rac ute (< 12 h), corre cti on can be rapi d . Otherw i se , aim for gradual correc ti on of p l as ma sod i um l e vel s (over 1–3 d ays ), parti c ul arl y i n c hroni c cases (> 2 days ' d urati on), to av oi d ce reb ral oe dem a t hrough sudde n l oweri ng of os mol al i ty . A rate of p l as ma sod i um l owe ri ng <0.7 mm ol /h has been sugge ste d.

Hypovolaemia If hypovol aem i a i s acc omp ani ed by haem ody nam i c al t erati ons, us e c ol l oi d i ni t i al l y to re store the ci rcul a ti on. Otherw i se , use i sotoni c sal i ne. Art i fi ci al col l oi d s ol uti ons consi st of hyd rox yet hyl st arc hes (e .g. Hes pan, El oHAES) or gel ati ns (e. g. Gel ofus i n, Haem acc el ) di ssol ve d i n i sotoni c sal i ne .

Normal total body Na (water loss) Wate r rep l ac ement e i t her PO (ad di t i on t o enteral fee d) or as 5% g l ucos e IV. Up t o 5l /d ay may be nec ess ary . If c rani a l d i ab ete s i nsi pi dus (CD I): re stri c t s al t and g i ve thi azide di ureti cs. Compl ete CDI wi l l re qui re desm opress i n (10µg bd i ntranas al l y or 1–2µ g b d IV) whereas part i al CD I m ay requi re d esm opress i n but often res ponds to d rugs that i ncreas e t he rat e of ADH sec ret i on or end-organ resp ons i ve nes s t o ADH, e. g. chl orp rop ami de, hy drochl ort hi azi de If nephrog eni c D I: manage by a l ow sal t d i et and t hi a zi des . High dose d esm opress i n may be effec ti v e. Cons i d er removal of causati v e agents, e. g. l i t hi um, dem ecl ocy cl i ne.

Low total body Na (Na and water losses) Tre at hype ros mol ar non-ke tot i c di a bet i c cri si s, uraemi a as appropri a te. Otherw i se consi der 0. 9% sal i ne or hy pot oni c (0.45%) sal i ne. Up t o 5 l /day may be ne eded .

Increased total body Na (Na gain) Wate r rep l ac ement e i t her PO (ad di t i on t o enteral fee d) or as 5% g l ucos e IV. Up t o 5l /d ay may be nec ess ary . In addi ti on, furos emi de 10–20 m g IV p rn may be ne ces sary. P.417

Causes of hypernatraemia

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Type Low total body Na

Aetiology Renal losses: diuretic excess, osmotic diuresis (glucose, urea, mannitol)

Extra-renal losses: excess sweating Normal total body Na

[Na + ] >20 mmol/l isoor hypotonic [Na + ] <10 mmol/l hypertonic

Renal losses: diabetes insipidus

Extra-renal losses: respiratory and renal insensible losses Increased total body Na

Urine

[Na + ] variable hypo-, iso- or hypertonic [Na + ] variable hypertonic

Conn's syndrome, Cushing's syndrome, excess NaCl, hypertonic NaHCO 3

[Na + ] >20 mmol/l isoor hypertonic

See also: Hae mo(d i a)fi l trati on (1), p62; Haemo(di a )fi l trat i on (2), p 64; Enteral nut ri ti on, p80; Parent eral nut ri t i on, p 82; El e ct rol yte s , p 146; Uri nal y si s , p 166; Cryst al l oi ds, p176; Col l oi ds, p180; Di ure ti c s, p212; El ec trol yt e m anagem ent , p414; Di abe ti c ket oac i dosi s , p 442; Hy perosm ol a r d i abet i c emerge nci es, p444 P.418

Hyponatraemia Clinical features Nausea, v omi ti ng, headac he, fat i g ue, weakne ss, muscul ar tw i tc hi ng, obt undat i on, p syc hos i s, se i zures and c oma. Sym ptoms dep end on the rate as wel l as t he mag ni t ude of fal l i n the pl asm a [N a + ].

Treatment Rate and degree of correction In c hroni c hyponat rae mi a corre cti on shoul d not e xce ed 0.5 mmol /l /h i n the fi rs t 24 h and 0. 3 m mol /l /h thereafter. In acut e hyponat rae mi a the i deal rate of corre cti on i s controversi al though el evati ons i n pl a sma Na + can be fast er, but < 20 mmol /l /day. A p l as ma N a + of 125–130 m mol /l i s a reas onab l e targe t for i ni ti a l c orrec ti on of b oth acute and chroni c st ate s. Att emp ts to achi ev e normo- or hype rnatraemi a rapi dl y shoul d b e avoi ded . Neurol ogi cal compl i cati ons , e. g. central ponti ne m yel i nol ys i s, are rel a ted to the d egree of c orrec ti on and (i n chroni c hyponat rae mi a ) the rate . Prem enopausal wom en are more prone to t hes e c omp l i cat i ons.

Extracellular fluid (ECF) volume excess If s ymp tom ati c (e.g . s ei z ure s, agi tat i on), and not oede matous, 100 m l ali quot s of hype rtoni c (1.8%) s al i ne can be g i ve n, che cki ng pl a sma l e vel s e very 2–3 h. If s ymp tom ati c and oed emat ous , c ons i d er furose mi d e (10–20 m g IV b ol us p rn), m anni tol (0.5g/k g IV over 15–20 mi n), and rep l ac eme nt of uri nary s odi um l os ses wi th al i quots of hyp ert oni c s al i ne . Check pl asm a l eve l s eve ry 2–3 h. Hae mofi l t rat i on or di al ysi s m ay be nece ssary i f renal fai l ure i s est abl i s hed. If not sym ptomat i c, re st ri c t w ate r t o 1–1. 5 l /day. If hyponat rae mi a pe rsi st s, consi d er i nappropri a te ADH (SIAD H) sec ret i on. If SIADH l i k el y , g i ve i s otoni c s al i ne and consi der de mec l oc ycl i ne . If SIADH unl i ke l y, consi der furosemi de (10–20 mg IV bol us prn), manni tol (0.5 g/kg IV ov er 15–20 mi n), and rep l ac ement of uri nary s odi um l os ses wi th al i quots of hyp ert oni c s al i ne. Chec k p l as ma l ev el s re gul arl y. Hae mofi l t rati on or d i al ysi s m ay be nec ess ary i f re nal fai l ure i s est abl i s hed .

Extracellular fluid volume (ECF) depletion

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If s ymp tom ati c (e.g . s ei z ure s, agi tat i on), gi ve i sot oni c (0.9%) sal i ne . C ons i de r hype rtoni c (1.8%) s al i ne. If not sym ptomat i c, gi ve i sotoni c (0. 9%) saline.

General points Equati ons that cal cul ate ex ces s w ater are unrel i abl e. It i s safer to perform freq uent e sti mat i ons of p l as ma sodi um l e vel s. Hype rt oni c s al i ne may be dangerous i n the e l de rl y and t hos e w i th i m pai red cardi ac funct i on. An alte rnati v e i s t o use furose mi d e w i th re pl acem ent of uri nary sod i um (and pot ass i um ) l oss es eac h 2–3 h. T hereafter, s i mp l e wat er res tri ct i on i s us ual l y suffi c i ent. Many pati e nts ac hi e ve normonatraem i a by s pontaneous w ate r d i uresi s. Use i s otoni c sol ut i ons for rec ons ti tut i ng drugs , p are nte ral nutri ti on, et c. Hyponat rae mi a may i nte nsi fy the cardi ac effect s of hy perkal aem i a. A t rue hy ponatraemi a m ay occ ur wi t h a normal osmol al i ty i n the p res enc e of abnormal s ol utes e. g. ethanol , ethy l ene g l yc ol , gl uc ose . P.419

Causes of hyponatraemia Type

ECF volume depletion

Aetiology

Renal losses: diuretic excess, osmotic diuresis (glucose, urea, mannitol), renal tubular acidosis, salt-losing nephritis, mineralocorticoid deficiency

Extra-renal losses: vomiting, diarrhoea, burns, pancreatitis Modest ECF volume excess (no oedema) acute and chronic renal failure ECF volume excess (oedema)

Urine [Na + ] >20 mmol/l <10 mmol/l

water intoxication (NB post-operative, TURP syndrome), inappropriate ADH secretion, hypothyroidism, drugs (e.g. carbamazepine, chlorpropamide), glucocorticoid deficiency, pain, emotion.

>20 mmol/l

nephrotic syndrome, cirrhosis, heart failure

<10 mmol/l

>20 mmol/l

Causes of inappropriate ADH secretion Neop l as m, e.g . l ung , p anc reas, l ym phoma Most pul monary l esi ons Most ce ntral ne rvous sys tem l e si ons Surgi c al and em oti onal s tre ss Gl ucoc ort i c oi d and thyroi d defi c i ency Idi opathi c Drugs, e. g. chl orp rop ami de, carbamazepi ne, narcoti c s

See also: Hae mo(d i a)fi l trati on (1), p62; Haemo(di a )fi l trat i on (2), p 64; Enteral nut ri ti on, p80; Parent eral nut ri t i on, p 82; El e ct rol yte s , p 146; Uri nal y si s , p 166; Cryst al l oi ds, p176; Col l oi ds, p180; Di ure ti c s, p212; Acut e renal fai l ure—di ag nos i s, p332; Ac ute re nal fai l ure— managem ent , p 334; El ect rol yt e m anag eme nt, p414; Di abe ti c ke toaci d osi s, p442; Hyperos mol ar di a bet i c eme rge nci es , p 444 P.420

Hyperkalaemia Pl a sma potas si um d epe nds on the balance bet wee n i ntake, exc re ti on and t he di stri buti on of p otassi um across c el l mem branes . Excreti on i s normal l y control l ed by the ki dne ys.

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Causes Reduced re nal ex cre ti on (e.g . c hroni c re nal fail ure , ad re nal i nsuffi c i ency, di abe tes , p otassi um spari ng di uret i cs ) Int rac el l ul ar pot ass i um re l ease (e.g . aci d osi s, rapi d trans fus i on of ol d b l ood, cel l l ysi s i nc l ud i ng rhab domy ol y si s, haem ol y si s and t umour l ys i s , K + channel ope ners (ni c orandi l )) Potassi um poi soni ng

Clinical features Hyp erk al a emi a m ay c aus e d ang erous arrhyt hmi as i ncl udi ng c ard i ac arre st. Arrhythmi a s are more cl os el y re l at ed to the rate of ri s e of p otassi um than t he abs ol ute l ev el . Cl i ni cal fe atures such as paraes the si a e and are fl e xi c we akne ss are not c l earl y rel a ted to the de gre e of hyperkal aem i a but us ual l y occ ur aft er ECG chang es (tall ‘T’ waves , fl at ‘P’ wav es, prol onge d PR i nterval and w i de QR S).

Management Pot ass i um re st ri c ti on i s need ed for al l c ase s and hae modi afi l t rat i on or haemodi a l ys i s may be ne eded for resi st ant cas es.

Cardiac arrest associated with hyperkalaemia Sod i um bi carbonat e (8.4%) 50–100 m l s houl d be gi ven i n add i t i on to st and ard CPR and ot her t reatme nt det ai l ed bel ow.

Potassium >7 mmol/l Cal ci um c hl ori de (10%) 10 m l s houl d be gi v en urg ent l y i n add i ti on to tre atm ent de tai l ed be l ow . Al thoug h c al c i um chl ori de does not red uc e the p l as ma pot ass i um , i t s tabi l i se s t he myocardi um agai nst arrhythmi a s.

Clinical features of hyperkalaemia or potassium >6 mmol/l with ECG changes Gl ucose (50 ml 50%) and s ol ubl e i nsul i n (10 i u) shoul d be gi ven IV ove r 20 m i n. Bl ood gl uc ose shoul d b e moni t ored eve ry 15 mi n and more gl ucos e g i ve n i f nece ssary. In ad di t i on, c al ci um resoni um 15 g qd s PO or 30 g bd PR can be consi dered. P.421

See also: Hae mo(d i a)fi l trati on (1), p62; Haemo(di a )fi l trat i on (2), p 64; Enteral nut ri ti on, p80; Parent eral nut ri t i on, p 82; El e ct rol yte s , p 146; Uri nal y si s , p 166; Cryst al l oi ds, p176; Di ure ti c s, p212; Cardi ac arres t, p272; Brad yarrhy thm i as , p 318; Acut e renal fai l ure— di a gnosi s , p 332; Ac ut e renal fail ure —manage ment, p334; El ec trol y te managem ent , p 414; Rhabdomyol ys i s, p528 P.422

Hypokalaemia Pl a sma potas si um d epe nds on the balance bet wee n i ntake, exc re ti on and t he di stri buti on of p otassi um across c el l mem branes . Excreti on i s normal l y control l ed by the ki dne ys.

Causes Inad equate i ntak e Gas troi nt est i nal l os ses (e. g. vom i ti ng , di arrhoea, fi stul a l os ses ) Renal l oss es (e. g. di a bet i c ket oac i dosi s , C onn's syndrome, se condary hype ral dos teroni sm, Cushi ng' s s ynd rome, renal tub ul a r aci d osi s, met abol i c al kal os i s, hy pom agne sae mi a , d rug s i nc l ud i ng di ureti cs, st eroi ds , t heophy l l i ne s) Haem ofi l trat i on l osse s Potassi um trans fer i nto cel l s (e. g. acute al k al osi s , g l uc ose i nfus i on, i ns ul i n t reatme nt, fami l i al p eri odi c paral y si s )

Clinical features Arrhyt hmi as (SVT, VT and Torsades de Poi nt es) ECG change s (ST dep res si on, ‘T’ wave fl a tte ni ng, ‘U’ wav es) Metabol i c al kal osi s Cons ti pat i on Il e us Weak nes s

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Management Whereve r p oss i b l e, the c aus e of potas si um l oss s houl d be t re ated . Potassi um re pl a cem ent shoul d b e i ntrave nous wi th ECG moni t ori ng whe n t here i s a cl i ni cally si gni fi cant arrhyt hmi a (20 m mol ov er 30 mi n, repe ate d ac cordi ng to l ev el s ). Sl ower i ntravenous re pl a cem ent (20 mm ol ove r 1 h) shoul d be us ed whe re the re are cl i ni cal fe atures wi thout arrhyt hmi as. Oral s upp l em ent ati on (to a t otal i nt ake of 80–120 mm ol /d ay, i ncl udi ng nut ri t i onal i nput ) c an be g i ve n w here there are no cl i ni cal fe atures . P.423

See also: Ent eral nut ri t i on, p 80; Parent eral nutri ti on, p82; El e ctrol y tes , p 146; Uri nal y si s , p 166; Cryst al l oi ds, p176; Di ure ti c s, p212; Steroi d s, p262; C ard i ac arres t, p272; Tac hyarrhythmi as, p316; El e ctrol y te managem ent , p 414; M etabol i c al k al osi s , p 436; Di ab eti c k etoaci dos i s, p442; Pos t-operati ve i nt ens i ve care, p534 P.424

Hypomagnesaemia Causes Exce ss l oss, e. g. d i uret i cs , othe r c aus es of pol yuri a (i ncl udi ng poorl y control l ed di a bet es mel l i tus ), seve re di a rrhoea, p rol ong ed vomi ti ng, l a rge nasog ast ri c as pi rat es Inad equate i ntak e, e.g . s tarvat i on, p are nte ral nutri ti on, al cohol i sm, malab sorpt i on sy ndromes

Clinical features Mag nes i um i s pri m ari l y an i nt rac el l ul ar i on i nvol ved i n the p rod uct i on and uti l i s ati on of energy st ore s and i n t he med i at i on of ne rve trans mi s si on. Low pl asm a l eve l s, whi ch do not nece ssari l y refl ect ei ther i nt rac el l ul ar or whol e bod y s tores, may t hus be ass oc i at ed wi t h fe atures rel a ted to these functi ons: Confusi on, i rri tab i l i ty Sei zures Musc l e weakne ss, l e thargy Arrhyt hmi as Symp tom s rel ate d t o hy poc al c aem i a and hy pokalae mi a whi ch are resi st ant to calci um and potas si um sup pl e ment at i on re spe cti vel y Normal pl asm a l eve l s range from 0.7–1.0 mmol /l ; s eve re sym ptoms do not usual l y occ ur unt i l l ev el s drop bel ow 0.5 mmol /l .

Management Where p oss i b l e, i d ent i fy and t reat t he cause. For sev ere , s ymp tom ati c hypomagnesaemi a, 10 mmol of magne si um s ul p hat e c an be gi v en IV ove r 3–5 mi n. T hi s can be rep eat ed onc e or t wi c e as ne ces sary. In l es s acut e s i tuati ons or for asym ptomat i c hyp omag nes aem i a, 10–20 mm ol MgSO 4 s ol uti on can be gi v en ove r 1–2 h and rep eat ed as nec ess ary , or ac cordi ng to rep eat pl asm a l evel s. A c ont i nuous IV i nfus i on (e .g. 3–5 m mol MgSO 4 s ol uti on/h) c an be gi v en; how eve r, thi s i s usual l y rese rve d for therap eut i c i nd i cati ons whe re sup ranormal pl asm a l evel s (1.5–2 mmol /l ) of magne si um are sought , e .g. tre atm ent of sup rav ent ri cul ar and ve ntri cul ar arrhythmi a s, pre -ec l am psi a and ecl amp si a , b ronchospasm. Oral m agnesi um sul phate has a l axati ve e ffe ct and may cause se vere d i arrhoea. Hi g h p l as ma l eve l s of mag nes i um may de vel op i n renal fai l ure; cauti on s houl d be app l i ed w hen ad mi ni st eri ng IV magnesi um. P.425

See also: Ent eral nut ri t i on, p 80; Parent eral nutri ti on, p82; Cal c i um, m agnesi um and phosp hat e, p148; D i uret i cs , p 212; As thm a—ge neral manage ment, p296; T achyarrhythmi a s, p316; El ec trol yt e m anageme nt, p414; Ge neral i sed se i z ure s, p372; Pre -ec l am psi a and e cl amps i a , p 538 P.426

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Hypercalcaemia Causes Mal i gnanc y (e .g. my el oma, bony m etastati c di sease, hy pernep hroma) Hype rparat hyroi di s m Sarcoi dos i s Exce ss i ntak e of calci um, vi tam i n A or D Drugs, e. g. thi azi des , l i t hi um Immobi l i s ati on Rare l y, thyrotox i c osi s, Add i son's di se ase

Clinical features Usual l y b ecome app are nt when total (i oni sed and un-i oni sed ) p l as ma l ev el s >3.5 m mol /l (normal rang e 2.2–2.6 mmol /l ). Sym ptoms depe nd on the pati e nt' s age, the d urati on and rat e of i ncreas e of pl asm a c al c i um, and the pre sence of concurrent m edi cal c ondi ti ons . Naus ea, vomi t i ng , w ei g ht l os s, pruri tus Musc l e weakne ss, fati g ue, l e thargy Depres si on, mani a, ps ychosi s Drowsi nes s, com a Abd omi nal pain, const i pati on Acute pancre ati ti s Pept i c ul cerati on Pol y uri a, re nal calcul i , renal fail ure Arrhyt hmi as

Management 1. Identi fy and treat cause whe re pos si b l e. 2. Care ful l y moni tor haem ody nam i c vari ab l es , uri ne outp ut, and ECG morphol og y wi th frequent est i m ati ons of pl a sma Ca 2+ , PO 4 3- , Mg 2+ , Na + and K + . 3. Int rav asc ul a r v ol ume rep l et i on—thi s i nhi b i ts proxi mal t ubul ar re abs orp ti on of c al c i um and ofte n l owers the pl a sma cal ci um by 0.4–0.6 mm ol /l . It shoul d prec ede di ure ti c s or any other the rap y. Ei t her col l oi d or 0.9% sal i ne shoul d b e used , de pendi ng on t he pre sence of hypovol aem i a-rel ate d feat ure s. 4. Cal c i ures i s— aft er ade quate i nt rav asc ul a r v ol ume rep l et i on, a force d d i ures i s wi t h furosem i de pl us 0.9% s al i ne (6–8 l /day ) may b e atte mpt ed. An effect i s us ual l y se en w i t hi n 12 h. Loop d i uret i cs i nhi bi t calci um reabsorp ti on i n the asc end i ng l i mb of the l oop of Henl é. More aggres si v e furosemi de re gi m ens can be at tem pte d b ut can pote nti al l y res ul t i n c ompl i c ati ons . T hi a zi des shoul d not b e used as tubul ar reabsorp ti on m ay b e reduced and hype rc al c aemi a w ors ene d. 5. Di a l ys i s/hae mofi l t rat i on—may b e i ndi cat ed at an earl y stage i f the pat i e nt i s i n est abl i s hed ol i go-anuri c renal fai l ure ± fl ui d ove rl oade d. 6. Ste roi ds can be effect i v e for hype rcalc aemi a rel ated to haematol ogi cal cance rs (l y mphoma, m yel oma), v i tami n D overdos e and sarcoi dos i s . 7. Cal c i t oni n has the mos t rap i d ons et of acti on wi t h a nadi r often re ached wi t hi n 12–24 h. It s acti on i s us ual l y short-l i v ed and re bound hype rcalc aemi a m ay occ ur. It ge neral l y d oes not d rop the p l as ma l ev el more t han 0.5 mmol /l . 8. Bi p hos phonat es (e.g . p ami dronat e) and IV phosp hat e s houl d onl y b e gi ven after sp eci al i st ad vi c e i s t ake n i n vi ew of thei r toxi c i t y and p ote nti al com pl i cati ons. P.427

Drug dosage

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Diuretics

Furosemide 10–40 mg IV 2–4 h (may be increased to 80–100 mg IV every 1–2 h)

Steroids

Hydrocortisone 100 mg qds IV or prednisolone 40–60 mg PO for 3–5 days

Pamidronate

15–60 mg slow IV bolus

Calcitonin

3–4 U/kg IV followed by 4 U/kg SC bd

See also: Cal ci um, mag nes i um and p hos phate, p148; Di ure ti c s, p212; Steroi d s, p262; Acut e renal fai l ure—d i ag nos i s, p332; Ac ute re nal fai l ure— managem ent , p 334; Pancreat i t i s, p354; El e ctrol yte manage ment, p414; D i ab eti c ket oaci dosi s , p442; Thy roi d e mergenci e s, p446; Hypoadrenal c ri si s , p 448 P.428

Hypocalcaemia Causes Ass oci ate d w i th hy perphosphataemi a: Re nal fail ure Rhabd omy ol y si s H ypop arathyroi di sm (i ncl udi ng s urgery), ps eudohyp oparat hyroi d i s m Ass oci ate d w i th l ow/norm al phos phate: Cri t i cal i l l nes s i nc l ud i ng se psi s, burns Hypom agnesaemi a Panc reati t i s Oste omalac i a Over-hyd rati on Mass i v e bl ood trans fus i on (c i t rat e-b i nd i ng ) Hype rve nti l a ti on and the re sul ti ng resp i ratory al k al osi s may reducet he i oni se d p l as ma cal ci um frac ti on and i nd uce cl i ni cal fe atures of hy poc al c aem i a

Clinical features The se usual l y appe ar whe n t otal p l as ma c al ci um l eve l s <2 mmol /l and the i oni sed fract i on i s <0.8 mmol /l . Tetany (i ncl udi ng carpop edal s pas m) Musc ul ar weak nes s Hypotensi on Peri oral and peri p heral parast hes i ae Chvoste k & Trous seau's si gns Prol onged QT i nterval Sei zures

Management 1. If res pi ratory al k al osi s i s p res ent , adjus t vent i l ator s ett i ng s or, i f sp ont aneousl y hype rve nti l a ti ng and agi tat ed, cal m ± sed ate . R ebreat hi ng i nto a bag may be benefi ci al . 2. If s ymp tom ati c, gi ve 5–10 ml 10% c al c i um chl ori d e s ol uti on over 2–5 mi n. Rep eat as ne ces sary. 3. Correc t hypom agnesaemi a or hypok al a emi a i f p res ent . 4. If asym ptomat i c and i n re nal failure or hyp oparat hyroi d, c ons i d er ent eral/p are nte ral calci um suppl ementat i on and vi t ami n D anal ogue s. 5. If hypotensi v e or c ard i ac output i s dec reased fol l owi ng ad mi ni s trati on of a calci um ant agoni s t, gi v e 5–10 ml 10% cal ci um c hl ori de s ol uti on over 2–5 m i n. P.429

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See also: Ent eral nut ri t i on, p 80; Parent eral nutri ti on, p82; Cal c i um, m agnesi um and phosp hat e, p148; D i uret i cs , p 212; Ac ute renal fai l ure— di a gnosi s , p 332; Ac ut e renal fail ure —manage ment, p334; Hypotensi on, p312; Panc re ati ti s , p 354; El e ct rol yte manage ment, p414; Rhab dom yol ysi s, p528 P.430

Hypophosphataemia Causes Cri ti c al i l l ne ss Inad equate i ntak e Loop di ureti c t herapy (i ncl udi ng l ow dose dop ami ne) Pare nte ral nutri ti on— le vel s fall rapi d l y duri ng hi gh dos e i nt rav enous g l ucos e t herapy , es pec i a l l y wi th i ns ul i n Al c ohol i s m Hype rparat hyroi di s m

Clinical effects Hyp ophosp hat aem i a i s ass oci ate d w i th muscl e w eakness ; howe ver, t hi s i s rarel y c l i ni c al l y apparent, eve n i n p ati ent s wi t h s eve re hyp ophosp hat aemi a w here p l as ma l ev el s may drop <0. 1 m mol /l .

Treatment Phosphate suppl eme nts (5–10 mmol ) shoul d be gi ven by i ntravenous i nfus i on ov er 6 h and re peated ac cordi ng t o t he pl a sma phosp hat e l eve l . P.431

See also: Ent eral nut ri t i on, p 80; Parent eral nutri ti on, p82; Cal c i um, m agnesi um and phosp hat e, p148; D i uret i cs , p 212; Ac ute weaknes s, p368 P.432

General acid–base management Inc re ased i ntake, al t ered p rod uc ti on or i mpaire d/e xce ssi ve exc ret i on of aci d or bas e l eads to de rangem ent s i n b l ood pH. Augme nte d renal e xcreti on of H + i ons m ay res ul t from hyp okal aem i a. Wi th ti me, res pi rat ory and renal adj ust ments correc t the pH tow ard s norm al i ty by al t eri ng the p l as ma l eve l of PCO 2 or HCO 3 - .

Increased intake Aci d: asp i ri n overdos e Bas e: N aHC O 3 adm i ni strat i on, antac i d ab use , buffe red re pl a cem ent fl ui d (haem ofi l trati on)

Altered production Inc reased ac i d produc ti on: l ac ti c ac i d osi s (usual l y s econdary to hyp operfus i on), di abet i c ket oac i d osi s Inc reased bas e p rod uc ti on: c hroni c hype rcapni c resp i ratory fai l ure, permi s si ve hype rc apni a Dec reased bas e p rod uct i on: c hroni c hype rve nti l at i on

Altered excretion Inc reased ac i d l os s: vomi ti ng, l a rge gastri c as pi rate s, di uret i c s, hyp eraldoste roni sm , c ort i c ost eroi ds Inc reased bas e l os s: d i arrhoea, s mal l b owel fi st ul a , uret hroent erostomy, proxi mal re nal tubul ar aci dosi s Dec reased aci d l os s: renal fai l ure, di s tal renal t ubul ar ac i dosi s , acet azol am i d e Dec reased bas e l oss : c hroni c hypercapni c resp i ratory fai l ure, permi s si ve hype rcapni a

Principles of management Correc t (w here p oss i bl e) the ab normal i ty , e .g. hy pop erfusi on Cons i de r addi ti on of ‘ subst rat e’ and physi ol ogi c al corre cti ve functi ons NaCl i nfus i on for v omi ti ng-i nd uce d al kal os i s; i nsul i n, Na + and K + i n d i ab eti c k etoaci dos i s Correc t p H i n s pec i fi c c i rcum stance s onl y , e .g. NaHCO 3 i n renal fai l ure

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P.433

See also: Bl ood gas anal y si s , p 100; Lact ate , p 170; Sodi um b i c arb onate, p178; Res pi ratory fai l ure, p282; Chroni c ai rfl ow l i mi t ati on, p286; Met abol i c ac i dosi s, p434; Me tab ol oi c al kal osi s, p436 P.434

Metabolic acidosis A s ubnormal arteri al bl ood pH wi th a b ase defi ci t >2 m mol /l . Outcome i n cri ti cal l y i l l p ati ent s has bee n l i nk ed to the sev eri ty and durat i on of me tab ol i c aci d osi s and hyp erl ac tat aemi a.

Causes Ti s sue hy pope rfusi on, e.g . heart fai l ure, hypovol aem i a, se psi s. The ani on gap i s rel a ted to producti on of l ac ti c and other org ani c aci ds. Anaerobi c m etabol i sm contri b ute s i n p art to thi s met abol i c ac i d osi s althoug h othe r cel l ul ar mec hani sm s are i nv ol v ed. Ti s sue ne crosi s , e .g. bowel , musc l e. Hype rc hl orae mi a , e. g. exc ess i ve sali ne i nfusi on. Ketoaci dos i s —hi gh l ev el s of β-hydroxy but yrate and ac etoace tat e rel a ted to unc ont rol l e d d i ab ete s m el l i t us, starvati on and alc ohol i s m. Renal fai l ure—ac cumul ati on of organi c ac i d s, e.g . s ul p huri c . Drugs— in parti cul ar, as pi ri n (sali cyl i c aci d) ove rdose, ac etazol ami de (carboni c anhyd ras e i nhi bi t i on), amm oni um chl ori de. Vasop res sor ag ent s m ay be i mp l i c ate d, pos si b l y by i nd uc i ng re gi onal i s chaemi a or, i n the case of epi nephri ne, ac cel erated gl ycol ys i s . Ing est i on of poi sons, e.g . p aralde hyd e, ethyl e ne gl y col , m ethanol . Bi c arb onate l os s, e.g . s eve re di a rrhoea, s mal l b owel fi st ul a e, l arge i l e ost omy l osse s. Type B l ac ti c aci d osi s—no e vi d enc e of t i ss ue hyp ope rfusi on.

Causes of type B lactic acidosis Ac ute i nfec ti on Di abet es mel l i tus Drugs , e. g. phe nformi n, met formi n, alcohol s Gl ucose-6-phosp hat ase de fi c i ency Hae mat ol ogi c al mal i gnanc y Hep ati c fai l ure Pancre ati ti s Renal fai l ure Short bow el syndrome (D-l ac tat e) Thi ami ne defi ci enc y

Clinical features Dys pnoe a Haem ody nam i c i ns tab i l i ty A rapi dl y i ncreasi ng met abol i c aci d osi s (ove r m i nutes to hours ) i s not due to renal fai l ure. Ot her cause s, parti c ul a rl y s evere t i s sue hyp ope rfusi on, sep si s or t i ss ue nec ros i s shoul d b e s usp ect ed when there i s as soc i a ted sys temi c det eri orati on

Management 1. The und erl yi ng cause s houl d be i d ent i fi ed and treat ed w here p oss i bl e rat her than admi ni ste ri ng alkali or mani pul at i ng mi nut e v ol ume t o norm al i se the arte ri a l p H. 2. Urg ent hae mo(di a )fi l trati on may be nec es sary i f ol i g uri a p ers i s ts. 3. Reve rsal of t he met abol i c ac i dosi s (othe r t han si mpl e b ufferi ng wi t h b i c arb onat e) i s generall y an i ndi cat i on of suc ces sful t herapy . An i ncreas i ng b ase defi ci t sug ges ts that t he the rap eut i c manoeuvre s i n operati on are ei the r i nadequate or wrong . 4. The benefi ts of buffers s uch as Carbi carb and THAM (t ri s-hydroxy -met hyl -am i nomet hane) remain unp rov ed and are not ge neral l y avai l ab l e. P.435

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P.436

Metabolic alkalosis A s upranormal arte ri a l b l ood p H w i th a bas e e xces s >2 m mol /l caused ei the r b y l oss of (non-c arb oni c) aci d or gai n of base. As the k i dney i s usual l y e ffi ci e nt at exc ret i ng l arg e q uant i t i es of bi carbonate , p ers i st enc e of a metabol i c al kal osi s usually de pends on ei t her chroni c re nal fai l ure or a d i mi ni s hed ex tracel l ul ar fl ui d vol um e wi t h s evere d epl eti on of K + . The pat i ent i s usual l y asym ptomati c though, i f s pontaneous l y breat hi ng, wi l l hypoventi l ate . A me tab ol i c al k al osi s wi l l cause a l eft shi ft of the oxyhaemogl obi n curve , reduci ng oxyg en availabi l i t y t o t he ti s sue s.

Causes Los s of total body fl ui d, Na + , C l + , K + us ual l y due to: d i ureti cs l arg e nasogas tri c aspi rates , v omi ti ng Sec ond ary hyp erald ost eroni s m w i th potas si um d epl eti on Use of hae mofi l t rat i on re pl a cem ent fl ui d containi ng exc es s b uffe r (e.g . l act ate ) Renal c omp ens ati on for chroni c hyp erc apni a. Thi s can de vel op wi t hi n 1–2 w eek s. Al t hough more apparent when the pat i ent hype rve nti l a tes , or i s hype rve nti l at ed to normoc apni a, an ove rc ompe nsated me tab ol i c alkalos i s can occ asi onally be se en i n t he chroni c state (i . e. a rai s ed pH i n an othe rwi se st abl e l ong term hype rc apni c pat i ent) Exce ss adm i ni st rat i on of bi carbonate Exce ss adm i ni st rat i on of ci trate (l a rge bl ood trans fus i on) Drugs, i ncl udi ng l ax ati ve abus e, corti cos teroi d s Rare l y, Cushi ng' s, Conn's , Bartte r's sy ndrome

Management 1. Repl ace ment of fl ui d, sod i um , c hl ori de (i .e . g i ve 0. 9% sal i ne ) and p otassi um l osse s are ofte n s uffi ci ent t o res tore aci d –base bal anc e. 2. Wi t h d i st al renal causes rel a ted to hyp eraldost eroni s m, add i ti on of spi ronol a ctone (or potas si um c anrenoate ) can be c ons i d ere d. 3. Act i ve treat ment i s rare l y nec ess ary. If s o, gi v e ammoni um c hl ori d e 5 g tds PO. Hydrochl ori c aci d has bee n used on occasi on for sev ere me tab ol i c alkalos i s (pH >7.7). It s houl d be g i v en v i a a c ent ral ve i n i n a c onc ent rat i on of 1 mm ol HCl pe r m l w ate r at a rat e not exc eed i ng 1 mmol /kg /h. 4. Comp ens ati on for a l ong-s tandi ng resp i ratory aci dos i s, fol l owed by corre cti on of t hat ac i d osi s, e.g . wi th mechani cal ve nti l a ti on, wi l l l ead to an uncom pensat ed m etabol i c al kal osi s. Thi s usuall y c orrect s w i th ti me though treat ment s s uc h as ac etazol ami de can be consi dered. Me chani c al ‘hy pov ent i l ati on’ , i .e. mai nt ai ni ng hype rc apni a, can al so be consi d ered. P.437

See also: Hae mo(d i a)fi l trati on (1), p62; Haemo(di a )fi l trat i on (2), p 64; Bl ood gas anal ysi s, p100; Sod i um bi carbonate , p 178; Bl ood trans fus i on, p 182; Ac ute re nal failure—di agnosi s, p332; Ac ut e renal fail ure —manag ement, p334; Vom i t i ng /gas tri c stasi s, p338; Hyp okalae mi a , p 422; Gene ral ac i d–bas e m anagem ent , p432 P.438

Hypoglycaemia Causes Inad equate i ntak e of c arb ohy drate Exce ss i nsul i n or sul phonyl urea Li v er fai l ure w i th de pl e ti on of g l yc oge n s tores Al c ohol Hypoadrenali sm (i nc l udi ng Addi son's di sease), hy pop i tui t ari sm Qui ni ne, asp i ri n

Clincal features

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Naus ea, vomi t i ng Inc reased sy mpat het i c ac ti v i ty , e .g. sw eat i ng , t achycardi a Al t ere d b ehavi our and consc i ous l eve l Sei zures, focal ne urol og i cal s i g ns

Management 1. Moni tor c are ful l y wi t h regul ar be dsi de est i mati ons . T he freq uency shoul d be i ncrease d i n c ond i t i ons k nown to pre ci p i tate hyp ogl ycaemi a, e.g . i nsul i n i nfus i on, l i v er fai l ure, qui ni ne t re atme nt of mal ari a. 2. Adm i ni ste r 25 m l 50% gl ucos e s ol uti on i f t he bl ood gl ucos e i s: ≤ 3 m mol /l or ≤ 4 m mol /l and the p ati ent i s sy mpt omati c or W i thi n the normal rang e b ut the pati e nt i s sym ptomat i c (us ual l y l ong-s tandi ng p oorl y control l ed di a bet i cs ) Re peat as nece ssary eve ry few mi nute s unti l symp tom s abat e and the bl ood gl ucose l ev el has normal i s ed. 3. If t he bl ood gl ucos e i s 3–4 mmol /l and t he pat i ent i s non-sym ptomati c, ei the r reduce the rate of i ns ul i n i nfusi on (i f pre sent), or i ncreas e calori e i ntak e (e nte ral l y or parenteral l y). In i nsul i n dep end ent di abe tes me l l i tus, the i ns ul i n s houl d conti nue wi t h adeq uat e g l uc ose i ntak e. 4. A c ont i nuous parenteral i nfusi on of 10%, 20% or 50% gl ucos e s ol uti on v ary i ng from 10–100 ml /h may be req ui red, de pendi ng on t he d egree of conti nui ng hypogl y cae mi a and t he p ati ent's fl ui d balance/uri ne out put . 5% gl ucos e s ol uti on onl y contains 20Cal /100 ml and s houl d not be us ed to pre vent or t reat hypogl y cae mi a . 5. In t he rare i ns tance of no v enous acc ess , hypogl y cae mi a may be te mporari l y re versed by gl ucagon 1 mg g i v en ei t her IM or SC . 6. Cont i nui ng hypog l yc aem i a i n the face of adeq uat e t reatme nt and l a ck of s ymp tom s s houl d be confi rmed wi th a form al l ab oratory b l ood s ugar e st i mati on t o ex cl ude mal funct i oni ng of the be dsi de tes ti ng equi pm ent . P.439

See also: Nut ri ti on—use and i ndi c ati ons , p 78; Ent eral nutri t i on, p 80; Pare nte ral nutri ti on, p82; C rys tal l oi ds , p 176; Ac ute l i ver fai l ure, p360; Gene ral i s ed sei zures, p372; Hyp oadrenal c ri si s , p 448; Parac etamol poi soni ng, p456 P.440

Hyperglycaemia Causes A c ommon occurrenc e i n c ri t i c al l y i l l pat i e nts due t o a com bi nati on of i mp ai red gl ucos e t ol e rance, i nsul i n res i st anc e, hi g h c i rcul ati ng l ev el s of endog enous c at echol a mi nes and corti cos teroi d s, and re gul ar adm i ni st rat i on of s uch drugs whi c h antag oni se the effec t of i nsul i n Panc reati ti s re sul ti ng i n i sl et cel l dam age

Clinical features None i n t he short term, other than p ol y uri a from the osmoti c di ure si s. The pat i e nt may com pl a i n of thi rs t or s how si gns of hyp ovol ae mi a i f fl ui d balance i s al l owe d t o b ecom e t oo neg ati ve.

Metabolic effects Rel ati ve l ac k of i nsul i n preve nts ce l l ul a r g l uc ose up tak e and uti l i s at i on re sul ti ng i n: Inc reased l i pol ysi s Al t ere d c el l ul ar met abol i s m Inc reased ri sk of i nfect i on (d ecreas ed neut rophi l acti on)

Prognostic significance St ri c t m ai ntenanc e of g l yc aemi c control (app rox . 4–7 m mol /l ) re sul ted i n s i gni fi cant outc ome i m provem ent i n a surgi cal IC U p opul at i on. W het her thi s i s rel at ed t o p rev ent i on of hy pergl y cae mi a and/or an effec t rel a ted to ad di t i onal adm i ni st rat i on of i nsul i n rem ai ns unc ert ai n.

Management 1. Tre atme nt shoul d be gi ven i f bl ood gl ucose el e vat i ons p ers i s t (> 7–8 mm ol /l ). 2. A s hort-acti ng i ns ul i n i nfusi on (e. g. act rap i d) shoul d b e us ed and ti trate d t o maint ai n norm ogl ycaemi a (4–7

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mmol /l ). Usually 1–4Uni ts /h are re qui red thoug h m ay need to be much hi g her i n di abe ti cs who bec ome cri ti cally ill . R egul ar be dsi de moni tori ng of b l ood s ugar s houl d be performed ; thi s shoul d b e undertaken hourl y i f unst abl e. 3. Oral hypogl y cae mi c ag ent s s houl d be g ene ral l y avoi de d i n t he ICU pati e nt bec aus e of thei r p rol ong ed durati on of act i on and unpredi ctabl e ab sorpti on. P.441

Key trial Van den Be rg he G , e t al. Int ens i ve i nsul i n therapy i n cri ti cal l y i l l p ati ent s. N Engl J Med 2001; 345:1359–67

P.442

Diabetic ketoacidosis Thi s m ay occ ur de novo i n a previ ous l y und i ag nos ed d i abet i c or fol l ow an acute i ns ul t (e.g. i nfec ti on) i n a k now n di a bet i c pat i e nt.

Clinical features Exce ss fat me tab ol i sm to fat ty aci ds wi t h k etone produc ti on An osmoti c d i uresi s w i t h l arg e l oss es of fl ui d (up to 6–10l ), s odi um (400–800 mmol ), pot ass i um (250–800 mm ol ) and mag nes i um Sym ptoms res ul t from hyp ovol ae mi a , m etab ol i c aci dos i s and el ect rol yt e i mbal ance w i t h pol yuri a. Hyp erv ent i l a ti on i s a p rom i ne nt feature. Com a ne ed not ne ces sari l y be prese nt for l i fe to be threat ene d. Pl a sma am yl a se comm onl y e xce eds 1000U/l but doe s not i nd i c ate pancreat i ti s. If sus pec ted , p erform an ab dom i nal ul t rasound.

Monitoring Ade quate i nv asi ve moni tori ng i s ess ent i al , p art i c ul a rl y i f the p ati ent has c i rcul atory i ns tab i l i ty or cardi ac dys functi on. Uri ne out put , b l ood g ase s and pl a sma el ect rol yte s s houl d al s o b e m oni tored fre que ntl y.

Fluid and electrolyte management 1. Fl ui d and el e ct rol yte re pl e ti on s houl d be tai l ored to i nd i v i dual nee ds. Tradi ti onal re gi mens (e .g. 3–4 l wi thi n t he fi rst 3–4 h) i ncre ase the ri sk of ce reb ral oe dema, c ard i ac and/or renal fai l ure. 2. Col l oi d fl ui d c hal l enges shoul d b e g i ve n t o rest ore the c i rc ul ati ng bl ood vol ume i n ti ssue hypoperfus i on. 3. Fl ui d rep l ac eme nt wi t h 0.9% sal i ne s houl d be g i ve n at a rate of 200 ml /h unti l the sal t and wat er deb t has bee n rep l eni shed. 4. Hypotoni c (0. 45%) s al i ne res usc i t ati on may be app rop ri a te i n the non-s hoc ked pat i e nt i f the pl asm a s odi um i s ri s i ng rapi dl y (shi ft of water and p otassi um i nt o c el l s and sod i um out). 5. Sub sti tut e 5% g l uc ose sol ut i on (100–200 ml /h) aft er rep l aci ng t he sod i um de bt; usual l y when the b l ood s ugar fal l s to <10 mmol /l . 6. Care ful l y moni tor K + repl ac ement. Bot h aci dos i s and exc ess i v e K + adm i ni st rat i on cause hy perkal aem i a whi l e fl ui d and i nsul i n wi l l produc e hypok al a emi a. Che ck l eve l s frequent l y to m ai ntai n normokalem i a. Infus i on of 10–40 m mol /h KCl wi l l be need ed. 7. Care ful l y moni tor m agnesi um rep l ac eme nt: 3–5 m mol /h M gSO 4 i s usual l y suffi c i ent.

Hyperglycaemia Correc t s l owl y at a rate of 2–4 mm ol /h b y adjus ti ng the short ac ti ng i ns ul i n i nfusi on (usual l y 1–5U/h). Moni t or bl ood gl ucos e hourl y . Conti nue IV i nsul i n (w i th gl ucose aft er achi ev i ng normogl y cae mi a ) unti l heav y ke tonuri a has di s app eared and the b ase defi c i t normal i se d.

Other aspects of managing ketoacidosis 1. Seek a pre ci p i t ati ng cause and treat as i ndi c ate d. App rox i matel y 50% are re l at ed to und erl yi ng d i se ase , e .g. seps i s , m yoc ard i al i nfarcti on, s troke, i nfec ti v e g ast roe nte ri t i s . 2. Onl y g i ve ant i b i ot i cs for p rov ed or hi g hl y suspe ct ed i nfe ct i on. 3. Abd omi nal pain shoul d not b e di sm i ss ed as part of t he s ynd rome. 4. A nasog ast ri c t ube shoul d b e i nse rte d, as gas tri c empt yi ng i s oft en d el ayed and acut e g ast ri c di l a tat i on i s comm on. 5. Avoi d bi c arb onate, eve n for sev ere ac i dosi s (p H < 7.0). It c aus es an i nc re ase d i ntrace l l ul a r aci d osi s and

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depres sed re spi rat i on due t o a re l at i ve CSF al kal os i s. Sodi um overl oad m ay also oc cur. 6. Low mol ecul ar we i ght hepari n 5000U SC od i s i ndi cat ed i n i mm obi l e or com atos e p ati ent s. P.443

See also: Central v enous cat het er— use , p 114; Ce ntral venous cathe ter—i nse rti on, p116; El e ctrol y tes , p 146; Bact eri ol ogy, p158; Uri nal ys i s, p166; Cry stalloi d s, p176; Fl ui d c hal l enge, p274; Anti c oag ul a nts , p 248; Ant i m i crobi al s, p260; Ol i g uri a, p330; Vomi t i ng/g ast ri c st asi s, p338; Abdomi nal sep si s , p 350; Hyp erk al a emi a, p420; Hyp okalae mi a , p 422; Hypomagnesaemi a, p424; Hyp erg l yc aem i a, p440; Met abol i c aci d osi s, p434; Infect i on—di ag nos i s, p480; Infect i on—treat ment, p482 P.444

Hyperosmolar diabetic emergencies Thi s i s more c ommon i n e l de rl y, non-i ns ul i n dep ende nt di abet i c s t hough can prese nt de nov o i n y oung adul ts. Pre ci pi t ati ng fac tors are si m i l ar to ket oaci dosi s , e .g. se psi s, myocardi a l i nfarc ti on

Clinical features Fl ui d depl et i on i s great er, bl ood gl ucose l ev el s often hi ghe r, com a m ore freque nt and mortali ty m uch hi gher than in di a bet i c ket oac i dosi s . Confusi on, ag i tati on and drowsi nes s t hat may p ers i st for 1–2 wee ks. A me tab ol i c aci dos i s may be prese nt but i s not usually profound ; ke toaci d osi s i s not a major feat ure . Hype ros mol al i ty may predi sp ose to thromb oti c events ; thi s i s the m ajor cause of mortalit y. Sev ere hype ros mol al i ty does not al w ays oc cur. Focal neurol ogi cal si gns and d i ss emi nat ed i nt ravasc ul ar coagul ati on are oc cas i onal l y recogni se d.

Management As for di abe ti c k etoaci dos i s; howeve r: 1. Unl ess the pati ent shows si gns of hyp ovol ae mi a and t i ss ue hyp operfusi on, i n whi ch cas e c ol l oi d chal l enges shoul d be gi ven for promp t resusc i tati on, fl ui d rep l ac eme nt shoul d be more gradual as t he ri s k of c ere bral oede ma i s hi g her. T hi s c an b e w i th ei the r 0.9% saline or, i f the pl asm a s odi um i s hi g h, 0.45% sal i ne at a rat e of 100–200 ml /h. 2. The pl a sma sodi um ri s es wi t h t reatme nt, eve n w i th 0. 45% saline, and can often i ncreas e i n t he fi rst few day s t o 160–170 mm ol /l b efore gradually de cl i ni ng the reafter. Ai m to corre ct sl owl y . 3. Serum phos phate and magne si um l eve l s fal l rapi dl y wi th thi s condi t i on; repl ace ment m ay b e need ed as gui ded by freq uentl y taken pl asm a l eve l s. 4. Pati ent s may be hyp ers ens i ti ve to i ns ul i n and re qui re l ow er dos es. 5. Unl ess ot herwi s e c ont rai ndi cat ed, these pati e nts shoul d b e ful l y hepari ni s ed unt i l ful l rec overy (whi ch may take ≥5 d ays ). P.445

See also: El e ct rol yte s , p 146; Bact eri ol ogy, p158; Uri nal ys i s, p166; Cry stalloi d s, p176; Anti coagul ant s, p248; Ant i mi crobi al s , p 260; Fl ui d chall eng e, p 274; Ol i guri a, p330; Vomi ti ng/gas tri c s tas i s , p 338; Abd omi nal se psi s, p350; Hy pernat raemi a, p 416; Hyp onatraemi a, p418; Hype rkalae mi a , p 420; Hypok al a emi a, p422; Hyp omagne sae mi a , p424; Hypop hos phatae mi a , p430; Hyp erg l yc aem i a, p440; Di abet i c ke toac i d osi s, p442; Infec ti on—di a gnosi s , p 480; Infec ti on—t re atme nt, p482 P.446

Thyroid emergencies Thyrotoxic crisis Pre sents as an exacerbat i on of the cl i ni cal feat ure s of hype rthyroi di sm (e. g. pyrexi a, hyp erd ynam i c ci rcul at i on, heart fai l ure, confus i on). The re i s usual l y a prec i pi tat i ng factor s uc h as i nfec ti on, surge ry, ke toac i d osi s, myocardi a l i nfarc ti on or chi l db i rth. It may pres ent wi th exhaust i on i n t he e l d erl y wi th few fe atures of hyp erthy roi di s m. The di a gnosi s i s c onfi rm ed by standard thy roi d func ti on t est s.

Management Pyre xi a shoul d b e c ont rol l e d b y surface cool i ng (avoi d asp i ri n whi ch di s pl a ces thyroxi ne from pl asm a p rot ei ns).

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Cate chol am i ne effec ts shoul d be re duc ed by β bl oc kade (e .g. propranol ol 1–5 m g IV t hen 20–80 mg qds PO). Thes e s houl d be use d w i th cauti on i f the re i s acute heart fai l ure. Bl ockade of t hyroxi ne synthe si s i s achi eve d by potas si um i odi de 200–600 m g IV over 2 h t hen 2 g/day PO and carbi m azol e 60–120 mg/day PO. Bl ockade of p eri phe ral T 4 t o T3 conve rsi on i s ac hi e ved by dex amet has one 2 mg qds IV. Care ful fl ui d and e l ec trol y te managem ent i s es senti a l .

Myxoedema coma Pre sents as an exacerbat i on of the fe atures of hy pot hyroi d i sm (e .g. hyp othermi a , c oma, brady cardi a, m etabol i c and res pi rat ory ac i dosi s , anae mi a ). There m ay be a prec i pi tat i ng factor (e.g . c ol d , i nfe cti on, surg ery , my ocardi al i nfarc ti on, CVA, central nerv ous sy ste m d epress ant drugs ). Di a gnosi s i s c onfi rm ed by thy roi d func ti on t est s.

Management Tre atme nt of the compl i cati ons of sev ere hy pot hyroi d i sm (e .g. hyp ote nsi on, he art fail ure , hypot hermi a, bradyc ard i a, se i zures ) i s m ore i m portant t han thyroi d hormone repl ace ment. Thyroxi ne rep l aceme nt shoul d be wi th l ow doses (0.1–0.2 mg PO or PR unl ess i s chaemi c heart d i s ease i s poss i b l e, then start at 0.25 m g). There are no defi ni te adv ant age s t o us i ng T 3 repl ace ment, hi g h d ose re pl a cem ent re gi m ens or i ntravenous tre atm ent . Ste roi ds (hy drocorti s one 100 m g q ds IV) shoul d b e g i ve n s i nc e c oex i st i ng hy poadre nal i sm i s maske d b y myxoede ma.

Sick euthyroid/low T3 syndrome Thi s i s a frequent compl i c ati on of c ri ti c al i l l ne ss wi t h l ow T3 and T4 and hi gh re verse T 3 (rT3) l eve l s. These corre l at e wi t h t he sev eri ty of di s eas e and a poor out com e. The re i s bot h reduced TSH s ecreti on and al tered peri p heral thy roi d met abol i s m. A t ri al of thy rox i ne adm i ni st rat i on i n c ri t i c al l y i l l pat i ents produced a negati v e outc ome al though those sufferi ng from the si ck eut hyroi d sy ndrome we re not i d ent i fi ed. Treat ment of t hi s sy ndrome thus rem ai ns unknown. P.447

See also: Hyp ote nsi on, p312; Tachy arrhyt hmi as, p316; Bradyarrhyt hmi as, p318; Acute coronary syndrome (1), p320; Ac ute coronary syndrome (2), p322; Heart fail ure —as ses sme nt, p324; Heart fai l ure—m anagem ent , p 326; Di arrhoea, p340; Fai l ure t o open bowel s, p342; Acute w eak nes s, p368; Gene ral i s ed sei zures, p372; Hyp erc al c aem i a, p426; Di abet i c ket oac i dosi s , p 442; Hy poadre nal cri s i s, p448; Sys tem i c i nfl am mat i on/mul ti -organ failure, p484; Hypothe rmi a, p516; Pyrexi a (1), p518; Pyrexi a (2), p520 P.448

Hypoadrenal crisis Clinical features Primary hypoadrenalism Gl ucoc ort i c oi d defi c i ency (e.g . w eak nes s, vomi ti ng, di arrhoe a, abd omi nal pain, hy pogl yc aemi a) Mi neraloc ort i coi d defi c i ency (e.g . d ehy drati on, hyp onatraemi a, wei ght l oss, postural hy pot ens i on, hype rkalae mi a ) Ski n p i gm ent ati on due to ACT H e xce ss

Secondary hypoadrenalism May be due to cri ti cal i l l ness , s teroi d wi thdrawal aft er 2 w eek s' tre atm ent , hypopi t ui t ari sm or et omi dat e us e No s ki n pi gme ntati on Feat ure s of m i ne ral ocorti coi d defi ci enc y m ay b e abse nt

Diagnosis Di agnosi s i s c onfi rm ed by pl a sma corti sol , ACTH l e vel s and a negati v e T etracosac tri n (ACT H anal ogue) t est , alt hough treatm ent shoul d b egi n on c l i ni c al sus pi ci on. A d ose of 250µg IV shoul d p rod uce a > 200 nm ol /l ri se i n pl as ma corti sol . In p ri m ary hy poadre nal i sm l e vel s remain bel ow 600 nm ol /l . Howe ver, b asl i ne l evel s m ay be normal or el e vat ed i n the re l at i ve ad renal defi ci enc y s een i n se psi s and other cri ti cal i l l ness es. De xam ethasone m ay be use d for ste roi d rep l ac eme nt for 48 h b efore an ACT H t est i s pe rforme d s i nc e othe r s teroi d treat ments are de tec ted i n the pl a sma corti sol assay.

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Management Sal t and wate r d efi ci enc y s houl d be c orrec ted urgentl y . Ini t i a l fl ui d repl ace ment s houl d be wi t h c ol l oi d i f there i s hypotensi on, or evi dence of poor t i ss ue perfus i on. Othe rwi se 4–5l /d ay 0.9% s al i ne wi l l b e need ed for sev eral days . Fl ui d managem ent shoul d b e c are ful l y moni tored to ensure adeq uat e repl ace ment wi thout fl ui d ove rl oad. Gl ucoc ort i c oi d re pl a cem ent shoul d b e wi th hyd roc orti s one 50–100 m g t ds IV on day 1 t hen 20–50 mg td s on days 2–3. Hy drocorti sone m ay b e c hanged to equi v al e nt dos es of d examet has one before the ACTH te st has bee n performed. The rel at i ve hyp oad renal i sm re l at ed to s eps i s can b e t reated wi t h hydroc ort i sone 50 mg q ds for 7 day s, and then a re duc i ng d ose ove r t he nex t 5–7 days . Studi e s have shown more rapi d resol ut i on of shock and an i mproved outc ome i n those showi ng a s ubopti mal re sponse to sy ntheti c ACTH, d esp i te rais ed b ase l i ne l ev el s . P.449

See also: Bl ood presure moni tori ng, p110; Ce ntral venous cathe ter—us e, p114; El e ctrol y tes , p 146; Calc i um , m agne si um and phosphate , p 148; Crys tal l oi ds, p176; Col l oi ds , p180; St eroi ds , p 262; Fl ui d chall eng e, p 274; Hypotensi on, p312; Di a rrhoea, p 340; Hy ponatraemi a, p418; Hyp erc al c aem i a, p426; Hyp ogl yc aemi a, p438

Ovid: Oxford Handbook of Critical Care

Ed itors:

Si nge r, M ervyn; We bb, An dre w R.

Ti tle : O xf ord Ha ndbook of Cr itic al Car e, 2nd Ed ition Cop yri ght © 1997,2005 M. Si nge r and A. R. W ebb , 1997, 2005. Publ i shed i n the Uni te d Stat es by Oxford Uni ve rsi ty Press Inc > Tab le of Co n te n ts > P oi son in g

Poisoning Poisoning—general principles Poi soni ng shoul d b e c ons i d ere d i n p ati ent s p res ent i ng wi th al t ered c ons ci ous nes s, res pi rat ory or cardi ovascul ar dep res si on, vom i ti ng , hypot hermi a or s ei z ure s. The hi story usual l y m ake s d i ag nos i s obv i ous althoug h c l i ni c al si g ns may be confus ed due to i nges ti on of m ul t i pl e p oi s ons or ab sent i f e ffe cts are d el a yed . It s houl d be rem embe red that poi sons m ay ent er the body v i a routes ot her than i ng est i on, e.g. i nhal at i on or trans dermal l y. Sali cyl ate and parace tam ol are ex tre mel y c ommon agents i n sel f-p oi s oni ng and pati e nts often prese nt wi t h no alte rat i on of consci ousne ss.

Investigation Al l p ati ent s requi re urea and el ect rol yt e, b l ood g l ucos e and b l ood g as est i mati ons. Rapi d be dsi de ki t s d ete ct the pre sence of com mon age nts such as parace tac ol , as pi ri n, and sev eral recreat i onal drugs . Uri ne s ampl es and gastri c asp i rate shoul d b e saved for p oss i bl e l ate r t oxi col og y anal y si s. Sal i cy l at e and parace tam ol l ev el s are nece ssary due to the common l ack of earl y si g ns and to al l ow sp eci fi c earl y t reatment. Ot her drug l ev el s may he l p i n di agnosi s b ut treatm ent i s often supporti ve. Earl y s upp ort from t he l oc al Poi sons Inform ati on Servi c e s houl d be sol i ci te d.

Supportive treatment Tre atm ent of cardi ovascul ar and resp i ratory com promi s e and neurol ogi cal di sturb anc e i s b y s tandard me thods out l i ned el sewhere i n the b ook . In t he unc ons ci ous pat i ent, opi ate s and benzod i az epi nes may be re versed te mporari l y to al l ow ass ess ment of underl y i ng ne urol og i cal s tatus .

Gastric elimination Consi d er gas tri c emp tyi ng i f the poi son i s not a c orrosi ve or hyd roc arb on and has be en i ng est ed <4h previ ous l y. If sal i c yl a tes or tri c ycl i cs have been i nges te d gast ri c em pty i ng i s us eful for 12h after i nges ti on. The re are no cl ear adv ant age s for forced eme si s (i pec acuanaha 30m l i n 200m l w ate r) or gas tri c l avage. Force d em esi s may be del aye d for 30mi n and t hen may be i ntract abl e. Asp i rati on i s a s eri ous ri sk wi t h e i ther form of g ast ri c em pty i ng therapy; the pat i ent s houl d be i nt ub ated for airway protec ti on i f c ons ci ous nes s i s at all imp ai red .

Activated charcoal Ac ti v ate d c harcoal i s p rob abl y m ore effect i v e t han gas tri c emp tyi ng to pre vent d rug ab sorpti on. A charcoal :poi son wei ght rati o of 10:1 i s req ui red. Poi sons may be el i mi nat ed aft er abs orp ti on v i a the sm al l bowel wi t h act i vated charc oal 50–100g fol l owe d b y 12.5g/h NG. Acti vat ed charcoal i s parti cul arl y useful for be nzodi a zep i ne s, ant i c onvul s ant s, tri cyc l i cs, theop hyl l i ne, phe not hi a zi nes and anti hi s tam i ne s.

Forced diuresis and dialysis

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Forced di ure si s wi th ap propri ate uri nary aci di fi c ati on or al k al i ni sat i on (s ee t abl e) i s use ful for w ate r-s ol ubl e poi sons whi ch are di st ri b ute d p red omi nantl y ex tracel l ul arl y. Force d d i uresi s s houl d not be us ed i f renal functi on i s abnormal . Small mol ec ul e s m ay also be re mov ed b y haem odi al y si s (e .g. et hyl ene gl ycol , met hanol , oxali c aci d , form i c aci d). P.453

Forced alkaline diuresis Used for s ol ubl e ac i d i c drugs (e. g. sal i cy l at es) Furosem i de or manni tol to maint ai n uri ne outp ut >200ml /h Int rav enous c ry stalloi d to pre vent hypovol aemi a Avoi d exce ss i ve pos i t i ve fl ui d balance Use 1.26% bi c arb onate to mai ntain uri nary p H > 7 Stop b i carbonat e i f arte ri a l p H > 7.5 and use 0.9% sali ne Al t ernate bi carbonate /saline w i th 5% gl ucose Moni tor and repl ac e potas si um and mag nes i um careful l y

Forced acid diuresis Used for s ol ubl e basi c d rug s (e.g. am phe tam i ne s, qui ni ne, phe ncy cl i di ne) Furosem i de or manni tol to maint ai n uri ne outp ut >200ml /h Int rav enous c ry stalloi d to pre vent hypovol aemi a Avoi d exce ss i ve pos i t i ve fl ui d balance Use 750g N H 4 C l i n e ach 500ml 5% gl ucose to m ai ntai n uri nary p H < 7.0 Al t ernate 0. 9% sal i ne wi th 5% g l ucos e Moni tor and repl ac e potas si um and mag nes i um careful l y

See also: Venti l at ory support— ind i c ati ons , p 4; Endot rac heal i ntubat i on, p 36; ECG moni t ori ng, p108; Bl ood press ure moni t ori ng, p110; Tox i col og y, p162; R esp i ratory s ti mul ant s, p188; Basi c res usc i tati on, p270; Re spi rat ory fail ure , p 282; Hyp ote nsi on, p312; Tachy arrhyt hmi as, p316; Bradyarrhyt hmi as, p318; Sal i cy l at e p oi s oni ng , p454; Parace tam ol poi soni ng, p 456; Sedati v e p oi s oni ng, p458; Tri cyc l i c anti dep res sant p oi s oni ng , p460; Amphetami nes i nc l ud i ng Ecs tas y, p462; Coc ai ne, p464; Inhaled poi sons, p466; House hol d c hem i cals, p468; Met hanol and et hyl ene gl ycol , p470; Org anophosphate poi soni ng, p472; R hab domy ol y si s, p528 P.454

Salicylate poisoning Seri ous, l i fe-threat eni ng tox i ci ty i s l i kel y afte r i nge sti on of >7.5g s al i cy l at e. Asp i ri n i s the most com mon form i ng est ed though sali cyl i c aci d and met hyl sal i c yl a te are occ as i onal l y i mpl i c ated . Los s of c ons ci ous nes s i s rare but m etabol i c derang eme nts are c omp l ex (e. g. res pi rat ory al kal osi s d ue to res pi ratory centre st i m ul a ti on, dehydrati on due to salt and wat er l os s, re nal bi carbonate ex cre ti on and hyp ert hermi a , hyp okalae mi a , me tab ol i c aci dos i s due to i nterferenc e w i th carbohyd rat e, l i pi d and am i no ac i d met abol i s m, hyp ert hermi a due t o uncoupl i ng of ox i dati v e p hos phoryl ati on and i ncre ase d m etabol i c rat e). The re may al so be p ul monary oed ema due to capi l l a ry l eak, and bl e edi ng due to re duc ed prothromb i n l ev el s . Al though gas tri c erosi ons are common w i th as pi ri n treat ment , b l e edi ng from thi s sourc e i s rare i n ac ute poi soni ng.

Management Gastric elimination Due to de l ay ed gas tri c e mpt yi ng g ast ri c e l i m i nati on i s w ort hwhi l e for up t o 24h aft er i ng est i on. Act i vated charc oal (12.5g /h) shoul d be gi ven NG to ad sorb s al i cyl at e remai ni ng i n the bowel and ad sorb any sal i cy l at e b ack - d i ffusi ng across t he b owe l m ucosa. Insol ubl e aspi ri n m ay form a gas tri c m ass that i s di ffi cul t t o remove b y g ast ri c l avage.

Salicylate levels Rep eat ed l eve l s shoul d b e t aken si nc e these may c ont i nue t o ri se as ab sorpti on conti nues . Leve l s taken aft er 12h may underest i mate the de gre e of toxi c i t y due t o t i s sue bi ndi ng. If salic yl a te l ev el s are < 3.1mmol /l aft er 1h of i ng est i on and t here i s no m etabol i c derang eme nt the n obse rvati on, fl ui ds and repe at l ev el s are all that i s req ui red. Uri ne al k al i ni zat i on i s requi re d i f l eve l s are >3. 1mm ol /l or t here i s m etabol i c derangeme nt but no re nal failure. Lev el s >6.2m mol /l (or >3. 1mm ol /l w i th re nal failure ) re qui re hae mod i al ysi s.

Alkaline diuresis The al kal i ni sati on rather than t he forced di ure si s i s more i mp ortant for s al i cy l at e e xcreti on. Uri nary pH mus t b e > 7.0

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wi t hout arte ri al al k al osi s (p H < 7.5). Potassi um l os s w i l l occur w i th the b i carbonat e i nfusi on, due to the d i uresi s and as a t oxi c e ffec t of t he sal i c yl a te. Pot ass i um l evel s mus t b e moni t ored and corre cte d i n a hi gh depe nde ncy env i ronme nt. Al kal i ni zati on, i f suc ces sful , shoul d c ont i nue unti l s al i cy l at e l eve l s <3. 1mm ol /l . Cal c i um l evel s may drop w i th prol onge d alkali ni z ati on.

Haemodialysis Ind i c ati ons i ncl ude sal i c yl a te l ev el s >6.2mm ol /l or renal fai l ure. P.455

See also: Bl ood gas anal y si s , p 100; Toxi c ol ogy, p162; Hy pok al a emi a, p 422; Metabol i c ac i dosi s , p 434; Poi soni ng—g ene ral pri nc i pl es, p452 P.456

Paracetamol poisoning Seri ous, l i fe-threat eni ng tox i ci ty i s l i kel y afte r i nge sti on of >15g parac etamol , p art i c ul a rl y wi th co-i ng est i on of enzyme -i nduc i ng drugs (e .g. anti c onv ul s ant s, ant i -T B t herap y) and/or al c ohol . Parace tam ol i s rap i d l y abs orb ed from the s tom ach and uppe r s mal l b owel and i s metabol i s ed by c onj ugati on i n t he l i ver. Hepat i c ne crosi s oc curs due to the toxi c i t y of an al kyl ati ng met abol i t e t hat i s normall y remov ed by conjug ati on wi t h g l ut at hi one; gl utat hi one i s rapi d l y dep l et ed wi t h overdos e and m ay al read y b e l ow i n s tarvat i on, al c ohol i c s and, pos si bl y , HIV di s eas e, thus p red i sp osi ng these group s t o an i ncreas ed ri s k of t oxi ci t y. Tox i ci ty i s us ual l y asy mpt omat i c for 1–2 days al though l aborat ory ass es sment of l i ve r func ti on may bec ome abnormal aft er 18h. Hep ati c fai l ure, i f mani fes t, dev el ops aft er 2–7 days, an earl i er ons et bei ng ass oci ate d w i th more sev ere tox i c i ty .

Management If i ng est i on has occurred <4h previ ous l y, gas tri c el i mi nat i on te chni ques shoul d be em pl oyed. Parac etamol l e vel s m ay be tak en to c onfi rm i nge sti on but shoul d not be i nt erp ret ed for toxi c i t y unti l afte r 4h from i nges ti on. The mai ns tay of treatm ent i s wi th N-ac et yl c yst ei ne t o rest ore he pat i c gl utat hi one l ev el s by i ncreas i ng i ntracel l ul ar cy ste i ne l e vel s.

N-acetylcysteine Tre atm ent i s most effect i ve i f st art ed wi t hi n 10h of i nge sti on but i s c urrent l y adv i se d for up to 36h of i ng est i on. Tre atm ent i s requi re d i f t he parace tamol l eve l s are i n t he t oxi c range (see fi gure) or >15g parac et amol has b een i ng est ed. It s houl d be c ont i nued unt i l parac etamol i s not d ete cte d i n t he bl ood. N-ac ety l cy st ei ne i s g i ve n b y conti nuous IV i nfusi on (150mg /kg ove r 15mi n, 50m g/kg i n 500ml 5% gl ucose ove r 4h t hen 50mg/k g i n 500m l 5% gl ucos e 8-hrl y).

Complications The major compl i cati on i s hepati c (± re nal ) fai l ure . A ri se i n prothrom bi n ti me, IN R and b i l i rubi n are e arl y w arni ng si gns of si gni fi c ant he pat i c dam age and thi s shoul d p rom pt earl y referral to a s pec i al i s t c ent re.

Guidelines for referral to a specialist liver centre Art eri al pH <7. 3 INR >3 on day 2 or > 4 t hereafter Ol i guri a and /or ri si ng cre ati ni ne Al t ere d c ons ci ous l ev el Hypogl y cae mi a

Guidelines for liver transplantation Art eri al pH <7. 3 Pl us al l of t he fol l ow i ng : PT > 100, INR >6.5 Creati ni ne >300µ mol /l Grade 3–4 enc ephal opat hy Hi g h l act ate l e vel s (>3.5mmol /l at 4 and 12h) and l ow fac tor V l e vel s are al s o associ a ted wi th a p oor out come i f not trans pl a nte d.

Graph for predicting treatment requirement Tre atm ent i s requi re d at l ower l evel s i f the pat i e nt i s a known al cohol i c, prote i n-depl et ed, HIV p osi ti v e, or i s tak i ng enzyme -i nduc i ng drugs , e .g. pheny toi n.

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P.457

Figure. No Caption Available.

See also: Li ver funct i on te sts , p 152; Coagul ati on moni tori ng, p156; Toxi col og y, p 162; Acut e renal fai l ure—d i ag nos i s, p332; Ac ute re nal fai l ure— managem ent , p 334; Ac ut e l i ve r fai l ure , p 360; Hep ati c e nce phalop athy, p362; Poi s oni ng—general pri nc i pl es, p452 P.458

Sedative poisoning Pat i ents present w i t h al te rat i on of consc i ousne ss, re spi ratory fail ure and, i n som e cases , c ardi ovas cul ar di s turbance . Aft er prol onge d i mmob i l i ty the p oss i bi l i ty of rhabdom yol ysi s shoul d be consi dered. In mos t cas es tre atm ent i s sup porti ve.

Benzodiazepine poisoning Benzod i az epi nes are c ommon agents use d for sel f-p oi s oni ng but se vere feature s are unc ommon, exc ept at extreme s of age. Fl um aze ni l may b e used as a s pec i fi c ant i dote (0. 2–1.0mg IV g i ve n i n 0.1mg i ncreme nts ). Fl um aze ni l i s s hort acti ng so benzod i azepi ne rev ers al may be te mporary. Rapi d reve rsal of b enz odi aze pi nes may l e ad to anxi ety at tac ks or sei zures .

Opioid poisoning Tre atme nt i s supporti ve wi t h atte nti on parti c ul arl y t o resp i ratory d epres si on and c ardi ovas cul ar di s turbance . Nal oxone m ay b e used as an anti d ote (0. 2–0.4m g IV) al t hough rap i d re versal i s not d esi red i n ab use rs. Nal oxone i s s hort act i ng so re versal may be te mporary. Cons i de r HIV i nfec ti on and end ocardi ti s i n IV d rug ab use rs. In i at rog eni c p oi s oni ng nal oxone wi l l reve rse the p ai n re l i ef t hat op i oi ds were g i ve n for. In these cases res pi ratory dep res si on i s bet ter re versed by the non-s pec i fi c res pi ratory sti mul ant d oxap ram (1.0–1.5mg/k g over 30s IV fol l owed by 1.5–4. 0mg /mi n).

Barbiturates Tre atm ent i s support i ve wi th parti c ul a r att ent i on to re spi rat ory and c ard i ov asc ul a r d epres si on. Vas odi l at ati on may be ext rem e requi ri ng fl ui d support and , i n s ome cases , i not rop i c sup port. Phe nob arb i t al may be el i mi nate d b y forc ed al k al i ne di ure si s . P.459

See also: Venti l at ory support— ind i c ati ons , p 4; Bl ood gas anal ysi s, p100; Bl ood p res sure m oni tori ng, p110; Toxi c ol ogy, p162;

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Res pi ratory st i mul ants, p188; Opi oi d anal g esi cs , p 234; Sed ati ves , p 238; Basi c res usc i tati on, p270; Poi soni ng —ge neral pri nc i pl es , p452; R hab dom yol ysi s, p528 P.460

Tricyclic antidepressant poisoning Tri cy cl i c anti dep re ssants are p res cri bed to pati e nts who are at gre ate st ri s k of a sui ci de att emp t. The y are rap i dl y abs orb ed from t he gas troi nt est i nal tract, al though gastri c emp tyi ng i s de l ay ed.

Clinical features Ant i chol i nergi c e ffec ts (di l a ted pupi l s, dry mouth, i l eus, ret ent i on of uri ne). Arrhyt hmi as (parti cul arl y ass oci ate d w i th prol onge d QT i nte rval and QRS waves ). Hypotensi on rel ate d t o arrhythmi a s and/or c ardi a c d epress i on through Na + c hannel bl ock ade . Hype r-refl exi a w i th ex tensor pl ant ars , v i s ual halluci nati ons, coma and s ei z ures. Drug l ev el s do not c orrel a te wi t h seve ri ty. Metabol i s m i s usually rapi d and i mprove ment c an be e xpe cte d w i thi n 24h.

Management 1. There i s no s pec i fi c tre atm ent for t ri c ycl i c anti d epress ant poi s oni ng. 2. Pati ent s req ui re ECG moni tori ng d uri ng the fi rs t 24h and unt i l EC G c hanges hav e d i sappe are d for 12h. 3. Gas tri c e l i mi nati on i s worthw hi l e for 24h aft er i nges ti on s i nc e t ri cyc l i c s sl ow gast ri c em pty i ng . 4. Act i vated charc oal vi a a nasog ast ri c tube wi l l adsorb tri cy cl i cs re mai ni ng i n t he bow el . 5. Card i ac arrhythmi a s are more c ommon i f t here i s aci d osi s. Bi carbonate shoul d b e used to ac hi e ve an arte ri al pH of 7.5 urg ent l y. If arrhy thm i as oc cur wi th no aci dosi s and fai l to re spond to tre atm ent wi th ami odarone or phenytoi n, bi carbonat e (25–50ml 8. 4% IV) may st i l l b e useful . 6. Sei zures are be st managed wi th benzod i azepi nes and p henytoi n. P.461

See also: Venti l at ory support— ind i c ati ons , p 4; Bl ood gas anal ysi s, p100; ECG moni tori ng, p108; Bl ood p res sure moni tori ng, p110; Tox i col og y, p162; Sodi um bi carbonate , p 178; Basi c resusci tat i on, p270; Tac hyarrhyt hmi as, p316; Generalis ed sei zures , p 372; Poi soni ng—g ene ral pri nci p l es , p 452 P.462

Amphetamines including Ecstasy Amp het ami nes , i nc l ud i ng 3, 4-m ethyl e nedi oxy met ham phe tam i ne (MD MA, ‘ Ecs tas y’) and 3,4-me thy l enedi oxy ethamphetami ne (‘Ev e’), are s ti mul ant s t ake n p red omi nantl y for recreat i onal use , or as appe ti t e sup press ant s. The se d rugs are hal l uci noge ni c at hi ghe r d ose s. MDM A has bee n s how n t o cause rapi d de creas es i n central nervous s yst em 5-hy droxyt ryp tam i ne and 5-hyd rox yi ndol e-3-ac eti c aci d l evel s and i nc re ase s i n d opam i ne rel eas e.

Clinical features of overdose Agi tati on, hyp eracti vi t y, hyp ert ens i on, hal l uc i nati ons, paranoi a fol l owed by exhaus ti on, com a, convul si ons and hyp ert hermi a. Idi os ync rat i c res ponses to Ec stasy and Ev e are m ore common, wi t h numerous reports of mortalit y and major morbi d i t y fol l owi ng i ng est i on of jus t 1–2 tab l e ts. These app ear re l at ed to i ng est i on i n hot envi ronments , e. g. ni g ht cl ubs, and c onc urrent de hyd rat i on. F eat ure s i ncl ud e profound hy perthe rmi a (>40°C), ag i t ati on, se i zures , m usc l e ri gi d i ty , hype rte nsi on, tachy cardi a, s weati ng, com a, di s sem i nated i ntravas cul ar coagul at i on and rhab dom yol ysi s. The se com pl i cat i ons l ead t o hy pov ol a emi a, el e ctrol y te i mb al a nce (p art i cul a rl y hy perkal aemi a) and a met abol i c aci dos i s . Som e p ati ent s t aki ng Ecs tas y or Eve hav e be en adm i tt ed wi t h w ate r i ntoxi c ati on and ac ute hy ponatraem i a fol l owi ng i ng est i on of l a rg e am ounts of wate r.

Management 1. Sup porti v e c are i ncl udi ng ai rway protec ti on, fl ui d re sus ci tat i on, e l ec trol yt e c orrec ti on and, i f nee ded , m echani cal vent i l ati on. 2. Earl y stages of amp het ami ne poi soni ng can ofte n be control l ed wi th tep i d spongi ng, chl orpromaz i ne, β -bl ock ade . Forc ed aci d d i ures i s to i nc rease uri nary excret i on i s rarel y need ed. 3. Seve re com pl i cati ons shoul d be manage d as t hey ari se , e .g. rapi d cool i ng for hy perpyrexi a, ant i convul s ant s for sei zures, force d alkaline d i uresi s ± fasci ot omi es for rhabdomyol ys i s , pl at el e t and fres h froz en pl asma i nfus i ons for coagul opathy .

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4. Dant rol ene may b e g i ve n t o t reat t he hype rp yre xi a at a d ose of 1mg /kg IV, repe ate d t o a cumul ati ve maxi mum dose of 10mg/k g, parti cul arl y i f t he tem perature i s >40°C. P.463

See also: Venti l at ory support— ind i c ati ons , p 4; Bl ood gas anal ysi s, p100; ECG moni tori ng, p108; Bl ood p res sure moni tori ng, p110; Tox i col og y, p162; Bas i c res usc i t ati on, p270; Hy pertensi on, p314; Tac hyarrhythmi as, p316; Gene ral i s ed sei zures , p 372; Poi soni ng—g ene ral pri nci p l es , p 452; Hyp ert hermi a , p 522 P.464

Cocaine poisoning Modes of action Bl ocks re upt ake of dop ami ne (causi ng eup hori a, hy peract i vi ty) and noradre nal i ne (c aus i ng vasoc ons tri ct i on and hype rt ens i on) Bl ocks Na + channel s , resul t i ng i n a l oc al anaest het i c act i on and m yoc ard i al de pre ssi on Pl at el et act i vati on

Complications Ches t p ai n re l at ed to myocardi a l i sc hae mi a or i nfarcti on. Local chest pain gui del i nes shoul d be fol l owed. EC G abnormali ti e s ofte n resol ve wi thi n 12h. Arrhy thm i as s houl d be t re ated conve nti onall y, t hough avoi di ng β-bl ock ers . Heart fai l ure from myocardi al depres si on or a cardi omy opat hy Sei zures Cere brovas cul ar ac ci d ent s Pneumot horax Rhab dom yol ysi s Prem ature l ab our—ab rupti on Agi tat ed del i ri um , hy pertherm i a Thermal i njury from sm oke i nhal ati on

Management 1. Oxyg en 2. Di a zep am for agi tat i on, d el i ri um, chest pain 3. Asp i ri n for che st pai n, CVA 4. Ni t rat es for chest pain, he art failure 5. Sod i um bi carbonate and forc ed d i ures i s for rhabd omy ol y si s 6. β-bl ock ers s houl d be avoi ded P.465

See also: Oxy gen therapy, p2; Vent i l a tory s upp ort —i ndi cat i ons, p4; Bl ood g as analys i s, p100; ECG moni t ori ng, p108; Bl ood pre ss ure moni t ori ng, p110; T oxi col ogy , p 162; Basi c res usc i tati on, p270; Hy pertensi on, p314; Tac hyarrhythmi a s, p316; Acute coronary syndrome (1), p320; Ac ute coronary sy ndrome (2), p 322; Gene ral i se d s ei z ures, p372; Stroke, p380; Poi soni ng —ge neral pri nc i pl es, p452; Hype rtherm i a, p522; Rhabdomyol ys i s, p528 P.466

Inhaled poisons Carbon monoxide Carbon monoxi de poi soni ng s houl d be c ons i d ere d i n anyone found i n a sm oke fi l l e d, enc l os ed space. Carbon monox i de di s pl ace s oxyge n from haemog l ob i n, t o whi c h i t has 200 ti mes great er affi ni ty and thus pre vent s oxyg en carri age. The re i s al s o a di rec t toxi c effe ct on mi t ochond ri al oxi dat i ve phosp horyl a ti on as i t c omp ete s wi th oxy gen for t he sam e bi ndi ng si t e on c ytochrome oxi das e.

Clinical features Fati gue , head ache, vomi ti ng, di zzi nes s, confus i on, dys pnoe a.

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A c herry red ap pearance of t he ski n and muc osae are c l a ssi cal but not com mon. PaO 2 wi l l be normal unl es s the re i s res pi rat ory dep res si on and pul se oxi met ry i s mi sl e adi ng. The hal f l i fe of carboxyhaemogl obi n i s 4h when bre athi ng room ai r and 50mi n w hen breat hi ng 100% oxy gen.

Management Carb oxy hae mogl ob i n l ev el s shoul d b e m easure d by a co-oxi met er and treat ment st arted i m medi at el y wi th oxyg en at the max i mum c onc ent rat i on t hat can be de l i v ere d (FIO 2 1.0 i f venti l at ed and 0.6–1. 0 i f sel f-ve nti l a ti ng). If c arboxy hae mog l ob i n l ev el s >25% or c arbon monoxi de poi soni ng i s as soc i a ted wi th ment al di sturbance , t he opti mal t reatme nt i s hyp erb ari c oxyg en at 3 at mos phe res for 30mi n, rep eat ed 6-hrl y i f l e vel s remain >25%. Deat h i s l i k el y wi th carbox yhaemog l ob i n l e vel s >60%. Hi g h c onc ent rat i on ox ygen treat ment s houl d conti nue unti l carboxyhaem ogl obi n l eve l s <10%.

Cyanide Seve re cyani d e p oi s oni ng has an ex tre mel y rapi d onse t and occ urs i n some cas es of s mok e i nhalat i on. Survi v al may be ass oci ate d w i th anoxi c b rai n d amage. Di a gnosi s must be made cl i ni call y si nc e a bl ood cyani d e l eve l t ake s > 3h t o p erform .

Clinical features Cl i ni cal fe atures i ncl ude anx i et y, agi tat i on, hype rve nti l at i on, head ache, l os s of c ons ci ousness , d ysp noe a, weak nes s, di z zi nes s and vomi ti ng. The s ki n re mai ns pi nk and hypotensi on m ay be sev ere . An unexp l ai ne d me tab ol i c aci dos i s i s sug ges ti ve.

Management Hi g h c onc ent rat i on ox ygen shoul d b e g i ve n, but i s onl y trul y effect i ve when gi v en at hype rbari c p res sures. In m i l d c ase s rapi d, nat ural d etoxi fi cati on red uce s c yani de l e vel s b y 50% w i thi n 1h, al l ow i ng support i ve therapy onl y. Sod i um thi os ul p hat e (150mg/k g i ntrave nousl y fol l owed by 30–60mg/k g/h) c onve rt s c yani de to thi oc yanate and shoul d be use d i f t here i s unc ons ci ousness . It i s, how eve r, sl ow-ac ti ng. Ni t ri t es produc e m ethaem ogl obi nae mi a and may p ote nti al l y w ors en cyani d e t oxi ci t y. Di c obalt ede tat e (300m g IV) i s the sp eci fi c anti dot e t o c yani de but i s s everel y t oxi c (v omi ti ng, urti c ari a, tac hyc ard i a, hy pot ens i on, d ysp noea, c hes t p ai n) i n t he abs enc e of cy ani de. It i s t herefore b est av oi d ed unl ess cyani d e toxi c i t y i s l i ke l y. P.467

Key trial Weaver LK , e t al . Hype rb ari c oxyg en for acute carbon monox i de poi soni ng. N Engl J M ed 2002; 347:1057–67

See also: Oxy gen therapy, p2; Vent i l a tory s upp ort —i ndi cat i ons, p4; Bl ood g as analys i s, p100; ECG moni t ori ng, p108; Bl ood pre ss ure moni t ori ng, p110; T oxi col ogy , p 162; Basi c res usc i tati on, p270; Inhal ati on i nj ury, p 306; Me tab ol i c aci dos i s, p434; Poi soni ng —ge neral pri nc i pl es P.468

Household chemicals Corrosives St rong ac i d s and al k al i s are i nc reasi ngl y av ai l ab l e i n the househol d and i nge st i on may l e ad to shock and bow el perforati on. Gast ri c el i mi nat i on t echni q ues must be avoi ded si nc e as pi rat i on of corrosi v es may cause sev ere l ung dam age . Earl y s urg i cal rep ai r of perforat i on may be ne ces sary.

Petroleum Al though not s tri ctl y a house hol d c hem i cal, acc ess t o pe trol e um i n t he hom e i s e asy .

Clinical features Gas troi ntes ti nal i nges ti on and absorp ti on g i ve s c l i ni c al feat ures si m i l a r t o t hos e of alcohol i ntox i cati on w i th more sev ere ce ntral nervous s yst em dep res si on.

Management

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Gas tri c e l i mi nati on tec hni que s m ust be avoi d ed s i nce a fe w d rop s of pe trol e um s pi l l i ng i nto the l ungs can l ead to a se vere p neumoni ti s. Thi s i s due to the l ow s urface te nsi on and vapour p res sure of p etrol e um al l owi ng rap i d spread through the l ungs . Tre atme nt i nvol ves sup porti ve the rap y and 250m l l i q ui d paraffi n oral l y.

Paraquat Paraquat i s wi d el y av ai l abl e as a se l ec ti v e w eedk i l l er whi ch i s i nac ti v ate d on contact wi t h t he soi l . A dos e of 2–3g i s usual l y fatal (equi valent t o 80–120g of granul es or 10–15ml of i nd ust ri a l l i q ui d conce ntrate ).

Clinical features Very l i tt l e of the i nges ted paraq uat i s ab sorbed from the gut b ut a l arg e dose wi l l l ead rapi dl y to shock wi th wi de spread ti ss ue nec ros i s. A b urni ng se nsati on i n t he mouth and abd ome n i s m ore common i n p oi s oni ng, as i s the d evel op ment of painful mout h ul c ers and, afte r s eve ral days, a rel ent l es s, prol i ferati ve al v eol i ti s causi ng d eat h b y pul monary fi bros i s.

Management Tre atme nt shoul d be gi n on cl i ni cal g rounds i n vi ew of the se veri ty of tox i c i ty and t he t i m e taken for l aborat ory confi rmat i on. Urg ent gas tri c emp tyi ng i s req ui red wi th i ns ti l l a ti on of 500ml water containi ng 150g F ul l er's earth and 25g magnesi um sul phate aft erw ard s. Seve re di arrhoe a may e nsue requi ri ng careful fl ui d managem ent . If p araquat p oi s oni ng i s confi rme d 200–500ml of 30% Ful l er's earth i s gi ven 2-hrl y for 24h vi a a nas ogastri c tub e. A forc ed d i ures i s shoul d be st art ed to enc ourage re nal ex cre ti on. Pul monary fi b ros i s i s more sev ere whe n b reathi ng hi gh oxyg en concentrati ons; i f ox yge n i s requi re d t he l ow est conc ent rati on p oss i bl e s houl d be gi v en acc ept i ng a l ow PaO 2 . Li posom al sup eroxi d e d i sm utase and gl utathi one peroxi das e have bee n us ed exp eri mental l y . P.469

See also: Tox i col og y, p162; Poi soni ng —ge neral pri nc i pl es, p452 P.470

Methanol and ethylene glycol Methanol Tox i ci ty mai nl y ari s es due to oxi dat i on of me thanol to formi c aci d and form al d ehyd e. The ox i dati v e p athway i s an enzymati c proce ss i nvol vi ng alcohol de hyd rog enas e b ut procee ds at 20% of the rate of ethanol oxi d ati on.

Clinical features Cl i ni cal fe atures of poi soni ng i ncl ude bl i nd nes s (due to conce ntrati on of met hanol i n the vi tre ous humour), sev ere met abol i c ac i d osi s, headac he, nausea, v omi ti ng and abd omi nal pain.

Management Metabol i s m of me thanol i s sl ow so tre atm ent wi l l nee d t o b e prol ong ed (sev eral d ays ). Tre atme nt i ncl udes gastri c emp tyi ng (wi thi n 4h of i nge sti on), s odi um bi c arb onate ti t rated to corre ct art eri al pH and ethanol t o s aturat e t he oxi dat i ve pathw ay. On p re sentat i on 1m l /kg et hanol (50%) i s gi v en oral l y fol l owed by 0.5ml /kg 2-hrl y for 5 day s. Al t ernati vel y, met abol i s m c an be bl ocke d b y 4-met hyl py razol e (fomep i z ol e ) whi ch can b e i nfused or i njec ted 12-hrl y. If m ethanol l eve l s are >1000mg/l haemodi a l ys i s i s us ed unt i l l ev el s are < 250mg/l .

Ethylene glycol Ethyl e ne gl y col i s p art i al l y met abol i s ed by al c ohol d ehy drogenase to oxali c ac i d whi ch i s re sponsi bl e for a se vere met abol i c ac i d osi s, renal fai l ure and sei zures .

Clinical features Cl i ni cal suspi ci on i s arouse d b y od ourl es s drunke nnes s, oxalat e c rys tals i n the uri ne or bl ood and t he seve re aci dos i s . As l i ttl e as 50ml can b e fatal .

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Management Tre atm ent i s as for m ethanol . P.471

See also: Uri nal ys i s, p166; Tox i col og y, p162; Sod i um bi carbonate , p 178; Acut e renal fai l ure — m anageme nt, p334; Vom i t i ng /gas tri c stasi s, p338; Met abol i c ac i d osi s, p434; Poi s oni ng—general p ri nci pl e s, p452 P.472

Organophosphate poisoning Organophosphate pe sti ci des are t he m ajor c aus e of s ui c i dal p oi s oni ng i n de vel opi ng countri es and are use d as ne rve age nts i n te rrori st att ack s (e.g . Sari n, Tab un, VX, GF). Thei r mode of acti on i s vi a c hol i ne rgi c t oxi ci ty.

Cholinergic (anticholinesterase) syndrome Sal i vati on, l ac ri mat i on Vomi ti ng, di arrhoe a Bradyc ard i a Bronchosp asm Mei osi s

Management Atropi ne— ant agoni s es ace tyl chol i ne at m usc ari ni c rece ptors . A dos e of 2mg shoul d be gi ven eve ry 15m i n unt i l the mouth i s dry Pral i d oxi me— reacti vat es i nhi bi te d enzym es i f gi v en before the ag ent pe rmanentl y bi nds t o the e nzy me Di a zep am—neuroprot ect i on P.473

See also: Oxy gen therapy, p2; Vent i l a tory s upp ort —i ndi cat i ons, p4; ECG moni tori ng, p108; T oxi col ogy , p 162; Bronchodi l ators , p186; Chronotropes , p 206; Brad yarrhy thm i as , p 318; Vomi t i ng/gastri c st asi s, p338; Di arrhoea, p340; Poi soni ng —ge neral pri nc i pl es , p452

Ovid: Oxford Handbook of Critical Care

Ed itors:

Si nge r, M ervyn; We bb, An dre w R.

Ti tle : O xf ord Ha ndbook of Cr itic al Car e, 2nd Ed ition Cop yri ght © 1997,2005 M. Si nge r and A. R. W ebb , 1997, 2005. Publ i shed i n the Uni te d Stat es by Oxford Uni ve rsi ty Press Inc > Tab le of Co n te n ts > I n f ect ion an d I n f lam mati on

Infection and Inflammation Infection control—general principles Infect i on ac qui re d wi thi n the IC U i s a maj or cause of m ort al i ty , m orb i di ty and i ncrease d d urati on of s tay . T here are rem ark abl e v ari ati ons i n p rac ti c e for whi ch the l a ck of a good evi dence bas e i s c hi e fl y re sponsi bl e . Exam pl e s i ncl ud e di fferent pol i ci e s w i th re gard t o p ati ent i s ol a ti on, mi crobi ol og i cal s urvei l l a nce , hand was hi ng p roc edures , use of i mp reg nat ed vas cul ar cat het ers, the durat i on of i ndwel l i ng cat het ers , and fre que ncy of change of di sposab l es such as i nt ravenous gi vi ng s ets and fi l t ers . It i s neve rthel ess ac cep ted that adeq uat e hand was hi ng b efore and aft er pat i ent contac t and stri c t asep ti c te chni q ue w hen pe rformi ng proced ure s are mandat ory .

ICU design Amp l e wash hand bas i ns wi th el b ow ope rat ed mi x er tap s, soap and anti sep ti c d i sp ens ers Sep arate c l e an-t re atme nt and sl ui ce are as Some i s ol ati on cub i cl es wi t h p osi ti ve/e xhaust ai r fl ow faci l i t y Amp l e space around bed areas

Staff measures

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Remove w atc hes and j ewel l e ry, re move l ong-sl e eve whi te coats and jacke ts, rol l shi rt sl eev es up to el b ow Hand and fore arm was hi ng before and after touchi ng pati e nt Wear di sp osabl e aprons and g l ov es i f i n contac t w i t h pati ent Wear gl ove s and aprons when hand l i ng any bod y fl ui d and eye protec ti on w hen any dange r of fl ui d or d rop l et spl ash Stri ct as ept i c te chni que for i nv asi ve proced ure s (e.g . c ent ral ve nous c atheter i nse rti on) and c l ean t echni q ue for basi c proced ure s, e.g . e ndot rache al suc ti on, changi ng venti l at or ci rcui ts or drug i nfusi ons Prev i ous i mmuni sat i on ag ai nst hep ati ti s B, t ube rcul os i s Ste thoscopes shoul d b e c l eaned bet wee n p ati ent s Cl ear s i g n-post i ng of precauti ons to be tak en on cub i cl e d oors

Visitors Non-ICU med i c al and parame di cal st aff, rel a ti v es and fri ends shoul d ad here t o t he g ui del i ne s i n forc e regardi ng the pat i ent b ei ng v i s i te d, e.g . hand was hi ng, gow ns and gl oves as di re cte d. Traffi c t hrough the ICU s houl d be mi ni mi se d.

Cross-infection Inform the Infec ti on C ont rol nurs e s houl d cross-i nfect i on ari s e wi th more t han one p ati ent i nfec ted by the same strai n of bac te ri a . Affe ct ed p ati ent s shoul d ge neral l y b e s ource i sol at ed, es pec i al l y i f the organi s m i s mul t i re si stant; treat ed w i t h anti bi oti cs and topi c al ant i s ept i cs i f ne ces sary; and barri er-nursed . If c ross-i nfect i on pe rsi st s/s pre ads , ot her s ources shoul d b e s oug ht, e. g. t aps , s i nks, re usabl e eq ui p ment (reb reathi ng bag s, venti l at ors ).

Protective isolation Some pati e nts c arry p ote nti al l y c ont agi ous or i nfec ti ve organi sms and requi re sourc e i sol ati on, e. g. tub erc ul osi s. Immunos upp res se d pati ent s, e.g . when neutropeni c fol l ow i ng chemothe rap y, are at ri sk of acq ui ri ng i nfec ti on.

Microbiological surveillance Pol i c i es vary; som e ICUs routi nel y s cre en sputum , b ronchoal v eol ar l av age , b l ood, uri ne and drai n fl ui d ev ery 3–7 day s w hi l e othe rs screen onl y whe n i ndi cat ed, e. g. det eri orati ng c ardi ores pi ratory st atus, pyrexi a, neut rophi l i a . Send sam pl e s p rom ptl y t o t he l ab for anal ysi s. P.477

See also: Bac teri ol og y, p158; Vi rol og y, serol ogy and ass ays , p 160; Anti mi crobi a l s, p260; Acute che st i nfect i on (1), p288; Acut e che st i nfect i on (2), p290; Infect i on—di agnosi s, p480; Infe cti on—treat ment , p 482; ICU l ayout, p566 P.478

Routine changes of disposables Care of intravascular catheters Si t es shoul d be covered wi t h t ransparent s emi permeabl e dress i ng s t o all ow obse rvati on and pre vent s ecreti ons from ac cum ul a ti ng. Rout i ne chang es of i nt rav asc ul a r c at het ers are no l onge r rec omme nde d. As the ri sk of i nfect i on does i nc re ase cons i d erabl y after a w eek in si tu, cat het ers s houl d be removed as soon as c l i ni c al l y feas i b l e. Cathete rs can be chang ed over a gui dew i re i f the s i t e l ooks cl ean but s i g ns sug ges ti v e of mi l d to mod erate i nfect i on are p res ent el sew here, (e.g . p yre xi a or unexp l ai ned ne utrophi l i a) but wi thout maj or cardi ores pi rat ory di s turbance. Cathete rs shoul d be chang ed to a fres h s i te i f: t he ol d si te app ears i nfe cte d t he pat i ent s hows s i gns of s evere i nfe cti on a pos i t i ve growt h i s obtaine d from a b l ood c ul t ure d rawn through the cathe ter or from the ti p of t he p rev i ous c athete r

Routine changes of disposables

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Frequency Ventilator circuit (if using bacterial filters)

Between patients unless soiled

Ventilator circuit (if using water bath humidifier)

Daily

Endotracheal tube catheter mount and bacterial filter

Between patients unless soiled

Disposable oxygen masks

Between patients unless soiled

CPAP circuits

Between patients unless soiled

Rebreathing bags and masks

Between patients unless soiled

Intravenous infusion giving sets

48h

Parenteral nutrition giving sets

Daily

Enteral feeding giving sets

Daily

Arterial/venous pressure transducer sets

48h

Wound dressings

Depends on type of dressing

Tracheostomy site

As necessary

Urinary catheter bags

Weekly

P.479 P.480

Infection—diagnosis Infect i on i s b oth a c omm on cause of admi ssi on to i ntensi v e c are and the m ajor s econdary com pl i cat i on. C ri t i c al l y i l l pat i ents are predi sp ose d t o furt her nosoc omi al i nfect i ons as m any of the i r nat ural barri e rs and de fence mec hani sm s hav e b een l os t, al tered or penetrate d. They are ofte n heavi l y i nstrume nte d, sed ate d and i mmobi l e. They ofte n dev el op i mmune hypores ponsi veness as part of t hei r cri ti cal di sease proces s, not wi t hst and i ng any t herape uti c i mm une suppress i on t hey may have rece i ve d. The hi gh ant i bi ot i c l oad g i ve n t o t hes e si ck pat i e nts encourag es col oni sati on b y pathogeni c organi sm s and s ub seq uent de vel opm ent of i nfec ti ons by mul ti d rug resi stant and /or aty pi c al (e. g. fungi ) organi sm s. Sep si s i s d efi ned as the s yst emi c resp ons e t o an i nsul t of proven or hi gh l i k el i hood of i nfec ti on. Where as i nfect i on can be ap pl i ed to a l ocalis ed phe nom enon, s eps i s i ni ti at es a sy ste mi c i nfl ammatory res pons e t hereby affec ti ng d i st ant org ans .

Diagnosis Oft en p rob l e mati c i n the cri ti cally i l l pat i ent as focal s i gns m ay b e l ack i ng and/or c amoufl age d by concurrent di s eas e (e .g. ve nti l at or-ass oci at ed p neumoni a on top of ARD S). Sy mpt oms are ofte n notfort hcomi ng d ue t o t he pati ent's me ntally i ncom pet ent st ate . In addi ti on, al l of t he t radi t i onal cl i ni cal and b i oc hem i cal m ark ers of i nfec ti on are non-sp eci fi c . T hes e i ncl ud e pyrexi a, neut rop hi l i a and alte red sp utum. Furthe rmore, the freq uent p res enc e of col oni s i ng organi sm s e .g. M RSA on s ki n, Pseudom onas aeruginosa i n the resp i ratory tract, does not i m pl y concomi t ant i nfec ti on. As a cons equenc e, many p ati ent s are over-t reated wi t h anti bi oti cs, enhanci ng t he ri sk ofov erg row th of res i st ant /at ypi cal organi s ms. Mark ers of i nfl a mmati on (C-react i v e prot ei n, p roc al c i t oni n) m ay be use ful , t hough s tudi e s have produc ed confl i cti ng res ul ts as to the i r spe ci fi c i ty /se nsi ti v i t y i n di ag nos i ng underl yi ng i nfect i on. The val ue of routi ne s cre eni ng (mi crobi ol ogi c al survei l l anc e) i s not proven, t hough thi s m ay hel p t o i denti fy i nfect i ng organi sm s e arl i er. For cas es of sus pec ted i nfec ti on, app rop ri ate sam pl es s houl d be tak en for anal y si s i ncl udi ng bl ood, sp utum, wound s wab s, drainage fl ui d, as pi rate d p us, cathe ter ti ps , c ere brospi nal fl ui d, etc . T hes e shoul dg eneral l y be take n b efore new ant i bi ot i cs are c omm enc ed. Cons i de r l es s c ommon c aus es of i nfect i on such as end ocardi ti s or oste omye l i ti s , p art i c ul a rl y i f the p ati ent fails to s ett l e aft er a s tandard c ourse of the rap y.

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Differential diagnosis of pyrexia Infe ct i on Non-i nfect i ve cause s of i nfl amm ati on, e. g. trauma, s urg ery , b urns, myocardi a l i nfarct i on, vasc ul i ti s, hep ati ti s, acal cul ous c hol ecy sti ti s, pancre ati ti s Adv ers e d rug re act i ons Exce ss i ve amb i ent heat i ng Mi s cel l aneous c aus es, e. g. neop l as m P.481

Definitions Infection Mi c robi a l p henomenon charac teri s ed by an i nfl amm atory res ponse to the prese nce of mi cro-organi sm s or t he i nv asi on of normal l y ste ri l e hos t t i ss ue by those org ani sms

Bacteraemia The prese nce of vi abl e b act eri a i n t he bl ood.

Sepsis The sy ste mi c re sponse to i nfec ti on. Defi ni ti on as for SIRS but as a res ul t of i nfec ti on.

Sites of infection before and after admission to an ICU Organ

Primary site of infection needing admission to ICU

Secondary site of infection acquired while in ICU

Brain

+

+

Sinuses

-

+

Cannula/wound sites

++

+++++

Other skin and soft tissue

++

+

Chest

++++

++++

Urogenital tract

++

+

Abdomen

++++

++

Bone

+

+

Heart valves

+

+

Key paper Ame ri can Col l e ge of C hes t Phys i ci ans /Soci e ty of Cri ti c al Care M edi ci ne C ons ens us Conferenc e: d efi ni t i ons for se psi s and organ failure and gui de l i nes for the use of i nnovat i v e t herapi es i n sep si s . C ri t Care Med 1992; 20:864–74.

See also: Bac teri ol og y, p158; Vi rol og y, serol ogy and ass ays , p 160; Pyre xi a (1), p 518; Pyre xi a (2), p 520 P.482

Infection—treatment Treatment Drain pus Change cannul a s i te s i f nece ssary

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App rop ri a te ant i bi ot i c the rap y after l aborat ory sp eci mens t ake n—t hough t hi s m ay not be nec ess ary for m i l d i nfect i ons w here t he c aus e has bee n removed, e. g. an i nfect ed cat het er Radi ol ogi cal and/or surg i cal i nte rve nti on i f i ndi c ate d Reg ul a r i nput from mi crobi ol ogi c al ± i nfe cti ous di sease spe ci a l i sts i s re comm end ed to adv i se on bes t opti ons for emp i ri c the rap y and for pos si bl e mod i fi cati ons bas ed on e arl y c omm uni cat i on of l a boratory res ul ts (i ncl udi ng ant i bi ot i c sensi t i v i ty patte rns ). Emp i ri c ant i bi oti c the rap y i s g ui d ed on t he sev eri ty of i l l ne ss of t he pat i ent, l i kel y s i te of i nfec ti on and l i k el y i nfect i ng organi s m(s ), w het her the i nfe cti on i s com muni t y-ac qui re d or nosoc omi al (i ncl udi ng ICU-acq ui red ), p ati ent i mm unosup pre ss i on, and k now n anti bi oti c resi stance patte rns of hospi tal and l ocal c omm uni ty org ani sms . In g ene ral , cri ti cal l y i l l p ati ent s s houl d re cei ve p arent eral anti bi oti c s at appropri a te dos age, taki ng i nt o ac count any i m pai red hep ati c or renal c l e arance , or c onc urrent re nal re pl acem ent therapy. Broad -sp ect rum therapy may be i ni ti al l y need ed, wi t h refi nem ent , c ess ati on or change after 2–3 d ays dep end i ng on cl i ni cal resp ons e and org ani sms subse que ntl y i s ol a ted . The d urati on of t reatme nt rem ai ns hi ghl y contenti ous . Apart from sp eci fi c condi ti ons such as end ocardi ti s , tub erc ul osi s and meni ng i ti s, whe re prol onged therapy i s probab l y adv i sabl e , i t m ay be suffi c i ent t o s top wi thi n 3–5 day s p rov i de d t he pat i ent has shown adeq uat e s i gns of recovery. Al t ernat i ve l y, pat i e nts not resp ond i ng or det eri orati ng shoul d be consi dered to be ei t her treat ment fai l ure s or i nap propri at el y treat ed (i . e. no i nfe ct i on was pre sent i n t he fi rst pl ace ).As d esc ri bed earl i er, commonl y acc ept ed markers of i nfe cti on are poorl y s pec i fi c i n the i nt ens i v e c are pat i e nt. Indeed , p yre xi a may s ett l e on stoppi ng ant i bi oti c tre atm ent . Ce ss ati on or change of ant i bi oti c the rap y m ust be consi dered on i nd i vi dual m eri ts ac cordi ng t o t he pat i ent's condi ti on and any subse que nt l ab oratory res ul ts. An ad vantag e of ce asi ng the rap y i s t he abi l i ty to t ake further spe ci mens for c ul ture i n an anti bi oti c -free env i ronme nt. It may be nec es sary t o remov e i ndw el l i ng pacem ake rs, tunne l l ed v asc ul ar cat het ers , p ros the ti c joi nt s, pl ate s, i mp l ants , g rafts and st ent s i f t hes e are t he sus pec te d c aus e of i nfec ti on. Thi s s houl d be done i n c ons ul t at i on wi th mi c robi ol og i st s and the ap propri ate sp eci al i st as i ndi v i d ual ri sk and be nefi t need s t o b e c are ful l y wei ghe d up. P.483

Specimen antibiotic regimens (organism unknown)

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Sepsis of unknown origin

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2nd/3rd generation cephalosporin OR quinolone OR carbapenem OR piptazobactam ± aminoglycoside (if Gram negative suspected) ± metronidazole (anaerobic cover) ± glycopeptide or linezolid (if MRSA suspected)

Pneumonia—community acquired

2nd/3rd generation cephalosporin + macrolide

Pneumonia—nosocomial

3rd generation cephalosporin OR quinolone OR carbapenem OR piptazobactam ± aminoglycoside (if Gram negative suspected) + teicoplanin, vancomycin + rifampicin or linezolid (if MRSA likely)

Skin and soft tissue

Flucloxacillin (if MSSA likely) Glycopeptide or linezolid (if MRSA likely) Benzyl penicillin or clindamycin (if Streptococcus suspected)

Abdominal

2nd/3rd generation cephalosporin OR quinolone OR carbapenem OR piptazobactam ± aminoglycoside ± metronidazole

Gynaecological

2nd/3rd generation cephalosporin OR quinolone OR carbapenem OR piptazobactam ± aminoglycoside + metronidazole

Nephrourological

2nd/3rd generation cephalosporin OR quinolone OR carbapenem OR piptazobactam ± aminoglycoside

See also: Bl ood press ure moni t ori ng, p110; Bac teri ol ogy , p 158; Anti mi c rob i al s, p260; Acut e c hes t i nfe cti on (1), p 288; Ac ute che st i nfect i on (2), p290; Hypotensi on, p312; Abd omi nal se psi s, p350; M eni ngi ti s, p374; T etanus , p 390; Botul i s m, p392; Neutropeni a, p408; Sy ste mi c i nfl a mmati on/m ul t i -organ fai l ure , p 484; Se psi s and sep ti c shock —treat ment, p486; HIV re l at ed di s eas e, p488; M al a ri a, p 490; Pyre xi a (1), p 518; Pyre xi a (2), p 520; Pos t-op erati ve i nt ens i ve care, p534 P.484

Systemic inflammation/multi-organ failure Exp osure to an exog enous i ns ul t c an res ul t i n an ex agg erated , ge neral i se d and ofte n i nap propri at e i nfl amm atory res ponse. Thi s i s de scri be d as ‘ SIR S’ —the s yst emi c i nfl amm atory res ponse syndrome. St i mul at i on of i nfl a mmatory pat hways l eads to act i vati on of macrophages , e ndothe l i um, neutrophi l s , p l at el e ts, coagul at i on, fi bri nol y ti c and contac t s yst ems wi th rel eas e of i nfl amm atory med i at ors and e ffec tors (e.g . c ytoki nes, prost anoi ds , free ox yge n rad i c al s , p rot eas es, ni tri c oxi de, end othel i n). Thi s re sul ts i n mi c rovas cul ar obs truct i on and oc cl usi on, bl ood fl ow red i s tri but i on, i nt ers ti t i a l oedem a and fi b ros i s , and c el l ul ar mi t ochond ri al dys func ti on. The c ons eque nce s of t hi s may be org an dys functi on, varyi ng from ‘ mi l d’ to sev ere , and affe cti ng si ngl e or m ul t i pl e organs, resul ti ng i n cardi ovas cul ar col l a pse , g ast roi nt est i nal fai l ure, renal fai l ure, hep ati c fai l ure , e nce phalop athy, neurop athy,

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myopat hy, and /or di ss emi nat ed i nt rav asc ul a r c oag ul a ti on. Ac ute re spi rat ory di st res s s ynd rom e (ARD S) i s the res pi rat ory component of thi s pat hop hys i ol og i cal resp ons e.

Causes include: Infe ct i on Trauma, burns Panc reati ti s Inhal a ti on i njuri e s Mass i v e bl ood l oss /trans fus i on Mi s cel l aneous i ncl udi ng drug-rel ate d (i nc l ud i ng ov erd ose ), myoc ard i al i nfarct i on, d row ni ng, hyp ert hermi a, pul monary emb ol us

Treatment Largel y s up porti v e, though the c aus e shoul d b e removed /treat ed i f at all possi bl e . T reatme nt i nc l udes ant i b i ot i cs , drainage of pus , fi xati on of fe moral / pe l vi c frac tures and de bri de ment of ne croti c t i ss ue. An i mp ortant facet of organ support i s to mi ni mi se i a trogeni c trauma. It i s s uffi c i ent t o maintai n s urv i val w i th rel at i ve hom eos tas i s unt i l re cov ery takes pl ace rathe r t han at tem pti ng to achi ev e normal p hys i ol og i cal or b i oc hem i cal target value s. An exampl e of t hi s i s pe rmi ss i ve hyp erc apni a . Spe ci fi c treat ment regi mens remain contenti ous due to a l ac k of ad equate l y powe red st ud i es showi ng opt i mal hae mod ynam i c goals , i not rop i c/ press or age nts , anti bi oti c regi mens, etc . Local p ol i ci es may fav our the use of one or more of a range of ecl ect i c therapi e s t hat may offer a reasonabl e t heoret i cal b asi s for adm i ni st rat i on, or anec dot al suc ces s, thoug h t hes eal l remain ess ent i al l y unp rov en. Ex amp l es i ncl ude ant i ox i dants , p rot eas e i nhi bi tors, i mm unonut ri ti on, pl a smaphe res i s, vasod i l ators, and i mmunogl obul i ns. It i s ge neral l y agre ed that rapi d res uci tat i on and re storat i on of ox yge n de l i very, gl y cae mi c control and promp t removal of any treat abl e c aus e i s d esi rab l e i n pre venti ng t he ons et of SIR S. Bec aus e of non-s tandardi sat i on of de fi ni ti ons , outc ome data are confl i ct i ng , t hough si ngl e organ ‘fai l ure’ carri es an app rox i mate 20–30% mortalit y w hi l e ≥ 3 organ ‘ fai l ures’ l a sti ng ≥3 day s c arri e s a mortal i t y i n e xce ss of 50%. Rec ove ry i s oft en c omp l et e i n s urvi v ors , t hough rec ent st udi es are re vealing l ong te rm phy si cal and ps yc hol ogi cal seq uel ae i n a s i gni fi cant proporti on of p ati ent s. P.485

Current UCL Hospitals principles of management Respiratory

SaO 2 >90–95% (may have to settle for lower) Permissive hypercapnia

Cardiovascular

Maintain cardiac output/oxygen delivery and blood pressure compatible with adequate organ perfusion (e.g. no metabolic acidosis)

Renal

Maintain adequate metabolic and fluid homeostasis by intravascular filling, diuretics, vasoactive agents, and/or haemo(dia)filtration

Haematological

Maintain haemoglobin >7g/dl (unless cardiorespiratory problems), platelets >20–40 × 10 9 /l, INR <1.5–2.5

Gastrointestinal

Stress ulcer prophylaxis (generally by enteral nutrition), pancreatitis, acalculous cholecystitis

Infection

Antibiotics, pus drainage, good infection control

Nutrition

Preferably early and by enteral route

Pressure area/mouth/joint care

Frequent turns, low pressure support surfaces, nursing care and physiotherapy

Psychological

Support to both patient and family

Definitions Systemic inflammatory response syndrome (SIRS) Two or more of:

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Temp erature > 38° C or < 36° C Heart rat e >90bp m Resp i ratory rat e > 20 bre aths/m i n or PaC O 2 <32mmHg (4.3k Pa) WBC >12,000 c el l s/m m 3 , <4000/mm 3 , or >10% i m mat ure forms

Sepsis The sy ste mi c re sponse to i nfec ti on. Defi ni ti on as for SIRS but as a res ul t of i nfec ti on.

Severe sepsis Sep si s associ a ted wi th org an dys functi on, hy pop erfusi on or hyp otensi on. These may i ncl ude, but are not l i mi ted to, l ac ti c aci d osi s, ol i guri a or an ac ute al terati on i n mental st atus.

Septic shock Sep si s wi th hy pot ens i on, d esp i te ad equate fl ui d re sus ci t ati on, pl us prese nce of perfus i on ab normal i t i es .

Multi-organ dysfunction syndrome (MODS) Pre sence of al t ere d organ func ti on i n an acut el y i l l p ati ent s uch that home ost asi s cannot be mai ntaine d w i thout i nt ervent i on. Mul ti p l e org an fai l ure (MOF ) has not achi ev ed worl dw i de uni formi ty of defi ni ti on.

See also: Venti l at ory support— ind i c ati ons , p 4; Bl ood press ure moni t ori ng , p 110; Bac teri ol og y, p 158; Anti mi c rob i als, p260; Ac ute re spi rat ory di st res s s ynd rom e (1), p292; Acut e resp i ratory d i s tre ss syndrome (2), p294; Inhal a ti on i njury, p306; Hyp ote nsi on, p312; Ab domi nal s eps i s, p350; Panc reati ti s , p 354; Infec ti on c ont rol —g eneral pri nc i pl es , p 476; Sep si s and s ept i c shock —treat ment, p486; Mul ti pl e t rauma (1), p500; Mul ti pl e traum a (2), p502; Burns —fl ui d manage ment , p 510; Burns— general m anagem ent , p 512; Py rex i a (1), p518; Py rex i a (2), p 520 P.486

Sepsis and septic shock—treatment Principles of treatment As for ot her cause s of M ODS, outc ome i n se psi s i mprove s w i th: 1. Prom pt di agnosi s and t re atm ent of the underl yi ng cause 2. Rapi d resusc i tati on t o p rev ent prol onge d t i ss ue hyp oxi a 3. Good gl ycaemi c c ont rol 4. Stri ct i nfec ti on control 5. Recogni ti on and app rop ri ate treat ment of se condary i nfe cti ons 6. Ade quat e nutri t i on 7. Recogni ti on t hat ‘ normal ’ p hys i ol ogi cal /bi ochemi cal l evel s do not nec ess ari l y ne ed t o b e attaine d w hi l e t he pati ent i s c ri t i c al l y i l l , p rov i de d he/she i s not com promi s ed: e. g. a me an BP of 55–60m mHg i s oft en acc ept abl e unl ess evi de nce of poor p erfusi on or i sc hae mi a sugge sts hi gher l ev el s shoul d b e s oug ht 8. Avoi dance of pre ventab l e mi s hap s, e.g . p rol ong ed hyp ote nsi on, press ure sores , t hromboemb ol i sm 9. Temp erature c ont rol i n t he range 36–38. 5°C . 10. Prev ent i on of contract ures, earl y mob i l i sati on, etc . 11. Spe ci fi c tre atm ent s (see be l ow)

Specific treatments for severe sepsis/septic shock 1. Act i vated prote i n C s i gni fi cantl y i mprove s outc ome i n pat i ents wi th ≥2 organ d ysfunc ti ons i f com menced wi thi n 48h of ons et of s eve re sep si s. The PROWESS s tudy m ai nl y i ncl uded pati e nts prese nti ng from t he com muni ty and had num erous exc l us i on cri t eri a, parti cul arl y rel ated to those at i ncrease d ri s k of bl eed i ng . Sub seq uent s tud i es reve al e d < 15% of sep ti c p ati ent s p res ent i ng to IC Us meet both i ncl usi on and exc l us i on cri t eri a. 2. ‘Low-dose’ hy drocorti sone (50mg qd s) gi v en for 7 d ays i m proved outcomes i f commenced wi thi n 8h of s ept i c shoc k p res ent at i on, t hough onl y i n t he s ubs et wi t h an abnormal c ort i s ol res ponse to synthe ti c AC TH. Our c urrent practi ce i s to start hyd roc orti s one after pe rformi ng a Synacthen tes t and t o d i s conti nue thi s t herapy i f the t est i s normal . 3. For norepi nep hri ne (NEPI)-re si s tant s ept i c shock , i .e. hi gh-out put se vere hy pot ens i on not resp ond i ng t o adeq uat e fl ui d l oad i ng and a NEPI dos e >0.4µ g/k g/m i n, we consi der careful admi ni strati on of terl i pre ssi n or methyl t hi oni ni um c hl ori de. Unt i l more dat a are fort hcomi ng, the se age nts shoul d b e v i ew ed as res cue therapi e s rat her than a st raight alte rnati ve for NEPI. 4. We occasi onal l y us e pl as mapheresi s, prostagl a ndi ns or hi gh-outp ut hae mofi l t rati on for res i st ant cases of se pti c

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shoc k, parti cul arl y t hos e w i th l ow c ard i ac outputs . We re adi l y ack now l ed ge the evi de nce bas e for the se the rap i es i s sl i ght and our use i s based on anecd otal s ucc ess . P.487

Figure. No Caption Available.

Key paper D el l i nger RP et al . Surv i vi ng Sep si s Campaign gui de l i nes . Cri t Care M ed 2004; 32:858–73

Key trials Bernard GR, for the PROW ESS st udy group . Effi cac y and safety of rec omb i nant hum an act i vated prote i n C for seve re sep si s. N Engl J M ed; 344:699–709 Annane D, et al . Effe ct of t re atme nt wi t h l ow dos es of hydroc ort i sone and fl udrocorti sone on m ort al i ty i n pat i e nts wi t h s ept i c shock . JAMA 2002; 288:862–71

See also: Oxy gen therapy, p2; Vent i l a tory s upp ort —i ndi cat i ons, p4; Haemo(di a)fi l t rati on (1), p62; Haem o(d i a)fi l trati on (2), p64; Pl as ma exchang e, p68; Ente ral nutri ti on, p80; Pare nte ral nutri ti on, p82; Bl ood g as anal ys i s, p100; Bl ood pre ss ure moni t ori ng, p110; C ard i ac output—t hermod i l uti on, p122; Cardi a c outp ut—other i nv asi ve, p124; Cardi ac out put —non-i nvasi v e (1), p126; Cardi ac out put —non-i nvas i v e (2), p128; Bac teri ol og y, p 158; Lact ate , p 170; Inotropes , p 196; Vasopre ssors , p 200; Anti c oag ul a nts , p 248; Anti mi c rob i al s, p260; Steroi ds, p262; Nove l t herap i es i n sep si s, p266; Fl ui d c hal l enge, p274; Ac ute chest i nfec ti on (1), p288; Acute che st i nfect i on (2), p 290; Acut e res pi rat ory di stres s s ynd rom e (1), p292; Acut e resp i ratory di s tre ss syndrome (2), p294; Hyp ote nsi on, p312; Ac ute renal fai l ure— di a gnosi s , p 332; Ac ut e renal fail ure —manage ment, p334; Abdomi nal sep si s, p350; Infec ti on—d i ag nos i s , p480; Infect i on—treat ment, p482; Pyre xi a (1), p 518; Pyre xi a (2), p520 P.488

HIV related disease Affect ed pat i ents may prese nt el e cti vel y afte r d i ag nos ti c b i op si e s of b rai n or l ung , or w here el ec ti v e v ent i l a ti on i s nee ded postoperati vel y. Other cas es pre sent w i th compl i c ati ons of HIV rel a ted di sease, es pec i al l y pul monary i nfect i on (e .g. Pneum ocys ti s c ari nii, CM V) or sei zures (e. g. cerebral l y mphoma, ce reb ral ab sc ess , me ni ngi ti s ). HIV rel at ed d i s eas es are now consi dered to be chroni c m anageabl e condi ti ons wi t h an ofte n good short term p rog nos i s . It i s there fore reasonab l e that i nt ens i ve care s houl d be offere d.

Infection control The prote cti on of staff from t ransmi ssi on of HIV fol l ows bas i c measures. Body fl ui ds shoul d not be handl e d (wear gl oves ) and the fac e and eyes s houl d be p rot ec ted whe re the re i s a ri s k of sp l as h c ont ami nat i on. Nee dl e s s houl d be di s pos ed of i n app rop ri a te bi ns w i thout re-sheat hi ng. Any fl ui d s pi l l ag es shoul d be cl eaned up i mm edi ate l y. Robus t p roc edures are adhe red to whe re a p ati ent i s known HIV p osi ti ve; the re al ri sk i s i n the pati e nt of unk nown HIV s tatus . Re mem ber that pat i ents pre senti ng wi t h non-HIV re l at ed i l l nes s m ay be unknown posi t i ve s. It fol l ow s t hat precauti ons s houl d be t ake n for al l pati e nts .

Pneumocystis carinii pneumonia

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Thi s i s t he com mone st re spi rat ory di sorder affec ti ng HIV posi t i ve pati e nts . T he maj ori ty survi v e t hei r fi rst att ack but prognosi s i s not as good i n t hos e requi ri ng mec hani cal v ent i l ati on. Intensi v e, earl y sup port w i th CPAP and appropri a te che mot herapy may av ert the need for ve nti l at ory support . Tre atme nt i s us ual l y starte d w i thout waiti ng for l a boratory confi rmat i on. Fi rst l i ne t reatme nt i s wi t h hi g h-dose co-tri mox azol e or pentam i di ne wi t h adjuvant hi gh-dos e s teroi ds. Co-t ri m oxazol e has a fast er ons et of e ffe ct and a b roader sp ect rum of anti b act eri al ac ti v i ty coveri ng the c omm on sec ondary pat hog ens . Pent ami di ne i s usuall y us ed whe re co-tri mox azol e fai l s or whe re pat i ents cannot take co-t ri moxazol e. Methyl p re dni sol one i s us ed to sup pre ss peri bronchi al fi b ros i s and al veol ar i nfi l trate. It i s usual for the re to b e an ini ti a l d ete ri orati on on t reatme nt l as ti ng s eve ral days. Resp i ratory sup port i s p rov i de d w i th CPAP (5–10c mH 2 O) i f hy pox aemi c d esp i t e hi gh FIO 2 . Lower CPAP pre ssures shoul d be use d w here p oss i bl e as t hes e p ati ent s are at ri s k of p neumot horax. Mechani cal ve nti l a ti on i s rese rve d for those who hav e a ri si ng w i t h de teri orat i ng gas e xchang e and fati gue desp i t e CPAP. CXR change s resp ond ve ry sl owl y .

Lactic acidosis Nuc l eosi de reve rs e t ranscri pt as e i nhi bi t ors (N RTIs) are frequent l y use d anti -re trovi ral age nts . Howe ver, an ass oci at ed m i t ochondri a l i mpairm ent can c aus e a se vere l act i c aci dos i s and a hi g h m ort al i ty . Anec dot al use of L-c arni t i ne i s re ported to be of benefi t.

IV drug abusers IV drug abus ers are at hi g h ri sk for HIV rel ate d d i s ease , t hough pre sent m ore commonl y for ot her reas ons (e. g. drug wi t hdrawal s ynd rom es, ov erd ose , s eps i s, endoc ard i ti s, he pat i ti s B or C, rhabd omy ol y si s ). P.489

Drug dosages Co-trimoxazole

120mg/kg/day in divided doses IV for 10–14 days then PO to complete 21 days

Pentamidine

4mg/kg/day IV

Methylprednisolone

1g/day for 3 days

See also: Venti l at ory support— ind i c ati ons , p 4; Endot rac heal i ntubat i on, p 36; Conti nuous p osi ti ve airway pre ssure , p26; Bac teri ol og y, p158; Vi rol og y, serol ogy and ass ays , p 160; Anti mi crobi a l s, p260; Ste roi ds, p262; Ac ute chest i nfec ti on (1), p 288; Acut e c hes t i nfe ct i on (2), p 290; Pneumothorax , p 300; Infe ct i on control — general p ri nci pl e s, p476 P.490

Malaria Mal ari a s houl d be sus pec ted i n any p ati ent re turni ng from endem i c areas wi t h a fe bri l e i l l ne ss whi ch may hav e cerebral , ab dom i nal, l ung or renal feat ures. Rarel y, p eop l e l i vi ng near ai rports may b e bi tt en by a trans porte d Anophe les mosqui to. T here m ay be c ons i d erabl e de l ay (we eks to months ) b etw een the mosqui t o bi te and si gns of i nfect i on. It i s caused by protozoal i nfe cti on wi t h t he Pl asm odi um g enus. The most sev ere form i s P. falc iparum whi ch causes malig nant, terti an mal ari a. Other forms (P. m alariae, P. viv ax, P. ovale ) rare l y cause si g ni fi cant l i fe threat eni ng di sease and wi l l not be di s cusse d furt her.

Pathophysiology P. fal cip arum i nvades erythroc yte s regardl es s of ag e. Hi g h l eve l s of parasi tae mi a >5% are c ons i de red se vere i n non-i m mune t rav el l ers . T he cel l s may haemol ys e or be de stroye d i n l i v er or spl een. Anae mi a may be se vere. Inc re ased vascul ar p erm eabi l i ty, cy tok i ne re l ease, re d c el l ag gl uti nat i on and i ntravascul ar coagul at i on (D IC) may al so occ ur.

Clinical features Symp tom s i nc l ud e headache , feve r w i th ri gors, myalgi a, abd omi nal pain, vomi t i ng and d i arrhoea. Si gns i ncl ude spl enomegaly, jaund i ce , t end er hep atomeg al y and anaem i a. Hy ponatraemi a i s comm on. Onl y a mi nori ty of pat i ents wi th P. falci parumhave parox ysms of fe ver wi th ‘col d’ and ‘ hot ’ s tag es.

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If > 5% parasi tae mi a , feat ure s i ncl ude : Cere bral m al a ri a, causi ng c oma, de l i ri um, sei zures or foc al defi c i ts . Coug h and haem opt ysi s or acute res pi ratory di s tress Bl a ckw ater fe ver i s as soc i a ted wi th mass i v e i ntravascul ar haemol ys i s, jaund i ce , haem ogl obi nuri a, col l aps e and renal fai l ure Acute renal dys functi on occ urs i n a thi rd of adul t ICU pati e nts Acute cardi ovas cul ar col l a pse (‘alg i d mal ari a’) and me tab ol i c aci dos i s Thrombocyt ope ni a , D IC and sp ont ane ous bl eed i ng

Diagnosis Pl as mod i a see n i n R BC i n thi ck or thi n s mears of peri pheral bl ood. The paras i t aemi a i nt ens i ty may vary from hour t o hour and may b e sc ant y i n numb er. The s mear s houl d be careful l y sc ruti ni se d and rep eat ed i f doub t persi s ts. Leucoc ytosi s i s not a fe ature of m al a ri a Spl enomegaly i s al mos t i nvari a bl e duri ng t he sec ond we ek of i l l nes s

Treatment 1. Earl y IV qui ni ne i nfusi on i s the mai ns tay of tre atm ent of se vere malari a . Level s shoul d be moni t ore d dail y and dosage adj ust ed as app rop ri a te. Compl i cati ons i nc l ude hypogl ycae mi a and t i nni t us. Artem ether shoul d be cons i d ere d i n c ase s of l i ke l y qui ni ne resi st anc e. 2. A 2–3l exc hange trans fus i on shoul d b e c ons i de red i f the p ati ent i s se verel y i l l or i f p arasi tae mi a l e vel s >10–20%. 3. Care ful at tenti on m ust be paid to fl ui d and el ect rol yt e balance and manag ement of renal fai l ure . 4. Tre atme nt of hyp ogl ycaemi a, renal fai l ure, coagul opathy , m etab ol i c aci dos i s, se i z ure s, ARD S, anaemi a and hype rpy rex i a fol l ow conve nti onal l i nes 5. Ste roi ds are not recomme nded for c ere bral oede ma. 6. Sus pec t c oi nci d ent Gram neg ati ve i nfect i on wi th ci rcul at ory col l aps e. P.491

Drug dosage First line Quinine

20mg quinine salt/kg IV over 4h, then 10mg/kg infusion over 4h, repeated 8-hrly until the patient can swallow, then tablets (10mg quinine salt/kg 8-hrly) to complete 7 days' treatment. Halve maintenance dose to 5mg salt/kg 8-hrly if continuing parenteral therapy for >48h.

Artemether

3.2mg/kg IM followed by 1.6mg/kg daily

Second line after asexual parasites eliminated Sulfadoxine 500mg/pyramethamine 25mg

3 tablets once

Doxycycline

200mg then 100mg daily for 7 days

See also: Hae mo(d i a)fi l trati on (1), p62; Haemo(di a )fi l trat i on (2), p 64; Bl ood transfusi on, p182; Fl ui d c hal l enge, p274; Ol i guri a, p330; Acute renal fai l ure— di a gnosi s , p 332; Ac ute re nal fai l ure—manage ment , p 334; Ge neral i se d s ei z ure s, p372; Jaundi ce, p358; Anaemi a, p400; Hae mol ysi s, p404; Pl a tel et di s ord ers , p 406; Infec ti on—di a gnosi s , p 480; Infect i on—t reatment, p482; Pyre xi a (1), p518;Pyre xi a (2), p 520 P.492

Rheumatic disorders

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Rheumatoid arthritis A d ebi l i tat i ng arthri t i s that m ay pre sent t o i nte nsi ve care t hrough pul monary i nvol ve ment or t hrough compl i cati ons of treatm ent (e .g. re nal failure, i m munosuppress i on, b l e edi ng di s ord ers ). Pl e uro-pul monary i nvol ve ment may p rec ede the arthri t i c sym ptoms and i s more com mon i n those wi t h acti ve rhe umatoi d d i s ease and m i dd l e age d m en. Care i s req ui red whe n i ntubat i ng p ati ent s w i th rheum atoi d art hri ti s s i nc e t he nec k j oi nts may subl ux.

Rheumatoid pleurisy Rhe umatoi d p l euri s y, oft en wi t h e ffus i on, i s mos t c ommon and i s usual l y asym ptomat i c. Howev er, effusi ons may b e rec urrent or c hroni c and m ay i mp ede res pi rat ory funct i on. T he effusi on i s an exud ate , l ow i n gl ucos e and oft en hi g h i n chol es te rol .

Rheumatoid lung Rhe umatoi d l ung i s a di ffus e i nte rst i t i al pneum oni ti s wi th bi -bas al fi b roti c chang es on the CXR . T he condi t i on may b e di ffi c ul t t o d i st i ng ui sh from i di opat hi c pul monary fi brosi s and produc es a rest ri cti ve pul monary de fec t. The mai ns tay of tre atm ent i s earl y sy ste mi c st eroi d therapy, al though chroni c cas es do not re spond.

Systemic lupus erythematosis (SLE) A non-org an spe ci fi c aut oi m mune d i se ase characte ri sed by ant i nucl ear anti b odi es wi t h hi gh ti tres of ant i doubl e-s trand ed D NA ant i b odi es. A vas cul i t i s i s promi nent , althoug h c utaneous and ce ntral nervous s yst em i nv ol v eme nt are not v asc ul i ti c. SLE may pres ent to i ntensi v e c are through pul monary , renal or c ent ral ne rvous sys tem i nvol vem ent .

Renal failure Renal fai l ure i s v asc ul i ti c i n ori gi n and may p rog res s t o e nd stage renal fai l ure requi ri ng l ong term d i al ysi s. Earl y treatm ent wi th sys tem i c st eroi ds and i mmunos upp res si v es may hal t di s eas e p rog res s.

Lupus pleurisy and pericarditis Unl i ke rheum atoi d pl e uri sy the p l eural i nvol vem ent i n SLE i s ofte n p ai nful and associ a ted wi th l arge pl e ural effusi ons .

Pulmonary haemorrhage Pul monary haemorrhage i s as soc i at ed wi t h renal fai l ure and m ay be l i fe t hre ate ni ng. Pl a sma exc hange may be hel pful .

Interstitial pneumonitis Int ersti ti a l p neumoni ti s i s unc omm on i n SLE. It i s m ore l i kel y t hat parenchy mal i nfi l trate s are i nfect i ve i n ori g i n sec ond ary to i m munosuppress i ve therapy.

Pulmonary thromboembolic disease Pat i ents typ i c al l y have a p rol ong ed act i vated parti al throm bop l as ti n ti me due to ci rcul a ti ng l upus anti coagul ant . b ut are more prone to thromb oti c e pi s ode s. Lup us ant i c oagul ant i s ass oci ate d w i th anti c ard i ol i p i n ant i bodi e s and a fal s e pos i t i ve VD RL. Rec urrent p ul m onary embol i may be as soc i at ed wi t h c hroni c p ul m onary hype rt ens i on. T reatment i s l ong t erm anti c oag ul ati on. P.493

See also: End otracheal i ntubat i on, p 36; Pl a sma exc hange, p68; Non-op i oi d anal ges i cs , p 236; Steroi d s, p262; Haem opt ysi s, p304; Acute renal fai l ure— di a gnosi s , p 332; Ac ute re nal fai l ure—manage ment , p 334; Up per gastroi nte sti nal hae morrhage, p344; Vascul i t i d es, p494 P.494

Vasculitides Vas cul i t i s shoul d b e susp ect ed i n any pat i ent w i th mul t i sy ste m d i se ase , e spe ci a l l y i nvol vi ng t he l ungs and ki dne ys.

Wegener's granulomatosis A s yst emi c vasc ul i ti s c harac teri se d b y necroti si ng granul omas of the uppe r and l ow er res pi ratory tract , gl omerul onep hri ti s and small ves sel vascul i ti s . W ege ner's granul omatos i s i s as soc i at ed wi t h p osi ti v e c ore ant i ne utrop hi l cy top l as mi c anti bodi es (c-ANC A), parti cul arl y granul ar wi t h c ent ral atte nuati on on i mm unofl uore sce nce . Inte nsi ve care admi ss i on i s us ual l y bec aus e of renal and/or p ul m onary i nv ol v eme nt.

Renal failure Foc al nec rot i s i ng gl ome rul one phri ti s l eads to progre ssi ve renal fai l ure. Treatm ent wi th ste roi ds and cyc l op hos phami d e m ay gi v e c ompl et e remi ssi on.

Upper airway disease Mos t p ati ent s w i l l have nas al sym ptoms i nc l udi ng e pi s tax i s, nasal di sc harge and sep tal pe rforat i on. Int ens i ve care adm i ss i on may b e requi re d rare l y for se vere e pi s tax i s. Ul cerat i ng l e si ons of the l a rynx and t rache a may c aus e

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sub gl ott i c ste nos i s. Thi s i s us ual l y i ns i d i ous b ut may present p robl e ms on atte mpt ed i nt ubati on.

Pulmonary involvement Usual l y associ ate d wi th hae mop tys i s, dy spnoea and c oug h wi th round ed opac i t i es on the CXR. The re may be cav i tati on. Nod ul es m ay be sol i tary. Al veol ar haemorrhage may b e l i fe threateni ng . T he mai nst ay of t reatme nt i s ste roi ds and c ycl ophosp hami de whi ch may produce com pl e te rem i ss i on. Pl as ma exc hange may be hel pful .

Polyarteritis nodosa (PAN) PAN i s a nec rot i s i ng vascul i t i s affect i ng s mal l and medi um si zed muscul ar arteri e s. Int ens i ve care admi ss i on may be provok ed by renal fai l ure, i sc hae mi c he art di sease, hy pertensi ve c ri si s and b ronchospasm, al though true pul monary i nv ol v eme nt i s unc omm on. Di agnosi s m ay be c onfi rmed by mes ent eri c angi ograp hy or renal b i opsy . Treat ment i nv ol v es renal rep l aceme nt the rap y, hi g h d ose st eroi d s and c ycl op hos pham i d e.

Goodpasture's syndrome Ant i g l om erul ar basem ent me mbrane (anti -GBM ) anti bod i es bi nd at the gl ome rul us and al veol us . Pati ent s p res ent wi th a p rol i fe rat i v e gl ome rul onephri t i s and haemopty si s . D i ag nos i s i s confi rme d b y p osi ti v e anti -GBM anti bod i es and renal bi opsy . T reatme nt i s wi t h i mmunos upp res si ve the rap y and p l as ma exc hange. P.495

See also: Pl a sma ex change , p68; Ai rway obst ruc ti on, p280; Ste roi ds, p262; Hae mop tys i s, p304; Ac ute re nal failure—di agnosi s, p332; Acute renal fai l ure— managem ent , p 334; Rheumati c d i sorde rs, p492 P.496

Anaphylactoid reactions Mi nor react i ons t o al l e rge ns (i t chi ng, urti cari a) are c omm on b efore a s evere reac ti on occ urs ; any s uc h hi st ory shoul d be tak en seri ousl y and p ote nti al al l ergens av oi d ed. Most reacti ons are acut e i n onse t and cl e arl y rel ated to the causat i ve al l erge n. Howe ver, s ome com pl ement-m edi ate d reac ti ons may take l ong er to dev el op.

Clinical features Resp i ratory— laryng eal oe dema, b ronchospasm, pul monary oede ma, pul monary hy pertensi on Card i ov asc ul ar— hyp ote nsi on, tachy cardi a , g ene ral i se d oede ma Other— urt i c ari a, ang i o-oede ma, ab domi nal c ram ps, ri gors

Management 1. Stop al l i nfusi ons and b l ood t ransfusi ons and wi thhol d any p ote nti al drug or food al l ergen. Bl ood and bl ood produc ts shoul d be re turned to the l aborat ory for anal ysi s. 2. Start oxy gen (FIO 2 0.6–1. 0). If there i s evi de nce of persi ste nt hyp oxae mi a consi der urgent i nt ubati on and mechani cal ve nti l a ti on. 3. If t here i s l aryng eal ob struct i on, b ronchosp asm or fac i al oe dem a g i ve IM or neb ul i se d e pi nephri ne and IV hydroc ort i sone. If there i s not rapi d rel i ef of ai rway ob struct i on, c ons i d er urg ent i ntub ati on or, i n ex tre mi s , emergency cri cothy roi dot omy or tracheos tom y. Pers i s tent b ronchospasm may re qui re an epi nep hri ne i nfusi on, ami nophyl l i ne i nfusi on or assi st ed e xpi rat i on (m anual che st com pre ssi on). 4. Hypotensi on s houl d be treate d w i th ep i ne phri ne IV/IM and rapi d c ol l oi d i nfusi on. Large vol ume s of c ol l oi d may b e req ui red to rep l ac e t he pl a sma vol ume de fi c i t i n se vere anaphyl a xi s . Seve re oede ma may coe xi s t w i t h hy pov ol a emi a. Pl as ma v ol ume has not b een ade quatel y repl ace d i f t he hae mog l ob i n i s hi g her than normal . Hetastarch i s the m ost ap propri ate fl ui d for c ol l oi d resusci tati on unl e ss the re act i on i s due t o a hydroxye thy l s tarch. 5. Pers i s tent hypotensi on s houl d be tre ate d wi th further epi nep hri ne, hy drocorti sone and c ol l oi d i nfusi on g ui d ed by cent ral v enous p re ssure ± c ard i ac output m oni tori ng . An e pi nephri ne i nfusi on may be req ui red to ove rcome myoc ard i al d epress i on. T he use of mi l i t ary anti s hoc k t rousers or nore pi nephri ne shoul d be consi dered to di v ert bl ood c ent rally and i ncreas e p eri phe ral resi stance . 6. Urt i cari a re qui re s c hl orphenami ne IV or PO d epe ndi ng on the sev eri ty of the re act i on. 7. Aft er control of t he anap hyl act oi d reac ti on, adv i ce shoul d b e s oug ht from the i mmunol ogy l a boratory and appropri a te sam pl e s t aken for c onfi rmati on. 8. Reac ti ons to l ong-acti ng drugs or fl ui d s w i l l requi re conti nue d s upp ort (p erhaps for m any hours). P.497

Drug dosages

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Laryngeal oedema and bronchospasm Initial dose

Continued treatment

Epinephrine

0.3–0.5mg IM or 0.5mg nebulised

Start at 0.05µg/kg/min

Hydrocortisone

200mg IV

Hypotension Initial dose

Continued treatment

Epinephrine

0.5–1.0mg IM or 0.05–0.2mg IV

Start at 0.05µg/kg/min

Hetastarch 6%

500ml

According to response

Hydrocortisone

200mg IV

200mg IV qds

Chlorphenamine

10mg IV tds

Urticaria Chlorphenamine

10mg IV tds or 4mg PO tds

Hydrocortisone

50–100mg IV tds

Prednisolone

20mg PO daily

See also: Venti l at ory support— ind i c ati ons , p 4; Endot rac heal i ntubat i on, p 36; Col l oi ds , p180; Bl ood trans fus i on, p 182; Inotropes , p 196; Bl ood p rod uct s, p252; Ste roi ds, p262; Bas i c re sus ci t ati on, p270; F l ui d c hal l e nge , p274

Ovid: Oxford Handbook of Critical Care

Ed itors:

Si nge r, M ervyn; We bb, An dre w R.

Ti tle : O xf ord Ha ndbook of Cr itic al Car e, 2nd Ed ition Cop yri ght © 1997,2005 M. Si nge r and A. R. W ebb , 1997, 2005. Publ i shed i n the Uni te d Stat es by Oxford Uni ve rsi ty Press Inc > Tab le of Co n te n ts > Tr a u ma an d Bu r n s

Trauma and Burns Multiple trauma (1) Suc h p ati ents are adm i t ted ei the r afte r s urg ery or for c l os e obse rvati on and medi cal m anag eme nt. The p ri nci pl e s of manage ment are t o: Mai ntai n or qui ckl y rest ore ad equate ti ssue p erfusi on and gas e xchange Cont rol pain Sec ure haemos tas i s and c orrect any c oagul opat hy

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Prov i d e ad equate nutri ti on Moni tor c l os el y and d eal prompt l y wi th any com pl i cati ons

Circulatory management Pati ent s are oft en col d and vas oconst ri c te d on ad mi s si on. Thi s serves to camoufl ag e c onc urrent hypov ol a emi a and com promi s e t i s sue perfusi on. Ade quat e m oni tori ng m ust be i nsti tut ed at an earl y stage. Deve l op ment of a persi sti ng ti ssue oxyge n d ebt has b een shown to l ead t o s ubs equent mul ti pl e organ dysfunc ti on whi ch may not be com e c l i ni call y ap parent for 3–7 day s. The refore , adequate pe rfusi on m ust be res tored prompt l y by rep eat ed fl ui d challe nge s. Add i ti on of a v asodi l ati ng age nt, e. g. gl y ceryl tri ni trate, may b e bene fi c i a l . An i nc reasi ng m etabol i c aci dos i s shoul d p rom pt sus pi c i on of i nade quate res usc i t ati on, covert haemorrhag e or ti s sue ne crosi s . M yoc ard i al de press i on or fai l ure may al so b e i mpl i c ate d.

Respiratory management Cons i de r t he pos si bi l i t y of a fractured , unst abl e neck , e spe ci a l l y i n unconsc i ous p ati ent s. Thi s s houl d be excl ud ed b y appropri at e radi ol ogy and an ex pert opi ni on. Unti l t hen the neck shoul d b e i mmobi l i se d. If v ent i l ate d, e nsure hae mod ynami c st abi l i ty, re moval of any metabol i c ac i dosi s , adeq uat e rewarmi ng and sat i sfact ory gas e xchange be fore atte mpt i ng to wean. If the pati e nt rem ai ns unst abl e, i t i s ad vi s abl e t o d el a y extubat i on i n c ase urgent s urg ery i s re qui red . If s pontaneousl y breat hi ng, gi ve s upp l e ment al oxy gen to provi de adeq uat e arte ri al oxyg enati on, enc ourage de ep bre athi ng to prevent atel ec tas i s and se condary i nfe cti on, and ensure suffi c i ent anal ges i a, al bei t not too much to sup pre ss venti l atory dri ve.

Haematological management Mai ntai n haem ogl obi n > 7g/dl (hi ghe r w i th cardi oresp i ratory d i se ase ) t o as si st oxy gen trans port. Cross-mat che d bl ood s houl d be readi l y avai l ab l e for se condary haem orrhag e. Correc t any c oag ul opat hy wi t h fres h frozen pl a sma, ± pl atel et s, and , oc cas i onal l y, ot her bl ood products (e .g. cry opreci pi t ate ) or acti vat ed fac tor VII.

Peripheries Inj ury to the l i mb may resul t i n nerve i nj uri es , ob st ruc ti on of t he vas cul ar sup pl y , or m usc l e dam age whi ch may l e ad to com partme nt syndrome and rhabd omyol ys i s . A hi gh l ev el of s us pi c i on shoul d b e hel d and c orrect i ve surg ery und ert ake n p rom ptl y i f nece ssary. P.501

See also: Venti l at ory support— ind i c ati ons , p 4; Che st drai n i nserti on, p42; Nutri ti on—use and i ndi cat i ons, p78; Bl ood gas analys i s , p100; Bl ood press ure moni t ori ng, p110; Ful l b l ood c ount, p154; C oag ul a ti on m oni tori ng, p 156; Lact ate , p170; Cry stalloi ds , p 176; Col l oi d s, p180; Bl ood t ransfusi on, p182; C oag ul a nts and anti fi b ri nol yti cs, p254; Bas i c res us ci t ati on, p270; Fl ui d challe nge , p 274; Pneum othorax, p300; Hae mot horax, p302; Hyp ote nsi on, p312; Anaem i a, p400; General aci d –base managem ent , p 432; Metabol i c ac i dosi s , p 434; Infec ti on—d i ag nos i s , p 480; Infect i on—t reatment, p482; Mul ti p l e trauma (2), p 502; Head i njury (1), p504; Head i njury (2), p506; Rhabdomyol ys i s, p528 P.502

Multiple trauma (2) Analgesia Ade quat e anal ges i a i s i m perati ve to avoi d c i rcul atory i ns tabi l i ty and d ecreas ed che st wal l e xcursi on, es pec i al l y fol l owi ng chest , ab dom i nal or s pi nal traum a. Inc reased us e of re gi onal te chni q ues (de pendi ng on abse nce of i nfect i on and c oag ul opat hy) and pati ent-c ont rol l ed anal g esi a has fac i l i tat ed pai n rel i ef and we ani ng. Opi ate s are rec omme nde d for i ni ti al analge si a . N on-s te roi dal s are parti c ul arl y e ffec ti ve for bony p ai n thoug h may occ asi onall y prec i pi tat e c oag ul opat hi e s, stres s ul ce rat i on and renal fai l ure . Agi tat i on may b e due t o c aus es other than p ai n, e .g. i nfec ti on, i nt rac rani a l l esi on.

Nutrition Earl y nut ri ti on has bee n s hown to re duc e p ost -op erati v e c omp l i c ati ons . T hi s s houl d i de al l y b e e nte ral , an approac h

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whi ch has be en demonst rated to be safe, even after ab dom i nal l aparot omy for t rauma.

Infection Depe ndi ng on the si te of trauma, t he typ e of wound (op en/cl osed , c l ean/d i rt y), and t he need for s urg ery, prophyl ac ti c te tanus and anti b i ot i c cover varyi ng from 1 dos e t o 1–2 week s m ay b e need ed. The trauma pati e nt i s at hi gh ri s k of de vel opi ng sec ond ary i nfec ti on, i n parti cul ar chest , wound si tes , i nt rav asc ul a r c athete r i ns ert i on si tes , p ost -ab dom i nal t rauma, i ntra-ab dom i nal absc ess es. Preve nti ve measures and stri c t i nfe cti on control shoul d be undertak en. Int rav asc ul a r c athete rs i nserted duri ng e mergency res usc i t ati on und er non-ste ri l e condi t i ons s houl d be rep l ac ed.

Prophylaxis Att ent i on shoul d b e p ai d to press ure areas ; t hi s may i nvol ve the us e of s pec i al i s ed m att re sse s or s upp ort be ds. Cl ear i ns tructi ons s houl d be obtaine d from the s urg eon re gardi ng c are of the wound and d rai n s i t es. Esp eci al l y afte r orthopaedi c p roc edures on the p el v i s and l ower l i mb, or i f the p ati ent wi l l rem ai n i mmob i l i se d, hepari n p rop hyl axi s agai nst de ep venous thromb osi s shoul d be i nsti tut ed.

Review Regul ar revi ew of t he pat i ent i s nece ssary to ens ure compl i cati ons are de tec ted and d eal t w i th promp tl y . T hi s may req ui re repe at l ap arotom y, ul t ras ound or C T s canni ng. Lat er com pl i cat i ons i nc l ud e p anc reati t i s , ac al cul ous chol e cys ti t i s , and mul ti p l e org an dys functi on (i ncl udi ng ARD S). P.503

See also: Nut ri ti on—use and i ndi c ati ons , p 78; Spe ci a l s upp ort s urface s, p86; Opi oi d anal g esi cs , p 234; Non-op i oi d anal ges i cs , p236; Ant i c oagul ants , p 248; Anti m i crob i al s, p260; Acut e resp i ratory d i s tre ss syndrome (1), p292; Acute res pi ratory di s tress sy ndrome (2), p 294; Infe cti on—di a gnosi s , p 480; Infec ti on—tre atm ent , p 482; Mul ti pl e traum a (1), p500; Head i njury (1), p504; Head i nj ury (2), p506; Pai n, p532 P.504

Head injury (1) The he ad may be i nj ure d w i th or wi thout si g ni fi c ant traum a t o ot her part s of the b ody . Pri ori ty i n managem ent of the mul ti pl y i njured pat i ent m ust be pl ace d on s ecuri ng adeq uat e gas e xchang e and ci rcul at ory re sus ci t ati on, and d eal i ng wi t h any l i fe-t hre ate ni ng i njury, e. g. an art eri al i njury, b efore defi ni ti ve t re atme nt for he ad i nj ury . The pati e nt wi l l usual l y b e ad mi t te d t o the ICU aft er CT s canni ng has i d ent i fi ed the ext ent of i njury. The ne ck shoul d al s o b e i mag ed by C T, parti cul arl y i f t he pat i ent i s v ent i l ate d. It i s al s o l i ke l y that s urg ery wi l l have b een undertak en for any s i gni fi cant s pac e-occupyi ng l es i on or for e l ev ati on of a d epress ed fracture.

General management An uns tab l e nec k frac ture s houl d be ass umed unti l e xcl ude d b y an ex pert opi ni on and appropri at e i nve sti gati ons. Most he ad i nj ury pati e nts ad mi t ted to non-neurosurgi cal ICUs wi l l have di ffuse or l oc al brai n i njury for whi ch a non-ope rat i ve ap proach has b een adopte d. The Reg i onal Neuros urgery Ce ntre s houl d be contac ted i f rai s ed i nt rac rani al pres sure i s p res ent as l ocal pol i cy may enc ourage earl y bone fl ap de com pre ssi on or re ferral for i nv asi ve m oni tori ng (e.g. i ntracrani al press ure , j ugul ar ve nous bul b O 2 s aturat i on). If a basal sk ul l frac ture i s s usp ect ed (e. g. X-rays , rhi norrhoe a, otorrhoea), avoi d nasal i ns ert i on of fee di ng or endotracheal tubes . Det eri orati on i n c ons ci ous l e vel , d evel opi ng neurol og i cal d efi ci t s or focal s i g ns (e.g . uni l at eral p upi l l ary di l atati on) shoul d promp t urge nt rep eat CT sc anni ng for l ate compl i cati ons, e. g. sub dural hae mat oma.

Complications Act i ve l y manage rai se d i ntracrani al press ure . Act i ve l y tre at sei zures wi th ant i convul sants to preve nt furthe r hypoxaem i c ce reb ral damag e, reduce cerebral oxyg en req ui reme nts and ICP. The pati ent shoul d b e l oade d w i th IV pheny toi n as p rop hyl axi s agai nst furt her fi ts. Cons i de r addi ti onal c aus es suc h as hypogl y cae mi a , de vel opm ent of a new space-occ upy i ng l e si on, rec reati onal drugs and i nfec ti on. Di a bet es i ns i pi dus s ugg est s hypot hal ami c i nj ury and c arri es a poor p rog nos i s. De smopre ssi n 1–4µg IV shoul d be gi v en d ai l y t o m ai ntai n uri ne out put of 100–150ml /h. Act i ve l y manage hyp erp yre xi a . Some st udi es show l ong -te rm benefi t from i nduc ed hypothe rmi a b ut thi s nee ds to

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be aggress i v el y i nsti tut ed as earl y as pos si b l e aft er the i njury t o b e e ffec ti ve. Act i ve l y manage hyp erg l yc aem i a wi t h i ns ul i n, and avoi d hyp ogl ycaemi a. P.505

Key papers Rov l i a s A, K ots ou S. The i nfl uenc e of hy pergl yce mi a on neurol ogi cal outc ome i n pat i e nts wi th sev ere head i njury. Neuros urgery 2000; 46:335–42 Cl i fton GL, M i l l er ER, Choi SC et al . Lack of e ffe ct of i nd uct i on of hy pot hermi a aft er acute brain i njury. N Engl J M ed 2001; 344:556–63

See also: Ant i c onv ul s ant s, p242; Ne uroprote cti ve agents , p 244; Ge neral i sed se i zures , p 372; Intracrani al haem orrhage, p376; Rai sed i ntracrani al pre ssure, p832; M ul t i p l e trauma (1), p 500; Mul t i pl e t rauma (2), p520; He ad i nj ury (2), p 506; Spi nal c ord i njury, p508 P.506

Head injury (2) Analgesia Ade quat e anal ges i a (us ual l y opi ate s) mus t b e g i ve n t o t he head -i njured pat i ent as p ai n and agi t ati on wi l l i nc rease i nt rac rani a l p res sure, the reb y c aus i ng a sec ond ary i nsul t. Short-act i ng se dat i on shoul d b e used as thi s enabl e s rapi d asse ssm ent of the underl y i ng consc i ous l eve l and any focal neurol ogi cal de fi c i t.

Respiratory management Agg res si v e hype rve nti l at i on i s no l onge r rec omme nde d apart from short -te rm managem ent of raise d i ntrac rani al pre ssure. If venti l at ed, ai m t o maintai n t he PaCO 2 at 3.5–4kPa. Face or ne ck i nj uri es may have requi red emergency cri cothy roi dot omy or tracheos tom y t o ob tai n a patent ai rway. If orotracheal l y i ntub ate d, ens ure l ocal sw el l i ng has s ubs i d ed (nas end osc opy , air l eak around defl at ed cuff) b efore extubat i on. Seve re agi tat i on and c onfusi on may l a st for se veral week s; thi s w i l l ofte n de l ay we ani ng and ext ubati on. Judi ci ous se dat i on, e .g. wi t h c hl orp rom azi ne, may be ne ces sary.

Circulatory management Hypotensi on s houl d be avoi de d w i th ad equate fl ui d re sus ci t ati on ± v asopre ssor t herapy . El e vate d b l ood p res sures may be tol erate d unl e ss exc ess i ve . β-bl ock ers may b e useful i n red uci ng the my ocardi al effect s of ex ces si ve c at echol a mi ne l evel s.

Other drug therapy Ant i bi oti c prophy l ax i s i s not routi nel y rec omme nde d. Hi g h-dose ste roi d the rap y has not yet be en shown t o b e b ene fi c i al . Tri al s of ot her ne uroprotec ti v e agents, e. g. fre e radi cal sc ave nge rs, have als o fail ed t o s how be nefi t.

Indications for consideration of intracranial pressure monitoring Indications GCS ≤8 and any ab normal i t y on CT sc an GCS ≤8 and a normal CT scan b ut any tw o of the fol l owi ng: Age >40 ye ars Hypotensi on Dec ere brate pos turi ng GCS >8 but : Requi ri ng ge neral anae st hes i a for treat ment of ot her i njuri e s Requi ri ng treat ment l i ke l y to i nc rease ICP, e .g. hi gh l ev el s of PEEP

Contraindications

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Coag ul opat hy Infe ct i on? ICP moni t ori ng shoul d be conti nue d: As l ong as t he ICP i s el e vat ed Duri ng ac ti v e m anageme nt of ICP For up to 3 d ays i n the ab sence of si g ni fi c ant el evat i on P.507

See also: Venti l at ory support— ind i c ati ons , p 4; Endot rac heal i ntubat i on, p 36; Int racrani a l p res sure m oni tori ng, p134; Jug ul a r venous bul b sat urati on, p136; Hypotensi on, p312; Rai sed i ntracrani al pre ssure, p382; Pai n, p 532 P.508

Spinal cord injury Spi nal i njury, wi th or wi t hout d amag e t o t he cord, may be app are nt soon afte r admi ssi on to hos pi t al ; howeve r, det eri orati on may occ ur, requi ri ng a hi gh i ndex of suspi ci on and careful m oni tori ng.

Immobilisation The spi ne shoul d be i m mob i l i se d unti l a se ni or s urgi c al /ort hop aed i c opi ni on has confi rmed that no uns tab l e frac ture i s pre sent, bot h radi ol ogi cal l y and cl i ni cal l y . Pl ac e a hard cervi c al col l a r i f a ne ck fracture i s pos si b l e . Thi s does not st abi l i s e t he spi ne; ei the r s kul l t racti on or operati ve st abi l i s ati on wi l l be need ed for an unstabl e fract ure . Move the p ati ent by ‘l og-rol l i ng’ or st rai ght -l i fti ng , usi ng at l eas t four st aff mem bers. Exe rci se care w i t h ne ck mani pul at i on; i ntubat i on shoul d b e p erform ed b y an e xpe ri e nce d operator.

Circulatory instability So-c al l ed ‘s pi nal shock’ may oc cur w i th marke d hy pot ens i on due t o s ymp atheti c outfl ow di sturbance . Hypovol aem i a shoul d be exc l uded fi rst . C ons i de r d amage t o othe r organs/ves sel s, e.g . s pl e en, aorta. Vas opress or the rap y m ay b e nece ssary i f evi dence of t i s sue hy pop erfusi on persi s ts , e. g. ol i guri a , m etabol i c aci dos i s. Post ural hyp otensi on and ci rcul at ory i nst abi l i t y (i nc l udi ng s ymp tomati c b rad ycardi a) i s com monpl a ce for the fi rs t few week s. Aut onomi c dy sfunct i on affec ts 50% of ce rvi cal and hi gh thoraci c c ord i njuri es .

Respiratory management Hi g h c erv i cal c ord i njury abov e C5 resul ts i n l oss of di a phragm ati c func ti on, whe reas abov e C8 can resul t i n l oss of i nte rc ost al functi on. Thi s may compromi se or pre vent b reathi ng and weani ng from IPPV. When ab l e, the p ati ent shoul d b e m anaged i n an upri g ht pos ture. Ate l ec tas i s i s common and requi re s regul a r p hys i ot herapy . Earl y trache ost omy may faci l i t ate support and com fort.

General measures Care ful l y moni tor neurol ogi cal funct i on to enabl e e arl y d ete cti on of s pi nal cord com pre ssi on and re ferral for urg ent re medi al surge ry. Gi v e LMW hepari n SC for t hromboemb ol i sm prophy l ax i s . The i nc i d enc e of st re ss ul c erati on i s hi g h. Ide al l y, ent eral nutri t i on shoul d b e i nst i tuted at an earl y st age thoug h thi s m ay p rov e unsucce ss ful . D rug s (e.g . s ucral fate , H 2 bl ocke rs ) may b e neede d. Ent eral feedi ng may be di ffi cul t t o i ns ti t ute i ni t i al l y as gas tri c d i s tensi on and paral y ti c i l eus i s c omm on fol l owi ng spi nal cord i nj ury . A NG tube shoul d be i nserted for g ast ri c d ecompress i on. An e nte ros tom y m ay e ventually be need ed to enabl e l ong-t erm fe edi ng. Bowe l and bl a dde r func ti on m ay be derang ed. Long-t erm si l a sti c b l ad der cathe ters and reg ul ar l ax ati ve and enem a t herapy shoul d b e i nst i tuted at an earl y st age . Spe ci a l c are i s ne ede d t o p rev ent press ure sores . Ins ti t ute re gul ar exe rci se s t o p rev ent contract ure s. Psyc hol ogi cal s upp ort for p ati ent and fami l y i s cruci al , parti cul arl y i f l ong-t erm di sab i l i ty i s l i kel y.

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Hi g h-dose ste roi d the rap y may b e b enefi c i al i f st art ed wi t hi n 8h, t hough thi s sti l l re mai ns controversi a l . Hype rbari c oxyge n t herapy i s of unproved be nefi t. Aft er spi nal i njury, mus cl e rel a xant s m ay cause sev ere hyp erkal aemi a. Ste roi ds hav e b een shown to be useful but t hi s re mai ns controversi al . P.509

Key trial Brack en M B, et al . Ad mi ni s trati on of m ethyl p red ni s ol one for 24 or 48 hours or ti ri l az ad mes yl a te for 48 hours i n the treatm ent of ac ute sp i nal c ord i njury. Res ul t s of t he Thi rd Nat i onal Ac ute Sp i nal C ord Injury R and omi zed Control l ed Tri al . N ati onal Acut e Spi nal Cord Injury St udy . JAMA. 1997; 277:1597–604

See also: Spe ci al sup port s urface s, p86; Bl ood press ure moni t ori ng, p110; H 2 bl ocke rs and proton p ump i nhi b i tors, p218; Suc ralfate, p220; Ant i coagul ants , p248; St eroi ds , p 262; Fl ui d chal l eng e, p274; Hyp ote nsi on, p312; Ac ute weakne ss, p368; Met abol i c ac i dosi s , p 434; Mul t i pl e t rauma (1), p500; Mul ti pl e trauma (2), p502; Head i njury (1), p504; Head i nj ury (2), p506 P.510

Burns—fluid management Maj or the rmal i njuri es (i .e . > 20% bod y s urface area) are ad mi tte d t o an i ntensi ve c are uni t , usually sp eci al i si ng i n the manag ement of b urns, for me ti c ul ous att ent i on t o fl ui d resusci tat i on, pre vent i on of i nfec ti on, and the freq uent nee d for mec hani cal v ent i l a ti on.

Monitoring The fl ui d l oss from major burns requi re s c are ful as ses sme nt of i nt rav asc ul a r v ol ume status . T he tradi t i onal mark ers of fl ui d resusci tat i on i n burns of ce ntral venous press ure, uri ne out put and haematoc ri t are gene ral l y i nadequate . Ei t her i nvas i ve or non-i nvas i v e c ard i ac output m oni tori ng i s ne ede d for acc urate ti t rati on of fl ui d. Thi s i s parti c ul a rl y ap pl i cabl e i n the p res enc e of a hyp erd ynami c , v asodi l ate d c i rcul ati on whi ch oft en com menc es wi t hi n 1–2 day s. Al though i nfec ti on i s not nec ess ari l y present, vas opress or therapy m ay be need ed to mai ntain adeq uat e s yst emi c b l ood p res sures . Pul monary art ery and c ent ral ve nous c athete rs shoul d not b e i nse rt ed t hroug h affec ted sk i n are as i f at al l poss i b l e. Ins ert i on of i ntravas cul ar cat het ers, uri nary c athete rs and NG tubes shoul d b e c arri ed out s oon after ad mi s si on as rapi d ons et s wel l i ng wi t hi n a few hours may make t hes e p roc edures i mpos si bl e .

Fluid management The ext ent of i njury wi l l have been es ti mate d b y p l as ti c s urg eons who w i l l al so det ermi ne t he p roporti on of ful l thi ckness de rmal i njury to cal cul ate the approxi mat e fl ui d resusc i tati on requi red. Fl ui d res usc i tati on i n the UK oft en fol l ows t he M ount Vernon (al bum i n-bas ed) formul a w hi l e t he Parkl a nd (cryst al l oi d -based ) formul a i s oft en use d i n t he US. Col l oi ds may reduce oed ema at non-burn si t es and re store bl ood v ol ume fas ter than cry stall oi d s. Thes e form ul a e onl y provi de an approxi mat e g ui de and fre que ntl y unde res ti mate l oss es b oth i nto the i nte rst i ti al spac es and through the l ost ski n barri e r. Evaporati ve l os ses are approxi mat el y 2m l /k g/h. Water l oss es may be i nc reased i f wounds are not cov ere d. Los ses i ncreas e furt her wi th i nhal a ti on i njury. Overze al ous fl ui d i nfusi on shoul d be av oi d ed to m i ni mi se oed ema. The i nc re ase d pe rme abi l i ty and fl ui d l e ak phas e l as ts app rox i matel y 1–2 d ays . Afte r 2–5 day s, a d i ureti c phas e usual l y c omme nce s w hen ex ces s t i ss ue fl ui d i s l ost and the body swe l l i ng re duc es. El e ctrol y te l ev el s (e spe ci a l l y K + and Mg 2+ ) can fl uc tuate wi d el y i n both peri od s requi ri ng moni t ori ng and rep l ac ement as nece ssary. Though som e haemol ys i s may oc cur, bl ood t ransfusi on req ui reme nts are usuall y l ow, but de bri dem ent wi l l re sul t i n major b l ood l oss often re qui ri ng major t ransfusi on (>8–10 uni ts ). A coagul op athy w i l l often oc cur, i n p art d ue to a di l uti onal effect of the albumi n i nfus i on. P.511

Fluid resuscitation regimen (adapted from Mount Vernon formula) Not e: thi s regi men shoul d b e used as a g ui de onl y. 1. Di v i de fi rst 36h from the t i me of burn i nt o s i x consec uti ve peri od s of 4, 4, 4, 6, 6 and 12h. For eac h p eri od gi ve 0.5m l 4.5–5% al b umi n × body w t [kg] × %burn

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2. Gi v e bl ood as ne ces sary t o m ai ntai n haem ogl obi n > 10g /dl . 3. Comm enc e enteral nutri ti on as s oon as possi bl e 4. Gi v e 1. 5–2ml /kg/h 5% gl uc ose 5. Reas ses s c ard i ores pi ratory vari ab l es and uri ne outp ut at fre que nt i nt erval s t o d etermi ne whet her vol um e rep l ac ement i s i nadeq uat e or ex ces si ve. Ad jus t fl ui d i nput as nece ssary.

See also: Bl ood press ure moni t ori ng, p110; Cent ral ve nous c athete r—use, p114; Col l oi d osm oti c p res sure, p172; Crys tal l oi ds , p176; Col l oi ds, p180; Bas i c re sus ci t ati on, p270; F lui d c hal l e nge , p274; Hy pot ens i on, p 312; Ol i g uri a, p330; Burns —ge neral managem ent P.512

Burns—general management Surgery Esc harotomy m ay be need ed on hos pi t al adm i ss i on t o affec ted l i mbs , as w el l as to the neck and /or chest i f a ci rcum ferent i al burn i s prese nt. Debri d eme nt of necroti c ti s sue i s often be gun wi thi n t he fi rst few days as e arl y g rafti ng i s ass oci ate d w i th i mp rov ed outc ome . Cove rag e i s obtaine d usi ng e i ther spl i t sk i n grafts from the pati e nt' s own unaffec ted sk i n, donor sk i n grafts or even ex peri me ntal ‘ ski n’. Bl ood l os s m ay b e rapi d and mas si v e, e.g . 100m l p er 1% of b ody surface grafte d.

Wound care Earl y appl i c ati on of dre ssi ngs and F lam azi ne (si l ve r s ul p had i azine) c re am w hi c h has ant i -b act eri al prope rti es agai ns t G ram neg ati ve bac teri a may us eful l y preve nt sec ond ary i nfec ti on. Earl y grafti ng oft en t ake s p l ac e w i thi n the fi rs t 2–3 days t o provi de a s ki n prote ct i ve barri er.

Nutrition Ent eral nutri ti on shoul d b e comme nce d s oon aft er adm i s si on as s tud i es have s how n t hat earl y enteral nut ri ti on i mp rov es outc ome . Target i ntak e i s p rot ei n of 1g/kg + 2g/%b urn and a calori e i nt ake of 20Cal /kg + 50Cal /%b urn.

Infection Prop hyl ac ti c anti b i ot i c s are oft en not gi v en to burn p ati ent s. Bod y te mpe rat ure ri se s on d ay 1–2 as hi g h as 40°C , m ay p ers i s t for sev eral d ays and does not i ndi c at e sec ondary i nfect i on. Li k el y i nfec ti ng agents i nc l ude s trept ococci , s tap hyl ococci and Gram ne gat i ve bacte ri a such as Pseudom onas. App rop ri a te ant i bi ot i c tre atm ent shoul d b e g i ve n as i ndi cat ed.

Other considerations Any suspe cte d i nhalat i on i njury s houl d be di a gnosed and t reated . Ens ure ade quate analge si a (opi a tes ). Ketami ne i s a us eful anae stheti c as i t has analge si c prop ert i es i n ad di t i on. Tetanus toxoi d s houl d be gi v en soon after hosp i tal admi ssi on. Reduce heat and fl ui d l os ses by pl aci ng the pati e nt on a heate d air fl ui d i se d b ed and by earl y cov erage of b urnt ski n t hrough ap pl i cat i on of oc cl usi ve d res si ngs and p l ac ement of affe cte d l i mb s i n t ransparent p l asti c b ags . Stress ul cerat i on can us ual l y be avoi de d t hrough promp t resusc i tati on and earl y ent eral nutri t i on. Pres sure sores and contract ure s s houl d be pre vented by careful nursi ng and phy si othe rap y. Sux amet honi um shoul d b e avoi ded from 5–150 d ays ' p ost -burn bec aus e of t he ri s k of rapi d and s eve re hype rkalae mi a . Inc reasi ng resi st anc e t o non-d epol ari si ng mus cl e rel a xants may be see n. β-bl ock ade has b een ass oc i at ed wi t h outc ome i mp rov eme nt i n chi l d ren sustaini ng burn i nj ury . P.513

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See also: Ent eral nut ri t i on, p 80; Spe ci a l s upp ort surfaces , p 86; Opi oi d anal g esi cs , p 234; Non-opi oi d anal ges i cs , p 236; Muscl e rel axants , p 240; Anti mi crobi a l s, p260; Hyp erk al a emi a, p 420; Infe cti on control — gene ral p ri nci p l e s, p476; Infect i on—di ag nos i s, p480; Infect i on—treat ment, p482; Burns—fl ui d managem ent , p 510; Py rex i a (10; Pyre xi a (2), p520; Rhab dom yol ysi s, p528; Pai n, p532

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Ed itors: Si nge r, M ervyn; We bb, An dre w R. Ti tle : O xf ord Ha ndbook of Cr itic al Car e, 2nd Ed ition Cop yri ght © 1997,2005 M. Si nge r and A. R. W ebb , 1997, 2005. Publ i shed i n the Uni te d Stat es by Oxford Uni ve rsi ty Press Inc > Tab le of Co n te n ts > P h y sica l Diso r d er s

Physical Disorders Hypothermia Clinical features Above 33°C —shi ve ri ng i s usual l y m ark ed i n an att emp t t o c orrect body temp erature. Bel ow 33° C—ne urol og i c al si g ns of dys art hri a and sl owne ss app ear. Bel ow 31° C—hy pertoni c i ty and s l ug gi s h refl exe s w i th cardi ovascul a r d ysfunc ti on b ecome l i fe t hre ate ni ng. Bel ow 28° C—arteri a l p ul s es oft en bec ome i mp al pabl e. Hyp otherm i c ri gi d i t y i s d i ffi cul t to di s ti ngui sh from death. Prog nos i s de pend s on t he deg ree and d urati on of hy pot hermi a.

ECG changes Si nus brady cardi a i s fol l owed by at ri a l fl ut ter and fi bri l l at i on wi th ventri cul ar ec top i cs . T he PR i nt erv al , QR S c omp l ex and QT i nterval are p rol ong ed. At ri al act i vi ty eve ntual l y c eas es. The ‘ J’ wave i s most oft en see n <31° C and ventri cul ar fi bri l l ati on i s com mon <30°C , gi vi ng way to asy stol e <28°C.

Complications Hyp oxaemi a i s c ommon d ue to hyp oventi l at i on and v ent i l a ti on–p erfusi on mi s mat ch. Hy pov ol a emi a and metabol i c aci dos i s are c ommon. Renal tub ul a r d amage m ay res ul t from renal bl ood fl ow reducti on. Ac ut e pancreat i t i s, rhabdomyol ys i s and gastri c erosi ons are c omm on.

Management 1. Oxyg en (FIO 2 0.6–1. 0) t o m ai ntai n SaO 2 >95%. 2. Fl ui d rep l ac eme nt wi t h c are ful moni t ori ng. 3. Rewarmi ng— Al l hypot hermi c p ati ent s w i th no ev i de nce of other fat al di s eas e s houl d be ass ume d ful l y rec overabl e. In the ev ent of cardi ac arrest ful l re sus ci t ati on shoul d c ont i nue unti l t he pat i ent i s normothermi c (ventri cul ar fi bri l l ati on i s res i s tant t o d efi bri l l ati on bet ween 28 and 30°C ). T he tec hni que us ed for re warmi ng depe nds on the c ore te mpe rat ure (me asured wi th a l ow readi ng rect al the rmomet er) and t he cl i ni c al ci rcum stance .

Rapid central rewarming In cas es whe re the te mperat ure i s <28°C (<33°C wi th acute exp osure hypothe rmi a), or where there i s cardi ac arres t, rap i d re warm i ng may b e achi eve d by pe ri toneal di al y si s , g ast ri c or b l ad der l a vag e wi th warmed fl ui d s. The se tec hni ques m ay achi ev e rewarmi ng rat es of 1–5° C/h. Act i ve surface rewarmi ng wi t h a he ate d b l anket or warm air bl a nke t c an achi ev e rate s of 1–7° C/h and i s l e ss i nvasi ve. Haemodynami c c hanges may be dramati c duri ng act i ve rew arm i ng , requi ri ng careful moni tori ng and sup port. If ext rac orporeal re warmi ng i s avai l ab l e, rates of 3–15° C/h may be achi ev ed wi t h t he addi ti on of c ardi ovas cul ar sup port.

Spontaneous rewarming Spontaneous rew arm i ng proce eds at a rat e i nve rse l y proporti onal t o the d urati on of hypothe rmi a. Wi t h g ood i ns ul ati on (sp ace bl anke t), re warmi ng rate s of 0.1–0.7°C/h c an b e achi eve d. Core t empe rat ure may fal l duri ng spontaneous rew arm i ng as col d bl ood i s ret urned from t he peri phery to the c ent ral ci rc ul a ti on.

Causes of hypothermia Coma and i mmob i l i ty Col d water i m mersi on

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Exposure Hypothy roi di sm Hypopi t ui tari sm Sep si s Ery throde rma P.517

See also: Venti l at ory support— ind i c ati ons , p 4; Endot rac heal i ntubat i on, p 36; Defi bri l l at i on, p 45; Peri toneal d i al ysi s, p66; EC G moni tori ng, p108; Bas i c res usc i t ati on, p270; Card i ac arres t, p272; F lui d c hal l e nge, p274; Tachy arrhyt hmi as, p316; Bradyarrhyt hmi as, p318; Pancre ati ti s , p 354; Thyroi d eme rge nci es , p 446; Rhabd omyol ys i s , p 528 P.518

Pyrexia (1) Mec hani sm s unde rl yi ng a ri se i n tem perature are poorl y unde rst ood . It refl ect s t he bal anc e b etw een heat l oss and heat p rod uct i on. T here m ay be i nabi l i ty to l ose heat (e.g. hi gh amb i ent t emp erature), ‘t hermos tat ’ d ysreg ul a ti on wi t hi n t he hypothalam us or i nc re ased he at generati on (e.g . d ue t o m i tochondri a l uncoupl i ng ). The re i s som e l ab oratory e vi d enc e t hat a rai sed te mpe rat ure may b e be nefi ci al i n te rms of whi te cel l res ponse, he at s hoc k p rot ei n act i vati on and mi t ochond ri al protec ti on. Sep ti c p ati ent s p res ent i ng wi th a l ow tem perature hav e a poorer prognosi s. An exc ess i ve te mpe rat ure may b e unpl eas ant to the pati e nt (e. g. ri g ors ), wi l l i nc rease met abol i c rate and there fore oxy gen dem and , m ay i nd uce exc es si v e vasod i l atati on and sal t and wate r l os s. At very hi gh te mperat ure s, bi oche mi c al functi on i s di srupte d w i th al tered enzyme funct i on and i ncreas ed cel l b reakdown (e.g . rhab dom yol ysi s).

Causes Infection The commones t c aus e i n t he ICU pat i ent, though ov er-di a gnosed . Main si tes are c hes t and i nt rav asc ul a r c athete r si tes . Uri nary tract i nfec ti ons are di ffi cul t to di a gnose i n the prese nce of a uret hral cat het er. Si mi l arl y, the res pi rat ory tract i s rout i ne l y col oni sed wi th bac teri a wi t hi n a few days of ICU admi ss i on; d i ffere nti ati on bet wee n col oni si ng and pat hog eni c bac teri a i s di ffi c ul t. See k malari a i n pati e nts who have vi s i t ed e nde mi c areas . Anti bi oti c the rap y m ay i ts el f be a c aus e of p yre xi a .

Inflammation Infl am mat i on unrel ate d t o i nfe cti on wi l l usual l y g ene rat e a pyrexi c res ponse, e.g . s yst emi c i nfl am mat ory re sponse syndrome, post-cardi a c s urgery, p ost -burns, pos t-my ocardi al i nfarcti on, vascul i ti s , g l om erul onephri ti s , hepati t i s , acalcul ous chol ec yst i ti s. Ot her than spe ci fi c the rap y, e.g . i mmnosuppress i on for v asc ul i ti s, managem ent i s ge neral l y sym ptom-ori e ntated to i ncl ude cool i ng.

Adverse drug reaction Num erous drugs may i nduc e an i di osyncrati c p yre xi a , i ncl udi ng ant i b i ot i cs , s edati v es, paral ysi ng age nts , and amp het ami nes . Usually re mov al of t he offend i ng drug i s suffi c i e nt but more acti ve measures may have t o b e t ake n, i nc l udi ng acti ve cool i ng and dantrol ene.

Adverse reaction to blood transfusion Thi s m ay be rel ate d t o an i mmunol ogi cal re act i on to one of the c el l ul ar consti tue nts , or t o c ont ami nat i on wi th an org ani sm, bacte ri al cel l p rod uct s or other pyrogen.

Ambient heating Exc ess i ve he ati ng or pre venti on of heat l oss may cause pyrexi a. Consi d er strong sunl i ght, exc ess te mpe rat ure control set ti ngs on sp eci al i sed be ds or mat tre sse s, and he at-ret ai ni ng be d c l ot hi ng.

Miscellaneous Other causes of py rex i a i nc l ude neop l as m and pos t-c ere bral i nsul t (e. g. head i njury, ce reb rov asc ul a r acc i de nt). P.519

Key paper C i rci umaru B, e t al. A p ros pec ti ve s tud y of fever i n t he i nt ens i ve care uni t. Int ens i ve Care Med 1999; 25:668–73.

P.520

Pyrexia (2) At prese nt, the op ti mal te mperat ure to targe t i n d i se ase st ate s i s not known, other than c ere bral i ns ul t s w here normo- or eve n hypothe rmi a appe ars to offer neurop rotec ti on b y reduci ng c ere bral m etabol i c rate. In other condi ti ons i t see ms reasonabl e t o acce pt mi l d p yre xi a provi ded thi s i s tol erate d b y t he p ati ent.

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Principles of management 1. Di a gnose t hen remov e or t reat t he offe ndi ng cause. For e xam pl e , s eek and treat i nfec ti on, st op b l ood i nfusi on and send d i sc ont i nued bag to l a boratory for anal y si s , use ant i -i nfl amm atory ± i mmunos upp res si v e agents for vasc ul i ti s. 2. Cool i ng ai ds sym ptomat i c re cove ry, reduc es met abol i c rate and l owers p res sor requi re ments: Increas e e vaporat i v e l oss es, e. g. t epi d spongi ng, wet sheet s, i c e packs Increas e c onv ect i ve l osse s, e.g . fanni ng to i m prove air ci rcul at i on Anti pyreti cs , e .g. parac etamol , as pi ri n, c hl orp rom azi ne M ore agg res si ve cool i ng i f t emp erature > 40° C Ai m to l ow er tem perature to <38. 5° C then reasse ss. P.521

See also: Bac teri ol og y, p158; Vi rol og y, serol ogy and ass ays , p 160; Bl ood t ransfusi on, p182; Ant i mi crobi al s , p 260; Acute che st i nfect i on (1), p288; Acute che st i nfect i on (2), p 290; Abdomi nal sep si s , p 350; Infect i on—d i ag nos i s, p480; Infect i on—t reatment, p482; Sys tem i c i nfl am mat i on/mul ti -organ failure, p484; Mal a ri a, p490; Vasc ul i ti des , p 494; Burns —ge neral managem ent , p 512; Pyre xi a (1), p 518; Hype rtherm i a, p522; Post-operat i ve i ntensi v e c are , p 534 P.522

Hyperthermia Hyp ert hermi a i s d efi ned as a c ore te mpe rat ure ab ove 41° C.

Clinical features Del i ri um and se i zures are associ ate d wi th tem perature s of 40–42°C Coma i s as soc i at ed wi t h t emp eratures above 42° C Tachycard i a Tachypnoea Sal t w ater d epl eti on Rhab dom yol ysi s Di s sem i nated i ntravas cul ar coagul at i on Heart fai l ure wi th ST de pre ssi on and ‘T ’ w ave fl a tte ni ng

Causes Hype rt hermi a may be an ext re me form of pyrog en-i nduced fe ver as soc i at ed wi t h i nfe cti on, i nfl ammati on, neop l as m or c ere brovas cul ar ac ci d ent . Heat st roke i s ass oci ate d wi th se vere ex erc i s e i n hi gh envi ronm ent al tem peratures and humi di t y. The re may be exce ss cl othi ng or hy povol ae mi a re duc i ng t he b ody 's abi l i ty to di s si p ate he at produc ti on. Mal i gnant hyp erthe rmi a i s a drug-i nd uce d m yopathy as soc i at ed wi t h a he red i tary cal ci um transfer defect i n pati ents rec ei v i ng vol at i l e anaes the ti c s, mus cl e rel a xants, anti d epress ant s, al c ohol or Ecs tas y. Heat product i on i s i nc reased by muscl e c atabol i sm , s pas m and peri pheral v asoconstri c ti on. The neurol ept i c mal i g nant s ynd rom e i s a drug-i nd uce d hypertherm i c syndrome sec ond ary to phenot hi azi nes or but yrophenone s. It i s as soc i at ed wi t h m usc l e ri g i d i ty , aki nesi a, i mp ai red consci ous nes s and aut onomi c dysfunc ti on and conti nue s for 1–2 wee ks.

Management 1. Rapi d c ool i ng s houl d be i ns ti t ute d w hen te mperat ure s e xcee d 41°C . 2. Sup porti v e t reatme nt i nc l ud es fl ui d re pl a cem ent and se i z ure control . 3. Cl ot hi ng shoul d be re move d and pat i ents shoul d be nurse d i n a cool env i ronme nt. 4. Surfac e c ool i ng may be ac hi e ved wi th a fan, tep i d spongi ng , we t s hee ts, i c e p ack s or a cool bat h. 5. Hand l i ng shoul d be mi ni m i se d and act i ve cool i ng measures shoul d be st opp ed when the c ore te mpe rat ure i s <39° C. 6. Int ernal cool i ng m ay be c ons i d ere d b y gastri c l a vag e or p eri toneal l a vag e us i ng c ool ed fl ui ds . 7. Phenothi az ines may be use d t o reduce temp erature and prevent s hi veri ng (not i n neurol ept i c mal i gnant synd rome).

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8. Musc l e re l ax ant s s houl d be use d i f t he p ati ent i s v ent i l a ted . 9. For mal i gnant hy perthe rmi a t he offend i ng drug shoul d be st opp ed and dantrol e ne 1mg/kg gi v en IV eve ry 5mi n t o a maxi m um dos e of 10mg/kg. 10. Mechani cal ve nti l a ti on w i th hi gh FIO 2 and t reatme nt of hyp erk al a emi a are requi red. 11. The neurol ept i c mal i g nant s ynd rom e i s t reated by st opp i ng the offendi ng d rug, g i v i ng dantrol e ne as abov e, and dopami ne agoni st s (e.g . L-dopa or b romocri p ti ne). P.523

See also: Venti l at ory support— ind i c ati ons , p 4; Bl ood press ure moni t ori ng , p 110; Coag ul ati on moni tori ng, p156; C ol l oi d s, p180; Sed ati ves , p 238; M usc l e rel axants , p 240; Basi c res usc i tati on, p270; Fl ui d chal l eng e, p274; Hyp ote nsi on, p312; Agi tati on/c onfusi on, p370; Generalis ed sei zures , p 372; Met abol i c ac i dosi s, p434; T hyroi d eme rg enc i es , p 446; Amp het ami nes i ncl udi ng Ecs tas y, p462; Pyre xi a (1), p 518; Pyre xi a (2), p520; Rhab dom yol ysi s, p528; Pos t-operati ve i nt ens i v e c are , p534 P.524

Electrocution The effec ts of e l ec trocuti on are due to the effec ts of the curre nt and the c onv ers i on of el ect ri c al ene rgy to he at ene rgy on passage t hroug h t he t i s sue s. Imp ort ant factors are : Energy del i v ere d—heat = ampe rag e 2 × resi stance × ti m e, i .e . t he ampe rag e i s t he mos t i mport ant det ermi nant of heat producti on. Resi st anc e t o current fl ow–ti s sue s are res i s tant t o c urrent fl ow i n the fol l owi ng d ecreas i ng order: b one, fat, tend on, sk i n, muscl e, bl ood ves sel s, nerves . A hi gh sk i n res i st anc e and short durati on of contac t c onc ent rat e t he effe cts l ocal l y . Howev er, sk i n contam i nants , m oi s ture and burni ng red uce re si s tance. Type of curre nt— al t ernat i ng curre nt i s more d ang erous than d i rect curre nt. Te tani c mus cl e contrac ti ons may pre vent the v i ct i m from rel eas i ng the c urrent sourc e w hereas the s i ng l e, st rong m usc l e contract i on wi th di rect current ofte n t hrows the vi cti m c l ear. Al ternat i ng current i s more l i k el y to re ach ce ntral ti s sues w i t h c ons eque nt sus tai ned ap noea and v ent ri c ul ar fi b ri l l a ti on (w i t h as l i tt l e as 50–100mA for 1–10m s). Current p athway— cardi ore spi rat ory arres t i s more l i ke l y the cl ose r t he contac t i s w i th the c hes t and heart. Li ght eni ng stri ke di ffe rs from c ont act el ect rocut i on i n that hi g h i nte nsi ty , ul tra-s hort d urati on of c urrent may p rod uce cardi ac arrest wi th l i t tl e t i ss ue des truct i on.

Clinical features Tachyarrhythmi a s—i ncl udi ng ventri cul ar tachy cardi a and fi bri l l at i on. Asy stol e— more l i ke l y wi t h hi gh current (>10A). Myoc ard i al i njury— heat i njury, coronary artery s pas m, arrhyt hmi as, my ocardi al spasm. Resp i ratory arrest —te tani c contract i on of the di aphragm, arrhy thm i as , c ere bral m edul l a ry dys functi on. Trauma— tet ani c mus cl e contract i on, fal l i ng or b ei ng t hrown c l e ar. Burns— to ski n and i nt ernal ti ssues.

Management Mos t s eve re el e ctri c al i nj uri es req ui re urg ent fi el d treat ment p ri or t o hosp i t al admi ss i on. 1. The fi rst pri ori t y i s t o ensure that t he s ource of the el ect ri cal i njury i s not a hazard to res cue rs. 2. Managem ent of cardi ore spi rat ory arre st. 3. Prev ent i on of further i nj ury, e .g. sp i nal p rotec ti on, rem oval of sm oul deri ng c l ot hes Aft er hos pi tal ad mi s si on and res torati on of the ci rc ul a ti on m anag eme nt i s di rec ted towards the com pl i cati ons. 1. Mai ntai n vent i l atory sup port. 2. Managem ent of hyp ovol ae mi a as soc i at ed wi t h b urn i njury. Fl ui d req ui rem ent s are usual l y g reater than for vi c ti m s of t hermal burns and requi re cl ose moni t ori ng . 3. Chec k c ard i ac enzym es for de gre e of my ocardi al i njury. T re at heart fai l ure and/or arrhyt hmi as as i nd i cated . 4. Managem ent of rhabdomyol ys i s and covert c omp art ment s ynd rom e. 5. Surgi c al deb ri deme nt of nec rot i c ti ssue and fi x ati on of b ony i njury. P.525

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See also: Venti l at ory support— ind i c ati ons , p 4; Endot rac heal i ntubat i on, p 36; Defi bri l l at i on, p 52; Cardi a c func ti on t est s, p150; Bas i c re sus ci t at i on, p 270; C ard i ac arre st, p272; Fl ui d challe nge , p 274; T achyarrhy thm i as , p 316; Ac ute coronary syndrome (1), p320; Acut e c oronary s ynd rom e (2), p322; Burns—fl ui d manage ment, p510; Burns—g ene ral manage ment , p 512; Rhab dom yol ysi s, p528 P.526

Near-drowning Fol l ow i ng ne ar-drowni ng the maj or com pl i cati ons are l ung i nj ury , hypothe rmi a and the effect s of p rol ong ed hyp oxi a. Al though hyp othermi a bes tow s p rot ect i v e effec ts agains t organ d amage, re warmi ng c arri es parti cul ar hazards.

Pathophysiology Prol onged i m mersi on usuall y resul ts i n i nhal at i on of fl ui d ; howev er, 10–20% of pati e nts de vel op i nt ens e l aryng osp asm l e adi ng to so-cal l ed ‘d ry drowni ng’ . T radi t i onal l y, fre sh wat er drowni ng was consi dered to l ead t o rapi d abs orp ti on of w ate r i nto the c i rc ul ati on wi t h haemol ys i s , hypo-osm ol a l i ty and pos si bl e el ect rol yte di st urb anc e whe reas i nhalat i on of hy pertoni c fl ui d from s ea wat er drowni ng produc ed a marke d fl ux of fl ui d i nto the al veol i . In pract i ce , t here s eems t o be l i tt l e di s ti nct i on be twee n fres h and sea wat er as bot h c aus e l oss of surfactant and se vere i nfl am mat ory di srupt i on of the al veol ar-capi l l a ry memb rane l ead i ng t o an AR DS-typ e p i ct ure. Ini ti a l l y, haem ody nami c i ns tabi l i ty i s often mi nor. A si mi l ar pi ct ure oft en dev el ops aft er ‘dry d row ni ng’ and subse que nt end otracheal i nt ub ati on. Ac ute hyp otherm i a oft en acc omp ani es near-d rowni ng wi th l oss of c ons ci ous nes s and haem ody nam i c al t erati ons .

Management 1. Oxyg en— FIO 2 0.6–1 s houl d be gi v en, ei the r b y face mas k i f t he pat i ent i s s pontaneousl y breat hi ng, or vi a mechani cal ve nti l a ti on. Comatos e p ati ent s s houl d be i ntub ate d. Earl y CPAP or PEEP may be use ful . 2. Bronchosp asm i s often prese nt and may re qui re neb ul i se d β 2 agoni s ts, and ei ther neb ul i sed or SC ep i ne phri ne . 3. Fl ui d rep l ac eme nt shoul d be di rec ted by app ropri ate moni t ori ng. Inotrope therapy may be nec ess ary i f hypoperfus i on pe rs i st s afte r adeq uat e fl ui d resusci tat i on. Int rav asc ul a r fl ui d overl oad i s unc ommon and the rol e of e arl y d i uret i c the rap y wi th a v i ew to l oweri ng i ntracrani al pre ssure i s controve rsi al . Haemol ys i s may oc cur and req ui re bl ood t ransfusi on. 4. Arrhyt hmi as may ari se se condary t o m yocard i al hy poxi a, hyp otherm i a and el ect rol yt e ab normal i t i es . T hes e shoul d be treat ed c onv ent i onal l y. 5. Metabol i c ac i dosi s may b e profound , b ut sod i um bi carbonate therapy i s rarel y i ndi cat ed as the ac i dosi s wi l l usual l y c orrect on re storat i on of ad equate ti ssue p erfusi on. 6. El e ctrol y te abnorm al i ti es are usual l y mi nor and shoul d b e manag ed convent i onal l y. 7. Rewarmi ng fol l ow s c onv ent i onal practi ce; cardi opul m onary b ypass may be consi dered i f core t emp erature i s <30° C. Cardi opul monary re sus ci tat i on i ncl udi ng cardi a c m ass age shoul d b e c ont i nued unt i l normot hermi a i s achi eve d. 8. Cere bral p rotec ti on usually fol l ows rai sed i ntracrani al pre ss ure protocol s t hough, as menti one d ab ove , t he rol e of di uret i c the rap y and fl ui d res tri ct i on i s c ont rov ers i al . Si g ns of b rai n d amage suc h as s ei z ure s m ay bec ome apparent and shoul d be treat ed as the y ari s e. 9. Ant i bi oti c the rap y (e .g. cl i ndamy ci n, or c efurox i me pl us met roni d azol e) shoul d be gi ven i f st rong e vi d enc e of aspi rati on e xi s ts. Ot herwi se, tak e s pec i me ns and treat as i ndi c at ed. 10. Dec ompres s t he s tomach us i ng a nas ogastri c tube to l es sen any ri sk of asp i rati on. Enteral fee di ng c an be i ni ti a ted afterwards. P.527

See also: Venti l at ory support— ind i c ati ons , p 4; Endot rac heal i ntubat i on, p 36; Pos i ti ve end ex pi ratory pre ss ure (1), p 22; Pos i t i ve end ex pi ratory pre ssure (2), p 24; Conti nuous p osi ti ve ai rway press ure , p 26; Bronchodi l at ors , p 186; Anti a rrhythmi cs, p204; Ant i mi crobi al s , p 260; Ac ute re spi rat ory di st res s s ynd rom e (1), p292; Acut e resp i ratory di s tre ss syndrome (2), p294; Met abol i c ac i dosi s , p 434; Hy pot hermi a, p 516 P.528

Rhabdomyolysis Breakd own of st ri a ted muscl e w hi c h m ay res ul t i n compartm ent sy ndrome , acut e renal fai l ure and e l ec trol yt e abnorm al i ti es (hyp erk al a emi a, hyp ocalcaemi a, hyp erp hos phatae mi a ).

Causes Trauma, es pec i al l y crush i njury Prol onged i mm obi l i sat i on, e .g. after fal l , drug ove rdose

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Drugs, e. g. opi ate s, Ecs tas y Hype rpy rex i a Vas cul ar occ l us i on (i nc l ud i ng l e ngt hy vas cul ar surge ry) Infe ct i on Burns/el e ctrocuti on Cong eni tal my opathy (rare )

Diagnosis Sug ges ted by di sproporti onatel y hi gh se rum creat i ni ne compared to urea (usual rat i o i s app roxi m atel y 10µ mol :1mm ol ). Rai s ed creati ne ki nas e (usuall y >2000IU/l ). Myog l ob i nuri a—t hi s produces a pos i ti ve uri ne di pst i ck to bl ood ; l aborat ory anal y si s i s requi re d t o c onfi rm myog l ob i n rat her t han bl ood or hae mog l ob i n. The uri ne i s usuall y red or bl a ck but may ap pear c l ear d esp i te si g ni fi cant rhabdomyol ys i s.

General management Prom pt fl ui d re sus ci t ati on. Hypocal cae mi a shoul d not be tre ate d unl e ss the pati e nt i s sym ptomat i c ; ad mi ni s tered cal ci um m ay form crys tal s wi t h t he hi g h c i rc ul a ti ng phos phate. Hype rkalae mi a may b e resi stant to med i cal m anageme nt and re qui re urgent haemodi a l ys i s or haem o(d i a)fi l trati on.

Compartment syndrome Sus pec t i f l i mb i s te nde r or p ai nful and p eri pheri es are cool . Loss of peri pheral p ul s es and te nse muscl es are l a te si g ns. Manomet ry i n mus cl e compartm ent s reve al pre ssure s >20–25mm Hg. Arm , l egs and b utt ock compartm ent s may b e affec ted . Managem ent i nvol ves ei the r p rop hyl act i c fas ci otomi e s i f at hi gh ri sk or cl ose moni tori ng (i ncl udi ng regul ar manomet ry) wi th dec ompres si on i f p res sures exc eed 20–25mmHg. Fasc i ot omi es may re sul t i n major b l ood l oss .

Renal failure Renal fai l ure i s t hought to be produc ed by a c omb i nati on of free rad i c al i nj ury , hypovol aemi a, hyp ote nsi on and , poss i b l y, my ogl obi n b l oc ki ng t he renal tub ul e s. Renal fai l ure may b e p rev ent ed b y p rom pt rehydrati on and a forced al kal i ne di ure si s wi th 6–10l 0. 9% s al i ne /day for 3–5 days, ai mi ng t o p rod uce an eq ui v al e nt amount of uri ne. The uri nary pH shoul d b e m ai ntai ned ≥6 and bl ood p H < 7.5 us i ng up to 500ml /h 1.24% s odi um bi c arbonate sol ut i on to i ncre ase uri nary exc ret i on of myog l ob i n. Furos emi de and /or manni tol may be ne ede d t o av oi d fl ui d ov erl oad and p otassi um, sodi um, cal ci um and mag nes i um l e vel s regul arl y moni t ore d and m anaged as app ropri ate . If renal fai l ure i s e stabl i shed, di al y si s or fi l trat i on te chni ques wi l l b e requi red, us ual l y for a p eri od of 6–8 we eks. P.529

Key paper Bet ter OS, Ste i n JH. Earl y manag ement of s hoc k and p rophyl axi s of acut e renal fai l ure i n t raumat i c rhabdomyol ys i s. N Eng l J Me d 1990; 322:825–9

See also: Hae mo(d i a)fi l trati on (1), p62; Haemo(di a )fi l trat i on (2), p 64; Pe ri t one al di al y si s , p 66; Uri nal ysi s, p166; Sod i um bi c arbonate, p178; Di ureti cs, p212; Ol i guri a, p330; Acute renal fai l ure—d i ag nos i s , p 332; Acute renal fai l ure—managem ent , p 334; Poi s oni ng—general p ri nci pl e s, p452; Am phet ami nes i ncl udi ng Ecs tas y, p462; C ocaine , p464; Mul ti p l e trauma (1), p500; M ul t i p l e trauma (2), p 502; Burns—fl ui d m anagem ent , p 510; Burns —ge neral manage ment , p 512; Hyp ert hermi a , p 522; El ec trocut i on, p 524

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Ed itors: Si nge r, M ervyn; We bb, An dre w R. Ti tle : O xf ord Ha ndbook of Cr itic al Car e, 2nd Ed ition

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Cop yri ght © 1997,2005 M. Si nge r and A. R. W ebb , 1997, 2005. Publ i shed i n the Uni te d Stat es by Oxford Uni ve rsi ty Press Inc > Tab le of Co n te n ts > P ai n a n d P o st- ope r at ive I n ten siv e C ar e

Pain and Post-operative Intensive Care Pain Pai n resul t s from many i nsul t s, e.g . t rauma, i nvasi ve proced ures, sp eci fi c organ di sease and i nfl a mmatory p roc ess es. Pai n rel i ef i s nec es sary for p hys i ol og i cal and psy chol og i cal reas ons : Anx i et y and l ac k of sl eep . Inc reased sy mpat het i c ac ti v i ty contri b uti ng to an i nc reased me tab ol i c d emand. The cap aci ty of the ci rc ul a ti on and res pi ratory sys tem to me et the dem and s of m etab ol i si ng ti s sues may not be adeq uat e. Myoc ard i al i schaem i a i s a s i gni fi cant ri s k. The end ocri ne resp ons e to i njury i s exag gerate d w i th conse que nt sal t and wat er ret ent i on. Phys i ol og i cal atte mpt s t o l i mi t p ai n may i ncl ud e i mmob i l i ty and musc l e spl i nt i ng and c ons equent re duc ti ons i n vent i l atory functi on and cough.

Pain perception The de gre e of ti ss ue damage i s rel at ed t o t he mag ni t ude of the p ai n st i mul us . T he si t e of i njury i s al s o i mport ant ; thorac i c and up per ab dom i nal i njury i s more p ai nful t han i njury el se where. How eve r, the perce pti on of p ai n i s dep end ent on ot her fac tors, e. g. s i m ul t ane ous se nsory i np ut, pe rsonal i t y, c ul tural bac kground and pre vi ous exp eri enc es of pai n.

Management of pain Systemic analgesia Opi oi d anal g esi cs form t he mai nst ay of anal ges i c drug tre atm ent i n i ntensi v e c are . Smal l , frequent IV doses or a conti nuous i nfusi on p rov i de the m ost st abl e b l ood l eve l s. Si nc e the d egree of anal ges i a i s de pend ent on bl ood l e vel s i t i s i mp ort ant that the y are m ai ntai ne d. Hi g her doses are requi re d t o t reat rather than p rev ent pain. The dos e of d rug re qui red for a parti cul ar i ndi v i dual dep end s on t hei r p erc ept i on of pain and whe the r t ol erance has bui l t up to previ ous anal g esi c use. The use of non-op i oi d d rugs may avoi d the ne ed for or red uc e the d ose re qui red of op i oi d d rug s. Thi s i nc l ud es paracet amol and non-st eroi dals, ke tam i ne and α 2 -ag oni sts such as cl oni di ne and d exm ede tom i di ne.

Regional analgesia Regi onal t echni ques reduce res pi ratory dep res si on b ut req ui re expe ri enc e t o ensure p roced ure s are performed safe l y. Epi dural analge si a may be ac hi e ved wi th l oc al anaest het i c age nts or op i oi ds . Opi oi d s avoi d t he vasodi l at ati on and hyp ote nsi on ass oc i at ed wi t h l ocal anaes theti c agents but do not prod uce as profound anal ges i a. The com bi nati on of opi oi d and l ocal anae stheti c i s s yne rg i st i c. Int rav enous opi oi d s s houl d be avoi ded or cl os e moni t ori ng shoul d c ont i nue for 24h aft er ce ssati on of ep i d ural opi oi d s d ue t o t he pot ent i al for l at e resp i ratory fai l ure . Samp l e reg i me ns are shown op pos i te . Loc al anae st het i c age nts may be us ed to bl ock sup erfi ci al nerves , e .g. i ntercostal nerv e b l oc k wi th 3–5ml 0. 5% bupi vac ai ne p l us adre nal i ne .

Non-pharmacological techniques Ade quate exp l anati on, posi t i oni ng and p hys i c al tec hni que s m ay all re duc e d rug re qui rem ent s. P.533

Regimens for epidural analgesia

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Lumbar LA

10–15ml 0.5% bupivacaine followed by an infusion of 5–20ml/h 0.125% bupivacaine

Thoracic LA

4–6ml 0.5% bupivacaine followed by an infusion of 6–10ml/h 0.125% bupivacaine

Opioid

5mg morphine gives up to 12h analgesia

Combined

An infusion of 3–4ml/h 0.125% bupivacaine with 0.3–0.4mg/h morphine or 25–50µg/h fentanyl

See also: Opi oi d anal ges i cs , p 234; Non-op i oi d anal ges i cs , p 236; Mul t i pl e t rauma (1), p500; Mul ti pl e trauma (2), p502; Head inj ury (1), p504; Head i njury (2), p506; Burns—g ene ral manag ement, p512; Pos t-op erati ve i nt ens i ve care, p534 P.534

Post-operative intensive care Pat i ents may be adm i t ted to the IC U afte r s urg ery , e i ther el e ct i ve l y (see op pos i te ) or afte r unexp ect ed peri -operati ve com pl i cati ons.

General care Ens ure surgi cal and anae stheti c p l an has b een ag ree d, e .g. ov erni ght v ent i l ati on, sp eci al pre cauti ons (e. g. wi re cut ters i f m and i bl e w i re d), mov eme nt al l owe d, haem ody nam i c target s, etc . Prov i d e ad equate anal g esi a. Ens ure ade quate rew arm i ng . Mai ntai n eugl yc aemi a. Prov i d e ap propri at e t hrombosi s prophyl a xi s . Bl ood gas , el ec trol yt e and haem ogl obi n m oni tori ng.

Post-operative respiratory problems Com mon i n those wi t h p re-exi sti ng re spi rat ory di sease, es pec i al l y wi th a reduc ed vi t al capac i ty or pe ak fl ow rate. Probl e ms i nc l ude: Exac erb ati on of chroni c che st di s eas e Retaine d s ecreti ons Bas al ate l ec tas i s Pneumoni a Uppe r airway probl e ms, e. g. l aryng eal oe dem a Anaest hes i a and surg ery (es pec i al l y up per abd omi nal s urg ery ) reduce func ti onal resi dual c apaci t y, thorac i c com pl i anc e and cough. There i s re duc ed mac rop hag e func ti on and sys tem i c i nfl am mat ory ac ti v ati on wi t h i nfe cti on and acute l ung i njury as pos si bl e conse quences .

Therapeutic aims Pre -op erati v e p rep arati on m ay hel p av oi d some of the probl ems : Cess ati on of smoki ng for >1 w eek Bronchodi l at ati on Resp i ratory mus cl e trai ni ng Ches t p hys i ot herapy Avoi dance of hyp ovol ae mi a i n the ni l -by-m out h p eri od Pos t-operati ve cl e arance of se cre ti ons and maint enance of bas al l ung e xpansi on are ve ry i mp ort ant . T hes e requi re effect i ve anal g esi a and che st phy si othe rap y. Cons i d er earl y use of non-i nvas i ve ve nti l at i on i f sp ont ane ous l y bre athi ng but re qui ri ng hi g h FIO 2 . Me chani c al venti l at i on as si s ts bas al exp ans i on and s ecreti on cl earanc e where anaes the ti c rec ove ry i s exp ect ed to be prol onged or whe re surgery ± pre-e xi s ti ng d i s eas e i ncreas e t he ri s k of s ecreti on ret ent i on and at el e ctasi s . Ens ure a p ate nt ai rway pri or t o ex tub ati on whe re i nt ubati on w as di ffi c ul t or after up per ai rway surgery.

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Post-operative circulatory problems Prev ent i on of hy pov ol a emi a i s c ruc i al i n av oi d i ng i nfl ammatory acti vat i on and, the refore , m any post-operat i ve comp l i cat i ons. Haem orrhag e i s usuall y ob vi ous and manag ed by res usc i tati on, corre cti on of c oag ul ati on di s turbance and surgery. Sub cl i ni cal hy povol ae mi a i s common p ost ope rat i ve l y. Hy pot hermi a and hi gh catec hol ami ne l ev el s he l p to mai ntai n CVP and BP de spi te conti nui ng hyp ovol aem i a. Av oi d i ng reduced st rok e vol um e or m etabol i c aci dos i s are the bes t i nd i cators of adequate re sus ci tat i on. Post -op erati v e fl ui d m anagem ent re qui res a hi g h d egree of s us pi c i on of hyp ovol ae mi a ; fl ui d c hal l enges wi th col l oi d s houl d be use d t o c onfi rm and t reat hypov ol a emi a w here t here i s any c i rcul atory di sturbance , m etabol i c aci dos i s or ol i guri a . P.535

Reasons for elective ICU admission Ai rway moni t ori ng: e. g. m ajor oral , head and neck surge ry Resp i ratory moni tori ng: e.g . c ard i ot horaci c s urgery, upp er abdomi nal surge ry, prol onge d anaes thesi a, pre vi ous res pi ratory di s eas e Card i ov asc ul ar moni tori ng: e.g . c ard i ac surge ry, vascul ar s urg ery , m ajor ab dom i nal s urgery, p rol onged anae sthesi a, previ ous cardi ovascul ar di sease Neurol ogi cal moni t ori ng: e. g. neuros urg ery , c ard i ac s urg ery wi th ci rcul at ory arres t El e cti ve vent i l ati on: e. g. cardi a c s urg ery , m ajor abdomi nal surgery, prol onged anaes the si a , p rev i ous resp i ratory di s eas e

See also: Venti l at ory support— ind i c ati ons , p 4; Endot rac heal i ntubat i on, p 36; Non-i nvas i ve re spi rat ory s upp ort , p 32; C hes t phy si othe rap y, p48; Pul s e oxi m etry, p90; Bl ood gas anal ysi s, p100; ECG moni tori ng, p108; Bl ood pre ssure moni tori ng, p110; Cent ral ve nous c athete r—use, p114; Ce ntral venous cathe ter—i nserti on, p116; C ard i ac out put —thermodi l uti on, p122; C ard i ac output—othe r i nvasi v e, p124; Cardi a c outp ut—non-i nvas i ve (1), p 126; C ard i ac out put —non-i nvasi v e (2), p128; El ect rol yte s , p 146; Ful l bl ood count , p 154; Coagul at i on moni t ori ng , p156; Col l oi ds , p 180; Bl ood trans fus i on, p 182; Bronc hod i l ators, p186; Re spi ratory s ti m ul a nts , p 188; Op i oi d anal ge si c s, p234; Non-opi oi d analge si c s, p236; Sed ati ves , p 238; M usc l e rel axants , p 240; Anti coagul ant s, p248; Coag ul a nts and anti fi b ri nol yti cs , p254; Fl ui d chall eng e, p 274; R esp i ratory fai l ure, p 282; Atel ect asi s and pul monary col l a pse , p 284; Chroni c airfl ow l i mi tat i on, p286; Hyp ote nsi on, p312; Ol i guri a , p 330; Met abol i c aci d osi s, p434; Hypothe rmi a, p516; Pai n, p532

Ovid: Oxford Handbook of Critical Care

Ed itors: Si nge r, M ervyn; We bb, An dre w R. Ti tle : O xf ord Ha ndbook of Cr itic al Car e, 2nd Ed ition Cop yri ght © 1997,2005 M. Si nge r and A. R. W ebb , 1997, 2005. Publ i shed i n the Uni te d Stat es by Oxford Uni ve rsi ty Press Inc > Tab le of Co n te n ts > Obs tetr ic E me r ge n ci es

Obstetric Emergencies Pre-eclampsia and eclampsia The hallm ark of pre-ec l a mps i a i s hyp ert ens i on wi th protei nuri a . It i s c ons i de red mi l d i f prote i nuri a i s 0. 25–2g/l and sev ere i f >2g/l . Ecl a mps i a i s the same condi t i on as soc i at ed wi t h s ei z ures. They are ass oci ate d w i th ce reb ral oe dem a and , i n s ome cases , haemorrhag e. A reduced pl asm a vol um e, rai sed pe ri pheral re si s tance and di sse mi nate d i nt ravas cul ar coagul ati on al l i mpai r ti s sue pe rfusi on, wi t h p oss i b l e renal and hep ati c fai l ure. Pul monary oed ema may occ ur sec ond ary to i ncreas ed p eri pheral resi st anc e and l ow col l oi d osmoti c p res sure.

Management Hyp ert ens i ve cri s es and convul si ons may c ont i nue for 48h pos t-p art um, duri ng whi ch ti m e c l os e m oni tori ng i n a hi g h dep end enc y or i nte nsi ve care area i s es senti a l .

Circulatory management Hi g h b l ood pres sure i s d ue to art eri ol a r v asospasm so control l ed p l asma vol ume ex pansi on i s e sse nti al as the fi rst l i ne t reatme nt.

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A s tandard fl ui d c hal l enge reg i me n m ay be used i n the i nt ens i ve care area wi th l i ttl e ri s k of fl ui d ov erl oad . Ol i guri a may coexi st wi t h reduced pl asm a v ol ume; control l ed vol ume exp ans i on i s us ual l y more appropri a te than di uret i c the rap y. If p l as ma vol ume ex pans i on fail s t o c ont rol hy pertensi on, ant i -hype rte nsi ves such as l ab etalol , ni fedi pi ne or hydral azi ne may be use d.

Convulsions Conv ul s i ons are bes t avoi ded by good b l ood p res sure control . Ini ti a l s ei z ure c ont rol may be ac hi e ved wi th small dos es of benzod i azepi nes . Magnesi um sul phate i s the t reatment of c hoi ce for ec l am pti c c onv ul si ons. Magnes i um l evel s shoul d be moni t ore d and kep t b etw een 2.5–3. 75m mol /l . Ab ove 3. 75m mol /l toxi ci ty wi t h p oss i bl e c ardi ores pi ratory arres t m ay b e seen. Prop hyl ac ti c anti c onv ul s ant therapy wi t h m agnesi um may al so b e c ons i d ere d i n p re-e cl amps i a . Exce ss sed ati on shoul d b e av oi d ed due to the ri sk of asp i rati on al t hough conti nued se i zure s may requi re el ec ti v e i nt ubati on, mec hani cal hype rve nti l at i on and furt her anti convul sant t herapy .

Early fetal delivery The de fi ni ti ve treatm ent for e cl a mps i a i s fet al del i v ery but t he need s of t he fetus m ust be balanced ag ai nst those of the mothe r. If fet al mat uri ty has be en reac hed i mmed i at e d el i very afte r c ont rol of se i z ure s and hype r-t ens i on i s nec ess ary . P.539

Drug dosages Labetalol

Start at 2mg/min IV or quicker if a rapid response is required. Labetalol is usually effective once 200mg has been given after which a maintenance infusion of 5–50mg/h may be continued.

Nifedipine

10mg SL is an often effective alternative, given every 20min if necessary.

Hydralazine

5–10mg by slow IV bolus, repeat after 20–30min. Alternatively, by infusion starting at 200–300µg/min and reducing to 50–150µg/min.

Magnesium

4g over 20min followed by 1–1.5g/h by intravenous infusion until seizures have stopped for 24h.

Key papers Mag pi e Tri al Col l aborat i on Group . D o women wi th pre -ec l am psi a, and thei r babi e s, benefi t from mag nes i um sul p hat e? The Magpi e T ri a l : a rand omi sed pl ace bo-c ont rol l e d t ri al . Lance t 2002; 359:1877–90 Whi ch ant i c onv ul s ant for women wi th ecl amp si a ? Evi d enc e from the C ol l aborat i ve Ec l am psi a T ri al . Lance t 1995; 345:1455–63

See also: Venti l at ory support— ind i c ati ons , p 4; Bl ood press ure moni t ori ng , p 110; Central v enous cat het er—use , p 114; Ce ntral venous cathe ter—i nserti on, p116; EEG/CFM moni tori ng, p138; Coagul ati on moni tori ng, p156; C ol l oi d os mot i c pre ss ure , p 172; Col l oi ds , p 180; Hy pot ens i ve age nts , p 202; Anti convul sants , p 242; Fl ui d chal l eng e, p274; Hyp ert ens i on, p 314; G ene ral i s ed s ei zures, p372 P.540

HELLP syndrome HELLP syndrome i s a p reg nancy rel ate d d i s ord er ass oci ate d w i th haemol ys i s, el evated l i ver funct i on te sts and l ow pl a tel et s. Cri teri a use d for the di agnosi s of HELLP are shown b el ow. Mi c roangi opathi c haem ol y si s re sul ts from d est ructi on of red ce l l s as they pas s t hrough damag ed s mal l vess el s. Hepati c d ysfunc ti on i s c haract eri se d b y pe ri portal ne crosi s and hyal i ne de pos i ts i n t he s i nusoi ds . In s ome cases hepati c necrosi s m ay procee d t o he pat i c hae morrhage or rup ture. Thrombocyt ope ni a re sul ts from i nc reased pl ate l et consumpt i on, althoug h p rot hrombi n ti m e and acti vat ed parti al thromb opl ast i n ti m e are normal , unl i ke i n DIC .

Clinical features

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Epi gas tri c or ri g ht upp er quadrant pai n w i th malai se. Naus ea and vomi t i ng . Gene ral i s ed oed ema i s usual but hy pertensi on i s l es s c omm on. Prese ntati on m ay occur p ost -part um.

Criteria for diagnosis of HELLP syndrome Haem ol y si s Abnormal b l ood fi l m H yperbi l i rub i naemi a LDH >600U/l El e vate d l i v er enz ymes AST >70U/l Thrombocyt ope ni a Pl at el e ts <100 × 10 9 /l

Management Pri ori ti es for manage ment i ncl ude basi c re sus ci tat i on and e xcl usi on of hep ati c haemorrhag e or rupt ure d l i ve r. In the l at te r c ase an earl y Cae sarean se cti on and de fi ni ti ve surgi cal re pai r are urg ent . Mi c roangi opathi c haem ol y si s and t hrombocyt ope ni a may re spond to pl a sma ex change and fresh froze n p l as ma i nfusi on. Pl at el et transfusi ons shoul d b e avoi ded unl es s t here i s acti ve bl e edi ng. P.541

See also: Pl a sma ex change , p68; Li ver funct i on te sts , p 152; Ful l bl ood count, p154; Coagul ati on moni tori ng, p156; Bl ood produc ts , p 252; Basi c re sus ci tat i on, p 270; Vom i ti ng/gas tri c stasi s , p 338; Hae mol ysi s, p404; Pl a tel et di s ord ers , p 406 P.542

Post-partum haemorrhage Usual l y d ue to i nc omp l et e uteri ne contrac ti on afte r d el i very, but may be due t o retaine d p rod uct s. The magni tud e of hae morrhage may be sev ere and l i fe threateni ng .

Resuscitation The pri nc i p l es of re sus ci t ati on are the s ame as those app l y i ng to any haemorrhagi c c ond i t i on. Bl ood t ransfusi on req ui rem ent s may b e m ass i ve and t here may t herefore be a ne ed to rep l ac e c oag ul a ti on fact ors . T here m ay be si gni fi c ant re tropl acental b l ee di ng whi c h m ay l ead to underest i mati on of b l ood v ol ume l os s. It i s safer to manage fl ui d and bl ood re pl a cem ent wi th hae mod ynam i c moni t ori ng.

Aortic compression Tem porary re duc ti on of haem orrhag e may b e achi eve d b y compress i ng t he aorta w i t h a fi s t p us hed fi rml y ab ove the umb i l i cus, usi ng the press ure be twe en the fi st and verte bral c ol umn to achi ev e c ompres si on. Thi s m anoeuvre m ay buy ti me whi l e defi ni ti ve s urgi c al rep ai r i s organi s ed.

Stimulated uterine contraction Prostagl andi n F 2α i nj ect ed l oc al l y i nto the uterus or IM i s an effect i ve met hod of st i mul at i ng uteri ne contract i on and may avoi d the ne ed for surge ry.

Arterial occlusion Ang i ographi c e mbol i s ati on or i nt ernal i l i ac artery l i g ati on may avoi d the ne ed for hys te rec tom y i n s ome cas es. The di s adv ant age s of t hes e p roc edures i ncl ude a s i gni fi cant del ay i n org ani sat i on and, i n the l a tte r c ase , t he hi g h fai l ure rat e. P.543

See also: Bl ood press ure moni t ori ng, p110; Cent ral ve nous c athete r—use, p114; Central venous cat het er— i nse rti on, p116; Ful l bl ood count, p154; Coagul ati on moni t ori ng, p156; Bl ood transfusi on, p182 P.544

Amniotic fluid embolus An unc ommon b ut dangerous compl i cati on of c hi l db i rt h.

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There i s a hi gh earl y mortal i t y associ a ted wi th acute pul monary hy pertensi on. The i ni ti al res ponse of the pul monary vascul a ture t o t he p re sence of amni oti c fl ui d i s i nt ens e v asospasm res ul t i ng i n se vere p ul m onary hyp ert ens i on and hypoxaem i a. Ri ght heart func ti on i s i ni ti al l y c omp rom i se d s eve rel y b ut ret urns t o norm al wi t h a se condary p has e duri ng whi ch there i s sev ere l e ft heart fai l ure and p ul monary oed ema. Amni ot i c fl ui d contai ns l i pi d -ri ch parti cul ate materi al whi c h s ti m ul a tes a sys tem i c i nfl am mat ory re act i on. In t hi s res pec t t he progre ss of the condi ti on i s s i mi l a r t o othe r c aus es of m ul t i p l e org an fai l ure w i th as soc i at ed cap i l l ary l eak and d i ss emi nat ed i nt ravas cul ar coagul ati on. Di a gnosi s i s support ed b y amni oti c fl ui d and fet al cel l s i n pul monary arte ry bl ood and uri ne , t hough thi s fi nd i ng i s not sp eci fi c for e mbol us .

Management Manage ment i s e nti rel y s upp ort i v e. If amni oti c fl ui d embol i sm occ urs pri or t o de l i very urge nt Caes are an sec ti on m ust be performed to prevent furthe r e mbol i s ati on.

Respiratory support Oxy gen (FIO 2 0. 6–1.0) mus t b e p rov i de d. In many cases CPAP or mec hani cal v ent i l a ti on w i l l b e requi re d.

Cardiovascular support St andard re sus ci t ati on pri nc i pl es app l y wi t h c ont rol l e d fl ui d l oad i ng and i not rop i c support bei ng starte d as requi re d.

Haematological management Manage ment of the c oag ul opat hy req ui res bl ood produc t t herapy gui de d b y l aborat ory as ses sme nt of coagul ati on ti mes. In ad di t i on, some cases i m prove aft er tre atm ent wi th cry opreci pi tat e, pos si b l e due to the effec ts of fi b ronect i n rep l ac eme nt. P.545

See also: Venti l at ory support— ind i c ati ons , p 4; Conti nuous pos i ti ve ai rway press ure , p 26; Pul m onary art ery cathe ter—us e, p118; Pul monary artery c athete r—i nse rt i on, p 120; Fl ui d chall enge , p 274; Pul m onary embol us , p 308; Heart fai l ure— ass ess ment, p324; Heart fail ure —manag ement, p326; Sys tem i c i nfl am mat i on/mul ti organ fai l ure, p484

Ovid: Oxford Handbook of Critical Care

Ed itors:

Si nge r, M ervyn; We bb, An dre w R.

Ti tle : O xf ord Ha ndbook of Cr itic al Car e, 2nd Ed ition Cop yri ght © 1997,2005 M. Si nge r and A. R. W ebb , 1997, 2005. Publ i shed i n the Uni te d Stat es by Oxford Uni ve rsi ty Press Inc > Tab le of Co n te n ts > Dea th an d th e Dyi n g P a tien t

Death and the Dying Patient Brain stem death The corre ct di agnosi s of brai n s tem death al l ows di sc ont i nuati on of fut i l e ve nti l at i on and e nab l es potenti a l retri e val of org ans for d onati on. Di a gnosi s of brai n st em death i s usual l y fol l owe d b y asys tol e w i thi n a few d ays . Before brain ste m func ti on t est i ng c an b e p erform ed to confi rm t he di a gnosi s the p ati ent must hav e an underl y i ng di agnosi s com pat i bl e w i th brai n s tem death. They mus t b e c omat ose and non-res ponsi v e for at l eas t 6h and the re shoul d be a mi ni mum of 2h fol l owi ng a c ard i ac arres t. The re mus t b e no hypot hermi a (t emp erature > 35° C), evi dence or sus pi ci on of dep res sant d rug s, si gni fi c ant me tab ol i c abnormalit y or m usc l e rel axant effect . T he performance of b rai n s tem death tes ts shoul d not p roc eed unti l rel a ti v es and al l m edi cal and nurs i ng st aff i nvol ved wi th the pati e nt hav e had a chance to take part i n d i sc uss i ons, al though the t est i t sel f d oes not requi re conse nt. Ce ssati on of me chani cal venti l at i on i s se en by m any l a y p eopl e as t he fi nal poi nt of death. Cl earl y, thi s fi nal st ep i s easi er i f al l are aware that i t i s to happ en. If organ donat i on i s consi dered, the t ransp l ant c oordi nator s houl d be i nv ol v ed at an e arl y s tage.

Brain stem death testing Proced ure s v ary i nternat i onal l y. In the UK cl i ni cal asse ssm ent of brai n st em refl ex es mus t b e p erform ed b y 2 doctors who have b een re gi s tered for >5 ye ars . An EEG i s req ui red i n ot her count ri e s.

Pupillary light reflex Pup i l s s houl d app ear fi xed i n si ze and fai l t o res pond to a l i g ht st i mul us .

Corneal reflexes The se shoul d be ab sent b i l ateral l y

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Pain response The re shoul d be no crani al res ponse to sup raorbi tal p ai n.

Vestibulo-ocular reflexes Aft er confi rmi ng that t he tym pani c memb ranes are cl ear and unob struc ted 20ml i ce d water i s s yri nge d i nto the e ar. The ey es woul d norm al l y d evi ate toward t he opp osi te di rect i on. Abs enc e of movem ent to bi l at eral c ol d st i mul a ti on confi rms an abs ent re fl e x.

Oculo-cephalic reflexes Al so cal l ed ‘d ol l 's eye ’ refl exe s. Wi t h t he eye l i d s hel d op en, bri sk l a teral rotat i on of the he ad normal l y produc es opp osi te rot ati on of the ey ebal l as i f to fi x the gaze on an obje ct. Thi s rotat i on i s l ost i n brai n st em deat h.

Gag reflex The gag refl ex i s abs ent i n brai n st em death. Howeve r, the gag refl ex i s oft en l os t i n p ati ent s w ho are i ntub ate d.

Apnoea test Whi l e the refl ex asse ssm ent s are bei ng performed the p ati ent shoul d b e p re-oxyg enated wi th 100% ox yge n. The venti l at or i s di s connec ted and 6l /m i n oxyg en i s pas sed i nto the trac hea vi a a cat het er. Ap noe i c oxy genati on can sus tai n SaO 2 for p rol ong ed peri od s b ut the re i s an i ne vi t abl e ri s e i n PaCO 2 whi ch shoul d st i mul at e resp i ratory effort . Aft er 3-15mi n of d i sc onnect i on bl ood gas anal yse s are performed unti l PaCO 2 > 6.7 kPa. Any re spi rat ory effort negates the di agnosi s of b rai n s tem de ath. P.549

See also: Bl ood gas anal y si s , p 100; EEG/C FM moni tori ng, p138; Ure a and c reati ni ne, p144; El ec trol yt es , p 146; T oxi col ogy , p 162; Op i oi d anal ges i c s, p234; Non-opi oi d analge si c s, p236; Sed ati ves , p 238; Muscl e rel axants , p240; Cardi a c arre st, p272; Hyp ogl ycaemi a, p438; Hypothe rmi a, p516; Care of the p ote nti al org an donor, p552 P.550

Withdrawal and withholding treatment Thi s i s arg uab l y the mos t d i ffi c ul t and s tre ssful dec i s i on that has to be mad e for the cri ti cally i l l p ati ent. Wi t hdrawal inv ol v es red uct i on or c ess ati on of v asoact i ve drugs and/or resp i ratory sup port. In som e ICUs the pati e nt i s heavi l y sed ate d and di s connec ted from the venti l at or. Wi thhol d i ng i nvol ve s non-c omm enc eme nt or non-esc al a ti on of treatm ent , e .g. ap pl y i ng an up per thres hol d d ose for an i not rop e and/or not start i ng re nal re pl a cem ent therapy. Before ap proachi ng the p ati ent /fami l y, the re shoul d i d eal l y be a c ons ens us among m edi cal and nursi ng s taff t hat quanti ty and /or qual i ty of l i fe are si g ni fi c ant l y com promi s ed and unl i k el y to re cov er. Often, t he p ati ent 's vi ewpoi nt i s very w el l -de fi ned and the carers may rue the fact that the di scussi on was not i ni t i a ted earl i er. Ethni c, cul tural and re l i gi ous fac tors w i l l i nfl uence b oth doctor and pat i ent/fami l y i n the ti mi ng and fre que ncy of such dec i s i ons. In som e soci eti es doc tors have a m ore paternal i s ti c ap proach wi th l i t tl e i nvol ve ment of pati e nt and /or fam i l y i n the d eci si on-m aki ng proces s. Ot hers are overl y i ncl usi v e, som eti mes to the p oi nt of ex ces si vel y ac qui es ci ng to the fami l y's de mands des pi t e obvi ous futi l i t y i n c ont i nui ng care. Cl earl y, a bal anc e needs to be st ruc k t hat se rve s the be st i nt erest s of the p ati ent . Al t hough pot ent i al l y awk ward , t he mental l y com pet ent pati e nt shoul d be i nvol ved i n the most i mp ort ant de ci s i on affec ti ng t hei r l i fe. Thi s s houl d be done as c ons i de rat el y as possi bl e , avoi di ng unnece ssary di s tress . A se ri es of d i sc us si ons ove r s everal days m ay be need ed, al l ow i ng ti me to contem pl a te. Consensus i s re ached wi t h > 95% of pat i ents/fam i l i es by the thi rd d i sc uss i on. It shoul d be st re sse d t o t he p ati ent and fami l y that c are i s not be i ng wi thd raw n/wi thhel d b ut that p ai n re l i e f, com fort, hyd rat i on and g ene ral nursi ng care are to be conti nued . Li ke wi s e, no dec i si on i s bi ndi ng but can b e am end ed dep end i ng on the p ati ent 's progre ss , e. g. mov i ng from wi t hhol di ng to wi t hdrawal, or re-i ns ti tut i on of ful l tre atm ent . A ‘ne got i at ed set tl ement’ i s oft en a useful i nt eri m comp romi s e for fami l i es unabl e to acc ept a wi t hdrawal d eci si on, whe reb y l i mi tat i on of treat ment i s i ns ti t ute d and sub seq uentl y re vi e wed Rel ati ves can s ome ti m es be very di st raught and, occ asi onally , i rrati onal on d i sc uss i ng wi thdrawal /wi t hhol d i ng . F or many, thi s w i l l be thei r fi rs t e xpe ri e nce of the dy i ng proc ess i n a l ov ed fami l y mem ber. A numbe r of ot her factors i nc l udi ng g ui l t, ang er and wi thi n-fami l y di s agreem ent s m ay al s o s urface . It s houl d be stress ed that t he wi t hdraw/wi t hhol d dec i si on shoul d not b e l eft to the fami l y al one as t hi s i s an unfair burden for t hem to carry . Rat her, i t i s t hei r pas si v e agre ement w i t h a med i cal rec omme ndati on t hat i s be i ng sought. The em phasi s of the di s cussi on i s to i nform them of t he l i kel y outc ome and to se ek t hei r vi e w of what the pat i e nt woul d w ant . T hey ne ed to be dealt wi t h b oth se nsi ti v el y and hone stl y, and they s houl d not fe el pre ss ure d t o gi ve i nstant dec i si ons . Di scussi ons shoul d i nvol ve the p ati ent 's nurse and ot her i nvol ved carers as appropri a te. It shoul d b e accurat el y doc ume nte d i n t he cas e note s t o ensure g ood communi c ati on bet wee n c are gi v ers and act as source data s houl d sub seq uent c omp l ai nt s s urface . P.551

See also: Com muni cati on, p564 P.552

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Care of the potential organ donor Pat i ents wi t h s us pec ted brai n st em deat h s houl d be consi dered c and i d ate s for org an d onati on unl e ss there i s evi de nce of: Canc er (ex cep t p ri m ary ce ntral nervous s yst em) HIV or he pat i ti s s urface anti g en pos i t i ve Hi g h ri sk for HIV Uncontrol l ed se psi s Si g ni fi cant sys tem i c di sease Sl ow vi rus i nfe cti on The trans pl ant co-ord i nator s houl d be c ont ac ted earl y (be fore t he fami l y are ap proached) to confi rm l i k el y sui t abi l i t y. If the fami l y are amenabl e, the trans pl ant co-ord i nator wi l l then i ni ti ate organ donati on proced ures. Do not rejec t those brain dead p ote nti al donors who, for exampl e, hav e ful l y t reated i nfec ti ons or acute renal fai l ure w i thout consul tati on wi th the t ranspl ant co-ordi nator.

Management 1. Confi rm brai n s tem death wi t h appropri at e t est i ng. 2. Lab oratory t est s for bl ood group, HIV and hepati ti s st atus and el e ctrol yte s. 3. Confi rm organ donat i on i s pe rmi ss i bl e b y t he corone r (or e qui val ent ). 4. Mai ntai n opt i mal c ard i oresp i ratory status wi th fl ui d ± i not rop es, op ti m al venti l at i on and physi ot herapy. Di ab etes i ns i pi dus shoul d b e t reated wi th DDAVP. 5. Cont act surg i cal and anae st het i c teams.

Organ suitability Ki dneys —Age 4–70, acce ptabl e U&E and cre ati ni ne Heart— Age 0–50, acc ept abl e C XR and EC G Lungs— Age 0–50, ac cep tab l e CXR and bl ood gases Li v er— Age 0–55, no al cohol or drug abus e, acc ept abl e LFTs Corneas —Ag e 0–100, no pre vi ous i nt raocul ar surge ry The trans pl ant co-ord i nator wi l l ad vi s e on ot her organ and t i s sue sui tabi l i t y, e.g. pancreas , t rache a, b owe l , ski n. P.553

See also: Bl ood gas anal y si s , p 100; Urea and creat i ni ne , p144; El ect rol yte s , p 146; Col l oi d s, p180; Inot rop es, p196; Vasop res sors, p200; F lui d c hal l e nge , p 274; Hy pot ens i on, p 312

Ovid: Oxford Handbook of Critical Care

Ed itors:

Si nge r, M ervyn; We bb, An dre w R.

Ti tle : O xf ord Ha ndbook of Cr itic al Car e, 2nd Ed ition Cop yri ght © 1997,2005 M. Si nge r and A. R. W ebb , 1997, 2005. Publ i shed i n the Uni te d Stat es by Oxford Uni ve rsi ty Press Inc > Tab le of Co n te n ts > I CU Or gan isa tio n a n d Ma n ag eme n t

ICU Organisation and Management ICU layout The i ntensi ve c are uni t shoul d b e easi l y acc ess i bl e b y d epartm ent s from whi ch pat i e nts are ad mi tte d and c l ose t o dep art ments whi ch share eng i ne eri ng servi ces . It i s d esi rabl e that cri ti cal l y i l l pati ent s are sep arated from t hos e req ui ri ng c oronary c are or hi gh dep end enc y c are whe re a q ui e ter envi ronm ent i s often ne ede d. It i s pos si b l e to provi d e i nt ens i ve care and hi g h d epe nde ncy care i n the same uni t s o l ong as pat i e nts can b e se parate d w i thi n the uni t. How eve r, the di ffe ri ng requi rements of the se pat i ents may l i mi t such fl e xi b i l i ty . T he fl oor si z es gi v en bel ow rep res ent a mi ni mum g ui d e.

Size Int ens i v e care bed re qui re ment s d epe nd on the ac ti v i ty of the hosp i tal w i th ad di t i onal bed s requi red for re gi onal

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spe ci al t i es such as cardi othorac i c surge ry or neuros urg ery. Very s mal l (< 6 b eds ) or v ery l a rge (>14 b eds ) uni t s m ay be di ffi c ul t t o manag e althoug h l arg er uni ts may be di vi d ed ope rat i onal l y and al l ow bet ter conce ntrati on of res ources .

Patient areas Pati ent areas must provi de unob struc ted passage around the be d w i th a fl oor space of 26m 2 per bed . C urt ai ns or screens are req ui red for pri vacy. Fl oors and ce i l i ng s m ust be const ruc ted to support heavy equi pm ent (some pi e ces may we i gh 1000k g). Doors mus t al l ow for p ass age of bul ky equi p ment as we l l as wi d e b eds . Every b ed shoul d have acc ess to a w ash hand bas i n. The spe ci fi c ati on shoul d i ncl ude 1 c ubi cl e p er 2 b eds wi t h 26m 2 fl oor area for i s ol ati on. Ai r c ond i t i oni ng shoul d al l ow for pos i t i ve and ne gat i ve press ure control i n cubi c l es and t emp erature and hum i di ty control . Servi c es mus t i ncl ud e ad equate el ect ri ci t y s upp l y (at l e ast 28 socket s per bed ) w i th em erg enc y b ack -up sup pl y. Oxyg en (4), me di c al ai r (2) and suc ti on (2) out l et s m ust be avail abl e for every b ed. The bed areas shoul d have nat ural dayl i g ht and pati e nts and s taff s houl d i de al l y have an out si d e v i ew . Comm uni cat i ons s yst ems i ncl ude an ade quate num ber of tel ep hone s t o avoi d all tel ephone s b ei ng i n use at onc e, i nt erc om sys tem s t o al l ow be d t o b ed com muni cati on and a s yst em t o c ont rol entry t o t he d epartm ent . Comp ute r netw ork s s houl d enabl e communi c ati on wi t h c ent ral hospi tal ad mi ni s trati on and l ab oratory s yst ems .

Other areas Other areas i ncl ude adeq uat e s torage sp ace , d i rty uti l i t y, cl ean uti l i ty, offi c es, l a boratory, se mi nar room, cl e ane rs' room, staff res t room , l ock er room, toi l et s, rel ati ves ' are a, b edroom and i nte rvi ew room. P.558

ICU staffing (medical) Int ens i v e care has ev ol v ed from t he e arl y s uc ces s i n s i mp l e mec hani cal v ent i l ati on of t he l ungs of pol i o vi c ti ms to t he pre sent d ay whe re pat i ents adm i tt ed to i nt ens i ve care wi l l usuall y have fai l ure or d ysfunc ti on of one or more organ sys tem s requi ri ng me chani c al sup port and moni tori ng. The i ntensi ve c are uni t shoul d have ded i c ated consul t ant ses si ons wi th addi ti onal allocat i on for m anagem ent , t eachi ng and audi t act i vi ti e s. The se ses si ons shoul d be di vi ded bet wee n s everal i ntensi v e c are sp eci al i st s. In add i ti on, the i nte nsi ve care s pec i al i s t s houl d be sup ported by juni or doc tors i n traini ng who can p rov i de 24h pe r d ay cov er on a rota whi ch provi des ade quate res t.

Required skills of intensive care medical staff Management Seni or i nte nsi ve care m edi cal st aff, assi ste d b y s eni or nursi ng and pharmacy col l eague s, com mand t he pri mary res ponsi bi l i t y for t he fi nanc i al manag eme nt of t he i nt ens i v e c are uni t. It i s through the i r ac ti ons that t reatme nt of t he cri ti cal l y i l l i s i ni ti a ted and p erp etuate d; t hey are ul ti mat el y resp ons i bl e for the ac ti v i ty of the uni t and pati ent out com e.

Decision making In the IC U m ost dec i s i ons are ul t i matel y m ade by te am c ons ens us. Cl i ni cal d eci si ons i n the i nte nsi ve care uni t can b e thought of unde r t hre e c ate gori es : (i ) d eci si ons re l at i ng t o common or rout i ne probl ems for w hi c h a uni t pol i c y exi sts ; (i i ) de ci s i ons rel ati ng to unc omm on p robl e ms req ui ri ng di sc uss i on wi th al l IC U and non-ICU st aff curre ntl y i nv ol v ed and (i i i ) de ci s i ons of an urge nt nat ure taken by i ntensi v e c are st aff wi t hout d el a y.

Practical skills Exp ert i s e i n t he m anagem ent of com pl e x e qui pme nt, moni t ori ng proced ures and performance of i nv asi ve proced ure s are re qui re d.

Clinical experience Med i cal s taff requi re ex peri ence i n the recog ni ti on, pre venti on and managem ent of cri ti cal i l l ness , i nfe ct i on control , anaest hes i a and organ support.

Technical knowledge The i ntensi ve c are sp eci al i st has an i mportant rol e i n t he choi ce of eq ui p ment used i n the i nte nsi ve care uni t .

Pharmacological knowledge Drug t herap y regi mens are c l e arl y open to the probl ems of drug i nt eract i ons and, i n add i t i on, p harmac oki net i cs are oft en sev ere l y al t ere d b y t he e ffe cts of major organ sys tem dy sfunct i on, p art i c ul a rl y i nvol vi ng the l i ver and ki dneys .

Teaching and training The modern i nte nsi ve care s pec i al i s t has acq ui red a numb er of s ki l l s that cannot be gai ne d outs i de the i nte nsi ve care uni t. It i s there fore nece ssary to be abl e to provi de thi s e duc ati on to juni or doct ors i n trai ni ng for i nt ens i ve care.

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P.559 P.560

ICU staffing (nursing) Cri ti cal l y i l l p ati ent s requi re cl os e nurs i ng supervi s i on. M any wi l l req ui re hi g h-i nte nsi ty nursi ng throug hout a 24h peri od whi l e ot hers are of a l ower d ependency and can s hare nurs es. In ad di t i on to the b eds i de nurse s, the dep art ment need s addi ti onal st aff to manage the d ay to day ope rat i on of the uni t , t o assi st i n l i fti ng and handl i ng of pat i ents , t o rel i eve bed si de nurses for rest pe ri ods and to col l e ct drugs and eq ui p ment. The se add i ti onal nurs es (or nurse ass i s tants) can b e te rme d t he ‘fi xed nursi ng est abl i s hme nt’ and t he nat ure of the i r duti e s i s s uch that the y w i l l usual l y b e hi gher grade nurse s. The bed si de nurses are a ‘vari abl e es tab l i shm ent ’ and the i r num bers are dep end ent on act i vi ty suc h t hat more pat i ents re qui re hi g her numbe rs. Most dep art ments fi x thei r vari a bl e es tab l i shm ent by ass umi ng an ave rag e ac ti vi t y.

Fixed establishment In the UK provi di ng 1 nurse pe r s hi ft c ont i nuous l y re qui res 5. 5 nurs es. In ad di t i on s taff handover, annual l eave, st udy l eave and si ckness are usually calcul a ted at 22% such that 1 ad di t i onal nurse i s re qui red . T hus , t he provi s i on of 1 nurse i n charg e of each shi ft and 1 nurse to sup port t he bed si d e nurs es req ui res 11 nurse s. In l arger uni ts t here may be a need for ad di t i onal support nurses .

Variable establishment The same pri nci pl es appl y for the provi si on of b eds i de nurs es. Thus, to provi de 1:1 nursi ng for a b ed req ui res 5.5 nurses and t o p rov i de 1:2 nurs i ng re qui re s 2.75 nurse s. The total number requi re d d epe nds on the oc cup anc y and the nurse to pat i ent rat i o for eac h occupi ed b ed. One of t he d i ffi c ul t i es i n s taffi ng an i ntensi ve c are uni t re l at es to the vari ab l e dep end enc y and occ upancy . An av erage dep end enc y we i ghted oc cup anc y (ave rag e oc cupanc y × av erage nurse to pat i ent rat i o) shoul d be us ed to set the e stabl i shm ent of be dsi de nurses wi th add i ti onal nurses be i ng draft ed i n from a bank or agency to cov er peak de mands.

Skill mix Nursi ng ski l l mi x i s t he s ubj ect of much controversy as the ne ed for econom y i s b al a nce d agai nst the need for qual i ty . As st ate d ab ove the fi xe d nurs i ng wi l l usual l y be of hi gher grade si nce the rol e i ncorporate s t he admi ni strati on of the uni t and sup erv i s ory nursi ng. The b eds i de nurse s w i l l be made up of t hos e w ho have re cei ved post-qualific ati on trai ni ng i n i ntensi ve c are and t hos e w ho have not. The rati o of trai ned to unt rai ned i ntensi v e c are nurse s s houl d be of the order of 3:1 t o faci l i t ate i n-se rvi ce teachi ng. P.561 P.562

Fire safety Fi res affect i ng the ICU are rare but are p art i cul arl y di ffi cul t i n t hat pati ent s are not eas i l y ev acuate d, yet thei r l i ves dep end on se rvi ces whi ch fi re may di srupt. Sm oke , w hi l e d ang erous to staff and the l e ss cri ti cal l y i l l p ati ent s w ho may be breat hi ng s pontaneous l y , i s l ess of a p robl e m t o those on me chani c al venti l ati on si nce thei r fresh gas s upp l y i s from outs i d e the affe cte d e nvi ronment. It the refore fol l ows t hat , i n the eve nt of fi re, the pri ori t y i s t o ensure safety and me ans of es cap e for t he st aff fi rst .

Control of smoke Smoke and toxi c gases are a com mon as soc i at i on wi th fi re and may , i n t hems el ves , be fl amm abl e, parti c ul arl y i n ass oci at i on wi th hi g h c onc ent rat i ons of oxyge n. The main tec hni que s for control of s mok e i ncl ude containm ent (e. g. fi re-resi st i ng walls , d oors and seals) and d i sp ers al (e. g. pos i ti ve pre ssure ai r c ond i ti oni ng), t he l at ter be i ng us ed i n pat i ent areas. The possi bi l i t y of fl amm abl e or t oxi c fume s s houl d be consi d ere d w hen equi p pi ng and furni s hi ng t he i nt ens i v e c are uni t.

Escape from fire Esc ape routes s houl d be w el l marke d and unobst ruc ted . The nat ure of cri t i cal i l l nes s i s s uch that not al l p ati ent s c an be evacuated . The staff shoul d es cap e fi rs t b y p roc eed i ng to the nearest ex i t away from the fi re. Pati ent s shoul d be evacuated i n the orde r of t he l east si c k fi rs t. Evac uat i on of pati e nts shoul d b e m anaged by som eone t rai ned i n the use of b reathi ng app aratus; i n m ost cases thi s w i l l be the fi re bri gade. If p ati ent s are to be evacuated they s houl d be mov ed to a pl ace of safet y on the s ame fl oor as the i nte nsi ve care uni t. Pat i ents shoul d not b e moved downs tai rs. In t he maj ori ty of fi res contai nme nt wi l l red uce the ne ed for ful l evacuati on.

Preventing fire Aut omat i c sm oke or heat alarms shoul d be provi ded i n al l areas. Cook i ng areas and l aborat ory areas mus t be s eparat ed from p ati ent areas by fi re doors.

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Fi re doors are p rov i d ed t o p rot ect s taff and p ati ent s and shoul d not b e we dge d open. If a cl ose d d oor woul d compromi se the care gi v en to p ati ents but i s es senti a l t o s eparat e fi re compartm ent s t hen an e l ec tro-me chani c al dev i c e shoul d hol d t he d oor op en and be di sab l ed by the fi re al a rm. Fi re ex ti ngui shers of the ap propri at e t ype s s houl d be readi l y avai l ab l e and st aff shoul d be prope rl y t rai ned i n thei r use . P.563 P.564

Communication Good c omm uni cat i on i s es senti al to the smooth runni ng of the IC U. Thi s i ncl ud es c omm uni cat i on b etwe en the IC U staff, pati e nts , v i si ti ng profes si onal s and rel ati ves .

Patient communication Cri ti cal l y i l l p ati ent s m ay s ti l l be abl e t o hear conversati on d esp i te se dat i on or ap parent unconsci ous nes s. Bed si de di s cussi ons shoul d t ake thi s i nt o account and all proced ures shoul d be exp l ai ned to the p ati ent i n si mp l e terms before start i ng . T he pat i ent who i s not com pet ent to conse nt to tre atm ent may ap pre ci ate verbal di sc uss i on or ex pl a nat i on.

Doctor–nurse communication It i s es senti a l t hat the m ul t i di sc i pl i nary app roach to i nt ens i v e c are i nvol ves med i c al and nursi ng staff i n dec i si on mak i ng . W ard round s are a forum for s uc h i nte rdi sci pl i nary com muni cati on and the consul tant l eadi ng t he round shoul d ensure t hat al l pre sent are trul y i nv ol v ed. The p l an for t he d ay can be se t on the w ard round but i s m ore l i kel y to suc cee d i f all invol ved i n effect i ng the p l an are i nvol ve d i n s ett i ng i t. Si m i l a rl y, al l chang es from t he p l an, w het her due to unforese en e mergenci es or d ue to fai l ure of t he pat i ent t o resp ond , s houl d be ful l y di s cus sed .

Communication with visiting teams The i ntensi ve c are st aff shoul d b e resp ons i bl e for the day t o d ay c are of cri t i cally i l l pat i ents, i ncl udi ng coordi nat i ng the i nput from vari ous non-ICU profes si onals i nv ol v ed i n the manage ment of p ati ent s and affe cti ng the treat ment pl a n. The ad mi t ti ng t eam shoul d b e i nvol ve d i n m ajor de ci si ons. Vi si ti ng m edi cal st aff shoul d not see pati e nts wi thout bei ng acc omp ani ed by a me mbe r of t he i nt ens i ve care med i cal s taff.

Communication with relatives Rel ati ves are ofte n ov erw hel med by the envi ronment of an i ntensi v e c are uni t, are w orri ed ab out the p ati ent and are eas i l y confused by the i nformati on t hey are gi ven ab out cri t i call y i l l pat i ents. Most com muni cati on s houl d be fac e t o fac e, avoi di ng l engthy d i sc uss i ons on t he tel ephone . W here s eve ral pe opl e are i mp art i ng i nformat i on, d i ffere nce s i n emp has i s or content d est roy any c hance of e ffe cti ve com muni cati on. It i s ess ent i a l t hat the b eds i de nurse i s prese nt whe n rel a ti v es are sp oke n t o s i nc e t here are ofte n q ues ti ons and conce rns whi c h c rop up l a ter and are d i rect ed to the nurse; i t i s wort h remem beri ng t hat the rel a ti v es have great er contac t w i t h t he nurses and often bui l d up a rel at i onshi p w i th them. Where adm i t ti ng t eam s need to com muni cate wi t h rel a ti ves about a s pec i fi c aspe ct of the i l l ne ss the be dsi de nurse and , i deally , a mem ber of the i nte nsi ve care m edi cal st aff, s houl d be pre sent. Mos t i nt ervi e ws w i t h rel a ti v es shoul d be away from the b eds i de al though i t i s often he l pful to i mp art si mpl e i nformati on at the be dsi de, parti cul arl y to dem ons trate parti c ul ar i ss ues . Agai n i t mus t b e remem bered that t he pat i ent m ay hear the conve rsati on. Whi l e i t i s he l pful to i nt erv i ew al l rel ati ves toget her thi s i s not al way s p rac ti c al , ei ther bec aus e the y c annot al l be prese nt at onc e or b ecause the y d o not rel ate to eac h othe r. Informati on oft en change s w hen del i ve red se cond hand so i t i s be tte r t o c omm uni cat e d i rect l y wi t h v ari ous re l at i ve s s eparat el y i n t hes e ci rcumst anc es. P.565 P.566

Medicolegal aspects The i ntensi ve c are uni t i s a s ource of many m edi col egal p rob l em s. Pat i ents are often not c ompe tent t o c ons ent to treatm ent . T hey may be ad mi t ted fol l owi ng t rauma, vi ol e nce or poi soni ng, al l of whi ch may i nvol ve a l egal p roc es s. Adm i s si on m ay als o fol l ow c omp l i c at i ons of treat ment or m edi cal mi shaps oc curri ng e l s ewhe re i n the hospi tal . T he nat ure of cri t i cal i l l nes s i s s uch that com pl i cat i ons are common and l i ti gati on m ay fol l ow.

Consent and agreement Many p roc edures i n i ntensi ve c are are i nvasi ve or i nvol ve si gni fi cant ri sk . T he pat i ent i s ofte n not com pet ent to consent for suc h t reatme nt and , i n m any count ri e s, surrogat e conse nt or ass ent cannot b e l egally gi ven by the nex t-of-ki n. It i s i m portant t hat the ri sk s and benefi ts of the proce dure are expl ai ned to the ne xt-of-k i n and that thi s di s cussi on i s doc ume nte d i n t he cas e records . F or major d eci si ons , p art i c ul a rl y those i nvol vi ng w i thdrawal or wi t hhol di ng of l i fe-p rol ong i ng t reatme nts , t he pat i ent s houl d i de al l y b e i nvol ve d i n d i sc uss i ons. If not fe asi bl e, rel at i ve s s houl d be aske d t o g i ve thei r vi ew of w hat the p ati ent woul d want i n thi s s i tuati on. Res earch pre sents consent p rob l em s i n t he cri ti cal l y i l l and req ui res cl ose et hi c al com mi t tee supervi s i on.

Note-keeping It i s i m pos si b l e to rec ord ev ery thi ng that happ ens i n i ntensi ve c are i n t he p ati ent 's notes . T he 24h obs erv ati on chart provi d es the most det ai l ed rec ord of what has hap pened but summary not es are es senti a l . Suc h note s m ust be factual wi t hout unsubst ant i a ted opi ni ons ab out the pati ent or about previ ous treat ment . Al l entri es mus t b e t i me d and

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si gned . R ecords of ward rounds must rec ord the name of the consul tant l eadi ng t he round. It must be rem emb ere d that t he not es may be use d l ate r i n l eg al procee di ngs. They m ay be use d ag ai nst you but, i f wel l k ept , w i l l us ual l y form t he bes t d efence. In the e vent of a med i cal m i s hap the ep i sode shoul d be cl earl y doc ume nte d afte r w i tness ed exp l anati on to rel ati ves .

Dealing with the police Mos t p ol i ce enq ui ri e s rel a te to pat i ents who are ad mi t te d after susp i ci ous ci rc ums tances . W hi l e t here i s a duty to pat i ent c onfi de nti al i ty i t may b e i n t he p ati ent's i nterest s t o i mpart i nformat i on ab out them. Thi s m ay be wi t h t he consent of t he pat i ent or t he next of ki n. Wri tt en statem ent s or ve rb al i nform ati on may be req ues ted . Any i nform ati on gi v en shoul d av oi d op i ni on and be st ri c tl y fact ual .

Dealing with the Coroner The Coroner mus t b e i nformed of any d eath where a deat h c erti fi cate cannot be i s sue d. Death certi fi c ate s c an b e i s sue d where the d eat h i s d ue to a natural cause and the p ati ent has b een se en p rofess i onal l y by the doc tor wi thi n 14 day s p ri or t o d eat h. The tabl e docum ent s t he condi t i ons requi ri ng the Coroner to be i nform ed. Where there i s any doubt the Coroner shoul d be i nformed . P.567

Deaths which must be informed to the Coroner Uni dent i fi ed body No d oct or att end i ng wi thi n pri or 14 day s Deat h w i thout recov ery from anaest hes i a Sud den or une xpl ai ned death Medi cal mi shap Ind ust ri a l acci de nt or di s eas e Vi ol ence, ac ci d ent or mi sad venture Sus pi c i ous c i rcum stance s Al c ohol i s m Poi s oni ng Deat h i n c us tod y P.568

Clinical governance Cl i ni cal governance i s a frame work t hrough whi ch he al t hcare org ani zat i ons are acc ountab l e for conti nuous l y i mp rov i ng t he q ual i t y of thei r s erv i ce s and safeguard i ng hi gh standards of care by c re ati ng an envi ronment i n whi ch exc el l enc e i n c l i ni c al care w i l l fl ouri s h. For the ICU c l i ni c al gov ernanc e requi res the cul ture, the s yst ems and t he sup port m echani sms t o ac hi eve good c l i ni c al performance and ens uri ng that qual i t y i mprove ment i s e mbed ded i nto the uni t' s routi ne. Thi s i ncl ud es act i on to ens ure ri sk s are managed , adve rse effec ts are rapi d l y det ect ed, op enl y i nv est i g ate d and l ess ons l earned , good practi ce i s rapi d l y di s se mi nate d and s yst ems are i n p l ac e t o e nsure conti nuous i mp rov ements i n cl i ni cal c are . There must be sys tem s t o e nsure al l cl i ni ci ans have the ri ght ed ucati on, trai ni ng , s ki l l s and compe tenci e s t o d el i ver t he c are ne ede d b y p ati ent s. The re mus t b e s yst ems i n pl ace to re cog ni s e and ac t on p oor performance.

Essential components of clinical governance Clear management arrangements Eve yone must know w ho t hey are account abl e t o, the l i mi t s of t hei r d eci si on maki ng and who m ust be i nformed i n the dec i s i on mak i ng proc ess .

Quality improvement Throug h t he proces s of c l i ni c al aud i t the st and ard of pract i ce i s moni t ored and change s e ffe cte d t o i mprove quali ty.

Clinical effectiveness Evi dence bas ed practi ce i s es senti a l w here ev i d enc e ex i st s to s up port c l i ni c al dec i si ons . Prot ocol s and gui de l i nes standardi se pract i ce .

Risk assessment and management A regi st er of cl i ni c al ri sks shoul d b e k ept , t o whi c h new ri s ks are app end ed as the y are ass ess ed. An ac ti on p l an shoul d be de vel ope d for m anagi ng e ach ri sk.

Staff and organisational development Inc l udi ng c ont i nued profes si onal ed ucati on, cl i ni cal supervi si on and p rofess i onal re gul ati on.

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Patient input Com pl a i nt s m oni tori ng s houl d be used to l e arn l ess ons and i mprove pract i ce wi thi n ICU. Pat i e nt and rel at i ve surve ys can be us ed to adap t q ual i t y i ni t i at i v es t o t he nee ds of pat i ents. P.569

See also: Aud i t , p 570 P.570

Audit Aud i t has b ecom e an e sse nti al part of m edi cal pract i c e. The mai n p urp ose i s t o i mprove quali ty of c are whi ch, i n t he i nt ens i v e c are uni t, must i nv ol v e al l memb ers of the m ul t i d i sc i pl i nary te am. Change i n pract i c e i n one d i sc i p l i ne w i l l i ne vi t abl y have a knoc k-on e ffec t i n others . Audi t m ay i nv ol v e a re vi e w of ac ti v i ty , p erform anc e agai nst pre det erm i ned i nd i cators or c ost -effec ti v ene ss. Audi t may focus on s pec i fi c t opi cs or may encom pas s t he p erformanc e of sev eral i nte nsi ve care uni t s. Succe ssful aud i t req ui res commi tme nt from se ni or staff t o e nsure pract i ce i s de fi ned, dat a are col l ec ted and c hange i s effect ed w here nece ssary. Where chang e i s s ugg est ed by aud i t a furt her re vi e w i s req ui red to ens ure t hat such change has oc curre d.

Data collection Ide al l y, a b asi c d ata se t s houl d be com mon to al l i nte nsi ve care uni t s nati onall y t o al l ow me ani ngful com pari sons to be mad e. T hi s requi re s t he dat a s et to be d etail ed enough to ans wer quest i ons p ose d b ut not so det ai l ed that col l e cti on bec omes unsustainabl e . R esourc es mus t b e provi de d i n t erm s of computer datab ase s and staff to c ol l ec t and anal y se dat a. T hos e c ol l ec ti ng t he dat a s houl d be p rovi d ed w i t h regul ar summary rev i ews t o ensure t hat ent hus i as m c ont i nues , and q ual i t y c ont rol i s maint ai ned. Me thods of dat a entry shoul d c ons i d er the ti me i nv ol v ed and the fact that m ost of those col l e cti ng dat a are not key board exp ert s. Typ ographi cal m i s take s d est roy the v al ue of col l e cte d d ata suc h t hat error t rap pi ng and dat a v al i dat i on must form p art of the house kee pi ng i n any dat abas e used . Som e audi t t opi cs re qui re dat a c ol l ect i on that i s not part of the basi c data set . C ol l ect i ng ap propri at e d ata req ui res cl ari ty i n set ti ng t he que sti on to be ans wered and care i n c hoosi ng dat a i tems t hat wi l l trul y ans wer the q ues ti on.

Audit meetings Reg ul a r audi t m eet i ng s s houl d fol l ow a pre defi ne d t i me tab l e. Thi s hel ps to ens ure maxi m um staff atte ndance and also set s t arget dat es for data col l ec ti on and analys i s . Audi t m eet i ng s s houl d be chaire d and hav e de fi ned ai m s. Di scussi on of the topi c be i ng audi t ed mus t l ead to re com mend ed change s i n p rac ti ce and the se mus t b e fol l owe d throug h afte r t he mee ti ng. It i s cl ear that al l st aff cannot at tend all mee ti ngs . D i ss emi nat i on of i nformat i on pri or t o i mp l em ent i ng prop osed chang es i s nec ess ary t o st and some chance of carry i ng them throug h. P.571

See also: Cl i ni cal governance, p568 P.572

ICU scoring systems Vari ous ICU sc ori ng sys tem s have evol ve d t o p rov i de : An i nd ex of d i se ase se veri ty , e .g. APACHE, SAPS. An i nd ex of w ork l oad and c ons ump ti on of resources , e. g. TISS. A me ans of compari s on for (i ) Aud i t i ng pe rformance —ei the r i n t he sam e ICU or b etw een ICUs. (i i ) Re search, e .g. ev al uati on of new produc ts or treatm ent re gi mens . Pati ent manag eme nt obje ct i ve s, e.g. se dat i on, p res sure are a c are . Other than t he Gl asg ow C oma Sc ore , t here i s no uni v ers al sys tem pract i s ed b y e very ICU. Whi l e APACHE i s t he pre dom i nant sys tem us ed i n the USA and UK for sc ori ng di s eas e s eve ri t y, SAPS i s more popul ar i n mai nl and Europ e. Int erpre tat i on of the same sys tem can also be hi ghl y v ari abl e.

TISS (Therapeutic Intervention Scoring System) Thi s s yst em att aches a sc ore t o proc edures and te chni q ues performed on an i ndi v i dual pat i e nt (e.g . use and numb er of vas oac ti v e d rug i nfus i ons, renal rep l aceme nt the rap y, adm i ni st rat i on of ent eral nut ri t i on). It has bee n used by some ICUs to de vel op a me ans of costi ng i nd i vi dual pat i ents by att achi ng a mone tary v al ue to e ach TISS poi nt sc ore d. It i s al s o used as an i ndex of workl oad act i vi ty. A d i sc harge TISS s core can be use d t o e sti mat e t he amount of nursi ng i nt erv ent i ons requi red for a p ati ent i n ste p-down fac i l i ti es (e.g . a hi gh dep end enc y uni t ) or on the g ene ral ward.

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TISS d oes not ac curat el y me asure nursi ng w ork l oad acti vi t y as i t fai l s t o c ate r for tas ks and duti e s s uc h as copi ng wi th the i rri t abl e or c onfuse d p ati ent , d eal i ng wi th gri ev i ng re l at i ve s, etc .

Glasgow Coma Scale Fi rst des cri be d b y T eas dal e and Jennett i n 1974, i t ut i l i se s e ye openi ng , b est motor re sponse and b est ve rbal res ponse to cat egori s e neurol ogi cal st atus. It i s the onl y sys tem us ed uni versal l y i n ICUs, though l i mi tat i ons e xi s t i n mec hani call y ve nti l a ted , s edat ed pat i ents . It c an be used for p rog nos ti cat i on and i s also frequent l y use d for the rap eut i c dec i s i on maki ng, e.g . el ec ti v e ve nti l a ti on i n p ati ent s p res ent i ng wi th a GCS <8.

Sedation A v ari et y of sy ste ms gauge and rec ord t he l eve l of s edati on i n a me chani c al l y v ent i l ated pati ent . Thi s as si s ts the staff to ti t rat e t he dos e of s edat i v e ag ent s t o avoi d e i ther ove r- or und er-sed ati on. The forerunner dev el oped i n 1974 was the Ramsay Sedati on Score w hi c h c ons i s ts of a 6-poi nt scori ng sys tem se parate d i nto 3 awak e and 3 as l ee p l ev el s where the p ati ent re sponds to a tap or l oud audi tory sti mul us wi t h e i t her bri sk , s l ug gi sh or no res pons e at all . The main probl e m l i es i n ac hi evi ng rep rod uci bi l i t y of the t ap or l oud audi tory s ti mul us. We curre ntl y use an 8-p oi nt sys tem de vel ope d i n-hous e. P.573

Glasgow Coma Scale Score

Eyes open

Best motor response

Best verbal response

6

—

obeys commands

—

5

—

localises pain

orientated

4

spontaneously

flexion withdrawal

confused

3

to speech

decerebrate flexion

inappropriate words

2

to pain

decerebrate extension

incomprehensible sounds

1

never

no response

silent

UCLH Sedation Score 3

Agitated and restless

2

Awake and uncomfortable

1

Aware but calm

0

Roused by voice, remains calm

-1

Roused by movement

-2

Roused by noxious or painful stimuli

-3

Unrousable

A

Natural sleep

P.574

ICU scoring systems—APACHE II APACHE (Acute Physiology And Chronic Health Evaluation) Devi se d by Knaus et al , t hi s sy ste m uti l i s es a p oi nt s core d eri ved from the deg ree of ab normal i ty of re adi l y obtainabl e physi ol ogi cal and l aborat ory vari a bl e s i n t he fi rst 24h of IC U admi ssi on, pl us ext ra poi nts for age and chroni c i l l healt h.

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The sum mat ed score provi d es a m eas ure of sev eri ty whi l e the pe rce ntage ri sk of s ubs equent de ath can b e comp ute d from sp eci fi c c oeffi ci ents app l i e d t o a wi d e rang e of admi ssi on di s ord ers (e xcl udi ng burns and c ard i ac surgery). APACHE I, fi rst de scri b ed i n 1981, uti l i s ed 34 phy si ol og i c al and bi ochemi cal vari a bl e s. A s i mp l i fi ed ve rsi on (APACHE II) uti l i si ng j ust 12 vari a bl e s w as pub l i s hed i n 1985 and ex tensi v el y valid ate d i n a numb er of countri es . A furt her re fi neme nt pub l i s hed i n 1990, APACHE III, cl ai ms to i mp rov e up on the st ati st i cal p red i c ti v e p ower by addi ng fi ve new phy si ol og i cal v ari abl es (al bum i n, bi l i rub i n, g l uc ose , urea, uri ne outp ut). Changi ng t hreshol d s and w ei g hti ng of exi sti ng vari a bl e s. Comp ari ng bot h admi ssi on and 24h s cores. Inc orp orati ng t he adm i ss i on sourc e (e.g . w ard , op erati ng the atre). Reas ses si ng e ffe cts of ag e, c hroni c heal th and sp eci fi c di sease cat egory. Wi de acc ept anc e of APAC HE III may be l i m i te d as i ts ri sk strati fi c at i on sy ste m i s p rop ri e tary and has to be purchase d.

Key paper K naus W A, et al . APACHE II: a s everi t y of di se ase cl ass i fi cat i on sy st em. Cri t C are Me d 1985; 13:818–29

P.575

Acute physiology score +4

+3

+2

+1 38.2–38.9

0

≥41

39–40.9

Mean BP (mmHg)

≥160

130–159

110–129

70–109

50–69

Heart rate (/min)

≥180

140–179

110–139

70–109

55–69

Respiratoryrate (/min)

≥50

35–49

If FIO 2 ≥0.5:A-aDO 2 (mmHg)

≥500

350–499

200–349

If FIO 2 <0.5:PO 2 (mmHg)

12–24

≥7.7

7.6–7.69

Serum Na + (mmol/l)

≥180

160–179

Serum K + (mmol/l)

≥7

6–6.9

155–159

10–11

3

32–33.9

4

6–9

<200

>70

Arterial pH

34–35.9

+2

Core temperature (°C)

25–34

36–38.4

+1

5

61–70

7.5–7.59

7.33–7.49

7.25–7.32

7

150–154

130–149

120–129

1

5.5–5.9

3.5–5.4

3–3.4

2.5–2.9

Serum creatinine (µmol/l)NB double points score if acute renal failure ≥300

171–299

121–170

50–120

<50

Haematocrit (%)

≥60

50–59.9

46–49.9

30–45.9

20–29.9

Leukocytes (/mm 3 )

≥40

20–39.9

15–19.9

3–14.9

1–2.9

Neurological points= 15 - Glasgow coma score

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Age points: Years

≤44

45–54

55–64

65–74

≥75

Points

0

2

3

5

6

Chronic health points 2 p oi nts for el ect i v e post-ope rat i ve ad mi s si on or 5 poi nt s i f e mergency ope rat i on or non-operati ve admi ss i on, i f pat i ent has ei t her: Bi opsy prove n c i rrhos i s , p ort al hyp ert ens i on or previ ous he pat i c fai l ure Chroni c heart fail ure (N YHA Grade 4), Chroni c hypox i a, hy percap ni a , s eve re exe rci se l i mi t ati on, 2° pol yc ythaem i a or pul monary hyp ertensi on Di a l ys i s-dep end ent re nal di sease Immunos upp res si on by d i s eas e or drug s P.576

ICU scoring systems—SAPS II Has a s i mi l a r rol e to APACHE II, but more wi d el y ut i l i sed i n mainl and Europe, the Si mp l i fi ed Ac ute Physi ol ogy Score (SAPS) was de vi s ed by LeGal l et al i n 1984 (SAPS I) and modi fi ed by the s ame group i n 1993 (SAPS II). A SAPS III score i s i n de vel opme nt. As for APACHE II, burns and cardi ac surgi cal pati e nts are e xcl ude d from analys i s . The ori gi nal ve rsi on use d 14 read i l y me asured cl i ni cal and b i oche mi c al vari ab l es whi l e the updated versi on, SAPS II, compri se s 12 p hys i ol ogy vari a bl e s, age , t ype of adm i ss i on (m edi cal , s che dul ed or uns chedul ed surgi cal ) and three unde rl yi ng d i se ase vari a bl e s. A p oi nt s core i s b ase d on t he d egree and prognost i c i m portance of d erange ment of t hes e vari abl es i n the fi rst 24h fol l ow i ng IC U admi ssi on. The p oi nt s cori ng was assi gned fol l owi ng l og i s ti c re gress i on mod el l i ng of d ata obtained from 8369 pat i ents i n 137 ad ul t IC Us i n bot h Europe and North Am eri ca and valid ate d i n a further 4628 pati ents. The cl ai m ed advantage of t hi s s yst em i s that i t e sti mat es the ri sk of death wi t hout havi ng to spe ci fy a pri mary di a gnos i s .

Key paper Le G al l JR, e t al. A new Si m pl i fi ed Acute Phys i ol og y Score (SAPS II) bas ed on a Europ ean/North Am eri can m ul ti c ent er study. JAMA 1993;270: 2957–63

P.577

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Point score in brackets Age

<40 (0); 40–59 (7); 60–69 (12); 70–74 (15); 75–79 (16);≥80 (18)

Heart rate (bpm)

<40 (11); 40–69 (2); 70–119 (0); 120–159 (4);≥160 (7)

Systolic BP (mmHg)

<70 (13); 70–99 (5); 100–199 (0); ≥200 (2)

Body temp (°C)

<39 (0); ≥39 (3)

PaO 2 /FIO 2 (kPa) only if ventilated or on CPAP

<13.3 (11); 13.3–26.5 (9); ≥26.6 (6)

Urine output (l/day)

<0.5 (11); 0.5–0.999 (4); ≥1 (0)

Serum urea (mmol/l)

<10 (0); 10–29.9 (6); ≥30 (10)

White cell count (/mm 3 )

<1 (12); 1–19.9 (0); ≥20 (3)

Serum K + (mmol/l)

<3 (3); 3–4.9 (0); ≥5 (3)

Serum Na + (mmol/l)

<125 (5); 125–144 (0); ≥145 (1)

Serum HCO3 - (mmol/l)

<15 (6); 15–19 (3); ≥20 (0)

Serum bilirubin (µmol/l)

<68.4 (0); 68.4–102.5 (4); ≥102.6 (9)

Glasgow Coma Score

<6 (26); 6–8 (13); 9–10 (7); 11–13 (5); 14–15 (0)

Chronic disease

metastatic cancer (9), haematological malignancy (10), AIDS (17)

Type of admission

scheduled surgical (0); medical (6); unscheduledsurgical (8)

P.578

ICU scoring systems—SOFA A l i m i tati on of t he APACHE and SAPS sc ori ng sys tem s i s that t hey were d esi gne d and val i dated on dat a obtaine d duri ng t he fi rst 24 hours of i nt ens i ve care adm i ss i on. Vari ous s yst ems hav e b een de vel oped to enabl e d ai l y s cori ng (e. g. Seq uenti a l Organ Fai l ure Asse ssm ent (SOFA), R i yadh Int ens i ve Care Program (R IP) sc ore , M ul t i pl e Org an Dys functi on Sc ore , e tc. ) t o al l ow a bet ter as ses sme nt of change i n the pati ent 's condi t i on. As the physi ol ogi cal and b i oc hem i cal s tat us of the pati e nt i s det erm i ne d i n p art by the d i se ase se veri ty , b ut al s o b y the de gre e of me di c al i nterventi on, the se seq uenti a l s cori ng s yst ems i ncorporate the use of v ari ous t herapi es and proced ures. The SOFA sys tem was i ni t i al l y de si g ned to i m prove p ati ent c haract eri sat i on for m ul t i c ent re drug t ri al s i n se psi s (SOFA i ni ti al l y s tood for Sep si s Organ Fail ure As ses sme nt) but has sub seq uentl y be en appl i e d t o i nte nsi ve care pat i ents i n general , wi th ‘Se que nti al ’ be i ng subst i t ute d for ‘Se psi s’ . Al though i t has not been valid ate d i n t he sense that a poi nt sc ore de not i ng se veri ty of dy sfunct i on i n one organ sys tem does not trans l at e d i rect l y to an e qui val ent se veri t y i n another organ, i t has b een us ed suc ces sful l y t o prognosti cate and to fol l ow chang es i n pat i ent s tat us throughout t hei r i nt ens i ve care stay. P.579

Point score in brackets

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0

1

2

3

4

Respiratory PaO 2 :FIO 2 ratio (mmHg)

>400

≤400

≤300

≤200*

<100*

Renal Creatinine (mg/dl) or Urine output (ml/d)

<1.2

1.2–1.9

2.0–3.4

3.5–4.9 or <500ml/d

≥5.0 or <200ml/d

Hepatic Bilirubin (mg/dl)

<1.2

1.2–1.9

2.0–5.9

6.0–11.9

≥12.0

Cardiovascular Mean arterial pressure (mmHg)

No hypo-tension

MAP >70

Dopamine≤5 or dobutamine (any dose)†

Dopamine>5 or epinephrine≤0.1 epinephrine≤0.1†

Dopamine>15 or epinephrine>0.1 epinephrine>0.1†

Haematological Platelet count(×10 3 /mm 3 )

>150

≤150

≤100

≤50

≤20

Neurological Glasgow Coma Score

15

13–14

10–12

6–9

<6

*With ventilatory support †Adrenergic agents administered for at least 1 h (doses in µg/kg/min)

Conversion factors: PaO 2 :FIO 2 to KPa: di vi d e b y 7.5 Creati ni ne t o µ mol /l : mul ti pl y by 88 Bi l i rubi n t o µ mol /l : mul ti pl y by 17.1

Key paper M ore no R, Vi ncent JL, Mat os R, e t al. The us e of maxi m um SOF A s core t o q uanti fy organ d ysfunc ti on/fai l ure i n i nt ens i ve care. Res ul ts of a prosp ect i v e, m ul t i c ent re study. Worki ng Group on Sep si s rel a ted Probl ems of the ESICM. Int ens i v e Care Med 1999; 25:686-96

P.580

ICU scoring systems—trauma Sc ori ng sys tem s have bee n d eve l op ed i n trauma for: Rapi d fi el d t ri age to di rec t t he pat i ent t o appropri at e l eve l s of care Qual i t y assurance Deve l op i ng and i mprovi ng traum a care sys tem s b y c ate gori s i ng pati e nts and i denti fyi ng p rob l em s w i thi n the sys tems Maki ng com pari s ons bet wee n g roups from d i ffere nt hos pi t al s , i n t he sam e hosp i tal over ti me, and/or undergoi ng di fferent treat ment s The Injury Seve ri t y Score (ISS) i s a s everi t y s cori ng sy ste m p ati ent s b ase d on t he anat omi cal i njuri e s s ust ai ned. The Rev i se d T rauma Score (RTS) uti l i s es measures of phys i ol og i cal abnormalit y t o p red i c t s urv i val. A c omb i nati on of ISS and RT S—T RISS—w as dev el oped to ove rcome the short com i ng s of anat omi cal or physi ol ogi c al sc ori ng al one. The TRISS met hod ol ogy use s ISS, RT S, pat i ent age and whether the i njury was b l unt or p ene trati ng to provi d e a measure of the probabi l i t y of survi val .

Injury Severity Score 1. Use AIS90 (Abbrevi ate d Injury Score 1990) di c ti onary t o s core i njury

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2. Identi fy hi g hes t abbrevi ate d i njury scale score for each of t he fol l ow i ng : Head and ne ck Abdomen and pe l vi c c ont ent s Bony pel vi s and l i m bs Face Chest Body surface 3. Add toget her the s quares of the three hi ghe st are a s cores. P.581

Revised trauma score Measure Respiratory rate (breaths/min)

Systolic blood pressure (mmHg)

Glasgow Coma Score

Coded value

10–29

4

>29

3

6–9

2

1–5

1

0

0

>89

4

76–89

3

50–75

2

1–49

1

0

0

13–15

4

9–12

3

6–8

2

4–5

1

3

0

× = Score weighting

0.2908

0.7326

0.9368

Total = revised trauma score

P.582

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07.11.2006 1:04