Pediatric Airway Surgery
Philippe Monnier
Pediatric Airway Surgery Management of Laryngotracheal Stenosis in Infants and Children
Editor Philippe Monnier University Hospital CHUV Otolaryngology, Head and Neck Surgery Rue du Bugnon 46 1011 Lausanne Switzerland
[email protected]
ISBN 978-3-642-13534-7
e-ISBN 978-3-642-13535-4
DOI 10.1007/978-3-642-13535-4 Springer Heidelberg Dordrecht London New York Library of Congress Control Number: 2010937958 © Springer-Verlag Berlin Heidelberg 2011 This work is subject to copyright. All rights are reserved, whether the whole or part of the material is concerned, specifically the rights of translation, reprinting, reuse of illustrations, recitation, broadcasting, reproduction on microfilm or in any other way, and storage in data banks. Duplication of this publication or parts thereof is permitted only under the provisions of the German Copyright Law of September 9, 1965, in its current version, and permission for use must always be obtained from Springer. Violations are liable to prosecution under the German Copyright Law. The use of general descriptive names, registered names, trademarks, etc. in this publication does not imply, even in the absence of a specific statement, that such names are exempt from the relevant protective laws and regulations and therefore free for general use. Product liability: The publishers cannot guarantee the accuracy of any information about dosage and application contained in this book. In every individual case the user must check such information by consulting the relevant literature. Cover design: eStudioCalamar, S.L. Printed on acid-free paper Springer is part of Springer Science+Business Media (www.springer.com)
To all of the children who have endured the nightmare of living with a tracheostomy cannula and to the family members who have gone though frightening experiences while caring for them at home. To my wife Dominique whose constant support and encouragement allowed me to complete this project and prosper in academic medicine. To my teacher and mentor, the late Professor Marcel Savary, who taught me the art of precise observation, documentation, and synthesis
Preface
Paediatric Airway Surgery is the fruit of experience gained over many years to improve the surgical outcome for children suffering from a variety of compromised airways. It focuses on the technical aspects of diagnosis and treatment to provide the reader not only with well-established treatment modalities, but also with new concepts of paediatric airway management. Some ideas may not be shared by all, but should stimulate new thoughts in search of better solutions in the future. This endeavour was induced by numerous foreign colleagues who visited the Lausanne ENT Department to study endoscopic and open surgical airway techniques, particularly cricotracheal resection and its variants. This book is also intended to provide insights into controversial issues pertaining to the most difficult airway reconstructions. The author does not claim to present definite solutions to the challenging problem of the compromised paediatric airway. Nonetheless his modest goal, based on the experience of pioneers, is to add a stone to the pyramid of knowledge in this field of research. With inputs from different horizons, it is hoped that this will one day lead to the full rehabilitation of most tracheostomized children suffering from various forms of laryngotracheal stenosis. Contributors to this book have all been directly implicated in the management of these children and they write from their vast experience. The lead author wishes for this book to reflect the necessary commitment that a paediatric airway surgeon must possess to acquire the stepwise knowledge of subtle diagnostic and therapeutic skills for providing the best possible care for his or her young patients. January 2010 Lausanne, Switzerland
Philippe Monnier
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Acknowledgments
I am thankful to the many colleagues who encouraged me to undertake the project of writing this book on the management of paediatric airway problems. My interest in this field matured with the pioneering work of my mentor, the late Professor Marcel Savary, who performed the first paediatric partial cricotracheal resection in 1978. I am deeply grateful to him for his open mind and his thoughtful and innovative work in endoscopy and head and neck surgery. Thanks to him, I had the opportunity to meet and exchange ideas with F. Griffith Pearson of Toronto, who has been very supportive of the Lausanne group over the years. It is a pleasure and honor to know such a keen and thoughtful thoracic surgeon, and I am greatly indebted to him for his valuable guidance. This book reflects the commitment of a group of colleagues who deal with paediatric airway problems as a team. Madeleine Chollet-Rivier deserves special recognition for being such a knowledgeable and skilled anaesthetist. She makes the management of difficult and compromised airways in infants and children both safe and easy. Marc-André Bernath takes over the skillfull part of anaesthesia for most airway reconstructions, and Jacques Cotting and Marie-Hélène Perez the postoperative care in the paediatric Intensive Care Unit. They all deserve recognition for their efficient and professional work. Mercy George from Vellore, India, played a special role as an independent reviewer of the surgical results of paediatric partial cricotracheal resections performed in Lausanne, focusing on different aspects of the problem. She also made thoughtful remarks about the manuscript that she read as a first editor, and deserves special acknowledgement. Finally, this project would never have been possible without the commitment of Kapka Batchvaroff, my secretary, who, with dedication and patience, and commitment performed the difficult tasks of word and reference processing. She must be congratulated for her hard work. No text dedicated to endoscopic and surgical techniques is self-explanatory without high-quality illustrations. Marion Brun-Baud and Anthony Guinchard have lent their master command of computer programs and their understanding of anatomical details to meticulously create the beautiful medical art work throughout the book. I am grateful for their contribution. Last but not least, I must express special thanks to my colleagues who ran the ENT department while I was working on Paediatric Airway Surgery.
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Contents
Part I Evaluation of the Compromised Paediatric Airway 1 The Compromised Paediatric Airway: Challenges Facing Families and Physicians . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
3
2 Applied Surgical Anatomy of the Larynx and Trachea . . . . . . . . . . . .
7
3 Clinical Evaluation of Airway Obstruction . . . . . . . . . . . . . . . . . . . . . .
31
4 Equipment and Instrumentation for Diagnostic and Therapeutic Endoscopy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
45
5 Endoscopic Assessment of the Compromised Paediatric Airway . . . .
77
Part II Congenital Anomalies of the Larynx and Trachea 6 Laryngomalacia (LM) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
99
7 Vocal Cord Paralysis (VCP) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 107 8 Congenital Subglottic Stenosis (C-SGS) . . . . . . . . . . . . . . . . . . . . . . . . . 119 9 Laryngeal Web and Atresia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 125 10 Subglottic Haemangioma (SGH) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 133 11 Ductal Cysts, Saccular Cysts and Laryngoceles . . . . . . . . . . . . . . . . . . . 141 12 Laryngeal and Tracheal Clefts . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 147 13 Congenital Tracheal Anomalies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 157 Part III Acquired Laryngeal and Tracheal Stenoses 14 Acquired Post-Intubation and Tracheostomy-Related Stenoses . . . . . 183 15 External Laryngeal Trauma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 199 16 Neoplastic Lesions of the Larynx and Trachea . . . . . . . . . . . . . . . . . . . 217
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Part IV Surgery for Laryngotracheal Stenosis 17 Preoperative Assessment, Indications for Surgery and Parental Counselling . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 231 18 Endoscopic Techniques for Laryngotracheal Stenosis . . . . . . . . . . . . . 241 19 Laryngotracheoplasty and Laryngotracheal Reconstruction . . . . . . . . 257 20 Partial Cricotracheal Resection . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 279 Part V Tracheal Surgery and Revision Surgery 21 Tracheotomy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 325 22 Tracheal Resection and Anastomosis . . . . . . . . . . . . . . . . . . . . . . . . . . . 337 23 Revision Surgery . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 349 Appendix . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 359 Index . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 361
Contents
Contributors
Marc-André Bernath, MD Clinical Instructor, Staff Department of Anaesthesiology, University Hospital CHUV, Rue du Bugnon 46, CH-1011 Lausanne, Switzerland Madeleine Chollet-Rivier, MD Clinical Instructor, Staff Department of Anaesthesiology, University Hospital CHUV, Rue du Bugnon 46, CH-1011 Lausanne, Switzerland Jacques Cotting, MD Clinical Instructor, Head of the Paediatric Intensive Care Unit, Department of Paediatrics, University Hospital CHUV, Rue du Bugnon 46, CH-1011 Lausanne, Switzerland Mercy George, MD Associate Professor, Department of Otolaryngology, Head and Neck Surgery, Christian Medical College, Vellore 632004, India Marie-Hélène Perez, MD Staff, Paediatric Intensive Care Unit, Department of Paediatrics, University Hospital CHUV, Rue du Bugnon 46, CH-1011 Lausanne, Switzerland
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Abbreviations
ACCG ACS AE ARDS ArF ARS ASA A-SGS BAL BiPAP BVCP CA CAA CCG CNS CO2 CPAP CS C-SGS CT CTR CTS CW D DNA DS DS-LTR DS-PCTR I-3C ECMO ENT EO EPP ET ET-CO2 ETT EXIT
Anterior costal cartilage graft Anterior cricoid split Aryepiglottic (folds) Acute respiratory distress syndrome Argon fluoride (laser) Airway reconstruction surgery American Society of Anesthesiology Acquired subglottic stenosis Broncho-alveolar lavage Bi-level positive airway pressure Bilateral vocal cord paralysis Cricoarytenoid Cricoarytenoid ankylosis Costal cartilage graft Central nervous system Carbon dioxide Continuous positive airway pressure Corticosteroids Congenital subglottic stenosis Computerised tomography Cricotracheal resection Cricotracheal stenosis Continuous working (laser) Digital Desoxyribonucleic acid Double-stage Double-stage laryngotracheal reconstruction Double-stage partial cricotracheal resection Indol-3 carbinol Extracorporal membrane oxygenation Ear-nose-throat Eosinophilic oesophagitis Epiglottic petiole prolapse Endotracheal End-tidal carbon dioxide Endotracheal tube Ex-utero intrapartum treatment xv
xvi
Extended PCTR Partial cricotracheal resection combined with an additional open airway procedure FEES Functional endoscopic evaluation of swallowing GOR Gastro-oesophageal reflux GORD Gastro-oesophageal reflux disease He-Ne Helium neon (laser) HPV Human papilloma virus Hz Hertz ICU Intensive care unit ILCSI Intra-lesional corticosteroid injection JORRP Juvenile-onset recurrent respiratory papillomatosis KTP Potassium-titanyl phosphate (laser) LASER Light amplification by stimulated emission of radiations LC Laryngeal cleft LM Laryngomalacia LSCTS Long-segment congenital tracheal stenosis LT Laryngotracheal LTOC Laryngotracheo-oesophageal cleft LTP Laryngotracheoplasty LTR Laryngotracheal reconstruction LTS Laryngotracheal stenosis MMC Mitomycin C MRI Magnetic resonance imaging MRSA Methicillin-resistant staphylococcus aureus Nd-YAG Neodymium: yttrium-aluminum-garnet (laser) NIBP Non-invasive blood pressure NIV Non-invasive ventilation NPO Nil per oral OA Oesophageal atresia OH Obstructive hypopnea OSA Obstructive sleep apneoa OSAS Obstructive sleep apneoa syndrome PCC Posterior costal cartilage PCCG Posterior costal cartilage graft PCTR Partial cricotracheal resection PEEP Positive end expiratory pressure PEG Percutanous endoscopic gastrostomy PGS Posterior glottic stenosis PICU Paediatric intensive care unit PPI Proton pump inhibitors RAE Ring-Adair-Elwin (tubes) RDA Recommended dietary allowances RDS Respiratory distress syndrome RLN Recurrent laryngeal nerve RRP Recurrent respiratory papillomatosis RSV Respiratory syncytial virus SAL Secondary airway lesion SEMAS Self-expandable metallic airway stent SG Subglottis, subglottic
Abbreviations
Abbreviations
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SGH Subglottic haemangioma SGS Subglottic stenosis SGSa Isolated subglottic stenosis SGSb Isolated subglottic stenosis with comorbidities SGSc Subglottic stenosis combined with glottic involvement SGSd Subglottic stenosis combined with glottic involvement and comorbidities SLN Superior laryngeal nerve SML Suspension microlaryngoscopy SpO2 Saturation in pulse-oxymetry SS Single-stage SS-LTR Single-stage laryngotracheal reconstruction SS-PCTR Single-stage partial cricotracheal reconstruction TC-CO2 Transcutaneous carbon dioxide TCI Target controlled infusion TIVA Total intravenous anaesthesia TNFL Transnasal fibre-optic laryngoscopy TOF Tracheo-oesophageal fistula UAR Upper airway resistance UVCP Unilateral vocal cord paralysis VC Vocal cord VCP Vocal cord paralysis W Watt
Part Evaluation of the Compromised Paediatric Airway
This first part of Paediatric Airway Surgery is dedicated to the clinical evaluation of airway obstruction and the assessment of the compromised paediatric airway. All too often, these preoperative investigations are not conducted in a precise, systematic, and rigorous manner (for example, there is an unclear assessment of vocal cord mobility, degree and extent of laryngeal stenosis, concomitant airway anomalies, and comorbidities). This may lead to inappropriate selection of operative procedures, and consequently, the failure of the initial airway reconstruction. Knowing that the patient’s best chances lie in the first operation, a thorough preoperative assessment is a prerequisite for a successful outcome.
In order to achieve this goal, part I of Paediatric Airway Surgery reviews relevant anatomical landmarks of the larynx and trachea with respect to surgical airway procedures, as well as the necessary equipment for diagnostic and therapeutic endoscopy. Finally, information on endoscopic techniques used for dealing with different degrees of paediatric airway comprise is provided, and the preoperative assessment of the tracheostomised child with known airway obstruction (the most common situation encountered prior to airway reconstruction) is explained in detail. This provides the reader with a surgical strategy before engaging in difficult airway procedures (please also refer to chapter 17, part IV).
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I
1
The Compromised Paediatric Airway: Challenges Facing Families and Physicians
Contents References............................................................................
Core Messages 5
›› Tracheostomy
›› ››
›› ››
in infants and children has a strong negative impact on the quality of life of parents and families due to: –– Fear of death from plugged cannula –– The frightening experience of changing tracheostomy tubes –– Anxiety about speech development –– A profound change of lifestyle –– Sibling rivalry and jealousy toward the tracheostomised child Surgery must be performed early to shorten tracheostomy dependence. Resection and anastomosis for severe subglottic stenosis (SGS) yield better operation-specific decannulation rates than laryngotracheal reconstruction. Expertise in endoscopy and open surgery is mandatory. The patient’s best chance lies in the first operation.
Paediatric laryngotracheal stenosis (LTS) encompasses a variety of congenital and acquired conditions that require precise assessment and tailored treatment for each individual patient. About 90% of acquired conditions are represented by subglottic stenosis (SGS) resulting as a complication of tracheal intubation [1, 14]. In this case, medical history often includes an extubation failure following an endotracheal intubation period in the paediatric intensive care unit (PICU), leading to tracheostomy. This procedure usually has a strong negative impact on the child’s family. P. Monnier (ed.), Pediatric Airway Surgery, DOI: 10.1007/978-3-642-13535-4_1, © Springer-Verlag Berlin Heidelberg 2011
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1 The Compromised Paediatric Airway: Challenges Facing Families and Physicians
As John Graham stated 20 years ago, ‘The child’s family enters a long tunnel of fear and apprehension, mixed with episodes of panic, isolation, militancy, and despair’ [7]. Despite considerable progress in the management of paediatric LTS over the past 30 years [2, 8, 12], primary surgery still fails in a significant number of complex LTS cases [9, 13]. In the most severe grades of SGS combined with glottic involvement, the primary surgery fails around 30% of the time, even with the latest available techniques [5]. In the worst-case scenario following failure, patients will require revision surgery with maintenance of the tracheostomy tube for months or even years. As far as the parents are concerned, the tunnel of fear continues. In tertiary care centres that handle only a few paediatric patients with compromised airways each year, it is frequently impossible to assemble the different medical professionals required to deliver comprehensive care for these difficult cases [15]. Families of tracheostomised children are often left alone with immense challenges at home. Medical practitioners frequently underestimate the responsibilities resting on the parents’ shoulders. Though not all cases are identical, many families report similar experiences. Parental anxiety results largely from the possibility of a plugged cannula, which can occur during the night with adverse outcomes. Despite in-home devices like oximeters and cardiorespiratory monitors, anxious parents tend to spend sleepless nights. As the literature reports a 1–3% risk of infant death from a plugged cannula in most series, it is clear that parents’ concerns are not unwarranted [15]. Another cause for concern among parents is the fear associated with changing the tracheostomy tube. Despite adequate training at the hospital, parents feel very uncomfortable when left to perform this procedure at home [6]. This experience is often terrifying: ‘It is important not to underestimate how it feels to be responsible for removing your child’s only way of breathing, and register, however briefly, his colour change and desperate struggle for breath. The emotional turmoil is awful’. Beyond these initial feelings of fear (‘I’ll do it wrong’), disgust (‘the wound makes me feel sick’), grief (‘why did this happen to me’), and anger (‘you’ve done this to my baby and now you want me to help’), the family must struggle through many other difficulties, all of which are major issues.
Families must cope with ‘seeing a hole in their child’s neck with a pipe stuck into it’, and ask themselves whether it will eventually be possible to get rid of it, whether the child will one day be able to speak, and how delayed speech is going to affect the child’s development. These questions hang over their heads like the sword of Damocles. The strain on the parents’ relationship as a result of a complete lifestyle change has a profound effect on the rest of the family. The negative impact of the tracheostomised child on his or her siblings is highlighted by the following thought: ‘Trying to provide security and be a supportive, loving parent for healthy siblings whilst worrying about a very sick child is virtually impossible’. This situation undoubtedly generates disturbed behaviour in siblings, who become jealous of the tracheostomised child. Establishing new relationships also becomes difficult, particularly for single women. Parents require supportive family members and friends to share the responsibility of changing the tracheostomy tube. However, it is difficult for others to accept this role, for fear that an adverse event should occur while they are taking care of the child. Only rarely does this shared anxiety strengthen a couple’s relationship. Parents are most often left alone with these responsibilities. Outside the hospital, they receive minimal professional support, and caregivers frequently lack special training in handling tracheostomised infants and children. Sooner or later, parents become more knowledgeable about tracheostomies than most nurses, and find that ‘They became better at sucking their child out than anyone else’. However, the possibility of returning to the hospital is considered a relief due to fear of being unable to cope in the long run. Peer group support for these parents does not exist in all communities. Often the parents themselves take the initiative and get to know other parents with similar challenges. Expressing one’s own feelings to someone ‘unofficial’ is of great relief: ‘It helps immeasurably to know that one is not alone’. Medical professionals facing challenging technical issues frequently ignore the family’s experience. As John Graham said [7], ‘Seldom can a small being provide such large problems for so many people for so long a period of time’. ENT surgeons, intensivists, anaesthetists, and nurses play a key role in the preoperative assessment, surgical management, and postoperative care of children undergoing surgery for
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References
LTS. In addition, inputs from pneumologists, gastroenterologists, cardiologists, neurologists, and geneticists are requested, depending on the associated comorbidities or congenital anomalies. Appropriate care for children with LTS requires a high level of integration of the aforementioned services, and the surgical management should be restricted to institutions with appropriate instrumentation and personnel. It is essential that the managing surgeon discusses every case with his or her team to avoid potential unforeseen complications during the course of the treatment. Finally, speech therapists should be involved in managing both voice and deglutition problems. They should also be part of the team assessing the child’s ability to cooperate before the surgery and supporting rehabilitation of speech and swallowing in the postoperative period. In many countries, families remain inadequately supported. This situation is unlikely to improve significantly, because the number of cases per year remains low in most institutions dealing with these problems. Contrarily, improving one’s own skills and techniques in endoscopy and surgery can shorten the time of tracheostomy dependence and relieve the whole family of this difficult time. The policy of waiting until the newborn’s body weight reaches 10 kg to perform primary surgery should not be the standard of care. Recent experiences in different medical centres [3, 10, 11] have shown that the post-operative results of partial cricotracheal resections (PCTR) in infants weighing less than 10 kg are as good as those in older children. Furthermore, selecting a resection and anastomosis technique (PCTR) for the treatment of severe (subtotal or total) SGS increases significantly the operation-specific decannulation rates [4, 9]. Even if the family has to spend a period of several weeks of intensive care at the hospital, the acceptance is high in comparison with repeated operations over several months or years. The light at the end of the tunnel is seen when the child is released of the tracheostomy tube. Only then can the whole family dream of a new and better life. The profound gratitude parents show the surgeon and the medical team is a testimony to the suffering they endured during a period of months or years. To cope with each possible situation, expertise in diagnostic and therapeutic endoscopies and adequate training in LTR and PCTR are mandatory. Therefore, the surgeon should be committed to make all possible
efforts to receive training in this sub-speciality so as to give the best care possible for LTS patients. The first operation is a great responsibility, as it is here that the patient’s greatest chance lies. Failure of the first surgical attempt inevitably worsens the outcome and prolongs tracheostomy dependence. Acknowledgments The content of this introduction is largely based on quotations from interviews made in 1986 by Mrs. Penny Jennings and reported in the Journal of Laryngology and Otology (Supplement 17) 1988:25–29. The sentences in quotation marks originate from the article entitled ‘The Parent’s View’, written by Mrs. Penny Gillinson [6]. We would like to express our gratitude to the authors for the permission to use their work.
References 1. Benjamin, B., Holinger, L.D.: Laryngeal complications of endotracheal intubation. Ann. Otol. Rhinol. Laryngol. 117(suppl 200) :2–20 (2008) 2. Cotton, R.T.: Management of subglottic stenosis. Otolaryngol. Clin. North Am. 33, 111–130 (2000) 3. Garabedian, E.N., Nicollas, R., Roger, G., et al.: Cricotracheal resection in children weighing less than 10 kg. Arch. Otolaryngol. Head Neck Surg. 131, 505–508 (2005) 4. George, M., Ikonomidis, C., Jaquet, Y., et al.: Partial cricotracheal resection in children: potential pitfalls and avoidance of complications. Otolaryngol. Head Neck Surg. 141, 225–231 (2009) 5. George, M., Jaquet, Y., Ikonomidis, C., et al.: Management of severe pediatric subglottic stenosis with glottic involvement. J. Thorac. Cardiovasc. Surg. 139, 411–417 (2010) 6. Gillinson, P.: Acquired subglottic stenosis in infants. The parent’s view. J. Laryngol. Otol. Suppl. 17, 41–44 (1988) 7. Graham, J.: Introduction. J. Laryngol. Otol. Suppl. 17, 1 (1988) 8. Gustafson, L.M., Hartley, B.E., Liu, J.H., et al.: Singlestage laryngotracheal reconstruction in children: a review of 200 cases. Otolaryngol. Head Neck Surg. 123, 430–434 (2000) 9. Hartnick, C.J., Hartley, B.E., Lacy, P.D., et al.: Surgery for pediatric subglottic stenosis: disease-specific outcomes. Ann. Otol. Rhinol. Laryngol. 110, 1109–1113 (2001) 10. Ikonomidis, C., George, M., Jaquet, Y., et al.: Partial cricotracheal resection in children weighing less than 10 kilograms. Otolaryngol. Head Neck Surg. 142, 41–47 (2010) 11. Johnson, R.F., Rutter, M., Cotton, R.T., et al.: Cricotracheal resection in children 2 years of age and younger. Ann. Otol. Rhinol. Laryngol. 117, 110–112 (2008) 12. Ndiaye, I., Van de Abbeele, T., Francois, M., et al.: Traitement chirurgical des sténoses laryngées de l’enfant. Ann. Otolaryngol. Chir. Cervicofac. 116, 143–148 (1999)
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13. Rizzi, M.D., Thorne, M.C., Zur, K.B., et al.: Laryngotracheal reconstruction with posterior costal cartilage grafts: outcomes at a single institution. Otolaryngol. Head Neck Surg. 140, 348–353 (2009) 14. Walner, D.L., Loewen, M.S., Kimura, R.E.: Neonatal subglottic stenosis-incidence and trends. Laryngoscope 111, 48–51 (2001)
15. Wetmore, R., Thompson, M., Marsh, R., et al.: Pediatric tracheostomy: a changing procedure? Ann. Otol. Rhinol. Laryngol. 108, 695–699 (1999)
2
Applied Surgical Anatomy of the Larynx and Trachea
Contents
Core Messages
2.1 Position of the Larynx and Trachea in the Neck.......
8
2.2 Laryngotracheal Framework......................................
9
›› Due to the rostral position of the thyroid carti-
2.3 The Larynx’s Intrinsic Musculature.......................... 11 2.4 Innervations of the Larynx......................................... 12
››
2.5 Vascular Supply of the Larynx and the Trachea...... 14 2.6 Endoscopic Anatomy................................................... 15 2.7 Morphometric Measurements of the Larynx and Trachea.................................................................... 16 2.7.1 Larynx Morphometry.................................................. 16 2.7.2 Trachea Morphometry................................................. 18 2.8 Laryngeal Stents........................................................... 2.8.1 Aboulker Stent............................................................ 2.8.2 Montgomery T-Tube................................................... 2.8.3 Healy Paediatric T-Tube.............................................. 2.8.4 Montgomery LT-Stent................................................. 2.8.5 Eliachar LT-Stent........................................................ 2.8.6 Monnier LT-Mold........................................................
19 19 20 21 22 22 23
2.9 Tracheal Stents............................................................. 24 2.10 Appendix 1.................................................................. 27
››
›› ››
››
2.11 Appendix 2.................................................................. 27 2.12 Appendix 3.................................................................. 27 References............................................................................ 28
›› ›› ›› ››
lage in the neck, laryngeal release procedures do not induce dysphagia and aspiration in infants and small children. When performing a vertical laryngofissure, it is important to transect the anterior commissure of the larynx, precisely in the midline. The conus elasticus creates a dome-shaped subglottis that cannot accommodate the proximal end of a Montgomery T-tube without causing significant complications. When a paediatric airway stenosis is resected, the length must be measured by the number of tracheal rings, and not in centimetres. In surgeries requiring resection of a diseased airway segment, the surgeon must have a detailed anatomical understanding of the larynx’s and the trachea’s blood and nerve supply. Surgeons and anaesthetists should use a chart detailing airway dimensions and their matching endotracheal tubes, tracheostomy cannulae and rigid bronchoscopes. Normal age-related endotracheal tubes are always slightly too large for the posterior paediatric interarytenoid glottis. Proper stents must be used for splinting airway reconstructions in order to avoid undue laryngotracheal damage. Tubular (cigar-shaped) stents are inadequate for splinting the glottis and subglottis. A dedicated, soft and atraumatic laryngotracheal stent is essential for preventing damage to the reconstructed airway.
P. Monnier (ed.), Pediatric Airway Surgery, DOI: 10.1007/978-3-642-13535-4_2, © Springer-Verlag Berlin Heidelberg 2011
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This chapter does not attempt to provide a comprehensive description of laryngotracheal anatomy, which has already been given in other textbooks [5, 26, 29, 30, 57, 60]. Instead, it highlights the relevant anatomical features that are specific to surgical or endoscopic airway procedures for paediatric airway surgeons. This chapter also examines airway dimensions in relation to endotracheal tubes (ETT), tracheostomy cannulae, rigid bronchoscopes and stents used in these procedures.
2.1 Position of the Larynx and Trachea in the Neck The larynx is suspended posteriorly at the skull base by the constrictor muscles and attached anteriorly to the hyoid bone and mandible by the thyrohyoid, digastric, stylohyoid, geniohyoid and mylohyoid muscles (Fig.2.1). Because of a shortened thyrohyoid membrane, the upper rim and the thyroid cartilage notch rest posterior or just inferior to the hyoid bone. Thus, a laryngeal release procedure (see Sect. 20.7, Chap. 20), combined with an airway resection, does not provoke
Fig. 2.1 Anterior muscular suspension of the larynx in the neck: One strap muscle, the thyrohyoid, suspends the larynx to the hyoid bone, while the suprahyoid muscles indirectly suspend the larynx to the mandible. Please note the high position of the thyroid cartilage in the neck and the ensuing long cervical trachea segment. Extrinsic laryngeal muscles: (1) digastric, (2) stylohoid, (3) mylohyoid, (4) sternocleidomastoid, (5) thyroidhyoid, (6)sternothyroid, (7) cricothyroid, (8) sternohyoid and (9) omohyoid
2 Applied Surgical Anatomy of the Larynx and Trachea
swallowing or aspiration problems in paediatric patients, provided that the vocal cord function is preserved. In infants and children, this procedure is markedly better tolerated than in adults. The high position of the infant larynx in the neck explains why the cervical trachea segment is proportionally longer than in adults. In newborns, there are approximately 10 tracheal rings above the sternal notch. In adolescents and young adults, there are approximately eight tracheal rings, while in older adults there are six or less, depending on individual anatomy [26]. Due to this greater number of tracheal rings, surgical airway resections are technically easier to perform in children than in adults. Children’s tissue elasticity also facilitates cranial mobilisation of the tracheal stump during surgery. On sagittal section, the infant larynx is located at the level of the third or fourth cervical vertebra, and it starts to descend at around 2 years of age, reaching the level of the sixth or seventh vertebra by adulthood [30, 34] (Fig.2.2). Phylogenetically, the newborn is similar to non-human primates [35]. The tip of the epiglottis rests behind the soft palate in both species. This anatomical situation allows simultaneous breathing and suckling without any risk of aspiration, also explaining
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2.2 Laryngotracheal Framework
a
b
Fig. 2.2 Sagittal section of the infant and adult larynges: (a) The infant larynx is positioned high in the neck at C3–C4 level. (b) As a result of the acquisition of articulated speech during the
phylogenetic evolution of species, the adult larynx is positioned at C6–C7 level
the preferential nasal breathing and absence of articulated speech (Fig. 2.3). Articulated speech was made possible only by the descent of the larynx at the time of Homo sapiens, during the evolution from primates to humans approximately 400,000 years ago. However, recent studies assign this acquisition to direct corticolaryngeal connections in humans [21, 22].
• In a full-term newborn baby, the length of the glottis is approximately 7 mm (range 6–8 mm), and the width of the posterior glottis is 3–4 mm. • Infant arytenoid cartilages are larger and longer, comprising slightly more than 50% of the anteroposterior glottis until 3 years of age. This ratio drops to 20% in adults. • The interarytenoid distance represents approximately 60% of the inner subglottic diameter in newborns, and more than 70% of this diameter in adults. • Cuneiform cartilages are proportionally larger in infants than adults; they are not directly connected with the arytenoid cartilages. • The cephalad half of the infant cricoid is V-shaped and becomes rounded at its lower level (Fig. 2.5b and c). • The cartilages of the infant larynx are softer and more pliable than in adults. • The mucosae of the supraglottis and subglottis are lax in infants and hence more prone to oedema when inflamed or injured.
2.2 Laryngotracheal Framework (Fig. 2.4) The infant larynx is different from the adult larynx, as summarised below [30]: • Its size is approximately one-third of the adult larynx. • The infant thyrohyoid membrane is much shorter, and the thyroid notch is behind the hyoid bone. • The thyroid cartilage is V-shaped in adults, but more rounded in children (Fig. 2.5a).
10
2 Applied Surgical Anatomy of the Larynx and Trachea
a
b
Fig. 2.3 Similarities of the newborn (a) and primate (b) larynges: The tip of the epiglottis rests behind the uvula of the soft palate in both species due to the high position of the larynx in
the neck. While simultaneous breathing and suckling are possible, articulated speech is not. (Reproduced from Laitman [35]. With permission)
SUPRAGLOTTIS
GLOTTIS
SUBGLOTTIS
a
b
Fig. 2.4 Frontal, axial, coronal and sagittal views of the infant larynx: (a) The thyroid cartilage is partially concealed behind the hyoid bone (frontal view). (b) The thyroid cartilage has a blunt, round-shaped curvature at the level of the anterior commissure (axial view). (c) The subglottis is larger than the glottis,
c
d
giving an inverted funnel shape to the subglottis in this section (coronal view). (d) The antero-posterior distance at the glottic level is much greater than the diameter of the subglottis at the cricoid level (sagittal view). The size of the arytenoid occupies approximately one-half of the glottic length
11
2.3 The Larynx’s Intrinsic Musculature
a
b
c
Fig. 2.5 Horizontal histological sections of the infant larynx. (Reproduced from Holinger, Chicago [32]. With permission.) (a) The thyroid cartilage is round and not V-shaped as in adults; the arytenoids are long, contributing to one-half of the glottic length; the cricoid plate is slightly V-shaped (section at the
g lottic level). (b) Due to the V-shaped configuration of the upper cricoid, the subglottic lumen is elliptical (section at the midportion of the cricoid cartilage). (c) At the lower level of the cricoid cartilage, the lumen is round-shaped
A thorough knowledge of the infant and child larynx calls for the following medical and surgical decisions:
• A postoperative mucosal oedema of the glottis and subglottis is more prominent in infants and children than adults. Therefore, there is a greater need for temporary postoperative intubation after singlestage PCTR in the paediatric age group.
• When performing a full laryngofissure or a partial cricotracheal resection (PCTR), the thyrohyoid membrane must often be sectioned along the thyroid cartilage’s upper rim to release the thyroid cartilage from its cranial attachment and move it into the operative field. • Performance of a precise vertical midline thyrotomy through the larynx’s anterior commissure can be difficult in a round-shaped anterior thyroid cartilage. This necessitates a vertical incision through the epiglottis at the level of the thyroid notch, which allows airway division under visual control without damaging the anterior commissure; this is especially relevant when the vocal cords are fused by a laryngeal web or synechia. • Owing to longer arytenoids, a shorter interarytenoid distance and a V-shaped cephalad cricoid, endotracheal intubation may damage the medial aspect of the arytenoids and postero-lateral portion of the cricoid ring (see Sect. 14.1, Chap. 14) [4]. • When performing a CO2-laser supraglottoplasty for laryngomalacia, part of the cuneiform cartilages must be vaporised to obtain a less bulky aryepiglottic fold and induce submucosal fibrosis. • The pliability of the thyroid cartilage allows the surgeon to increase the subglottic lumen during PCTR by performing an inferior midline thyrotomy; this permits a better adaptation of the larger tracheal ring used for the thyrotracheal anastomosis (see Sect. 20.3, Chap. 20).
The infant and child trachea has the same overall configuration as the normal adult trachea, except for its size [26]. From birth to late adolescence, the trachea more than doubles in length, triples in diameter and increases by sixfold in cross-sectional area, while maintaining the same architecture of 16–20 horseshoeshaped tracheal rings [60]. The posterior membranous trachea is flexible and consists of fibro-elastic and muscular tissue layers (Fig. 2.6).
2.3 The Larynx’s Intrinsic Musculature (Fig. 2.7) Of the intrinsic laryngeal muscles, the posterior cricoarytenoid muscle is the only abductor of the vocal cords. All other muscles are either adductors (paired lateral cricoarytenoid, unpaired interarytenoid) or tensors of the vocal cords (paired thyroarytenoid, including the vocalis muscle). It is worth noting that the function of each muscle changes slightly depending on the position of the vocal cords. During phonation, for example, the posterior cricoarytenoid muscle counteracts the thyroarytenoid muscle’s tensor function in order to stabilise the arytenoid cartilage. This type of interaction between agonist and antagonist muscles is essential for balanced
12
2 Applied Surgical Anatomy of the Larynx and Trachea Vocalis Lateral thyroarytenoid
Muscular process of arytenoid Transverse interarytenoid
Vocal ligament
Cricothyoid
Lateral cricoarytenoid Posterior cricoarytenoid
Fig. 2.7 Intrinsic muscles of the larynx (posterior to anterior superior view): In the infant, location and function of all intrinsic muscles are identical to those of the adult
Fig. 2.6 Infant trachea: The general configuration is similar to that of the adult with 16–20 horseshoe tracheal rings and a pars membranacea. Its size is only 50% in length, 36% in diameter and 15% in cross-sectional area, as compared to the adult’s
laryngeal function. Two other slip muscles, the thyroepiglotticus and the aryepiglotticus (not shown in Fig. 2.7), play minor additional roles: The former improves the sphincteric effect of the laryngeal vestibule and the latter shortens the vocal ligament, producing a low-pitched voice [57]. The cricothyroid, an extrinsic muscle of the larynx, also acts as a tensor of the vocal cords, and helps raise the voice’s pitch (Fig. 2.8). Therapeutic surgical or endoscopic interventions may enhance previous trauma (vocal cord palsy, cicatricial stenosis, etc.) and further damage the functions of these delicate muscles: • Laryngotracheal reconstruction (LTR) with anterior costal cartilage graft and PCTR both abolish the cricothyroid muscle’s function (see Chaps. 19 and 20). • During PCTR, the lateral cricoarytenoid muscle must be preserved in order to maintain stability of the arytenoid cartilage and prevent arytenoid
prolapse during phonation in the postoperative period. This is even more essential if a subglottic stenosis is combined with a posterior glottic stenosis (PGS). The procedure usually requires complete transection of the interarytenoid muscle to enlarge the larynx’s posterior commissure; this may eventually destabilise the arytenoids. Extended PCTR with intussusception of the thyrotracheal anastomosis preserves the lateral cricoarytenoid muscle’s function and helps prevent arytenoid prolapse (see Sect. 20.5, Chap. 20).
2.4 Innervations of the Larynx (Fig. 2.9) The sensory and motor nerve supply of the larynx originates bilaterally from the vagus nerve. Although the recurrent laryngeal nerve (RLN) provides the sensory supply to the infraglottis, its main function is to provide the motor supply to the intrinsic laryngeal muscles. The superior laryngeal nerve (SLN) predominantly provides the sensory supply to the supraglottis and glottis, but its external branch also provides the motor supply to the cricothyroid muscle. The ansa Galeni, an anastomosis between the SLN’s internal branch and one of the RLN’s branches, provides the accessory motor and predominant sensory supply to endolaryngeal structures. To preserve the larynx’s function, it is absolutely necessary that the laryngotracheal surgeon has detailed knowledge of the SLN’s and RLN’s courses in the laryngeal region.
13
2.4 Innervations of the Larynx
1/2 1/2
a
b
Fig. 2.8 Function of the cricothyroid muscle: (a) Resting position of the cricothyroid muscle. In infants, the anterior commissure of the larynx is positioned slightly below the mid-distance point between the thyroid notch and the inferior border of the
thyroid cartilage. (b) Contracting position of the cricothyroid muscle: During contraction, the cricothyroid distance is shortened, and the vocal ligament is stretched, raising the voice pitch. This function is lost in LTR and PCTR
Internal branch SLN Ansa Galeni
External branch RLN
Fig. 2.9 Innervations of the larynx:∙ SLN: The internal branch provides sensory function to the supraglottis and glottis– The external branch provides motor function to the cricothyroid muscle∙ RLN: Provides motor function to all intrinsic muscles– Provides sensory function to the infraglottis∙ Ansa Galeni: Provides weak motor and strong sensory functions to the endolaryngeal structures
Fig. 2.10 Relationship of the RLNs with the cricothyroid joint: horizontal section at the level of the cricothyroid membrane (diagram): (1) RLN, (2) cricothyroid joint, (3) cricoid plate, (4) posterior cricoarytenoid muscle, (5) cricothyroid muscle, (6) lateral cricoarytenoid muscle and (7) cricothyroid membrane. The RLNs are located immediately behind the cricothyroid joints
The RLN originates from the vagus nerve. On the left, in the thorax, the RLN separates from the vagus nerve, passes around the aortic arch, then travels back cranially in the tracheo-oesophageal groove, and eventually reaches the larynx just posterior to the cricothyroid joint. On the right, the RLN passes under the subclavian artery, runs cranially in the tracheo-oesophageal groove, as it does on the opposite side, and enters the larynx just behind the cricothyroid joint [58]. Due to their considerable length, both RLNs are at risk of injury during intra-thoracic surgery on the left side,
and laryngotracheal, pharyngo-esophageal and thyroid surgeries on both sides of the neck. The entry point of the RLN into the larynx is just behind and below the cricothyroid joint. At this level, it is protected by the inferior constrictor muscle and the cricothyroid muscle (Fig. 2.10). In about 90% of cases, the RLN divides into two to three branches just a few millimetres before entering the larynx underneath the inferior constrictor muscle [53]. The posterior branch runs just behind the mucosa of the posterior cricoarytenoid muscle, where it lies in close contact
14
with the cricoid plate’s lower edge. During a thyrotracheal anastomosis, the surgeon must be aware of potential nerve damage while placing stitches through the cricoid plate. The SLN leaves the vagus nerve trunk at the level of the nodose ganglion. It runs transversally behind the carotid artery, approaches the larynx with the superior laryngeal branch of the superior thyroid artery, then penetrates the thyrohyoid membrane anterior to the lateral thyrohyoid ligament and at mid-distance between the upper thyroid rim and the hyoid bone [13]. Before entering the larynx, the SLN provides a smaller external motor branch for the cricothyroid muscle that runs on the constrictor muscle’s outer surface, where it is at risk of injury during surgery [9]. The surgeon must know these precise anatomical landmarks in order to avoid potential irreversible sensory or motor damage to the larynx: • Laryngotracheal reconstruction with cartilage expansion is carried out with a vertical midline laryngofissure. This explains its popularity among paediatric otolaryngologists, who are wary of injuring the RLNs and SLNs during more complex surgical procedures, such as airway resection and anastomosis. • During PCTR, lateral reflection of the cricothyroid muscle, from the midline over the cricothyroid joint, protects the RLN and the inferior laryngeal artery (see Sect. 20.3, Chap. 20). • While performing the thyrotracheal anastomosis during PCTR, the posterior and postero-lateral stitches must always emerge in a subperichondrial plane on the cricoid plate’s outer surface to avoid injury to the RLNs (see Sect. 20.3, Chap. 20). • A laryngeal release procedure is best performed by sectioning the thyrohyoid muscles on the thyroid cartilage, and by incising the thyrohyoid membrane along the upper edge of the thyroid cartilage to reach the upper lateral cornu on both sides. The upper cornu can be sectioned at this level without risking damage to the SLN’s neurovascular bundle.
2.5 Vascular Supply of the Larynx and the Trachea The larynx is supplied by vascular branches of the superior and inferior thyroid arteries. The superior laryngeal artery, a branch of the superior thyroid artery,
2 Applied Surgical Anatomy of the Larynx and Trachea
penetrates the thyrohyoid membrane, together with the SLN, just anterior to the lateral thyrohyoid ligament, providing the blood supply to the supraglottis and glottis [56, 57]. The inferior laryngeal artery, a branch of the inferior thyroid artery, reaches the larynx at the level of the cricothyroid joint and provides the blood supply to the cricothyroid and inferior constrictor muscles, as well as the subglottis and glottis, where it anastomoses with capillaries of the superior laryngeal artery. During PCTR, lateral reflection of the cricothyroid muscle over the cricothyroid joint protects not only the RLN but also the inferior laryngeal artery, thereby preserving the subglottic vascular supply (see Sect. 20.3, Chap. 20). Although the superior thyroid artery gives no direct branches to the cervical trachea, it anastomoses with the inferior thyroid artery in and around the thyroid gland, and indirectly supplies the adjacent upper tracheal wall with small feeder vessels, originating from the thyroid gland capsule (Fig. 2.11). In its cervical segment, the trachea receives its blood supply from the inferior thyroid artery [40], and in its thoracic segment from the innominate-subclavian
Fig. 2.11 Vascular supply of the larynx and cervical trachea: The superior and inferior laryngeal arteries, originating from the thyroid arteries, supply blood to the larynx, with anastomoses in and around the thyroid gland. The inferior thyroid artery supplies blood to the cervical trachea and gives rise to the tracheal arteries. Their segmental distribution throughout the entire length of the trachea, with lateral longitudinal anastomoses and transverse intercartilaginous feeder vessels to the inner submucosal plexus, dictates the basic surgical principles for PCTR, as well as those for tracheal resection and anastomosis. (Adapted from Salassa [51]. Copyrighted and used with permission of Mayo Foundation for Medical Education and Research)
15
2.6 Endoscopic Anatomy
system and bronchial arteries [51]. Avoid ischemic complications after airway resection and anastomosis, precise knowledge of the arteries’ segmental distribution throughout the trachea is more relevant than that of the supply vessels’ origin. The inferior thyroid artery passes posterior to the carotid sheath on both sides and often gives rise to three branches that reach the tracheooesophageal groove laterally, travelling anterior or posterior to the RLN. Two tracheo-oesophageal branches, at times even one single vessel, supply the upper cervical trachea [51]. These vessels then divide into tracheal and oesophageal branches. The tracheal branches connect with one another over three to four interspaces, creating a complete longitudinal tracheal anastomosis. Each tracheal branch penetrates the trachea in the intercartilaginous soft tissue space then moves into the submucosa, where it provides a rich interanastomotic capillary bed to the endoluminal surface of the tracheal cartilages. This blood supply is independent from that of the posterior membranous trachea. The tracheal cartilages receive their blood supply on the inner, mucosal side. There is no capillary network on the outer surface of the tracheal cartilages (Fig. 2.12). Therefore, circumferential intraluminal compression of the tracheal mucosa may lead to ischemic necrosis of the tracheal cartilages. The segmental distribution of the feeder vessels to the thoracic trachea is similar to the cervical trachea’s segmental distribution. The bronchial arteries provide Lateral longitudinal anastomosis
Ant. transverse intercartilaginous a.
continual blood supply to the distal trachea and carina [8, 51]. The rest of the blood supply to the upper thoracic trachea is provided by numerous arteries of the innominate-subclavian system, namely, the supreme intercostal artery, the subclavian artery, the mammary artery and the innominate artery, with significant individual variations. The segmental supply from the tracheo-oesophageal grooves is similar to what has been described for the cervical trachea. Because of this segmental vascularisation of the trachea, the airway surgeon must adhere to the following principles during laryngotracheal surgery: • Preservation of the trachea’s lateral blood supply, except for the segment that needs to be resected • Outer anterolateral dissection of the cervical trachea in close contact with the cartilaginous rings, without compromising the blood supply passing through the tracheo-oesophageal groove • Minimal tracheo-oesophageal separation, consisting of a few millimetres, cranially and caudally from the resected tracheal segment • Preservation of the thyroid gland in contact with the trachea while the surgeon resects a tracheal stenosis below the thyroid isthmus • Sectioning of the thyrohyoid membrane along the thyroid cartilage’s upper rim for a laryngeal release procedure • Lateral reflection of the cricothyroid muscle over the cricothyroid joint in order to protect the RLN and inferior laryngeal artery during PCTR For a more comprehensive description of the trachea’s blood supply, the reader is referred to the work of Salassa et al. that has continued to be a valuable reference for over 30 years [51].
2.6 Endoscopic Anatomy (Fig. 2.13) The infant larynx differs from the adult larynx as follows [30]: Tracheoesophageal a.
Submucosal capillary plexus
Fig. 2.12 Schematic view of the tracheal microscopical blood supply: The rich vascular network beneath the endotracheal mucosa originates from the transverse intercartilaginous arteries derived from the lateral longitudinal anastomosis. (Adapted from Salassa [51]. Copyrighted and used with permission of Mayo Foundation for Medical Education and Research)
• The epiglottis is omega-shaped and projects posteriorly above the glottis at a 45° angle. • The lateral edge of the epiglottis is positioned slightly medial to the pharyngo-epiglottic fold. • The aryepiglottic folds are shorter. • The tubercle of the cuneiform cartilage is more prominent.
16
2 Applied Surgical Anatomy of the Larynx and Trachea
a
b
Fig. 2.13 Schematic endoscopic aspect of the adult and infant larynx: (a) Adult larynx: The ligamentous glottis represents approximately 80% of the entire glottic length; the aryepiglottic folds are long; the epiglottis is unfolded and projects vertically;
the subglottis is round-shaped. (b) Infant larynx: The entire glottic length is 50% ligamentous and 50% cartilaginous; the aryepiglottic folds are short; the epiglottis is somewhat tubular, omega-shaped; the subglottis is elliptical proximally
• The increased ratio of the cartilaginous to the ligamentous glottis accentuates the pentagonal shape of the glottis during inspiration. • The immediate subglottic lumen is elliptical, due to the V-shaped upper half of the cricoid cartilage.
during the first 6 years of life, in subjects who are asleep or resting quietly [27, 28]. These data have been correlated with recommended uncuffed ETT sizes for intubation [59] and with rigid bronchoscopes routinely used for diagnostic and therapeutic endoscopies.
2.7 Morphometric Measurements of the Larynx and Trachea
2.7.1 Larynx Morphometry
Benign stenoses of the larynx and trachea most commonly arise from iatrogenic complications following endotracheal intubation [54]. An improved understanding of airway dimensions at different developmental ages would allow the surgeon and anaesthetist to choose the correct endotracheal tube size, thus avoiding inadvertent damage to the larynx and trachea. Therefore, surgeons, anaesthetists, intensivists and neonatologists must be familiar with the paediatric larynx’s morphometric measurements. Iatrogenic complications from the use of oversized endotracheal tubes (ETT) for resuscitation and mechanical ventilation in the paediatric intensive care unit (PICU) could be largely prevented, but only a few studies are currently available in the medical literature [20, 52, 56]. The data in the following section come from studies on whole organ serial sections of the paediatric larynx during the first 5 years of life [14, 15], as well as CT-scan measurements of the paediatric trachea,
2.7.1.1 Subglottic Luminal Diameter and Recommended ET-Tube Sizes Eckel et al. [14, 15] published cross-sectional area measurements of the cartilaginous subglottis (cricoid ring) and subglottic airway (cricoid ring with mucosa) in 43 infant (n = 24) and child (n = 19) larynges. Crosssectional surfaces were converted into diameters for this work, in order to compare them with ETT sizes (Fig. 2.14). Anaesthetists only refer to the ETT’s internal diameters, which are relevant for ventilating the patient. However, the ETT’s outer diameters can differ depending on the manufacturer. These differences in outer diameter are significant when we consider the size of the corresponding airway (Table 2.1). Since a majority of medical professionals prefer the soft Portex blue line tube for prolonged endotracheal intubation in the PICU, we have used this device for comparison in the following tables. Only the median and minimal diameters of the subglottic airway are
17
2.7 Morphometric Measurements of the Larynx and Trachea
Table 2.2 Subglottic luminal diameters compared to recom mended endotracheal tube (ETT) sizes Age Subglottic Recommended (years) lumen (mm)* ett (mm)** Median
Minimal
Outer ø
Inner ø
0–1
4.6
3.7
4.4–5.1
3.0–3.5
1–2
5.5
4.9
5.9–6.6
4.0–4.5
2–3
6.7
6.2
6.6
4.5
3–4
6.8
5.8
6.6–7.3
4.5–5.0
4–5
7.0
6.2
7.3–8.0
5.0–5.5
From Eckel et al. [14] ** From Weyckemans [59] *
• The ETTs may be oversized at all ages. • If the larger recommended ETT is used, it will induce significant intubation trauma at all ages. Fig. 2.14 Cricoid ring and arytenoids: The diameters of the subglottis and interarytenoid space are pertinent for assessing the potential risks linked to ETT sizes during intubation Table 2.1 Diameters (mm) of endotracheal tubes (ETTs) Tube n° Malinckrodt Portex Rüsch (Lanz and Rae) ID OD OD OD 2
3
2.9
2.9
2.5
3.6
3.6
3.8
3
4.3
4.4
4.4
3.5
4.9
5.0
5.3
4
5.6
5.4
5.9
4.5
6.2
6.6
6.7
5
6.9
7.2
7.3
5.5
7.6
8.0
8.0
6
8.2
8.8
8.7
6.5
8.8
9.5
9.3
reported in Table 2.2. Maximum diameters were omitted, since they can readily accommodate recommended uncuffed ETT sizes. We can draw the following conclusions from these morphometric measurements: • The outer diameter of the recommended ETTs slightly exceeds the median luminal diameter of the subglottis.
Therefore, any slight trauma to the subglottic mucosa during intubation can induce severe dyspnoea in the infant (Fig. 2.15). According to Holinger [30], the width of the posterior glottis (i.e., the interarytenoid distance) corresponds to approximately 80% of the subglottic lumen. If the median interarytenoid distance is calculated at 80% of the subglottic lumen’s median diameter, then all recommended ETTs are oversized and cannot fit the posterior glottis without excessive pressure on the mucosa (Table 2.3). In order to avoid iatrogenic complications of intubation, anaesthetists and intensivists must be aware of these discrepancies between ETTs and paediatric airway sizes. The following principles should be respected: • At the slightest resistance met when introducing the ETT into the larynx, we recommend changing the ETT to a smaller size. • In the PICU, the smallest tube that will provide adequate ventilation for infant and child should always be chosen over the largest.
2.7.1.2 Cricoid Cartilage Diameter Compared to Recommended Sizes of Rigid Bronchoscopes For a short procedure like rigid bronchoscopy, the diameter of the cricoid cartilage is acceptable as a reference
18
2 Applied Surgical Anatomy of the Larynx and Trachea
Fig. 2.15 Infant subglottis and risk of dyspnea: The size of the infant subglottis has a maximum diameter of 5–6 mm and a cross-sectional area of 28 mm2. One millimetre of mucosal oedema reduces the diameter by 2 mm and the cross-sectional area (12.6 mm2) by nearly 50% (Reproduced with permission of Holinger, Chicago [31])
R
R
3 mm
2 mm
a
b
Table 2.3 Median interarytenoid distance compared to recom mended ETT sizes Age Median Recommended ETT (mm)** (years) interarytenoid Outer ø Inner ø distance (mm)* 0–1
3.7
4.4–5.1
3.0–3.5
1–2
4.4
5.9–6.6
4.0–4.5
2–3
5.3
6.6
4.5
3–4
5.5
6.6–7.3
4.5–5.0
4–5
5.6
7.3–8.0
5.0–5.5
From Eckel [14] From Weyckemans [59]
*
**
Table 2.4 Cricoid cartilage diameters compared to recom mended sizes of rigid bronchoscopes Age Cricoid cartilage Recommended rigid (years) diameter (mm)* bronchoscopes Median
Minimal
Outer ø
Storz ø
0–1
6.3
4.8
4.2–5.7
2.5–3.5
1–2
7.7
7.1
6.4
3.7
2–3
8.1
7.7
6.7–7.3
4.0–4.5
3–4
7.9
7.5
7.3–7.8
4.5–5.0
4–5
9.0
8.6
8.2
6.0
From Eckel [14]
*
since a temporary compression of the subglottic mucosa is tolerated. However, the presence of a pre-existing pathology that diminishes the subglottic lumen’s size should first be ruled out (Table 2.4). The outer diameter of the rigid bronchoscope’s recommended dimensions
is always smaller than that of the median cricoid cartilage diameter. The risk of trauma to a normal-sized subglottis is minimal during rigid bronchoscopy. Furthermore, a smaller size of endoscope can always be used if a slight resistance is met during the bronchoscope’s insertion into the larynx.
2.7.2 Trachea Morphometry The length and size of the trachea vary considerably depending on the artefacts induced by ex vivo (autopsy specimens) versus in vivo (CT-scan) measurements. The CT-scan studies of Griscom et al. [27, 28] on 130 infants and children are displayed in Fig. 2.16. The measured parameters (length, diameter, cross-sectional area, volume) correlated with body height, but in small children the correlation was higher with body weight. Until the age of 6 years, the antero-posterior diameter of the trachea is smaller than the lateral diameter. Later in life, the cross section of the trachea becomes rounder, taking on comparable antero-posterior and lateral diameters. The recommended uncuffed cannula for the child’s age usually fits the tracheal lumen (Table 2.5). Precise knowledge of airway dimensions or direct access to a chart with all relevant information is necessary to avoid major complications of endotracheal intubation: • Recommended ETT sizes are usually at the upper limit of the age-corresponding airway diameter (subglottic lumen, interarytenoid distance) or larger. Oversized tubes primarily induce pressure necrosis on the medial aspect of the arytenoids.
19
2.8 Laryngeal Stents
5.4
0–2 years
0 64
6.4
2–4 years
0 81 0 53
7.2
4–6 years
09 0 74
8.2
6–8 years
0 93 08
8.8
8–10 years
1 07 0 92
10
10–12 years
1 18 1 05
10.8
12–14 years
1 33 1 16
11.2
14–16 years
1 46 13
12.2
16–18 years
1 40 1 39
1 39
Fig. 2.16 Tracheal lengths and diameters [27, 28]: From birth to adolescence, the length of the trachea doubles, its diameter triples and its cross-sectional area increases sixfold Table 2.5 Tracheal diameters compared to recommended Shiley paediatric cannula sizes Age Tracheal diameter Cannula size (years) (mm)* (mm) Median
Minimal
Outer ø
Inner ø
0–1
4.6
4.1
4.5
3.0
1–2
5.3
4.1
5.2
3.5
2–3
6.7
6.4
5.9–6.5
4.0–4.5
3–4
7.4
5.8
7.1
5
4–5
7.8
7.5
7.7
5.5
From Griscom [28]
*
• Medical personnel involved in intubation and ETT management in the PICU should know the tube outer diameter corresponding to the patient’s age or be able to refer to a chart containing this information. • Although considerable progress has been made and incidences of postintubation laryngotracheal stenoses have dropped to less than 1–3%, this complication can be devastating for the individual patient and family.
2.8 Laryngeal Stents Because of the significance of the inner laryngeal contours for an adequate indwelling stent, this section has been included in the chapter on airway anatomy. Laryngotracheal stents are temporarily used to keep the airway expanded after surgical reconstruction (LTR or extended PCTR) for complex glottosubglottic stenoses. Although they support and immobilise tracheal grafts during the healing process,
they also act as foreign bodies in the reconstructed airway. If stents do not conform to the inner laryngeal contours or if their consistency is hard, mucosal injuries, granulation tissue formation and subsequent stenosis may occur. Ideally, a stent should conform to the airway contours and exert less than 30 mmHg mucosal pressure. Additionally, a stent should resist compressive forces, sustain airway anatomy, move with the larynx during respiration and deglutition, and be biocompatible [50]. Several laryngeal stents are currently available on the market. The basic devices, such as the finger cot and the rolled silastic sheet, are customised [19]. Over time, these devices have been largely replaced by the Aboulker stent [2], the Montgomery T-tube [43], the Healy-Montgomery paediatric T-tube and the Mont gomery [46] or the Eliachar laryngotracheal stents [16]. However, these stents do not truly meet the aforementioned requirements for safe use without potential damage to the reconstructed airway. Although stenting is still necessary after complex airway reconstructions involving the glottis, the shape of current stents has remained suboptimal considering the complexity of the inner laryngeal contours. For the management of complex airway stenoses in infants and children, these stents must be used with caution to achieve superior results following LTR or extended PCTR.
2.8.1 Aboulker Stent (Fig. 2.17) This cigar-shaped prosthesis, introduced in the early 1960s by the French otolaryngologist Aboulker, is
20
2 Applied Surgical Anatomy of the Larynx and Trachea
cords, this cigar-shaped stent cannot restore a sharp anterior laryngeal commissure, which has a negative impact on voice quality.
2.8.2 Montgomery T-Tube (Fig. 2.18) The Montgomery T-tube is a simple open silicone tube with a smaller lumen projecting from the side of the stent at a 90° angle. It is soft and pliable, allowing easy insertion through the tracheostoma [45]. Although the Montgomery T-tube is well tolerated by the underlying mucosa, its extremities are sharp with cut edges, promoting granulation tissue formation at the site of the shearing forces between the stent and the airway mucosa. This occurs primarily in the conic-shaped subglottis if the upper end of the stent is positioned below the vocal cords. Because of this, the upper end of the stent must be placed slightly higher than the level of the false vocal cords. Nonetheless, this position may also
Fig. 2.17 Aboulker stent: Cigar-shaped, hard-Teflon prosthesis, unsuitable for stenting glotto-subglottic stenoses
made of very hard Teflon and is available in a variety of outer diameters. Originally used in adults, the Aboulker stent is now primarily used in children to splint the airway after LTR. In the late 1960s, Aboulker reported a decannulation in three out of five children having undergone airway reconstruction [1]. After 1970, Grahne [25], Cotton [11] and Crysdale [12] began using this stent for stabilising the post-LTR airway in children, reporting favourable results. Sub sequently, other surgeons also started using this prosthesis for stenting airway reconstructions [3, 47, 62]. Although the highly polished Teflon of the Aboulker stent is well tolerated by tissues, this prosthesis is too hard and does not conform to the complex inner contours of the larynx. In 1992, Zalzal [63, 64] reviewed the complications with the Aboulker stent. These complications included granulation tissue formation occurring at the inferior or superior end of the stent, in addition to infection, stent migration, broken stents and pressure necrosis at the base of the epiglottis and on the medial aspect of the arytenoids. Furthermore, in cases of cicatricial fusion of the vocal
Fig. 2.18 Montgomery T-tube: Simple open silicone T-tube suitable for tracheal stenting but not for glotto-subglottic airway reconstructions
2.8 Laryngeal Stents
21
Fig. 2.19 Complications induced by the Montgomery T-tube: (a) In the subglottis, the upper cut edge of the prosthesis gets impacted into the conus elasticus during coughing, inducing ulcerations, granulation tissue formation and restenosis. (b) In the supraglottis, the opened proximal extremity of the prosthesis must be closed to avoid aspiration problems, although it may still induce ulcerations, granulation tissue formation and scarring
lead to the production of granulation tissue on the laryngeal aspect of the epiglottis and on the ventricular bands (Fig. 2.19). To protect the airway from aspiration, the stent’s upper extremity must be closed by sutures, a silicone glue plug or a cap. Although the Montgomery T-tube is an effective device for stenting simple tracheal stenoses, it is not always suitable for stenting airway reconstructions of the glottis and subglottis [10]. Similar to the Aboulker stent, its round-shaped configuration does not restore a sharp anterior commissure of the glottis. In children, the safety of the stent must be considered when sizes less than 8 mm in outer diameter are used. The prosthesis can become plugged with dried secretions that may be lethal, requiring prompt removal of the T-tube [7, 55]. Reported complications in children include self-removal of the T-tube by the child, expulsion of the tube due to upward migration, formation of granulation tissue and plugging [23].
2.8.3 Healy Paediatric T-Tube (Fig. 2.20) To overcome the Montgomery T-tube’s risk of clogging in children, Healy designed a paediatric T-tube with a 70° connecting angle, allowing the introduction
Fig. 2.20 Healy paediatric T-tube: This prosthesis comprises an inner cannula that can quickly be removed and changed in case of clogging by dried secretions. This inner cannula further diminishes the inner size of the prosthesis required for the passage of air
22
of a flexible inner cannula. Although this paediatric T-tube permits quick removal of plugged secretions in the inner cannula, it further diminishes the airway size in an already small T-tube. This paediatric counterpart of the adult tracheal stent shares all of the aforementioned drawbacks of the Montgomery T-tube when used in older children and adults.
2 Applied Surgical Anatomy of the Larynx and Trachea
only exists in two different sizes, which is largely insufficient when applied to the full spectrum of laryngotracheal stenoses in the paediatric age group. Currently, this stent is seldom used in paediatric airway reconstructions [44].
2.8.5 Eliachar LT-Stent (Fig. 2.22) 2.8.4 Montgomery LT-Stent (Fig. 2.21) Designed for the treatment of glotto-subglottic stenosis, this prosthesis is made of plain silicone and is quite hard; it was obtained by moulding cadaver larynges. However, its posterior interarytenoid distance is narrow, reproducing the cadaveric paramedian position of the vocal cords. Therefore, this prosthesis is not entirely appropriate for stenting airway reconstructions for subglottic stenosis combined with posterior glottic stenosis. In addition, the Montgomery LT-stent
Fig. 2.21 Montgomery LT-sent: Plain silicone, hard prosthesis for the stenting of posterior glottic stenoses. (a) Posterior view: The interarytenoid distance is too narrow and cannot stent the larynx in the abducted position of the vocal cords. (b) Lateral view: The supraglottic position of the stent is too small
Made of soft silicone, this prosthetic hollow stent is less traumatic to the laryngeal mucosa than the Montgomery LT-stent. It was initially designed for the management of chronic aspiration [16]. Its conformity to the inner laryngeal contours is superior to that of all the previously discussed stents, but its shape is not triangular at the level of the glottis. Although providing internal support to laryngeal airway reconstructions, it does not restore either a large interarytenoid distance or a sharp anterior commissure of the glottis. Moreover, the Eliachar LT-stent cannot be used in infants or
2.8 Laryngeal Stents
23
Fig. 2.22 Eliachar LT-stent: Soft silicone prosthesis designed for chronic aspiration management. Its general shape cannot restore a large interarytenoid distance or a sharp anterior commissure of the larynx
children, and its fixation system with the silicone strap through the tracheostoma may induce granulation tissue formation at the tracheostoma site.
2.8.6 Monnier LT-Mold (Fig. 2.23) (Table 2.6) This laryngotracheal prosthesis is made of silicone at a strength of 50 Shores-A. Because of its softness, it avoids pressure necrosis at the medial aspect of the arytenoids. The Monnier LT-Mold design was created after moulding cadaver larynges and increasing the
Fig. 2.23 Monnier LT-Mold: (a) Moulds of cadaver larynges with narrow interarytenoid distance due to the paramedian cadaveric position of the vocal cords. (b) The LT-Mold is triangular at the glottic level with a large interarytenoid distance. The supraglottic head of the prosthesis is larger than that at the glottic level, preventing accidental shifting into the distal airway
interarytenoid distance in order to obtain the intralaryngeal contours of a fully abducted larynx. This property is essential when treating a subglottic stenosis combined with a posterior glottic stenosis. After the publication of a pilot study in The Laryngoscope in 2003 [41], the LT-Mold was modified with a dedicated silicone cap for each prosthesis size to avoid granulation tissue formation at its distal extremity. The prosthesis exists in 10 different sizes, from 6 to15 mm in outer diameter, and four different lengths for each size (Fig. 2.24 and 2.25). It can be inserted into the airway during open surgery (intra-operative use) (see Sect. 20.4, Chap. 20) or after endoscopic resection of a laryngotracheal stenosis (see Sect. 14.3.3, Fig. 14.17, Chap. 14).
24 Table 2.6 LT-Mold dimensions (in mm)
2 Applied Surgical Anatomy of the Larynx and Trachea
Based on the experience gathered in 30 paediatric patients [42], the LT-Mold almost meets the ideal requirements except for voice production. Given that these patients have already undergone failed surgeries and often present with aphonia, a further delay of several months before successful decannulation and voice production is acceptable. Disclosure The author holds a financial relationship with the company whose product is mentioned in the text.
2.9 Tracheal Stents
In 1992, reviewing the essential features of an ideal stent, Zalzal [63] identified five major characteristics: (a) availability of different sizes and shapes to fit into the reconstructed areas; (b) placement that avoids any risk of respiratory passage obstruction; (c) absence of foreign body reaction, pressure necrosis or discomfort; (d) adequate voice production and swallowing without aspiration; (e) easy placement and removal.
Fig. 2.24 Monnier LT-Mold: The prosthesis exists in 10 different sizes (6–15 mm in outer diameter) for use in infants, children and adults
Benign congenital and acquired tracheal stenoses must be treated surgically. There is almost no justification for using self-expandable metallic airway stents (SEMAS) in the management of benign stenoses of adult and child airways. Numerous reports of severe complications from indwelling SEMAS in the trachea and bronchi [6, 17, 24, 36, 37, 39, 61] are found in the literature. Among long-term complications, granulation tissue formation with subsequent restenosis, mucostasis, stent-migration, stent-fracture, as well as massive and lethal haemorrhage are described. Even though their easy application and
2.9 Tracheal Stents
Fig. 2.25 Monnier LT-Mold: Per size, the prosthesis exists in four different lengths to accommodate different positions of the tracheostomy site
availability in many different sizes seemingly make them ideal prostheses, in only very rare cases is the endoluminal placement of SEMAS in the paediatric age group justified as a life-saving measure [36, 48]. Other options to alleviate benign tracheal obstructions in infants and children include: • Non-invasive mask ventilation with continuous positive airway pressure (CPAP) or bi-level positive airway pressure (BiPAP). This is a temporary measure for moderate obstruction, as seen in tracheobronchomalacia [18, 33]. • Tracheotomy with tracheal stenting by a long cannula. The tip of the cannula should be positioned just above the carina. • Tracheostomy with a Montgomery or Healy T-tube. This is the most commonly used technique that allows stenting of the trachea. In children, caution must be exercised when outer diameter size is less than 8 mm, due to the risk of suffocation if the stent becomes clogged with dried secretions. At the time of tracheostomy closure, anterior costal cartilage grafting is often necessary to rigidify a localised segment of malacia at the former stoma site.
25
• Stenting without tracheotomy. This technique can only be used for recurrent inoperable tracheal stenoses as a last-chance treatment, after resection and anastomosis and subsequent tracheoplasty with costal cartilage grafting have failed. This technique is not appropriate for infants and small children, whose airways are too small to tolerate a small-sized stent. This method of long-term tracheal stenting is appropriate in older children and adolescents when a silicone tube with an outer diameter of at least 8 mm can be inserted into the airway. Perfectly smooth on its outer surface, the silicone tube exerts only minimal pressure on the tracheal wall, thus allowing re-epithelialisation of the stenotic zone (Fig. 2.26a). The prosthesis is fixed to the trachea by a 3.0 Prolene suture (Fig. 2.27). Based on our experience (unpublished data), only the plain smooth silicone tube can be used for long-term tracheal stenting without tracheotomy. • The Dumon stent, anchored to the tracheal wall by studs on its outer surface, causes constant granulation tissue formation. This prevents complete reepithelialisation of the stenotic segment around the stent [38] during the management of benign tracheo-bronchial stenoses [49]. Shearing forces occurring at the stent-mucosal interface also generate granulation tissue formation at both extremities of the Dumon stent (Fig. 2.26b). • The covered SEMAS tends to get impacted into the tracheal wall, also preventing re-epithelialisation of the stenotic zone and promoting granulation tissue formation at both extremities of the stent (Fig. 2.28a). • By contrast, the plain silicone tube does not generate such complications provided that the chosen size is appropriate for the specific trachea. It is snugly fixed to the trachea by a 3.0 Prolene suture and moves with the trachea during respiration and coughing. This prevents granulation tissue formation at both of its extremities. The pressure on the tracheal wall is less than 30 mmHg, which is favourable for the re-epithelialisation process (Fig. 2.28b and c).
26
Fig. 2.26 Plain silicone tube and Dumon stents: (a) Plain silicone tube: The smooth outer surface of the plain silicone tube facilitates re-epithelialisation of the trachea around the stent. The prosthesis must be fixed endoscopically to the trachea with a 3.0 prolene suture. (b) Dumon stent: The outer surface of the Dumon stent presents several studs which help maintain the prosthesis in place. However, migration is common in benign stenoses, and re-epithelialisation around the stent is compromised by the irregular outer surface of the stent that causes mechanical trauma to the tracheal wall
Fig. 2.28 Recurrent tracheal stenosis after several failed resection-anastomoses and tracheoplasties in a 16-year-old adolescent. (a) Initial presentation: The self-expandable polyflex tube retains secretions and produces granulation tissue resulting in severe distal airway obstruction. (b) Status 1 year after replace-
2 Applied Surgical Anatomy of the Larynx and Trachea
Fig. 2.27 Endoscopic placement of a smooth silicone tube in the trachea to calibrate an inoperable benign stenosis: (a) A 3.0 (70 cm long) prolene suture is initially passed through the silicone tube: In SML, the prosthesis is fixed to the trachea by endoextralaryngeal stitches using a Lichtenberger needle-carrier. (b) Silicone tube in place and snugly fixed to the tracheal wall: The 3.0 prolene thread is tied under the skin after recapturing the threads through a small horizontal skin incision
ment of the expandable stent by a plain silicone tube fixed with a prolene suture: excellent tolerance of the stent without granulation tissue formation. (c) Long-term result 2 years after stent removal: stabilised airway at 70% of its normal size
27
2.12 Appendix 3
2.10 Appendix 1 Recommended uncuffed ET-tube sizes Patient age
Tube size (Portex®) ID (mm)
(OD mm)
Premature <1,000 g
2.0
2.9
Premature 1,000–2,000 g
2.5
3.6
Newborn to 6 months
3.0/3.5
4.4/5.0
6 months to 1 year
3.5/4.0
5.0/5.4
1–2 years
4.0/4.5
5.4/6.6
2 years and older
Age + 16 4
2.11 Appendix 2 Recommended uncuffed and cuffed ET-tubes for children 2 years and older Uncuffed ET-tube
Age + 16 4
Cuffed ET-tube
Age 4
+3
Length of insertion Oral (cm)
3 × ID (mm)
Nasal (cm)
3 × ID (mm) + 2
2.12 Appendix 3 Recommended tubes and scopes based on patient age Patient age
Bronchoscope
Oesophagoscope
Tracheostomy tube ISO
ETT ID
size
OD (mm)
Premature
2.5
4.2
4
2.0/2.5
2.5
Term newborn
3.0
5.0
4–5
3.0/3.5
3.0/3.5
6–12 months
3.5
5.7
5–6
3.5/4.0
3.5/4.0
1–2 years
3.7
6.4
6
4.0
4.0/4.5
2–3 years
4.0
6.7
6–7
4.0/4.5
3–4 years
4.5
7.3
7
5.0
4–5 years
5.0
7.8
8
5.0/5.5
Age + 16 4
28
References 1. Aboulker, B. : Traitement des Stenoses Tracheales. Problèmes Actuels d’oto-rhino-laryngologie, pp. 275–295. Librairie Maloine, Paris, France (1968) 2. Aboulker, P., Sterkers, J.M., Demaldent, E.: Modifications apportées à l’intervention de Rethi. Intérêts dans les sténoses laryngo-trachéales et trachéales. Ann. Otolaryngol. Chir. Cervicofac. (Paris) 83, 98–106 (1966) 3. April, M.M., Marsh, B.R.: Laryngotracheal reconstruction for subglottic stenosis. Ann. Otol. Rhinol. Laryngol. 102, 176–181 (1993) 4. Benjamin, B., Holinger, L.D.: Laryngeal complications of endotracheal intubation. Ann. Otol. Rhinol. Laryngol. 117, 2–20 (2008) 5. Bosma, J.F.: Anatomy of the infant head. Johns Hopkins University Press, Baltimore, MA (1986) 6. Burningham, A.R., Wax, M.K., Andersen, P.E., et al.: Metallic tracheal stents: complications associated with longterm use in the upper airway. Ann. Otol. Rhinol. Laryngol. 111, 285–290 (2002) 7. Calhoun, K.H., Deskin, R.W., Bailey, B.J.: Near-fatal complication of tracheal T-tube use. Ann. Otol. Rhinol. Laryngol. 97, 542–544 (1988) 8. Cauldwell, E.W., Siekert, R.G., Lininger, R.E., et al.: The bronchial arteries: an anatomic study of 105 human cadavers. Surg. Gynecol. Obstet. 86, 395–412 (1948) 9. Cernea, C.R., Ferraz, A.R., Nishio, S., et al.: Surgical anatomy of the external branch of the superior laryngeal nerve. Head Neck 14, 380–383 (1992) 10. Cooper, J.D.: Use of the silicone tracheal T-tube for the management of complex tracheal injuries. J. Thorac. Cardiovasc. Surg. 82, 559–568 (1981) 11. Cotton, R.T., Evans, J.N.: Laryngotracheal reconstruction in children. Five-year follow-up. Ann. Otol. Rhinol. Laryngol. 90, 516–520 (1981) 12. Crysdale, W.S.: Subglottic stenosis in children. A management protocol plus surgical experience in 13 cases. Int. J. Pediatr. Otorhinolaryngol. 6, 23–35 (1983) 13. Durham, C.F., Harrison, T.S.: The Surgical Anatomy of the Superior Laryngeal Nerve. Surg. Gynecol. Obstet. 118, 38–44 (1964) 14. Eckel, H.E., Koebke, J., Sittel, C., et al.: Morphology of the human larynx during the first five years of life studied on whole organ serial sections. Ann. Otol. Rhinol. Laryngol. 108, 232–238 (1999) 15. Eckel, H.E., Sprinzl, G.M., Sittel, C., et al.: Zur Anatomie von Glottis und Subglottis beim kindlichen Kehlkopf. HNO 48, 501–507 (2000) 16. Eliachar, I., Nguyen, D.: Laryngotracheal stent for internal support and control of aspiration without loss of phonation. Otolaryngol. Head Neck Surg. 103, 837–840 (1990) 17. Eller, R.L., Livingston 3rd, W.J., Morgan, C.E., et al.: Expand able tracheal stenting for benign disease: worth the complications? Ann. Otol. Rhinol. Laryngol. 115, 247–252 (2006) 18. Essouri, S., Nicot, F., Clement, A., et al.: Noninvasive positive pressure ventilation in infants with upper airway obstruction: comparison of continuous and bilevel positive pressure. Intensive Care Med. 31, 574–580 (2005)
2 Applied Surgical Anatomy of the Larynx and Trachea 19. Evans, J.: Laryngotracheoplasty. Otolaryngol. Clin. North Am. 10, 119–123 (1977) 20. Fearon, B., Whalen, J.S.: Tracheal dimensions in the living infant (preliminary report). Ann. Otol. Rhinol. Laryngol. 76, 965–974 (1967) 21. Fitch, T.: A cognitive biologist foresees breakthroughs in understanding vocal learning. Journal club. Nature 466, 163 (2010) 22. Fitch, T., Hauser, M.D.: Computational constraints on syntactic processing in a nonhuman primate. Science 303, 377– 380 (2004) 23. Froehlich, P., Truy, E., Stamm, D., et al.: Role of long-term stenting in treatment of pediatric subglottic stenosis. Int J Pediatr Otorhinolaryngol 27, 273–280 (1993) 24. Gaissert, H.A., Grillo, H.C., Wright, C.D., et al.: Complication of benign tracheobronchial strictures by selfexpanding metal stents. J. Thorac. Cardiovasc. Surg. 126, 744–747 (2003) 25. Grahne, B.: Operative treatment of severe chronic traumatic laryngeal stenosis in infants up to three years old. Acta otolaryngologica 72, 134–137 (1971) 26. Grillo, H.C.: Anatomy of the trachea. In: Grillo, H.C. (ed.) Surgery of the trachea and bronchi, pp. 40–59. BC Decker Inc, Hamilton; London (2004) 27. Griscom, N.T., Wohl, M.E.: Dimensions of the growing trachea related to age and gender. Am J Roentgenol 146, 233– 237 (1986) 28. Griscom, N.T., Wohl, E.B., Fenton, T.: Dimensions of the trachea to age 6 years related to height. Pediatr. Pulmonol. 5, 186–190 (1989) 29. Hast, M.: Anatomy of the larynx. Otolaryngology 3, 1–16 (1986) 30. Henick, D.H., Holinger, L.D.: Laryngeal development. In: Holinger, L.D., Lusk, R.P., Green, C.G. (eds.) Pediatric laryngology and bronchoesophagoscopy, pp. 1–17. LippincottRaven, Philadelphia; New York (1997) 31. Holinger, L.D.: Evaluation of stridor and wheezing. In: Holinger, L.D., Lusk, R.P., Green, C.G. (eds.) Pediatric laryngology and bronchoesophagology, p. 42. LippincottRaven, Philadelphia; New York (1997) 32. Holinger, L.D., Green, C.G.: Anatomy. In: Holinger, L.D., Lusk, R.P., Green, C.G. (eds.) Paediatric laryngology and bronchoesophagology, p. 23. Lippincott-Raven, Philadelphia; New York (1997) 33. Kirk, V., O’Donnell, A.: Continuous positive airway pressure for children: a discussion on how to maximize compliance. Sleep Med. Rev. 10, 119–127 (2006) 34. Laitman, J.T.: The anatomy of human speech. Natural History 93, 20–27 (1984) 35. Laitman, J.T. : L’origine du langage articulé. Recherche (Paris, 1970):1164–1173 (1986) 36. Lim, L.H., Cotton, R.T., Azizkhan, R.G., et al.: Complications of metallic stents in the pediatric airway. Otolaryngol. Head Neck Surg. 131, 355–361 (2004) 37. Madden, B.P., Loke, T.K., Sheth, A.C.: Do expandable metallic airway stents have a role in the management of patients with benign tracheobronchial disease? Ann. Thorac. Surg. 82, 274–278 (2006) 38. Martinez-Ballarin, J.I., Diaz-Jimenez, J.P., Castro, M.J., et al.: Silicone stents in the management of benign tracheo-
References bronchial stenoses. Tolerance and early results in 63 patients. Chest 109, 626–629 (1996) 39. Merrot, O., Buiret, G., Gleizal, A., et al.: Management of tracheobronchial stenoses with endoprostheses: experience with 103 patients and 11 models. Laryngoscope 118, 403– 407 (2008) 40. Miura, T., Grillo, H.C.: The contribution of the inferior thyroid artery to the blood supply of the human trachea. Surg. Gynecol. Obstet. 123, 99–102 (1966) 41. Monnier, P.: A New Stent for the Management of Adult and Pediatric Laryngotracheal Stenosis. Laryngoscope 113, 1418–1422 (2003) 42. Monnier, P.: Airway stenting with the LT-Mold™: Experience in 30 pediatric cases. Int. J. Pediatr. Otorhinolaryngol. 71, 1351–1359 (2007) 43. Montgomery, W.W.: T-tube tracheal stent. Arch. Otolaryngol. Head Neck Surg. 82, 320–321 (1965) 44. Montgomery, W.W.: The surgical management of supraglottic and subglottic stenosis. Ann. Otol. Rhinol. Laryngol. 77, 534–546 (1968) 45. Montgomery, W.W.: Silicone tracheal T-tube. Ann. Otol. Rhinol. Laryngol. 83, 71–75 (1974) 46. Montgomery, W.W., Montgomery, S.K.: Manual for use of Montgomery laryngeal, tracheal, and esophageal prostheses: update 1990. Ann. Otol. Rhinol. Laryngol. 150, 2–28 (1990) 47. Ndiaye, I., Van de Abbeele, T., Francois, M., et al.: Traitement chirurgical des sténoses laryngées de l’enfant. Ann. Otolaryngol. Chir. Cervicofac. 116, 143–148 (1999) 48. Nicolai, T.: Airway stents in children. Pediatr. Pulmonol. 43, 330–344 (2008) 49. Puma, F., Ragusa, M., Avenia, N., et al.: The role of silicone stents in the treatment of cicatricial tracheal stenoses. J. Thorac. Cardiovasc. Surg. 120, 1064–1069 (2000) 50. Richard, L.G., John, B.S.: Long-term stenting in the treatment of subglottic stenosis. Ann. Otol. 86, 795–798 (1977) 51. Salassa, J.R.: Gross and microscopical blood supply of the trachea. Ann. Thorac. Surg. 24, 100–107 (1977)
29 52. Schild, J.A.: Relationship of laryngeal dimensions to body size and gestational age in premature neonates and small infants. Laryngoscope 94, 1284–1292 (1984) 53. Schweizer, V., Dorfl, J.: The anatomy of the inferior laryngeal nerve. Clin. Otolaryngol. Allied Sci. 22, 362–369 (1997) 54. Shah, R.K., Lander, L., Choi, S.S., et al.: Resource utilization in the management of subglottic stenosis. Otolaryngol. Head Neck Surg. 138, 233–241 (2008) 55. Stern, Y., Willging, J.P., Cotton, R.T.: Use of Montgomery T-tube in laryngotracheal reconstruction in children: is it safe? Ann. Otol. Rhinol. Laryngol. 107, 1006–1009 (1998) 56. Tucker, G F., Tucker, J.A., Vidic, B.: Anatomy and development of the cricoid: serial-section whole organ study of perinatal larynges. Ann. Otol. Rhinol. Laryngol. 86, 766–769 (1977) 57. Tucker, H.M.: Anatomy of the larynx. In: Tucker, H.M. (ed.) The Larynx, p. 12. Thieme, Stuttgart; New York (1993) 58. Wang, C.: The use of the inferior cornu of the thyroid cartilage in identifying the recurrent laryngeal nerve. Surg. Gynecol. Obstet. 140, 91–94 (1975) 59. Weyckemans, F.: Equipement, monitoring, and environmental conditions. In: Bissonnette, B., Dalens, B. (eds.) Pediatric anesthesia: principles and practice, pp. 419. McGraw-Hill, Medical Pub. Division (2002) 60. Williams, P.L., Bannister, L.H.: Gray’s anatomy: the anatomical basis of medicine and surgery. Churchill Livingstone, New York (1995) 61. Zakaluzny, S.A., Lane, J.D., Mair, E.A.: Complications of tracheobronchial airway stents. Otolaryngol. Head Neck Surg. 128, 478–488 (2003) 62. Zalzal, G.H.: Use of stents in laryngotracheal reconstruction in children: indications, technical considerations, and complications. Laryngoscope 98, 849–854 (1988) 63. Zalzal, G.H.: Stenting for pediatric laryngotracheal stenosis. Ann. Otol. Rhinol. Laryngol. 101, 651–655 (1992) 64. Zalzal, G.H., Grundfast, K.M.: Broken Aboulker stents in the tracheal lumen. Int. J. Pediatr. Otorhinolaryngol. 16, 125–130 (1988)
3
Clinical Evaluation of Airway Obstruction
Contents
Core Messages
3.1 Degree of Respiratory Distress.............................. 32
›› Once
3.2 Site and Cause of Airway Obstructions................ 3.2.1 Pathological Respiratory Sounds.............................. 3.2.2 Variable Extrathoracic Obstruction)......................... 3.2.3 Variable Intrathoracic Obstruction............................ 3.2.4 Fixed Airway Obstruction........................................
››
33 33 34 34 34
3.3 Assessment of Laryngeal Functions)..................... 35 3.4 Medical History....................................................... 36 3.5 Physical Examination............................................. 37 3.5.1 In-Office Transnasal Flexible Laryngoscopy (TNFL)...................................................................... 37 3.5.2 Indication for Endoscopy Under General Anaesthesia............................................................... 37 3.6 Radiological Evaluation......................................... 38 3.7 Anaesthetic Techniques for MRI in Children with Obstructive Dyspnoea.................................... 3.7.1 Pre-anaesthetic Assessment...................................... 3.7.2 Anaesthesia for MRI in Children with Mild (Stage I and II) Obstruction...................................... 3.7.3 Anaesthesia for MRI in Children with a Fixed (³70%) Tracheal Stenosis............................... 3.7.4 Anaesthesia for MRI in Children with Stage III and IV Collapsible Upper Airway............................ 3.7.5 Sedation for MRI in Children with Compressible Intrathoracic Airway.................................................
40 40
››
››
››
40 41 42 42
››
3.8 Assessment of the Patient’s General Condition... 42 References............................................................................ 43
››
the degree of respiratory distress has been evaluated, proper management must be applied before the child becomes exhausted. If airway compromise does not require an immediate life-saving measure, then diagnostic endoscopy should always precede intubation or tracheotomy. Identifying the site and cause of obstruction is facilitated by the quality of the pathological respiratory sound (stridor, stertor and wheezing) and the phase of the respiratory cycle during which it is produced. Understanding the pathophysiological mechanism of extra- and intrathoracic airway obstruction avoids erroneous evaluation of the dyspnoeic child. The systematic assessment of laryngeal functions (respiration, phonation and protection of the lower airways) is a reminder that precise questions concerning voice, cry and aspiration must be asked. Age of onset, aggravating factors and the influence of body position on dyspnoea symptoms provide pertinent clues as to the potential aetiology of airway narrowing. Physical examination should be carried out in an orderly fashion (increasingly invasive) to prevent any agitation or crying in the child.
P. Monnier (ed.), Pediatric Airway Surgery, DOI: 10.1007/978-3-642-13535-4_3, © Springer-Verlag Berlin Heidelberg 2011
31
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3 Clinical Evaluation of Airway Obstruction
›› Precise observation and listening to the child’s
›› ››
››
››
›› ››
››
respiration provide essential information as to the severity of the respiratory distress and the location of the airway obstruction (supra- or infraclavicular retractions, prolonged respiratory cycle and type of pathological sounds) prior to proceeding to an intrusive physical examination. Additional inspection of the infant or child’s morphotype provides insight into possible syndromic or non-syndromic congenital anomalies. Transnasal fibreoptic laryngoscopy (TNFL) represents an integral part of the office examination in infants and children with mild to moderate obstructive dyspnoea. Anteroposterior and lateral neck X-rays as well as chest X-rays should be conducted routinely. Misinterpretation of airway narrowing is possible. X-ray interpretation should be compared with the patient’s medical history and physical examination. Sophisticated X-ray investigations (Helical CT scan and MRI with 3D reconstructions and digital subtractions) are very useful in planning the surgical approach in the case of complex cardiovascular anomalies of the mediastinum. Oesophagram is efficient in assessing fistulas, clefts and incomplete glottic closure. Ultrasound is a non-invasive method for assessing cervical masses (cyst versus solid masses) and is useful for the follow-up of vocal cord paralysis. Depending on specific medical problems, additional inputs from neonatologists, geneticists, neurologists, pneumologists, cardiologists and gastroenterologists offer the best comprehensive evaluation of the child prior to the undertaking of an airway reconstruction.
Any upper or lower airway obstruction generates a pathological respiratory sound resulting from the rapid, turbulent flow of air through the narrowed segment of the respiratory tract. Depending on the severity, duration and progression of the obstruction, other symptoms and signs of respiratory distress may occur such as dyspnoea, nasal flaring, supraclavicular, sternal, intercostal and subcostal retractions, grunting, life-threatening cyanotic episodes, somnolence and apnoea.
Before investigating the site and cause of airway obstruction, the degree of respiratory distress must be assessed carefully.
3.1 Degree of Respiratory Distress The initial careful observation of a dyspnoeic child provides valuable information on both the severity and the site of the airway obstruction. However, diagnostic airway monitoring is useful in establishing the need for any further endoscopic intervention in a child with mild to moderate dyspnoea [6]. In clinical practice, the symptoms of respiratory obstruction can be graded as follows: • Grade I –– Noisy breathing with mild to moderate dyspnoea and chest retractions –– No anxiety or restlessness –– Normal intake of food and drink –– Interest in playing • Grade II –– Noisy breathing with severe dyspnoea and chest retractions –– Anxiety and restlessness –– Refusal of food and drink –– No interest in playing • Grade III –– Exhausted child with decreased stridor and intercostal muscle retractions –– Slowing down of respiratory rate and heart rate –– Ashy-grey colour and perspiration –– Spells of somnolence If history and clinical examination reveal progressive respiratory distress in a child with an impending airway compromise, then immediate airway stabilisation is mandatory. As Chevalier Jackson mentioned in the 1950s [20, p. 135], ‘If tracheotomy is not done, the child will give up fight and sleep away’. Therefore, securing the airway at this stage is crucial and may be performed in either the endoscopy suite or the operating room in order to avoid a progression of the respiratory compromise towards grade III. A team of anaesthetists and otolaryngologists experienced in the management of difficult airways should immediately proceed
3.2 Site and Cause of Airway Obstructions
33
with endoscopy, intubation or tracheotomy [39] (see Sect. 5.1, Chap. 5).
3.2 Site and Cause of Airway Obstructions When dealing with a child in grade I respiratory distress, a thorough medical history and physical examination are mandatory, thereby providing information relating to the site and cause of the airway narrowing. Stern and Cotton’s statement is all the more pertinent, ‘Any pathological sound in an infant needs immediate attention and should be carefully evaluated’ [45]. The assessment of a dyspnoeic infant or child is based on the following factors: 1. Quality of pathological respiratory sounds 2. Phase of the respiratory cycle during which the pathological sounds are produced 3. Assessment of the three main functions of the larynx 4. Medical history
3.2.1 Pathological Respiratory Sounds (Fig. 3.1) • Stridor: a harsh respiratory sound caused by turbulent airflow through a restricted area. By definition, stridor should correspond to an audible inspiratory sound; however, other terms such as expiratory and biphasic stridor have also been used in the English medical literature to describe intrathoracic and fixed airway obstructions. • Stertor: a low-pitched inspiratory fluttering and snoring sound produced by nasal or naso-pharyngeal obstruction. By differentiating inspiratory stertor from stridor, the site of the narrowing in the upper airway can be localised. Stridor originates in the larynx and upper trachea, whereas stertor originates in the nasopharynx or oropharynx. • Wheezing: an expiratory whistling sound produced by turbulent airflow passing through constricted small airways (bronchioles).
Fig. 3.1 Pathological respiratory sounds Stertor (blue): Naso-oropharyngeal obstructions: –Adenoid hyperplasia –Tonsillar hyperplasia –Base of tongue mass –Glossoptosis, retrognathia –Pharyngeal mass Stridor (red): Laryngotracheal, variable extra-thoracic tracheal obstructions: –Laryngomalacia –BVCP bilateral vocal cord palsy –Soft tissue SGS –Cysts and laryngoceles –Cleft larynx –Glottic web Wheezing (orange): Variable intrathoracic obstruction of the tracheobronchial tree: –Tracheobronchomalacia –Extrinsic vascular compressions –Non-circumferential tracheal stenosis –Mediastinal masses
Though this term is often used in reference to asthma, wheezing or expiratory stridor can also be associated with other intrathoracic narrowings of the larger tracheobronchial airways. Airway obstruction is characterised by its propensity to change diameter during the respiratory cycle. This may be accounted for by the flaccid (pharynx, supraglottis), malacic or non-circumferential nature of the area involved. For instance, depending on the intraluminal pressure, the pars membranae of the trachea can alter the shape of the lumen. Variable airway obstruction is therefore influenced by atmospheric, intratracheal and intrapleural pressures during inspiration and expiration [23].
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3 Clinical Evaluation of Airway Obstruction
3.2.2 Variable Extrathoracic Obstruction (Fig. 3.2) Due to the Bernoulli effect [32, p. 385], inspiration generates negative pressure at the site of the extrathoracic narrowing. At this level, atmospheric pressure is higher than intratracheal pressure. During the expiratory phase, the outflow of air from the thorax generates positive intratracheal pressure in the neck, which is higher than atmospheric pressure. Variable extrathoracic obstruction of the airway produces: • An inspiratory pathological sound (stridor or stertor) • A prolonged inspiratory phase • A hindered inspiratory phase dependant on the severity of the obstruction
force transmitted from the lung parenchyma to the walls of the trachea and bronchi. The intrapleural pressure is lower than the intratracheal pressure. During the expiratory phase, contraction of the chest generates a high intrapleural and thus, extraluminal pressure, in comparison with the intratracheal pressure. The trachea and bronchi undergo circumferential compression and narrowing. Variable intrathoracic obstruction of the airway produces: • An expiratory pathological sound (wheezing) • A prolonged expiratory phase • A hindered expiratory phase dependant on the severity of the obstruction
3.2.4 Fixed Airway Obstruction 3.2.3 Variable Intrat horacic Obstruction (Fig. 3.3) During the inspiratory phase, the volume of the chest increases, expanding the central airways by the elastic
A fixed obstruction describes the situation in which intra- and extraluminal pressures do not affect the size of the narrowed segment of the airway. This is typically the case in congenital cartilaginous or acquired cicatricial subglottic stenosis.
a
b Ptr <Patm
Fig. 3.2 Variable extrathoracic obstruction (Reproduced from Kryger et al. 1976 [24]. With permission). (a) During inspiration, the intratracheal pressure (Ptr) is lower than the atmospheric pressure (Patm). This generates a prolonged inspiratory phase with an inspiratory pathological sound (stridor or stertor). (b) During expiration, the intratracheal pressure (Ptr) is higher than the atmospheric pressure (Patm). This maintains an almost normal expiratory flow rate, depending on the severity of the obstruction
Ptr >Patm
35
3.3 Assessment of Laryngeal Functions Fig. 3.3 Variable intrathoracic obstruction (Reproduced from Kryger et al. 1976 [24]. With permission). (a) During inspiration, the intratracheal pressure (Ptr) is higher than the pleural pressure (Ppl). This maintains an almost normal inspiratory flow rate, depending on the severity of the obstruction. (b) During expiration, the intrapleural pressure (Ppl) is higher than the intratracheal pressure (Ptr). This generates a prolonged expiratory phase and pathological expiratory sound (wheezing)
a
b Ptr >Ppl
A fixed obstruction of the airway produces:
Ptr
Respiration
Voice
• A typical biphasic stridor of equal intensity during both phases of the respiratory cycle • Variability in the inspiratory and expiratory phases, depending on the severity of the condition
3.3 Assessment of Laryngeal Functions (Fig. 3.4) During the evaluation, systematic testing of the three main laryngeal functions is mandatory. In addition to assessing respiration, as described in the previous paragraphs, attention should be paid to the sphincteric function of the larynx. Swallowing problems as well as feeding difficulties with aspiration (coughing, choking, gagging, regurgitation or aspiration pneumonia) are observed in laryngotracheo-oesophageal clefts (LTOC), oesophageal atresia with tracheo-oesophageal fistula (TOF), nerve palsies of the pharyngolarynx and to a lesser degree in unilateral vocal cord paralysis. Discoordinated pharyngolaryngeal function with no clear evidence of central nervous system damage can also cause feeding difficulties with aspiration [15].
Sphincter
Fig. 3.4 Main laryngeal functions as a mnemonic support for medical history taking
The quality and amplitude of the voice or cry should also be evaluated. A weak and breathy cry corresponds to incomplete glottic closure, as seen in unilateral vocal cord paralysis. A hoarse voice or aphonia is indicative of a vocal cord lesion, which may be due to inflammation, oedema, tumour or scarring. A muffled sound is suggestive of a supraglottic mass (e.g., cyst, lymphovascular malformation). A high-pitched cry can be seen in conditions such as bilateral vocal cord palsy, synechia or web of the vocal cords [45]. Unless it is very severe, tracheal stenosis does not influence voice quality and cry.
36
3 Clinical Evaluation of Airway Obstruction
3.4 Medical History In the absence of severe respiratory distress, and while taking the medical history, the physician should closely observe the infant or child in its parents’ arms. History and clinical examination must be supplemented with answers to the following questions: • Age of onset (Table 3.1): A compromised airway manifesting itself immediately at birth or during the neonatal period warrants questions regarding the pregnancy (e.g., foetal distress and prematurity) and delivery (e.g., difficult labour, asphyxia, apnoeic episodes, low Apgar scores, and birth injury). Several congenital anomalies are present at birth, whereas other conditions appear later on during the first few years of life.
–– Dyspnoea and stertor worsen during sleep in nasopharyngeal or oropharyngeal obstructions, as a result of muscular tone loss. –– Coughing and choking episodes increase during meals in tracheo-oesophageal fistulae and clefts. • Influence of body position (Table 3.3): Being in prone position usually reduces noisy breathing resulting from anterior compression of the airway (e.g., glossoptosis, median vallecular cyst and aberrant innominate artery). Conversely, in Table 3.2 Factors worsening airway obstruction in infants and children Worsening with crying, feeding or straining (laryngeal anomalies) –– Laryngomalacia –– Bilateral vocal cord paralysis
• Aggravating factors (Table 3.2):
–– Subglottic stenosis
–– Dyspnoea and stridor worsen during feeding, crying or in the case of agitation, due to increased airway demands.
–– Subglottic haemangioma Worsening during sleep (naso-oro-pharyngeal obstruction) –– Retrognathia with tongue base prolapse –– Epiglottic prolapse
Table 3.1 Pathological conditions relating to the age of onset in the case of respiratory symptoms
–– Adenotonsillar hypertrophy
Birth
Worsening with deglutition (deficient sphincteric function of the larynx)
–– Bilateral vocal cord paralysis –– Congenital cysts
–– Unilateral vocal cord paralysis
–– Laryngeal webs and atresia
–– Discoordinated pharyngolarynx (neurological disorder)
–– Choanal atresia
–– Tracheoesophageal fistula and cleft
–– Vascular mediastinal anomalies –– Severe subglottic stenosis Age: first few weeks of life
Table 3.3 Influence of the body position in the case of airway obstruction Decreased noisy breathing in prone position
–– Laryngomalacia
–– Laryngomalacia
Age: 1–4 months
–– Vallecular cyst
–– Moderate subglottic stenosis
–– Micro-retrognathia
–– Subglottic haemangioma
–– Macroglossia
Age: 1–3 years
–– Innominate artery compression
–– Croup
Decreased or worsened noisy breathing in lateral position*
–– Bronchiolitis
–– Unilateral vocal cord paralysis
Age: 3–6 years –– Membranous laryngo-tracheobronchitis
–– Lateral pharyngolaryngeal cyst, mass Symptoms diminish when the baby lies on the affected side and increase when the baby lies in the contralateral position *
–– Epiglottitis
37
3.5 Physical Examination Table 3.4 Mnemonic history of airway obstruction [17] S = severity: parents’ subjective impression regarding the severity of the obstruction P = progression: evolution of the obstruction over time E = eating: feeding difficulties, aspiration and failure to thrive C = cyanosis: cyanotic episodes, apparent life-threatening events S = sleep: disturbed sleep, suprasternal or chest retractions during sleep Reproduced by permission of LD Holinger, Chicago
unilateral vocal cord palsy and lateral pharyngeal masses, the airway improves when the infant lies on the affected side (the lateral position). Lastly, information about prior intubation or endoscopy and surgical interventions should be obtained. As proposed by Holinger [17], the mnemonic ‘SPECS’ for the history of airway obstruction is helpful in assessing the severity of the condition. It provides information as to the need for diagnostic and therapeutic endoscopy (Table 3.4).
3.5 Physical Examination The initial clinical examination in a child with noisy breathing and mild to moderate dyspnoea starts with a careful non-invasive inspection. This involves evaluation of dysmorphic facial features and the size and position of the mandible and tongue. The patency of nasal airways, flaring of ala nasi, mouth breathing and retractions of the accessory respiratory muscles (suprasternal, intercostal, subcostal and abdominal movements) is systematically determined. Auscultation of the lungs and heart should be conducted when the child is quiet. The physician should then proceed to an examination of the chest wall, sternum and neck, as well as the mouth and nose. This auscultation is very useful when the pathological respiratory sound is not clearly audible. Once again, attention should be paid to the intensity of the pathological sound and its relation to the respiration phase. At times, older children are seen to be breathing quietly at rest, yet history gives clear evidence of exertional dyspnoea. In this case, the child is asked to breathe rapidly through the open mouth (panting). The aim is to have him/her emit the pathological sound and prolonged phase of the respiratory cycle induced by the high-velocity
airflow through the narrowed segment of the respiratory tract. As a result, more accurate information about the relative patency of the airway may be obtained. Examining infants in various positions and observing the associated changes in the intensity of the pathological sound ensures a more accurate diagnosis (see Table 3.3). Only at the end should the examination of the nasal and oral cavities be carried out. In the case of a crying child, thanks to the deep and rapid inspiratory breaths emitted, the physician will obtain more precise information on the site of the airway narrowing.
3.5.1 In-Office Transnasal Flexible Laryngoscopy (TNFL) Transnasal flexible laryngoscopy is part of the inoffice examination in infants and cooperative older children [46]. Toddlers often refuse this examination and should not be forced to undergo it. Gentle restraints applied to infants by qualified personnel allow for an easy TNFL with no topical anaesthesia. Patency of the nasal cavities, choanae, nasopharynx and pharyngolarynx should be carefully assessed; the degree of dynamic functional narrowing of the airway at the naso-oropharyngeal junction and larynx during inspiration should also be determined. Inspection of the larynx is aimed at documenting the abnormalities of the supraglottis (e.g., laryngomalacia, lymphovascular malformations and cysts) as well as assessing the mobility of the vocal cords. If restricted abduction or true immobility is perceived, then a complete examination under general anaesthesia is justified in order to differentiate neurogenic bilateral vocal cord paralysis from posterior glottic stenosis, particularly when the medical history reveals a prior history of endotracheal intubation. Transnasal flexible laryngoscopy always yields incomplete information as the subglottis and trachea cannot be visualised.
3.5.2 Indication for Endoscopy Under General Anaesthesia We agree with Cotton that not all patients need direct laryngoscopy, particularly when a clear diagnosis of mild laryngomalacia is made following a comprehensive
38
3 Clinical Evaluation of Airway Obstruction
medical history and physical examination [45]. However, in the case of symptom progression, associated abnormalities or atypical clinical presentations, a complete laryngotracheobronchoscopy and oesophagoscopy must be performed under general anaesthesia. In the case of chronic stridor, clinical indicators such as feeding difficulties, failure to thrive, obstructive sleep apnoeas and cor pulmonale warrant further investigation and possible treatment under general anaesthesia. A detailed description of this examination is provided in Chap. 5.
3.6 Radiological Evaluation After a thorough medical history and physical examination, an appropriate radiological evaluation of the airways should be scheduled in the case of a noisy child with mild to moderate dyspnoea. Preference is given to plain films and a fast acquisition helical CT scan where, as opposed to MRI, sedation is not required [42]. A nurse or physician should closely observe the dyspnoeic or sedated child during the entire procedure. An experienced radiology team (technicians and physicians) is essential to ensure image quality and X-ray interpretation. The paediatric airway changes in size and configuration during both the respiratory cycle and deglutition. Proper technique is essential to avoid misinterpretations. Lateral and anteroposterior soft tissue (high-kilovoltage) X-rays of the neck and chest provide useful information as a first screening procedure of the compromised paediatric airway (Fig. 3.5). Plain radiographs are obtained using the following techniques: • Patient in upright position with the head fully extended • High-kilovoltage (120–150 KV) X-rays obtained during full inspiration • Anteroposterior and lateral neck and chest films The radiological report should always be correlated with the medical history and physical examination. In the case of a discrepancy or doubt as to the correct diagnosis, a helical CT scan using contrast medium is requested. Ultrafast acquisition of frames in less than 0.1 s [22] diminishes the blurring of the images on the films. A CT scan offers better spatial resolution than
Fig. 3.5 High kilovolt lateral neck X-ray: congenital web of the vocal cords with anterior subglottic cartilaginous component
MRI and is particularly useful in evaluating extrinsic compressions of the airway by cystic or solid masses. In the case of the chest, where the thymus completely fills the anterior mediastinum when seen on plain films, the CT scan provides a major contribution. With intravenous contrast medium, and by using a CT scan, abnormal mediastinal vessels narrowing the trachea can readily be demonstrated without sedating an infant [44, 26] (Fig. 3.6). Three dimensional (3D) reconstructions of the laryngotracheal airway offer useful information as to the location, extent and severity of the obstruction (Fig. 3.7). Virtual endoscopy cannot replace conventional laryngotracheal bronchoscopy. Indeed, this technique provides no information as to the quality of the mucosa (cicatricial versus inflammatory). Furthermore, trapped secretions below the stenosis may artificially increase the extent of the narrowing. In the case of a total obstruction of the airway, virtual endoscopy is helpful in visualising the distal portion of the airway [19].
39
3.6 Radiological Evaluation
An MRI is useful in assessing vascular compressions of the airway secondary to congenital cardiovascular anomalies. The contrast resolution is finer than the CT scans’, and MRI permits imaging in any desired plane with 3D reconstructions [30] (Fig. 3.8). Radiological examinations in moderately dyspnoeic infants and children require sedation. In our institution, an anaesthetist is present during the entire procedure, and the child’s vital signs are monitored using
pulse oximetry, electrocardiogram and an apnoea monitor. Post-sedation management is carried out in the recovery room.
Fig. 3.6 Contrast CT scan of the mediastinum: left pulmonary artery sling
Fig. 3.8 3D-MRI-scan reconstructions of a complete aortic arch with mirror-image branching and long-segment tracheal stenosis
Fig. 3.7 CT scan with 3D reconstruction of the cervical trachea: 2 cm long, concentric stenosis. (a) Lateral view. (b) Coronal view
a
b
40
3 Clinical Evaluation of Airway Obstruction
Of the ancillary radiological examinations, ultrasound and barium oesophagram are the most widely used. In the neck, ultrasound is capable of differentiating cystic from solid masses. The latter technique is also useful in the assessment and follow-up of vocal fold paralysis [14]. A barium or gastrograffin oesophagram is requested in the case unclear dysphagia with mild aspiration or recurrent pneumonia [21]. The site and extent of a potential oesophagotracheal fistula or cleft, as well as the function of the glottic sphincter should be clearly evaluated. A vocal cord motion impairment or discoordination of the pharyngolarynx may induce aspiration. These radiological examinations may be supplemented by a functional endoscopic evaluation of swallowing (FEES) [8, 47]. If aspiration is massive, then immediate broncho-oesophagoscopy is preferred to a barium swallow; the latter can contaminate the lower airways with contrast medium. An oesophagram can also reveal an indentation suggesting vascular compression.
complete obstruction. The level of airway obstruction is dependent on both the type of general anaesthetic used and the depth of anaesthesia. With propofol and sevoflurane, airway narrowing is dose-dependent, being more pronounced at the level of the epiglottis and in small children, with marked inter-individual variations [10, 12].
3.7.1 Pre-anaesthetic Assessment The type and degree of obstruction (Tables 3.5 and 3.6) must be assessed, based on a careful medical history and physical examination. Signs predicting a difficult intubation as well as associated cardiorespiratory problems must be searched for [7, 48]. Signs of mild cardiac dysfunction are not always obvious in children, and transthoracic echocardiography should be used in order to detect cardiac and vascular anomalies, which are frequently associated with congenital upper airway anomalies [1].
3.7 Anaesthetic Techniques for MRI in Children with Obstructive Dyspnoea Madeleine Chollet Rivier, MD, Marc-André Bernath, MD, Staff Anaesthesiologists
3.7.2 Anaesthesia for MRI in Children with Mild (Stage I and II) Obstruction (See Table 3.5) Obstructive disorders of the upper airways represent a continuum from simple snoring to obstructive sleep apnoea (OSA) as upper airway resistance (UAR) increases (Table 3.5) [7]. Three different situations may be encountered: • Collapsible upper airway, as seen in laryngomalacia or OSA • Fixed stenosis, as seen in congenital or acquired cicatricial laryngotracheal stenosis • Compressible intrathoracic airway, as seen in tracheomalacia or in the presence of a mediastinal mass Regardless of the type of obstruction, airway narrowing is the main cause for difficult ventilation and at times intubation. Tracheotomy is frequently necessary to secure the airway, particularly in children under 1 year of age [48]. In patients presenting with severe obstruction of the upper airway, appropriate oxygenation is the priority. General anaesthetics are known to increase airway narrowing, potentially leading to
Static and dynamic cine magnetic resonance imaging (MRI) techniques have been used to assess the causes of obstructive upper airways [16]. During MRI, sedation is required in order to ensure a relatively motionless patient and allow for successful imaging under spontaneous ventilation without using an artificial airway such as a tracheal tube, laryngeal mask or oral/ nasal airway. A thorough evaluation of upper airway dynamics and function is thus rendered possible [11]. Sedation under spontaneous respiration in a child without airway obstruction induces less atelectasis than endotracheal intubation with positive pressure ventilation during MRI [33]. In a recent survey, inhalation induction under sevoflurane was the method of choice selected by over 90% of paediatric anaesthesiologists [3]. This technique allows for preoxygenation of the patient and ensures airway control, while maintaining spontaneous respiration. After placing a venous line, a balanced hypnotic
41
3.7 Anaesthetic Techniques for MRI in Children with Obstructive Dyspnoea Table 3.5 Continuum of sleep-disordered breathing (Adapted from [7]). Normal
No snoring
Stage I
Stage II
Stage III
Stage IV
UAR
OH
OSA
Primary snoring
Upper airway resistance syndrome
Obstructive hypopnoea
Obstructive sleep apnea
Snoring
Increased UAR
Increased UAR
Intermittent
No daytime symptoms
Sufficient to cause symptoms
Sufficient to cause �PaCO2, ¯ SaO2
Upper airway obstruction
Table 3.6 Targeted pre-anaesthetic evaluation of upper airway obstruction Symptoms and signs Yes No Degree/type Since when Snoring Stridor (inspiratory, expiratory, biphasic) Voice modification (dysphonia) Preferred sleeping position (side, orthopnea, head position) Obstructive apneoa or hypoventilation Dyspnoea Cough Choking with feeds
haemodynamics [31]. Dexmedetomidine, which has been shown to simulate natural non-rapid eye movement sleep in animals studies [36], may be the best drug to assess obstructive phenomena, as the latter predominantly occur during sleep. Nevertheless, maintaining spontaneous respiration under sedation is only possible for patients with light Stage I and II symptoms of dynamic obstruction (Table 3.5) or fixed (less than 70%) stenosis, given that MRI is a relatively long-lasting procedure (~90 min). Monitoring during MRI sedation is done according to the ASA guidelines. In Lausanne, dedicated MRI non-magnetic monitoring (Maglife C Plus®, Schiller AG, Switzerland) with paediatric settings is used. During sedation, O2 (3 l/min) is given via a double channel nasal cannula, permitting simultaneous measurements of end-tidal CO2 (ET-CO2). In the immediate MRI room vicinity, there is a fully equiped anaesthesia cart, with proper equipment and medication for airway management and ressuscitation.
Infectious episodes Obesity Enlarged tonsils and/or adenoids Previous tracheal intubation
anaesthesia is most frequently used for sedation; opioid administration is not required, as the procedure is painless. The use of midazolam (0.1 mg/kg) associated with a low-dose propofol infusion is the technique of choice [5]. New sedative regimens have been reported, such as dexmedetomidine bolus (1 mg/kg) followed by infusion at a rate of 1 mg/kg/h and ketamine bolus (1 mg/kg) so as to counteract dexmedetomidine’s negative effects on
3.7.3 Anaesthesia for MRI in Children with a Fixed (³70%) Tracheal Stenosis At rest, clinical signs of obstruction become manifest when the stenosis exceeds 70% of the lumen. Owing to Poiseuille’s law, a 50% reduction in the airway radius is associated with a 16-fold increase in airflow resistance. To maintain the same oxygen flow, the pressure applied above the stenosis raises in exponential manner [4]. Suprastenotic ventilation is recommended in order to diminish the risk of complete obstruction [25], and positive pressure ventilation is
42
mandatory to ensure correct minute ventilation through the stenotic airway. Supraglottic devices such as laryngeal masks have been used for the management of laryngotracheal stenosis, with controversial results. Airway obstruction at or below the larynx is a relative contraindication to their use [2]. If the required inspiratory pressure to deliver oxygen through the stenotic airway is higher than the aperture pressure of the superior oesophageal sphincter, the risk of gastric distension and resultant hypoxia is significant. Furthermore, if a small jet ventilation catheter is passed beyond the stenosis to ensure manual oxygenation, gas trapping with overinflation of the lungs and complete obstruction may occur [13]. In the presence of severe fixed tracheal stenosis, the safest treatment options consist in either endoscopic dilation of the stenotic airway immediately after anaesthesia induction or performance of a tracheostomy.
3.7.4 Anaesthesia for MRI in Children with Stage III and IV Collapsible Upper Airway Positive pressure ventilation is required to mechanically stent the airway open and improve functional residual capacity as soon as the child has fallen asleep following administration of sedative drugs. Continuous positive airway pressure (CPAP) delivers up to 10 cm H2O of constant pressure to the airway. Bi-level positive airway pressure (BiPAP) applies inspiratory support (up to 15 cm H2O) and positive end-expiratory pressure. Both CPAP and BiPAP have been safely used in children under spontaneous respiration anaesthesia, using an adjusted facial or nasal mask and ventilator [43]. While there is not sufficient evidence to support any particular technique, the avoidance of a tracheal tube by using a supraglottic device may decrease postoperative coughing and the risk of unforeseen airway collapse.The laryngeal mask is probably the most common way to apply positive pressure ventilation under spontaneous respiration. If the inspiratory pressure is higher than 14 mmHg, the risk of gastric distension along with a dramatic fall in cardiac output is high, particularly in small children [2]. If a high inspiratory pressure is required to ensure airway patency, endotracheal intubation and intermittent positive pressure
3 Clinical Evaluation of Airway Obstruction
ventilation are mandatory. Avoidance of premedication and use of short-acting anaesthetic drugs are recommended [27].
3.7.5 Sedation for MRI in Children with Compressible Intrathoracic Airway When the collapsible airway is located in the thorax, increased dynamic compression of the airway and cardiovascular structures occurs in response to positive pressure ventilation. This situation is similar to that observed in patients with anterior mediastinal masses [34]. During inspiration, spontaneous ventilation and avoidance of muscle relaxation maintain airway patency, owing to the radial traction on trachea and bronchi exerted by the negative intrathoracic pressure. Active expiratory force helps overcoming obstruction during exhalation. Slow and quiet respiration is essential as agitated breathing may worsen dynamic intrathoracic airway collapse and increase airflow turbulence at the site of obstruction [38]. Cine magnetic resonance imaging is an important tool to evaluate the type and location of the airway obstruction, particularly when associated with cardiac and vascular anomalies [40]. When using the aforementioned anaesthetic techniques, cine magnetic resonance imaging is considered to be a safe examination, even in sick children [41].
3.8 Assessment of the Patient’s General Condition The medical history and physical examination should differentiate normal infants and children from those with disabilities. Some impairments are readily visible (e.g., prematurity, severe neurological deficits and congenital syndromic anomalies); others should be investigated by specialists (e.g., poor pulmonary reserve, gastro-oesophageal reflux and cardiac anomalies): • Congenital anomalies: A thorough physical examination by a geneticist facilitates the diagnosis of rare syndromic anomalies that may compromise the surgical results in the case of congenital or acquired
43
References
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•
•
subglottic stenosis. Karyotyping should be conducted in children with congenital anomalies if requested by the geneticist. Prematurity: History of prematurity in a child should always raise the possibility of poor pulmonary reserve as a sequela to hyaline membrane disease as well as neurological deficits secondary to periventricular leucodystrophy caused by brain haemorrhage. Neurological evaluation: Lack of coordinated breathing and swallowing in a mentally retarded child can preclude any surgical attempt at reopening the stenotic larynx. A thorough examination by a paediatric neurologist should help the decision-making process concerning the surgical intervention. Cardiac evaluation: If the airway obstruction is intrathoracic or if cardiac problems are associated with a subglottic stenosis, then electrocardiography and echocardiography will assist in the diagnosis and management of the airway problem. Pulmonary evaluation: Ideally, lung function tests and arterial blood gas evaluation should provide precise information as to the patient’s pulmonary reserve. However, spirometry data are not reliable in children with airway obstructions, particularly if they have previously been tracheostomised. The best estimate of pulmonary reserve may be obtained based on intentional episodes of apnoea during endoscopy under general anaesthesia. The rapidity with which the child recovers from temporary oxygen desaturation provides useful information on the quality of the gas exchanges in the lung parenchyma. This information can help decide if a singlestage or a double-stage surgery should be considered for the treatment of subglottic stenosis. Gastro-oesophageal investigation: Gastrooesophageal reflux (GOR) can induce chronic irritation of the pharyngolarynx, which in turn may cause or aggravate an upper airway stenosis. Twenty-four hour pH- [28, 35] or impedance pH monitoring [9, 29] and gastric emptying studies are useful in evaluating possible reflux. In practice, these tests are reserved for patients who do not respond to a trial of proton pump inhibitors, or when primary surgery for laryngotracheal stenosis has failed, possibly due to gastro-oesophageal reflux. Day-to-day variability in pH-recordings is, however, a limiting factor in assessing the severity of GOR [37].
References 1. Austin, J., Ali, T.: Tracheomalacia and bronchomalacia in children: pathophysiology, assessment, treatment and anaesthesia management. Paediatr. Anaesth. 13, 3–11 (2003) 2. Brimacombe, J.R., Brain, A.I.J., Berry, A.M.: Indications and contraindications. In: Brimacombe, J.R., Brain, A.I.J., Berry, A.M. (eds.) The laryngeal mask airway: a review and practical guide, pp. 114–116. W. B. Saunders, London (1997) 3. Brooks, P., Ree, R., Rosen, D., et al.: Canadian pediatric anesthesiologists prefer inhalational anesthesia to manage difficult airways. Can. J. Anaesth. 52, 285–290 (2005) 4. Bruce, I.A., Rothera, M.P.: Upper airway obstruction in children. Paediatr. Anaesth. 19(Suppl 1), 88–99 (2009) 5. Bryan, Y.F., Hoke, L.K., Taghon, T.A., et al.: A randomized trial comparing sevoflurane and propofol in children undergoing MRI scans. Paediatr. Anaesth. 19, 672–681 (2009) 6. Bull, P.D.: Evaluation of the pediatric airway by rigid endoscopy. In: Cotton, R.T., Myer III, C.H.M. (eds.) Practical pediatric otolaryngology, pp. 477–481. Lippincott-Raven, Philadelphia; New York (1999) 7. Carroll, J.L.: Obstructive sleep-disordered breathing in children: new controversies, new directions. Clin. Chest Med. 24, 261–282 (2003) 8. Chien, W., Ashland, J., Haver, K., et al.: Type I laryngeal cleft: establishing a functional diagnostic and management algorithm. Int. J. Pediatr. Otorhinolaryngol. 70, 2073–2079 (2006) 9. Condino, A.A., Sondheimer, J., Pan, Z., et al.: Evaluation of gastroesophageal reflux in pediatric patients with asthma using impedance-pH monitoring. J. Pediatr. 149, 216–219 (2006) 10. Crawford, M.W., Arrica, M., Macgowan, C.K., et al.: Extent and localization of changes in upper airway caliber with varying concentrations of sevoflurane in children. Anesthesiology 105, 1147–1152 (2006). discussion 1145A 11. Donnelly, L.F., Shott, S.R., LaRose, C.R., et al.: Causes of persistent obstructive sleep apnea despite previous tonsillectomy and adenoidectomy in children with Down syndrome as depicted on static and dynamic cine MRI. AJR Am. J. Roentgenol. 183, 175–181 (2004) 12. Evans, R.G., Crawford, M.W., Noseworthy, M.D., et al.: Effect of increasing depth of propofol anesthesia on upper airway configuration in children. Anesthesiology 99, 596– 602 (2003) 13. Fayoux, P., Marciniak, B., Engelhardt, T.: Airway exchange catheters use in the airway management of neonates and infants undergoing surgical treatment of laryngeal stenosis. Pediatr. Crit. Care Med. 10, 558–561 (2009) 14. Friedman, E.M.: Role of ultrasound in the assessment of vocal cord function in infants and children. Ann. Otol. Rhinol. Laryngol. 106, 199–209 (1997) 15. Froehlich, P., Seid, A., Denoyelle, F., et al.: Discoordinate pharyngolaryngomalacia. Int. J. Pediatr. Otorhinolaryngol. 39, 9–18 (1997) 16. Hofmann, U., Hofmann, D., Vogl, T., et al.: Magnetic resonance imaging as a new diagnostic criterion in paediatric airway obstruction. Prog. Pediatr. Surg. 27, 221–230 (1991) 17. Holinger, L.D.: Evaluation of stridor and wheezing. In: Holinger, L.D., Lusk, R.P., Green, C.G. (eds.) Pediatric lar-
44 yngology and bronchoesophagology, p. 45. LippincottRaven, Philadelphia; New York (1997) 18. Holinger, L.D., Lusk, R.P., Green, C.G.: Laryngeal development. In: Holinger, L.D., Lusk, R.P., Green, C.G. (eds.) Pediatric laryngology and broncoesophagology, pp. 1–17. Lippincott-Raven, Philadelphia; New York (1997) 19. Honnef, D., Wildberger, J.E., Das, M., et al.: Value of virtual tracheobronchoscopy and bronchography from 16-slice multidetector-row spiral computed tomography for assessment of suspected tracheobronchial stenosis in children. Eur. Radiol. 16, 1684–1691 (2006) 20. Jackson, C., Jackson, C L.: Obstructive laryngotracheal diseases. In: Jackson, C., Jackson, C.L. (eds.) Bronchoesophagology, p. 135. W. B. Saunders, Philadelphia; London (1950) 21. Jaffe, R.B.: Radiographic manifestations of congenital anomalies of the aortic arch. Radiol. Clin. North Am. 29, 319–334 (1991) 22. Kao, S., Smith, W., Sato, Y., et al.: Ultrafast CT of laryngeal and tracheobronchial obstruction in symptomatic postoperative infants with esophageal atresia and tracheoesophageal fistula. Am. J. Roentgenol. 154, 345–350 (1990) 23. Kryger, M., Bode, F., Antic, R., et al.: Diagnosis of obstruction of the upper and central airways. Am. J. Med. 61, 85–93 (1976) 24. Kryger, M., Bode, F., Antic, R., et al.: Diagnosis of obstruction of the upper and central airways. Am. J. Med. 61, 85 (1976) 25. Kussman, B.D., Geva, T., McGowan, F.X.: Cardiovascular causes of airway compression. Paediatr. Anaesth. 14, 60–74 (2004) 26. Lambert, V., Sigal-Cinqualbre, A., Belli, E., et al.: Preoperative and postoperative evaluation of airways compression in pediatric patients with 3-dimensional multislice computed tomographic scanning: effect on surgical management. J. Thorac. Cardiovasc. Surg. 129, 1111–1118 (2005) 27. Lerman, J.: A disquisition on sleep-disordered breathing in children. Paediatr. Anaesth. 19(Suppl 1), 100–108 (2009) 28. Littlem, J.P., Matthews, B.L., Glock, M.S. et al. : Extraesophageal pediatric reflux: 24-hour double-probe pH monitoring of 222 children. Ann. Otol. Rhinol. Laryngol. 169(Suppl ):1–16 (1997) 29. Lopez-Alonso, M., Moya, M.J., Cabo, J.A., et al.: Twentyfour-hour esophageal impedance-pH monitoring in healthy preterm neonates: rate and characteristics of acid, weakly acidic, and weakly alkaline gastroesophageal reflux. Pediatrics 118, 299–308 (2006) 30. Lowe, G.M., Donaldson, J.S., Backer, C.L.: Vascular rings: 10-year review of imaging. Radiographics 11, 637–646 (1991) 31. Luscri, N., Tobias, J.D.: Monitored anesthesia care with a combination of ketamine and dexmedetomidine during magnetic resonance imaging in three children with trisomy 21 and obstructive sleep apnea. Paediatr. Anaesth. 16, 782–786 (2006) 32. Lusk, R.P., Khosla, S.: Principles of fluid dynamics. In: Holinger, L.D., Lusk, R.P., Green, C.G. (eds.) Pediatric lar-
3 Clinical Evaluation of Airway Obstruction yngology and bronchoesophagoscopy, pp. 381–391. Lippincott-Raven, Philadelphia; New York (1997) 33. Lutterbey, G., Wattjes, M.P., Doerr, D., et al.: Atelectasis in children undergoing either propofol infusion or positive pressure ventilation anesthesia for magnetic resonance imaging. Paediatr. Anaesth. 17, 121–125 (2007) 34. Massullo, D., Di Benedetto, P., Pinto, G.: Intraoperative strategy in patients with extended involvement of mediastinal structures. Thorac. Surg. Clin. 19, 113–120 (2009). vii–viii 35. Matthews, B.L., Little, J.P., McGuirt Jr., W.F., et al.: Reflux in infants with laryngomalacia: results of 24-hour doubleprobe pH monitoring. Otolaryngol. Head Neck Surg. 120, 860–864 (1999) 36. Nelson, L.E., Lu, J., Guo, T., et al.: The [alpha]2-adrenoceptor agonist dexmedetomidine converges on an endogenous sleep-promoting pathway to exert its sedative effects. Anesthesiology 98, 428–436 (2003) 37. Nielsen, R.G., Kruse-Andersen, S., Husby, S.: Low reproducibility of 2 × 24-hour continuous esophageal pH monitoring in infants and children: a limiting factor for interventional studies. Dig. Dis. Sci. 48, 1495–1502 (2003) 38. Pullerits, J., Holzman, R.: Anaesthesia for patients with mediastinal masses. Can. J. Anaesth. 36, 681–688 (1989) 39. Rabb, M., Szmuk, P.: The difficult pediatric airway. In: Hagberg, C.A., Benumof, J. (eds.) Benumof’s airway management: principles and practice, pp. 783–833. Mosby Inc, Elsevier, Philadelphia (2007) 40. Sandu, K., Monnier, P.: Congenital tracheal anomalies. Otolaryngol. Clin. North Am. 40, 193–217 (2007) 41. Sarikouch, S., Schaeffler, R., Korperich, H., et al.: Cardiovascular magnetic resonance imaging for intensive care infants: safe and effective? Pediatr. Cardiol. 30, 146–152 (2009) 42. Schlesinger, A., Hernandez, R.: Radiographic imaging of airway obstruction in pediatrics. Otolaryngol. Clin. North Am. 23, 609 (1990) 43. Schwengel, D.A., Sterni, L.M., Tunkel, D.E., et al.: Perioperative management of children with obstructive sleep apnea. Anesth. Analg. 109, 60–75 (2009) 44. Singh, C., Gupta, M., Sharma, S.: Compression of trachea due to double aortic arch: demonstration by multi-slice CT scan (MSCT). Heart Lung Circ. 15, 332–333 (2006) 45. Stern, Y., Cotton, R.T.: Evaluation of the noisy infant. In: Cotton, R.T., Myer III, C.M. (eds.) Practical pediatric otolaryngology, pp. 471–476. Lippincott-Raven, Philadelphia; New York (1999) 46. Vauthy, P.A., Reddy, R.: Acute upper airway obstruction in infants and children. Evaluation by the fiberoptic bronchoscope. Ann. Otol. Rhinol. Laryngol. 89, 417–418 (1980) 47. Wiet, G.J., Long, F.R., Shiels, I.W., et al.: Advances in pediatric airway radiology. Otolaryngol. Clin. North Am. 33, 15–28 (2000) 48. Wrightson, F., Soma, M., Smith, J.H.: Anesthetic experience of 100 pediatric tracheostomies. Paediatr. Anaesth. 19, 659–666 (2009)
4
Equipment and Instrumentation for Diagnostic and Therapeutic Endoscopy
Contents
Core Messages
4.1
Endoscopy Suite...................................................... 46
›› Endoscopic management of the paediatric air-
4.2 4.2.1 4.2.2 4.2.3 4.2.4 4.2.5 4.2.6
Laryngoscopes......................................................... Parsons Laryngoscopes............................................. Benjamin–Lindholm Laryngoscopes........................ Kleinsasser Laryngoscopes....................................... Holinger–Benjamin Laryngoscopes......................... Suspension Microlaryngoscopy................................ Ancillary Instruments...............................................
46 47 47 47 48 48 49
4.3 Bronchoscopes......................................................... 52 4.3.1 Rigid Bronchoscopes................................................ 53 4.3.2 Flexible Bronchoscopes............................................ 54
›› ›› ››
4.4 Oesophagoscopes.................................................... 54 4.4.1 Rigid Oesophagoscopes............................................ 54 4.5
Documentation and Training................................. 55
4.6 4.6.1 4.6.2 4.6.3 4.6.4
Lasers in Paediatric Airway Management........... Laser Principles........................................................ Properties of Laser Light.......................................... Laser–Tissue Interactions......................................... Light Delivery Systems............................................
56 57 58 58 62
4.7 4.7.1 4.7.2 4.7.3 4.7.4 4.7.5 4.7.6
Laser Safety............................................................. Eye and Skin Hazards............................................... Skin Protection......................................................... Fire Hazards.............................................................. Fire Prevention.......................................................... Laser-Induced Accidents.......................................... Safety Recommendations.........................................
65 66 67 68 69 70 70
4.8 Ancillary Therapeutic Means................................ 71 4.8.1 Dilation..................................................................... 71 4.8.2 Microdebrider........................................................... 72 4.9
Appendix 1............................................................... 74
References............................................................................ 74
›› ›› ››
way requires a well-equipped endoscopy suite with versatile instrumentation and an ultrapulse CO2 laser. Knowledge of laser–tissue interactions is essential in selecting the appropriate laser with respect to the pathology. Choosing optimal CO2 laser parameters greatly diminishes collateral thermal damage. For benign cicatricial airway stenoses, the CO2 laser should be set to ultrapulse mode, 100– 150 mJ/cm2, 250-m spot size at 400-mm focal distance, with a 10-Hz repetition rate. Vascular or pigmented airway lesions can be treated using the argon or KTP laser. Before engaging in endoscopic laser procedures, all involved personnel must attend an educational programme on laser safety. Fire hazard is the most feared complication of endoscopic laser airway surgery. The risk can be minimised by: –– Adopting an appropriate anaesthetic technique (tubeless with spontaneous breathing or intermittent apnoeas) –– Strict adherence to safe gas mixtures (25% O2 and 75% N2) –– Working in a free operative field without any flammable material –– Using the CO2 laser in a pulsed or chopped mode –– Avoiding non-target strikes by proper alignment of the CO2 and He–Ne laser beams
P. Monnier (ed.), Pediatric Airway Surgery, DOI: 10.1007/978-3-642-13535-4_4, © Springer-Verlag Berlin Heidelberg 2011
45
46
4 Equipment and Instrumentation for Diagnostic and Therapeutic Endoscopy
›› Eye and skin hazards are the most dangerous
›› ››
injuries, potentially affecting patients and theatre personnel. They can be avoided by: –– Wearing appropriate goggles for the laser type –– Protecting the patient’s face with wet surgical towels For dilation of an airway stenosis, tapered bougies provide better tactile feedback than balloon dilators. For the treatment of recurrent respiratory papillomatosis, the microdebrider is more efficient and less traumatic than the CO2 laser.
Table 4.1 Paediatric difficult airway cart [15] • Assortment of laryngoscope handles and blades • Oxyscope • Endotracheal tubes 2–7 mm • Oral/nasal airways • Masks • Stylets • Endotracheal tube exchangers • Laryngeal mask airways: all sizes • Fibreoptic intubation equipment • Bronchoscopic swivel connector • Rigid bronchoscopes • Retrograde intubation kit
Management of the compromised paediatric airway may be challenging. In this situation, anticipating potential problems is most rewarding in terms of a successful outcome. In order to reach a high level of expertise in compromised paediatric airway management, the following arrangement is necessary: • A dedicated, well-equipped endoscopy room • Versatile instrumentation for paediatric laryngoscopy and broncho-oesophagoscopy • Well-maintained, up-to-date laser equipment • A multidisciplinary medical team specialised in problematic airway management The success of endoscopic procedures largely depends on the interaction between the surgeons and the anaesthetists. Both an accurate diagnosis of the airway problem and minimally traumatic endoscopic surgery contribute to a positive outcome. Overuse of lasers or dilators in the case of paediatric airway stenosis, particularly in infants, may induce intractable cicatricial sequelae, constituting a therapeutic challenge. This chapter focuses on the basic equipment needed for diagnostic and therapeutic endoscopy. It also provides detailed information on the use of lasers and dilation for airway stenosis management.
4.1 Endoscopy Suite In order to manage a difficult airway, this area must be well-equipped, with anaesthetic and emergency care facilities, along with cardiopulmonary resuscitation
• Magill forceps • Percutaneous cricothyrotomy kit
equipment (see Sect. 5.1, Chap. 5). The American Academy of Pediatrics strongly recommends that a specific cart or cupboard be designated for use by the anaesthetist for difficult cases in which intubation or ventilation must be used during airway stenosis management [15]. The list of useful items is shown in Table 4.1. The endoscopist must be prepared for suspension microlaryngoscopy using an operating microscope, a CO2 laser, different-sized endoscopes (direct laryngoscopes, bronchoscopes) and ancillary equipment (e.g., forceps, retractors, laser platforms, dilators).
4.2 Laryngoscopes In 2001, Benjamin published a comprehensive review of paediatric laryngoscopes [4].Optimal exposure using a wide range of paediatric endoscopes is a prerequisite for efficient diagnostic and therapeutic endoscopy. Anaesthetic intubation laryngoscopes are readily available in different sizes, equipped with interchangeable curved or straight blades. Though quite versatile, they provide poor light intensity. When used in conjunction with a bare 4-mm sinuscope, they provide good exposure with a panoramic telescopic view of the pharyngolarynx (Fig. 4.1). Useful in the case of bedside laryngeal examinations of intubated children, this instrument can replace Karl Storz general-purpose laryngoscopes [4] (Fig. 4.2).
47
4.2 Laryngoscopes
Diagnostic and operative laryngoscopes have two basic designs. They are equipped either with a side slot for the introduction of an endotracheal tube or bronchoscope, or with a modified open-tube with no side opening.
4.2.1 Parsons Laryngoscopes (Fig. 4.3) Parsons laryngoscopes offer the best design. Their tapered tip can be placed in the vallecula or behind the epiglottis for optimal exposure of the endolarynx. The side slot not only serves an intubation purpose, but also provides working space for endoscopic suturing, especially in the treatment of laryngotracheo-oesophageal clefts that extend below the cricoid plate into the cervical trachea (see Sect. 12.5.3, Chap. 12).
4.2.2 Benjamin–Lindholm Laryngoscopes (Fig. 4.4) Fig. 4.1 Panoramic view of the pharyngolarynx with a 4-mmdiameter sinuscope: (a) View of the pharyngolarynx. (b) 4-mmdiameter sinuscope
These laryngoscopes were designed to provide a larger view of the pharyngolarynx. The distal tip is placed at the base of the tongue in the vallecula. In suspension laryngoscopy, the pressure exerted against the median and lateral glosso-epiglottic folds elevates the epiglottis, resulting in optimal exposure of the pharyngolarynx for instrumentation as well as imaging purposes. This laryngoscope is highly suitable for treating all forms of pharyngolaryngeal pathologies, such as laryngomalacia, saccular cysts or vascular anomalies (see Sect. 6.6, Chap. 6).
4.2.3 Kleinsasser Laryngoscopes (Fig. 4.5)
Fig. 4.2 K. Storz general-purpose laryngoscopes: They are provided with a side slot for introducing an endotracheal tube or bronchoscope. The distal tip may be placed in front or behind the epiglottis
These straight laryngoscopes provide a wide exposure of the larynx in a direct line, well suited for CO2 laser. This contrasts with the hourglass-designed operating laryngoscopes, compromising direct access of the laser beam to all endolaryngeal structures. These laryngoscopes are quite suitable for cold-instrumentation surgery but less optimal in the case of paediatric laryngeal laser work (Fig. 4.6). The advent of the Lindholm selfretaining false cord retractor has improved the access to the subglottis, with a reduced risk of trauma as compared to the Benjamin subglottiscope, which is rarely used in our ENT department.
48
4 Equipment and Instrumentation for Diagnostic and Therapeutic Endoscopy
Fig 4.3 Set of Parsons laryngoscopes: (a) Infant and child sizes. (b) Adolescent and adult sizes
Fig. 4.5 Kleinsasser laryngoscopes: These straight scopes are suitable for laser work in the paediatric larynx
Fig. 4.4 Benjamin–Lindholm laryngoscopes: They are available in different sizes for infants and children, providing a panoramic view of the pharyngolarynx
4.2.4 Holinger–Benjamin Laryngoscopes (Fig. 4.7) These are small-diameter laryngoscopes that are slotted along the right side for intubation of a problematic airway. Their other function is to expose the anterior commissure and the subglottis in the case of difficult access, but they cannot be used for suspension microlaryngoscopy. They are available in three different sizes.
The purpose of all handheld or suspension laryngoscopes is to expose the pharyngolarynx or the endolarynx. During this manoeuvre, the Benjamin–Haves light clip, a versatile light carrier adapted to all laryngoscopes, provides proper illumination (Fig. 4.8). Detailed examination is then carried out using rigid Hopkins telescopes of different angulations and an operating microscope.
4.2.5 Suspension Microlaryngoscopy Proper exposure of the larynx is the key to successful endoscopic diagnosis and treatment. The surgeon should not hesitate to try different laryngoscopes until a good
49
4.2 Laryngoscopes
Fig. 4.6 Hourglass-shaped operating laryngoscopes: Despite providing ample space for the introduction of various instruments, these laryngoscopes are not optimal for laser work because of their narrow hourglass neck which prevents the delivery of the laser beam to all exposed sites in the operative field
view of the larynx is obtained. Suspension laryngoscopy is done using a laryngoscope holder on the support table. Visualisation of the anterior laryngeal commissure may be improved by using Elastoplast® as a ‘third hand’ in order to exert external pressure on the larynx (Fig. 4.9). To begin with, the larynx is examined by means of rigid rod-lens telescopes with different angulations in order to obtain a panoramic view of the pharyngolarynx as well as hidden structures such as the ventricles and subglottis. As proposed by Benjamin, a laryngeal lift manoeuvre, that is, the grasping and elevating of the thyroid cartilage, will provide ideal exposure of the hypopharynx and post-cricoid region [4]. The microscope is used for therapeutic procedures leaving both hands free to manipulate instruments during the operation. In the case of laser surgery, one hand holds a forceps in order to grasp the mucosa, while the other hand manipulates the joystick; in ‘cold instrument’ surgery, a pair of microscissors is used instead. Therefore, both hands are available for endoscopic suturing and knot-tying. The appropriate laryngoscope must be selected to perform specific tasks at the various levels of the larynx (supraglottis, glottis or subglottis).
4.2.6 Ancillary Instruments Besides cup forceps, grasping forceps and microscissors, which are available in different designs and orientations, other, less conventional instruments are very useful in paediatric airway management:
Fig. 4.7 Slotted small-diameter paediatric laryngoscope designed to expose difficult areas, such as the anterior commissure and subglottis
• The Lindholm self-retaining false cord retractor (Fig. 4.10): This is the most useful instrument in the case where a neurogenic bilateral vocal cord paralysis must be differentiated from a posterior glottic stenosis (see Sect. 5.3.3.2, Chap. 5). During laser surgery for different conditions such as cicatricial web-like stenosis or subglottic haemangioma, it also provides a wide access to the subglottis. In the paediatric larynx, this retractor should always be placed on the ventricular bands and not on the vocal cords to avoid injuring these delicate structures. • The Bouchayer heart-shaped grasping forceps (Fig. 4.11a): This paired (right and left), delicate, serrated, triangular, fenestrated forceps allows for precise holding of the laryngeal mucosa with minimal trauma. It is also useful in the treatment of laryngomalacia (see Sect. 6.6, Chap. 6).
50
4 Equipment and Instrumentation for Diagnostic and Therapeutic Endoscopy
Fig. 4.8 Proposed set of paediatric laryngoscopes to manage the most common situations: (a) Anaesthetist laryngoscope. (b) Kleinsasser laryngoscope. (c) Benjamin– Lindholm laryngoscopes. (d) Parson laryngoscope. (e) Benjamin–Haves light-clip. Only one size per laryngoscope is shown, with the exception of (c)
•
•
• Fig. 4.9 Suspension microlaryngoscopy set-up: Anterior neck pressure with a band of Elastoplast® improves visualisation of the anterior laryngeal commissure. It should be noted that the laryngoscope holder rests on the support table
• The endoscopic measuring device (Fig. 4.11b): This multipurpose instrument is used to measure lengths in the craniocaudal axis. It is useful in the measure-
•
ment of the distance from the vocal cords to the SGS or the tracheostoma site, in order to select the appropriate stent that will be placed endoscopically. The Zeitel injection needle (Fig. 4.11c): The distal angulation of the needle with respect to the shaft is ideal for injections into Reinke’s space and the subglottis. For instance, this needle is useful for injecting Cidofovir® in recurrent respiratory papillomatosis. The Bouchayer dissectors (Fig. 4.11d): This paired (right and left) instrument is ideal for testing passive mobility of the arytenoids in the case of vocal cord immobility. The Lichtenberger needle-carrier (Fig. 4.11e): This versatile instrument can be used to place endoextralaryngeal stitches under endoscopic visual control. It is also indicated for vocal cord lateralisation procedures and for fixing laryngeal prostheses such as a keel at the anterior laryngeal commissure or an LT-Mold. Despite its apparently large size, it is adapted to the infant’s larynx. Endoscopic suturing instruments (Fig. 4.12): Karl Storz and Microfrance needle holders can grasp a small ‘TF plus’ needle for endoscopic suturing of a
4.2 Laryngoscopes
51
Fig. 4.10 Lindholm false vocal cord retractor: a useful instrument to spread apart the vocal cords in order to assess the true width of the posterior laryngeal commissure and improve the access to the subglottis
Fig. 4.11 Set of useful laryngeal instruments: (a) Bouchayer’s triangular serrated forceps. (b) Endoscopic measuring device. (c) Zeitel’s injection needle. (d) Bouchayer’s dissectors. (e) Lichtenberger’s needle-carrier
laryngotracheo-oesophageal cleft. The Pilling pusher is used to tie the knots. • Laser platforms (Fig. 4.13): These exist in different shapes and sizes and are equipped with a side hole for suctioning laser plumes. They shield the normal
mucosa during laser surgery. The Pilling platform is especially designed to protect the contralateral vocal cord at the anterior commissure of the larynx. • The Kleinsasser laryngeal instrument set (Fig. 4.14): Among several instruments, the right-angle probe
52
4 Equipment and Instrumentation for Diagnostic and Therapeutic Endoscopy
Fig. 4.12 Indispensable instruments for endoscopic suturing: (a) Karl Storz or (b) Microfrance needle-carrier and (c) Pilling knot-pusher
4.3 Bronchoscopes Both rigid and flexible bronchoscopes are routinely used in paediatric airway management. Complementing each other, they are essential components of the standard instrument set used for the examination of a child’s airway.
4.3.1 Rigid Bronchoscopes
Fig. 4.13 Laser platforms for shielding the adjacent mucosa from the laser work: (a) Steiner’s platforms. (b) Pilling platforms
serves to palpate in the search for passive mobility of the arytenoids or for a laryngotracheo-oesophageal cleft. It is also useful for repositioning a luxated arytenoid (see Fig. 15.9, Chap. 15).
A wide range of open-tube rigid bronchoscopes is available. With a variety of shapes and sizes, they permit inspection of the tracheobronchial tree, from the premature infant to the adolescent and adult patient (Table 4.2). The open-tube is used in closed circuit for ventilation through a standard 15-mm side port, connected to the ventilation tube of the anaesthesiology cart. A 0° or angulated rod-lens telescope is inserted through a fenestrated rubber plug allowing for simultaneous ventilation of the patient. Inspection of the airway down to the basal bronchi is easily performed with long, slim telescopes, even in the case of premature babies (Fig. 4.15). The rigid outer tube is also used in open circuit with a jet ventilation system connected to the working channel. A prismatic light deflector illuminates the open-tube to provide a sufficient view of the trachea and bronchi; in the absence of visual control
53
4.3 Bronchoscopes Fig. 4.14 Kleinsasser set of laryngeal instruments: Different instruments can be adapted to the hand-holder. The right-angled probe is used to palpate the posterior laryngeal commissure when searching for a cleft
Table 4.2 Sizes of pediatric rigid bronchoscopes N° ID OD Length (cm) Storz (mm) (mm) 2.5
3.5
4.0
3.0
4.3
5.0
3.5
5.0
5.7
3.7
5.7
6.4
4.0
6.0
6.7
4.5
6.7
7.3
5.0
7.1
7.8
6.0
7.5
8.2
4.3.2 Flexible Bronchoscopes There are five types of flexible bronchoscopes used in paediatric airway interventions (Fig. 4.18):
20 cm 26 cm 30 cm
ID = internal diameter OD = outer diameter
with a telescope, insertion of suction catheters or various forceps is thus facilitated. Over the years, several types of optical forceps mounted onto telescopes have been developed to improve precision in removing foreign bodies and taking biopsies, even in the case of small infant airways. More recently, thin fibres used with the argon or KTP laser and hollow-core photonic bandgap fibres (see Sect. 4.6) used with the CO2 laser have widened the therapeutic possibilities in paediatric airway management. The fibre is simply fixed to the rod-lens optic, using Steri-Strips and is easily seen in the telescope’s field of vision in the trachea or bronchi (Fig. 4.16). This permits endoscopic curative excision of some benign tumours, thereby avoiding major open surgery (Fig. 4.17).
• The ultra-slim 1.9 or 2.2 mm-diameter bronchofibroscope (not a video-endoscope) with distal flexion, but with no working channel. • The 2.8 and 3.5 mm-diameter video-bronchoscopes with a 1.2-mm working channel. • The 4.9 mm-diameter video-bronchoscope, routinely used in children and adolescents. The distal 180° and 130° flexions improve visualisation of the segmental bronchi of the upper lobes. The sizes of the working channels are 2.0 and 2.2 mm in diameter, respectively. Both instruments offer adequately sized cups and grasping forceps. Although popularised by Woods 30 years ago [40], paediatric bronchofibroscopy is not a routine procedure in tertiary centres in the sedated, non-intubated child. Based on reports from various centres, the technique’s complication rate is low when performed by experienced hands [39]. Generally, otolaryngologists prefer to combine rigid and flexible bronchoscopy under general anaesthesia as this combination is convenient and safe [37, 39]. Both techniques complement each other. When assessing a stridorous, dyspnoeic child, transnasal flexible pharyngolaryngoscopy (TNFL) and bronchofibroscopy are routinely carried out through an anaesthetic face mask in order to evaluate the func-
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Fig. 4.15 Paediatric rigid bronchoscopes:(a) Set of eight Karl Storz bronchoscopes from size 2.5–6.0. (1) Light-cable connection. (2) Straight-forward telescope. (3) Prismatic light deflector for illumination of the open-tube. (4) Working/jet ventilation channel. (5) Standard 15 mm side port with connected rubber
pipe for anaesthesia. (b) Lateral and frontal views of a variety of optical forceps mounted on straight-forward telescopes. From top to bottom: scissors, biopsy, foreign body, cup-biopsy and grasping forceps
tional dynamics of the upper airway, larynx and trachea (see Sect. 5.2.2, Chap. 5).
4.4.1 Rigid Oesophagoscopes (Fig. 4.19)
4.4 Oesophagoscopes The advent of slim, flexible video-gastroscopes has improved the quality of the examination of the upper digestive tract. However, the utility of rigid oesophagoscopes in situations such as the removal of foreign bodies and tortuous stenoses at the upperoesophageal sphincter remains unsurpassed to this day.
With a built-in suction channel and air-inflation device supplied by a manual rubber bulb, the paediatric counterparts of the rigid Universal Storz adult oesophagoscope exist in different lengths and sizes (Fig. 4.19a). They all benefit from the built-in inflation device, which facilitates the proper examination of the oesophagus. Optical biopsy and grasping forceps of different shapes and sizes enhance the versatility of its use (Fig. 4.19b). Larger, straight, round-oval open-tubes of the Hasslinger type are extremely useful for removing foreign bodies lodged at the upper-oesophageal
55
4.5 Documentation and Training Fig. 4.16 Omniguide CO2 laser fibre: The fibre is simply fixed to the 0° telescope with Steri-Strips
Fig. 4.17 Haemangioendothelioma of the left main-stem bronchus in a 13-year-old girl: (a) Preoperative view. (b) After KTP laser excision-vaporisation. (c) Postoperative view after 3 years
sphincter. Both adult and paediatric sizes exist with a variety of strong and large optical forceps (Fig. 4.20). Holinger mentioned in his book on paediatric laryngology and broncho-esophagology that ‘no fewer than 60 variations of foreign body forceps have been designed to cope with the many mechanical problems of foreign body extraction’ [17]. Clearly, this description provides an invaluable insight into this challenging problem. In addition, laser fibres for the CO2, argon, KTP and Nd-YAG lasers are useful in certain rare conditions within the paediatric age group.
4.5 Documentation and Training Over the years, the efficacy of photography and video documentation has greatly improved, for the physician’s and the patient’s benefit. Currently, all endoscopies are performed with a 3 CCD-digital camera coupled with the optic rod lens of the endoscope or the operating microscope. These video cameras are small and lightweight with low-light sensitivity. During the entire endoscopic procedure, a cart with two swivelling monitors provides the attending surgeon, anaesthesia team, residents and nurses
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resolution overshadows this advantage when compared to a reflex digital camera. Nevertheless, the quality of the image is sufficient for storage and PowerPoint presentations. This technology also permits the transfer of images to CD-ROMs, USB drives and the Internet, improving communication between medical professionals for purposes of training and teleconferencing.
4.6 Lasers in Paediatric Airway Management Fig. 4.18 Flexible 2.2 mm bronchofibroscope and 4.9 mm video-bronchoscope
with an excellent view (Fig. 4.21). This facilitates the entire team’s work in managing a difficult airway and also results in substantial benefit for the patient. The digital video camera provides high-quality images and simplifies still photography. A simple touch on a knob registers the photograph with immediate quality control in terms of exposure and sharpness. Decreased
Fig. 4.19 Set of rigid paediatric oesophagoscopes and forceps: (a) Sizes 3 and 3.5 are 20 cm long; Sizes 4–6 are 30 cm long. (b) Optical forceps: same forceps as those used for bronchoscopy
Although lasers are routinely used in paediatric laryngeal and tracheal management, the details of their parameters for achieving optimal results without complications are insufficiently described in the medical literature. A thorough knowledge of the different types of lasers and their application in various conditions is of utmost clinical importance. The CO2 laser, which has been the workhorse in otolaryngology since the late 1970s, is used for treating different pathological conditions relating to the paediatric airway. As stated
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4.6 Lasers in Paediatric Airway Management Fig. 4.20 (a) Hasslinger oesophagoscopes: They exist in different paediatric and adult sizes. (b) Close up view: Strong optical grasping forceps are useful for foreign body extraction in the hypopharynx
previously, precise descriptions of CO2 laser parameters (power density, energy density and exposure time) essential for its efficient use are lacking. This section summarises the basic principles of lasers, including details on laser–tissue interactions and proper setting of CO2 laser parameters. For a comprehensive description of lasers in otolaryngology, the reader is referred to the textbook entitled Principles and Practice of Lasers in Otorhinolaryngology and Head and Neck Surgery published by V. Oswald and M. Remacle in 2002 [25].
4.6.1 Laser Principles
Fig. 4.21 Cart for videomonitoring and still photography: Two swivelling monitors can be positioned at different viewing angles for the benefit of the attending surgeon and anaesthesiology staff
All lasers consist of three essential components: a lasing medium, a pumping system provided by external energy and an optical cavity (Fig. 4.22). The lasing medium determines the laser’s wavelength and consequently, its interaction with biological tissues. The medium may be gas (CO2, argon, heliumneon), crystal (Nd-YAG, KTP), liquid (dyes) or a semiconductor (diode). The pumping energy is provided by an external excitation source (electrical discharge, laser light, etc.), which stimulates the emission and the amplification of photons in the optical cavity.
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Fig. 4.22 Laser tube: The lasing medium is confined inside the discharge tube equipped with two reflecting mirrors, one of which is only partially reflective
The optical cavity consists of a discharge tube with a totally reflecting mirror at one end and a partially reflecting mirror at the opposite end. The pumping energy excites the atoms or molecules of the lasing medium contained in the optical cavity. Since further energy is continuously pumped into the system, more atoms or molecules are in the excited state than in the ground state. This is known as a ‘population inversion’. The electrons revolving around the nucleus proceed toward a higher, unstable orbit from which they spontaneously decay to their ground state. The amount of energy lost by the excited, unstable electron is released in the form of a photon emitted spontaneously and randomly into the optical cavity. The mirrors at each end reflect the photons emitted in parallel to the axis of the tube. The photons collide with excited atoms or molecules and stimulate the emission of new photons. The stimulated light is emitted in the same direction as the radiant light, so that all the rays of light are parallel. The process repeats itself many times, resulting in an enormous surge in the number of photons. This is the ‘Light Amplification by Stimulated Emission of Radiation’ (i.e. LASER). The laser beam is the fraction of light leaking out of the optical cavity through the small aperture of one of the mirrors. The remaining fraction of light stays in the optical cavity, pursuing the lasing process.
4.6.2 Properties of Laser Light
one of its pertinent tissue interactions, that is, the specific absorption coefficient for a given tissue. In order to minimise collateral thermal damage, the surgeon must take this property into account in selecting the laser that emits the wavelength that is maximally absorbed by the tissue type to be treated. • Collimated laser light is directional and almost parallel, with little diversion. When passed through a lens, this pencil-sized beam of light focuses on the smallest possible spot, whereas the ordinary light of a tungsten lamp is scattered randomly from its source, focusing on larger images. • The collimated nature of laser light permits transmission of the beam to the surgical site by means of an optical fibre or an articulated arm. The beam can then be focused by a lens on the smallest of spots so as to deliver high energy density for tissue ablation and vaporisation. This property is essential for its use in medicine. • Coherent laser light means that all of the light waves are in phase, in both time and space. This property of coherence is not used for tissue ablation, but rather for the destruction of ureteral stones in urology; its other indications are the measurement of the motion of the tympanic-membrane as well as that of the vocal cords in otolaryngological laser interferometry.
4.6.3 Laser–Tissue Interactions
Laser light is monochromatic, collimated and coherent. • Monochromatic laser light is a single wavelength with a very narrow bandwidth, whereas the white light of a tungsten lamp is a mixture of the entire visible spectrum. Each laser medium is characterised by its specific wavelength, which determines
The effect of a laser beam on tissues depends on several parameters: • The laser wavelength • The absorption characteristics of the tissue • The tunable laser parameters
4.6 Lasers in Paediatric Airway Management
4.6.3.1 Laser Wavelength The laser wavelength is determined by the active lasing medium in the laser tube. Each laser is thus characterised by its wavelength. When a laser beam strikes the tissue, its energy undergoes four different interactions (Fig. 4.23): • Reflection: The energy reflected back from the surface of the tissue is minimal, but can be significant in the case of polished metal instruments. Therefore, the flammable anaesthetic tubes, the patient and the theatre personnel must be protected during laryngeal laser surgery. • Absorption: This property is essential for achieving the desired effect on the tissue. Absorption is strongly dependent on the laser’s wavelength as well as the tissue’s relevant biological properties. Following tissue absorption, the energy of the laser beam is converted into heat. Above 55°C, coagulation and denaturation of proteins generate irreversible tissue damage, eliciting a strong inflammatory response. With a further rise in temperature, the tissue suffers thermal necrosis and charring at around 100°C, followed by tissue disintegration (=vaporisation) when the temperature exceeds 250°C. Depending on the type of laser used and the energy density (Joules/cm2) delivered to the tissue, charring will line the crater. When this blackened carbon is hit by subsequent laser strikes, it may glow and further increase heat diffusion into the surrounding
Fig. 4.23 Effects of the laser beam on biological tissues:– Absorption is the desired effect –Scatter generates thermal damage –Reflexion is minimal on biological tissues –Transmission is dependent on tissue type
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tissues. This carbonisation effect should be avoided at all costs in paediatric airway management. • Transmission: This represents the amount of light that is transmitted through specific tissues. Depending on the type of laser and tissue, transmission without scattering can be limited or may be nearly complete, for example, transparent ocular fluids by the argon and KTP lasers, which are not absorbed by water at all. • Scatter: This corresponds to multiple reflections of the energy delivered by the laser within the tissue, causing unwanted thermal damage. The scattering properties of different lasers vary widely. The Nd-YAG wavelength displays strong scatter within mucous membranes, causing deep thermal damage; the CO2 laser generates minimal scatter and thermal damage in the same tissue.
4.6.3.2 Absorption Characteristics of the Tissue In paediatric endoscopic airway surgery, the relevant tissues are the mucous membranes, cartilage, scar tissue and pigmented vascular lesions such as haemangiomas. They are all composed of approximately 85% water; this percentage varies slightly between oedematous mucosa and scar tissue. The absorption coefficient of the different lasers with respect to the tissue spectral characteristics of water, haemoglobin and melanin are displayed in (Fig. 4.24): • The CO2 (10,600 nm), erbium-YAG (2,940 nm), holmium-YAG (2,100 nm) and argon fluoride (ArF) excimer (193 nm) lasers are all strongly absorbed by water-rich tissues, independently of their colour. They result in constant and reliable tissue interactions in the mucous membranes. • The argon (514 nm), KTP (532 nm) and tunable dye lasers (400–700 nm) are strongly dependent on the content of the pigments (haemoglobin and melanin) in the mucous membranes. Their absorption coefficient is extremely variable: absent in clear aqueous tissue such as the cornea, lens and vitreous humour of the eye, partial in white tissues such as skin or fat and significant in pigmented tissues such as vascular tumours. In otolaryngology, they are used to treat haemangiomas or melanomas of the skin and mucous membranes.
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Fig. 4.24 Absorption coefficients of water, haemoglobin and melanin with different types of lasers: The wavelength of the laser is indicative of its tissue effects (see text)
• The Nd-YAG (1,064 nm) and diode (980 nm) lasers are weakly absorbed by the mucous membranes. Their absorption coefficient is very weak in clear aqueous tissue, poor in non-pigmented lesions, but increased in pigmented, charred tissues. These lasers produce a very strong scattering effect, reaching up to 4 mm in depth in mucous membranes. They are well suited for haemostasis by coagulation and for vaporisation of large amounts of tissue. They cannot be used in paediatric airway management where precise, delicate incision and resection of tissue are required. • The penetration depth of the different lasers in mucous membranes is shown in (Fig. 4.25). Owing to the aforementioned laser–tissue interactions, the CO2 laser is considered the ultimate laser of choice in paediatric airway management. In the case of vascular tumours, the argon or KTP lasers may be used. However, the use of Nd-YAG or diode lasers in the treatment of paediatric airway lesions should never be justified simply because other lasers are unavailable (Table 4.3). In these cases, patients should be referred to tertiary centres equipped with the latest technology CO2 lasers (ultrapulse or superpulse modes).
4.6.3.3 Tunable Laser Parameters Even after choosing the right laser (i.e. CO2 laser) for paediatric airway management, the inappropriate selection of its parameters may adversely affect the outcome. The surgeon can control the delivery of the laser energy on the target tissue by adjusting the following parameters: • Output power • Spot size • Exposure time –– CW mode –– Pulsed mode –– Superpulse –– Ultrapulse The output power The output power expressed in watts is the rate at which the energy is delivered. It is of little relevance if it does not refer to the spot size on the target tissue. Therefore, knowledge of the power density (irradiance) and energy density (fluence) is essential.
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4.6 Lasers in Paediatric Airway Management Fig. 4.25 Penetration depth of different lasers into mucous membranes: The wavelength of the laser and the type of biological tissue determine the penetration depth (see text)
Table 4.3 Properties of different lasers Type of laser Vaporise Cut Coagulate CO2 :
10,600 nm
Argon :
514 nm
KTP :
532 nm
Nd-Yag :
1,064 nm
Diode :
980 nm
++
++
±
±
±
±
±
−
++
Fluence = energy density The energy density is a measure of the amount of work performed by the laser beam (power in watts × time in seconds = joules) divided by the crosssectional area of the laser beam expressed in cm2: Energy - density = power ´ time / area = watts ´ seconds ( joules ) / cm 2 CW mode
Irradiance = power density The thermal effect of the laser beam on the tissue depends on the output power of the machine measured in watts (W) divided by the cross-sectional area of the laser beam expressed in square centimetre. This is known as the power density or irradiance. The power density is inversely proportional to the square of the spot diameter: Power density = power / area = watts / cm 2 For the same amount of radiated energy, reducing the spot size increases the power density. As a result, more vaporisation and less coagulation necrosis are obtained in the target tissue (Fig. 4.26). A sharp laser incision on mucous membranes requires the smallest possible spot size for a given output power. This is achieved by sharply focusing the laser beam on the surface of the tissue (Fig. 4.27).
The laser beam can be delivered in the continuous working (CW) or pulsed mode. In the CW mode, the emission of the laser beam is continuous as long as the foot switch is activated, but the laser beam can be interrupted sequentially by a revolving mechanical shutter (at a speed of 1 s to 1 ms), in order to avoid repeatedly hitting the foot switch. This is known as the chopped or gated mode, and must not be confused with the pulsed mode. Pulsed Mode One of the technical innovations brought about by the use of the CO2 laser has been its ability to vaporise tissue with minimal collateral damage. The idea is to deliver high peaks (several hundred watts) of energy over extremely short periods of
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time (milliseconds to nanoseconds). The peaks are interspersed with ‘rest’ periods allowing for the tissue to cool down. In the superpulse technology, the frequency of pulses is less than 1,000 pulses per second. In the ultrapulse technology, the laser beam is excited by radio frequency waves, thereby producing an even higher frequency mode than by using the superpulse technology. This ‘more concentrated’, high-peak energy allows for more ‘resting’ time between the peaks, enabling the tissue to cool down. Given the same mean power, the CO2 laser in superpulse mode must deliver four to five pulses for each ultrapulse, whereas the CW chopped mode, delivering the same energy as in the ultrapulse mode, takes seven times longer (Fig. 4.28). As conduction of heat takes time (as exemplified by a brief versus long contact of one’s finger with a hot object), less thermal collateral tissue damage is expected when the energy delivery time is short. In the case of the ultrapulse mode, each laser pulse has sufficient energy to vaporise instantaneously any tissue it strikes, with no residual thermal damage to adjacent or deeper tissues (Fig. 4.29).
In clinical practice, there are two ways of preventing collateral tissue damage: • Using a laser with a short absorption length (i.e. the CO2 laser) • Using a pulsed laser to vaporise tissue quickly (i.e. the ultrapulse mode) When the paediatric surgeon wishes to incise or ablate tissue with precision, the CO2 laser in the ultrapulse mode should be used. Pulsed technology is not a mere technological gadget. The difference in collateral thermal damage can be significant when a CO2 laser is used with the parameters appropriate to working in paediatric airway management. Notwithstanding, and despite the obvious advantages of the CO2 laser, the diode laser is still in use in some centres for treating paediatric airway stenosis.
4.6.4 Light Delivery Systems Routinely used in endoscopy, the articulated arm, the micromanipulator and the waveguide fibres will now be presented.
In summary, the pulsed CO2 technology:
4.6.4.1 Articulated Arm
• • • •
The articulated arm is made of several hollow metal tubes assembled together with knuckle joints. Each joint contains an internal mirror that reflects the laser
Vaporises tissue quickly Avoids thermal damage Permits constant tissue ablation at any pulse Avoids charring and scarring
Fig. 4.26 Influence of spot size on power density (ex vivo experiment on liver tissue): With identical output power (25 W) and exposure time (0.5 s), whether focused (left) or unfocused (right), CO2 laser beams generate completely different tissue damages: (a) Focused beam: high energy density, precise
v aporisation and little thermal damage. (b) Slightly focused beam: medium energy density, medium vaporisation and medium thermal damage. (c) Unfocused beam: low energy density, no vaporisation and important thermal damage with coagulation necrosis
4.6 Lasers in Paediatric Airway Management
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Fig. 4.27 Influence of spot size on power density: For the same output power, the power density is inversely proportionate to the square of the spot diameter
Fig. 4.28 Comparison of ultrapulse, superpulse and chopped CW modes for a same mean power: (a) Ultrapulse highly concentrated energy peak (red). (b) Superpulse lasers must deliver four to five pulses for each ultrapulse (blue). (c) Chopped CW
mode is seven times longer than each ultrapulse for the same amount of energy (yellow). The time intervals between pulses correspond to the ‘resting’ time, enabling tissues to cool down
beam to the next tube until it reaches the distal end of the articulated arm. Proper alignment of all the mirrors is essential in order to transmit the laser beam without scattering. The distal end of the articulated arm can be connected to a hand-piece, a waveguide or a micromanipulator when used with the operating microscope. It should be noted that the articulated arm is highly vulnerable to impact or jerks, which can cause a misalignment of both the invisible CO2 laser beam and visible helium-neon pilot laser beam (Fig. 4.30).
Composed of a system of lenses, it focuses the laser beam on a swivelling mirror handled by a joystick (Fig. 4.31). The focal length of the lenses in the micromanipulator must be adjusted to the focal length of the objective lens in the operating microscope, which in turn determines the focal distance or the working distance to the target (200–400 mm). The suspension of the reflecting mirror is very sensitive, thereby allowing for a precise manipulation of the laser beam in the operative field, using the joystick. A lateral knob is used to adjust the focal length of the micromanipulator and can therefore modify the power density by changing the spot size on the target tissue. This manoeuvre serves to increase or decrease the coagulating properties of the CO2 laser. Additionally to the conventional micromanipulators, the digital AcuBlade robotic laser microsurgery
4.6.4.2 Micromanipulator Fixed to the objective of the operating microscope, this expensive device is connected to the articulated arm.
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Fig. 4.29 Comparison of ultrapulse and CW modes (ex vivo experiments on liver tissue) at a constant power density of 9,600 W/cm2(a) Macroscopic view: (1) Ultrapulse mode, 150 mJ/cm2: no charring. (2) CW chopped mode, 50 ms, 0.1 s: mild charring. (3) CW continuous mode: moderate charring. (4) CW continuous mode, slightly unfocused: severe charring. (b) Corresponding microscopic view: (1) No coagulation necrosis. (2) Mild coagulation necrosis. (3) Medium coagulation necrosis. (4) Severe coagulation necrosis
system has been developed. It is a sophisticated but expensive scanning micromanipulator, which provides automatic control over the orientation of selected incision and ablation patterns. The computer-controlled digital AcuBlade allows the laser beam to travel across its target as a straight or curved incision line or area for char-free ablation, vaporisation, excision or incision of soft tissue. This device is compatible with the new Lumenis® Acupulse and the Ultrapulse SurgiTouch CO2 laser systems. It further adds precision to char-free incision using the superpulse or ultrapulse technology.
Fig. 4.30 CO2 laser and articulated arm: Ultrapulse CO2 laser console and diagram of the articulated arm with mirrors at each knuckle joint
4.6.4.3 Waveguide (Fig. 4.32) Transmitting the CO2 laser beam through a flexible fibre was not possible until the development of hollow-core photonic bandgap fibres by the Massachusetts Institute of Technology in Boston. This new technology facilitates the transmission of the CO2 laser beam through small, flexible hollow fibres with a 0.2 mm spot size at the distal tip of the fibre and a small divergent angle (1.4 mm spot size at 1 cm distance from the fibre tip) (Fig. 4.33). Connected to the CO2 laser console, this
Fig. 4.31 Computer-controlled digital AcuBlade micromanipulator for the CO2 laser, coupled to the Wild-Leica® microscope: (a) The side knob is used to focus the laser beam on the target (white arrow). (b) The central joystick is used to move the laser beam in the operative field (black arrow)
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4.7 Laser Safety
obtained. Due to their high absorption in haemoglobin, these two lasers, with small fibres attached to the bare telescopes, are highly suitable for treating vascular malformations or haemangiomas of paediatric airways. This offers a panoramic view during the entire procedure.
4.7 Laser Safety
Fig. 4.32 CO2 laser console with the omniguide CO2 laser fibre
Fig. 4.33 Beam divergence at the distal omniguide CO2 fibre tip: The distance from the fibre tip to the target determines the power density for a same output power. Cutting or coagulating effects can be obtained by moving the fibre tip from the target
fibre can be used with telescopes in paediatric airway management (see Fig. 4.16). If used beyond the carina, air embolism from the coaxial CO2 cooling device of the fibre may occur. The shortest distance between the fibre tip and the target must be maintained to ensure an optimal cutting/vaporising effect. The fibre can be fixed with Steri-Strips to a bare telescope and used through a small bronchoscope in the treatment of tracheal or subglottic lesions. The argon (514 nm) and KTP (532 nm) lasers are easily transmitted through optical fibres that accommodate wavelengths between 250 and 2,500 nm for powers up to 10 kW. Their short wavelength facilitates the delivery of the green light to a small spot size. By modifying the distance from the fibre tip to the target, an increased coagulating or vaporising effect is
Before engaging in laser endoscopic procedures, both the surgeon and personnel must attend a laser safety educational programme providing them with appropriate knowledge on laser biophysics, tissue interactions and safety precautions, with supervised hands-on training (American National Standard for Safe Use of Lasers in Health Care Facilities. ANSI Standard Z-136.3) [23]. The aim of this section is not to provide comprehensive information on laser safety (dedicated courses are organised for this purpose), but rather to highlight the main risks incurred in endoscopic airway surgery. All medical lasers used for thermal tissue ablation fall under Class IV and are hazardous to the eyes and skin. When used in endoscopic airway surgery, they also present significant risks of fire hazards [34]. Although it is not possible for all centres to benefit from a laser protection adviser and supervisor, a biannual inspection and maintenance of their laser(s) are mandatory. It is the laser surgeon’s responsibility to test the laser beam’s effects prior to any intervention. With the CO2 laser, a test burn onto a wooden tongue depressor is used to verify proper alignment of both the invisible CO2, and the visible helium-neon aiming beams (Fig. 4.34). The test burn allows the surgeon to assess the power density using different spot sizes as well as the pulsed or CW chopped modes. With the CO2 laser, ‘what you see is what you get’. Identical laser strikes generate similar craters of vaporisation on a wooden spatula and the mucosa. When starting a new laser procedure, this rough preoperative estimate is sufficient in order to avoid any undesirable tissue effects. When laser beams are delivered through a fibre, this test becomes less relevant since the power density is greatly influenced by the distance from the fibre tip to the target; unless the fibre is deteriorated, the laser beam always emerges exactly from the centre of the fibre tip.
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Fig. 4.34 CO2 laser test burns on a wooden spatula: (a) Precise matching of the invisible CO2 and visible helium-neon laser aiming beams, allowing for safe laser use. (b) Misalignment of the two laser beams, rendering precise laser work impossible
Vaporising tissue generates laser plumes that are contaminated with toxic gas particles, blood, viruses and bacteria [9] [10]. The operating site is rapidly obscured by the plume, which is heavier than air (Fig. 4.35). To be efficient, a dedicated smoke evacuator [33] connected to a suction cannula held by the surgeon or fixed to the laryngoscope must be placed as close as 1 cm from the target. In clinical practice, two separate suction set-ups are often used, one connected to the laryngoscope, the other to the surgical suction tip held by the operating surgeon. Standard surgical masks do not provide adequate protection of the theatre personnel, hence only appropriate smoke evacuators can eliminate any risk to the operator and room attendants [32]. Fig. 4.35 Laser work in the pharynx without a smoke evacuator: The operative field is obscured by the laser plume
4.7.1 Eye and Skin Hazards (Fig. 4.36) Entryways to the laser operating theatre must display a warning sign with the signal words ‘Danger – Laser Light’ to prevent any unauthorised personnel from entering accidentally. The potential for eye damage depends on the wavelength of the laser: • Far-infrared (> 2,000 nm) and UV (< 200 nm) laser beams are strongly absorbed by water-rich tissues. The CO2 (10,600 nm), erbium (2,940 nm), holmium (2,100 nm) and argon fluoride excimer lasers (193 nm) are primarily cornea hazards [38].
• Lasers operating in the visible range (400–800 nm) are absorbed by pigmented tissues only. They are fully transmitted through the transparent cornea, lens and vitreous humour of the eye to the retina where the beam is completely absorbed. The argon (514 nm), KTP (532 nm) and tunable dye lasers (400–700 nm) thus cause retinal photocoagulation with potentially severe damage to the optic nerve or macula. Peripheral retinal damage is better tolerated as it does not interfere with central vision. • And lastly, near infrared lasers operating between 800 and 2,000 nm are the most dangerous. They can inflict thermal burns on the cornea, the lens and the
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4.7 Laser Safety
a strong lens that refocuses the slightly divergent beam delivered by the fibre of the Nd-YAG (1,064 nm) and diode (980 nm) lasers onto the retina. Significant power density is thereby generated and may cause photocoagulation damage to the retina [29]. The integrity of the fibre must be checked before it is used. Should a break occur at any point in the fibre, it will be immediately visible. In order to reduce the risk of ocular damage, it is mandatory to protect the eyes of the patient, the surgeon and all other personnel in the operating room. Appropriate goggles for the wavelength of the laser must be used [12]. For the CO2 laser, normal optical spectacles are sufficient, but side shields should be added for better protection. Fig. 4.36 Eye damage resulting from various laser wavelengths: (a) Far-infrared laser beams (CO2, erbium and holmium) (red) are fully absorbed by water-rich tissues. They are damaging to the cornea. (b) Near infrared lasers (Nd-YAG, diode) (blue) are partially absorbed by clear aqueous tissues and pigmented tissues. They may damage the cornea, lens and retina. (c) Lasers working in the visible range (argon, KTP) (yellow) are fully transmitted through the transparent aqueous tissues of the eye. They are strongly absorbed by pigmented tissues, thus damaging the retina
retina because they are partially absorbed by clear aqueous tissues as well as by pigmented tissues. Nearly 50% of Nd-YAG or diode laser radiation is transmitted through the ocular media to the retina. The structure of the eye anterior to the retina acts as
Fig. 4.37 General set-up for laser use in suspension microlaryngoscopy: All exposed skin and mucous membranes are protected with water-saturated surgical towels
4.7.2 Skin Protection Non-target strikes to the patient’s face and teeth are a real and common possibility. The patient’s exposed skin and mucous membranes must be protected with a double layer of water-saturated surgical towels, snugly fit around the laryngoscope (Fig. 4.37). For procedures of long duration, the towels should be moistened repeatedly in order to prevent them from drying. This also applies to the surgical field. Wet gauze or surgical pledgets must be remoistened constantly to avoid non-target mucosal burns. The operating theatre personnel are at a much
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lower risk of skin damage caused by non-target strikes originating from the CO2 laser beam. Should a nurse or an anaesthetist be inadvertently hit, he/she will instantaneously withdraw the exposed skin from the laser beam. In this case, severe damage is unlikely.
4.7.3 Fire Hazards Laser-induced endotracheal fire is the most feared and dreadful complication encountered in endoscopic airway surgery [19]. Its prevalence ranges from 0.4% to 1.9% of all airway laser interventions, representing nearly 14% of laser-related accidents [6, 21, 34]. Causal factors are always linked to a violation of the safety protocol. Given the dramatic consequences that such complications may have on the patient [19], it is essential to adhere strictly to the following principles: choice of the appropriate anaesthetic technique, use of laser-safe tubes whenever possible, respect of anaesthetic gas mixtures, avoidance of non-target strikes and preparation for flammability. Combustion requires a source of ignition, a gas mixture that supports combustion, and flammable material.
4.7.3.1 Source of Ignition
short distance from the operating tip. This diminishes the ignition risk of combustible material that is not located in the immediate surroundings of the fibre tip. As a general rule, lasers that operate in a pulsed mode have a much lower risk of igniting flammable material than lasers operating in the continuous working (CW) mode. In the paediatric airway where precise and delicate laser work is required, the CO2 laser should always be used in the pulsed mode.
4.7.3.2 Combustible Material The ET tube is the most critical combustible material. Conventional ET tubes are easily flammable when exposed to anaesthetic gas mixtures. For this reason, they should never be used unless the ET tube can be protected from the laser, and the laser target is remote from the tube. These conditions are encountered only during the treatment of lesions in the oral cavity or the pharynx. They are unlikely to be found in airway surgery; in this case, laser-safe ET tubes must be used if a closed circuit anaesthesiology technique is chosen as the best option for treating a specific condition (Fig. 4.38). Other combustible materials such as dry tapes, sponges, pledgets, naso-pharyngeal airway tubes, naso-gastric tubes are also in danger of being ignited by the laser in the operative field.
A source of ignition is provided by the laser. Highly collimated beams such as those of the CO2 laser retain a high power density over long distances and can ignite flammable materials inside or outside the surgical field. Other laser beams delivered through a fibre diverge from the fibre tip. Their power density is high over a
Oxygen, nitrous oxide (N2O) and volatile anaesthetic agents support combustion, whereas nitrogen (N2) and helium do not.
Fig. 4.38 Bivona laser-safe, cuffed ET tube used in the treatment of a left supraglottic lymphatic malformation (cystic hygroma) in combination with a CO2 laser: (a) Preoperative view: Supraglottic
obstruction prevents the use of a safe, tubeless anaesthesia during spontaneous respiration. (b) Postoperative view: The endolaryngeal obstruction has been completely removed
4.7.3.3 Combustion-Supporting Gas Mixture
69
4.7 Laser Safety
Total intravenous anaesthesia (TIVA) with a mixture of 25% of O2 and 75% of N2 is the preferred technique in paediatric airway surgery.
4.7.4 Fire Prevention
Tube has no cuff and therefore does not isolate the anaesthetic gases from the laser field. Strict adherence to safe gas mixtures during the entire laser procedure is mandatory to avoid fire hazards. This ET intubation technique should be used under specific conditions only (see Fig. 4.38). Other anaesthetic techniques are more suitable for use in the airways of small children or infants.
Four main anaesthesiological techniques are available to prevent the risk of airway fire (see Sect. 18.1, Chap. 18): (a) Closed circuit with a laser-safe ET tube (b) Intermittent apnoeas (c) Tubeless anaesthesia in spontaneous respiration (d) Jet ventilation
4.7.4.1 Closed Circuit Anaesthesia with a Laser-Safe ET Tube In the case of paediatric airway surgery, this technique presents several constraints. Because of the thickness of their walls, laser-safe tubes have a poor ratio of inner to outer diameter. They can only be used in older children and should be equipped with a cuff to isolate the anaesthetic gases from the surgical field. Protection of non-dedicated laser tubes with self-adhesive aluminium tape is unsafe and strictly contraindicated [35] [36]. Of all manufactured laser-safe tubes, the allmetal ET tubes by Oswald–Hunton [18], Mallinkrodt or the Bivona types are the safest for use in paediatric airway surgery (Fig. 4.39). The Oswald–Hunton ET
4.7.4.2 Intermittent Apnoeic Technique This technique allows for a free operative field during laser surgery. After induction of total intravenous anaesthesia (TIVA) using 100% oxygen and face mask ventilation, the larynx is exposed and suspended with the appropriate laryngoscope during a short apnoea. A soft Portex blue line tube is introduced through the laryngoscope under visual control, and the child is ventilated until oxygen saturation (SpO2) reaches the highest possible level above 90%. The tube is then removed, and the laser work is performed in the free operative field during an apnoeic period. Oxygen saturation is not allowed to fall below 90% before the ET tube is reintroduced into the trachea through the laryngoscope. This technique is adequate for short duration laser work, typically of 1 or 2 min, such as would be used for CO2 laser supraglottoplasty in laryngomalacia or vaporisation of a subglottic haemangioma. In both indications, an ET tube can easily be passed through the subglottis into the trachea. Because the ET tube cannot be passed beyond a cicatricial stricture without traumatising the mucosa, this technique is less appropriate for cases of subglottic stenosis. However, this intermittent apnoeic technique is very safe and flexible when used appropriately. It also allows for a fully immobile and free operative field, an advantage for precise lasering of delicate structures in an infant’s larynx [7].
4.7.4.3 Tubeless Anaesthesia in Spontaneous Respiration
Fig. 4.39 Laser-safe ET tubes: (a) Laser shield tube: This tube is less safe than the Oswald-Hunton, Mallinkrodt or Bivona tubes. (b) Mallinkrodt metallic tube with double cuffs. (c) Bivona metallic tube with foam-cuff
Total intravenous anaesthesia (TIVA) is titrated to enable the infant or child to breathe spontaneously. Topical anaesthesia of the larynx prevents wakeup phases in the patient when the mucosa is stimulated with instruments. A 25% enriched oxygen/air mixture
70
4 Equipment and Instrumentation for Diagnostic and Therapeutic Endoscopy
is supplied through a naso-pharyngeal airway tube [31]. This set-up offers optimal working conditions in the larynx and subglottis [3]. Although few cord motions occur, they can be eliminated using a Lindholm self-retaining false cord retractor placed at the level of the ventricular bands, in case the laser is used at the glottic or subglottic level. This technique is well suited for the treatment of webs and synechia of the vocal cords, cicatricial SGS, as well as endoscopic repairs of laryngotracheo-oesophageal clefts.
4.7.4.4 Jet Ventilation Anaesthesia Although this technique is routinely used in adults [20] and has also been reported in small children [22], it is potentially dangerous and may induce barotrauma or pneumothorax. When the metal jetting cannula is fitted to the operating laryngoscope, air pressure is delivered above the glottis, and constant vibration of the vocal cords ensues. When this technique is used with a percutaneous transtracheal catheter placed below the laryngeal narrowing, it may become extremely dangerous in the absence of perfect cooperation between the anaesthetist and the surgeon [30]. As a rule, a jet ventilation system should not be used beyond an airway obstruction in children unless a very experienced team is handling the situation [21, 22, 27, 28]. It is the surgeon’s responsibility to ensure free egress of air through the stenosis to avoid a barotrauma. Although jet ventilators are equipped with safety devices that immediately stop ventilation when a high pressure is registered at the tip of the catheter, their reliability is not absolute. In paediatric airway management, other anaesthesia techniques are available and preferred. Last but not least, a 60-cc syringe filled with saline should always be present on the surgeon’s support table in order to extinguish any possibility of an endotracheal fire immediately. In these situations, time is of the essence.
4.7.5 Laser-Induced Accidents Strict adherence to laser safety protocols and proper training of the medical staff and theatre personnel considerably reduces laser-induced hazards.
In the early 1980s, several reports of complications linked to the use of the CO2 laser were published in the relevant literature [1, 5, 8, 11, 21]. In fact, complication rates are rather low when strict laser safety protocols are followed. Ossoff reported a 0.1% complication rate in 7,200 laser surgical procedures [24] and Healy a 0.2% complication rate in 4,416 laser surgical procedures [16]. Current CO2 laser devices are perfectly safe and reliable. A lack of vigilance and insufficiently suitable training are the main factors causing complications [13, 14]. Standards for laser use and equipment in medicine are available and should be consulted prior to establishing a laser safety protocol [2]. Compliance to strict rules prevents most accidents [23].
4.7.6 Safety Recommendations A laser educational programme has been shown to be the single most effective measure to prevent complications. The following recommendations can be made: • Surgeons, anaesthetists and operating theatre personnel should receive appropriate laser safety education through dedicated training courses. • The laser equipment and the smoke evacuator device require biannual inspection and maintenance. • A warning sign with the signal words ‘Danger – Laser Light’ must be displayed in the entryways of all operating theatres. • Proper protection of the patient’s face and eyes with a double layer of water-saturated surgical towels is mandatory. • Hazard to the eyes is the most feared accidental injury affecting operating theatre personnel. Wavelength appropriate goggles should be worn by all theatre attendants. • Prior to any CO2 laser treatment, proper alignment of both the invisible CO2 and the visible heliumneon laser beams must be checked by directing the light onto a wooden spatula; the power density for a given spot size and desired laser parameters must also be verified. • The CO2 laser should be used in the pulsed or CW chopped mode in order to diminish the risk of fire hazards.
4.8 Ancillary Therapeutic Means
71
• An appropriate anaesthetic technique must be chosen for each specific airway intervention. • Total intravenous anaesthesia (TIVA) with spontaneous respiration or the intermittent apnoeic technique in the fully relaxed patient are most appropriately used for infants and children with small or compromised airways. • Strict adherence to safe gas mixtures (25% O2 and 75% N2) is a guarantee for safe laser procedures under total intravenous anaesthesia.
4.8 Ancillary Therapeutic Means Most endoscopic interventions in the paediatric airway deal with congenital anomalies, cicatricial stenoses and benign tumours. In addition to CO2 and KTP lasers routinely used in tertiary centres, laryngotracheal dilators and the microdebrider play an important role in the management of compromised paediatric airways.
Fig. 4.40 Savary-Gilliard tracheal dilators: The well-tapered nose allows for smooth and progressive dilation
4.8.1 Dilation Rigid bronchoscopes should not be used to dilate laryngeal, tracheal or bronchial stenoses. Although the procedure is meant to be carried out under direct vision, the bevelled tip of the outer tube may induce trauma to the mucosa. For this reason, dedicated semirigid tapered bougies or angioplasty balloon dilators are preferred.
4.8.1.1 Tapered Bougies The Savary–Gilliard oesophageal dilators may be modified for proper use in the airway. They consist of flexible, tapered, incompressible bougies ranging from 5 to 15 mm in diameter (Fig. 4.40). Their longitudinal flexibility adapts to the laryngotracheal contours, while their transverse hardness results in an efficient dilation. In clinical practice, the bougies are introduced into the airway during intermittent apnoeas. The resistance felt during dilation is an excellent indicator of the maximal size that should be used. These bougies
Fig. 4.41 Tracheal dilators with a metal rod and a tapered plastic head: These dilators are more traumatic and less versatile than the Savary–Gilliard dilators
are more versatile than the standard brass tracheal dilators, which are straight and rigid. Other tracheal dilators made of a metal rod and a tapered plastic head are also often used for dilatating subglottic stenoses in paediatric airways (Fig. 4.41).
72
4 Equipment and Instrumentation for Diagnostic and Therapeutic Endoscopy
4.8.1.2 Balloon Dilators This technique has gained wide acceptance over the last decade. The angioplasty balloons are expanded to increasingly larger sizes by augmenting their inside pressure by means of a syringe fitted with a manometer. The balloon dilation catheters are capable of reaching three distinct, and progressively larger (range 8–10 mm and 11–13 mm) diameters, when inflated with water at a pressure ranging from 3 to 9 atm. However, if confined to the recommended pressures, the balloon diameter cannot expand beyond a specified size (Fig. 4.42). Although balloon dilation sounds safe in theory, in practice it does not provide any tactile feedback when compared to dilation with bougies. In the rare cases of Fig. 4.42 Balloon dilation catheter with a dedicated syringe for inflation: (a) General set. (b) Deflated balloon (close-up view). (c) Inflated balloon (close-up view)
Fig. 4.43 Cicatricial stenosis of the left main-stem bronchus treated by balloon dilatations: (a) Preoperative view. (b) Postoperative view
stenotic lesions of the main-stem bronchi, the use of balloon dilators is indisputable (Fig. 4.43). For dilation of cicatricial subglottic stenosis, the author prefers the use of tapered bougies because of the tactile feedback. In clinical practice, to avoid coughing during the procedure, balloon dilators are used either under repeated apnoeas or during spontaneous respiration, following sedation and topical airway anaesthesia.
4.8.2 Microdebrider Routinely used in endonasal sinus surgery, this instrument was modified for the treatment of benign
4.8 Ancillary Therapeutic Means
73
paediatric airway lesions (papillomas, haemangiomas and granulation tissue) (Fig. 4.44). The microdebrider consists of an 18-, 22.5- or 27.5-cm long rod with a distal side hole of either 2.9 or 3.5 mm in diameter; it is also equipped with an inner rotating blade to cut the soft tissue sucked into the side hole during surgery (Fig. 4.45). The oscillating rotation of the cutting blade is set to 800–1,500 per minute. This device is very suitable for the management of laryngeal and tracheal papillomas (see Sect. 16.1.3, Chap. 16). It has also been used to remove subglottic haemangiomas [26] and granulation tissue in the subglottis and trachea.
Fig. 4.44 Microdebrider with dedicated console: general set-up
Fig. 4.45 (a) Suction cannula of the microdebrider. (b) Close-up view of the side opening with inside rotating blade
74
4 Equipment and Instrumentation for Diagnostic and Therapeutic Endoscopy
4.9 Appendix 1 CO2 laser : power density calculations (W/cm2) Power (Watts)
Spot size 0.1 mm
0.2 mm
0.3 mm
0.4 mm
0.5 mm
2
25.465
6.366
2.829
1.592
3
38.197
9.549
4.244
4
50.929
12.732
5
63.662
6
0.6 mm
1.0 mm
1.019
707
255
64
28
10
2.387
1.528
1.061
382
95
42
15
5.659
3.183
2.037
1.415
509
127
57
20
15.915
7.074
3.979
2.546
1.768
637
159
71
25
76.394
19.099
8.488
4.775
3.056
2.122
764
191
85
31
7
89.127
22.282
9.903
5.570
3.565
2.476
891
223
99
36
8
101.859
25.465
11.318
6.366
4.074
2.829
1.019
255
113
41
9
114.591
28.648
12.732
7.162
4.584
3.183
1.146
286
127
46
10
127.324
31.831
14.147
7.958
5.093
3.537
1.273
318
141
51
15
190.985
47.746
21.221
11.937
7.639
5.305
1.910
477
212
76
20
254.647
63.662
28.294
15.915
10.186
7.074
2.546
637
283
102
References 1. Alberti, P.W.: The complications of CO2 laser surgery in otolaryngology. Acta Otolaryngol. 91, 375–381 (1981) 2. American National Standards I, Council of National L, Information A (1980) Laser safety in the health care environment. The Institute, New York, N.Y. 3. Aun, C.S., Houghton, I.T., So, H.Y., et al.: Tubeless anaesthesia for microlaryngeal surgery. Anaesth. Intensive Care 18, 497–503 (1990) 4. Benjamin, B.: Pediatric laryngoscopes: design and application. Ann. Otol. Rhinol. Laryngol. 110, 617–623 (2001) 5. Burgess III, G.E., LeJeune Jr., F.E.: Endotracheal tube ignition during laser surgery of the larynx. Arch. Otolaryngol. 105, 561–562 (1979) 6. Chiu, C.L., Khanijow, V., Ong, G., et al.: Endotracheal tube ignition during CO2 laser surgery of the larynx. Med J Malaysia 52, 82–83 (1997) 7. Cohen, S.R., Herbert, W.I., Thompson, J.W.: Anesthesia management of microlaryngeal laser surgery in children: apneic technique anesthesia. Laryngoscope 98, 347–348 (1988) 8. Cozine, K., Rosenbaum, L.M., Askanazi, J., et al.: Laserinduced endotracheal tube fire. Anesthesiology 55, 583–585 (1981) 9. Dikes, C.N.: Is it safe to allow smoke in our operating room? Todays Surg. Nurse 21, 15–21 (1999) 10. Freitag, L., Chapman, G.A., Sielczak, M., et al.: Laser smoke effect on the bronchial system. Lasers Surg. Med. 7, 283– 288 (1987) 11. Fried, M.P.: A survey of the complications of laser laryngoscopy. Arch. Otolaryngol. 110, 31–34 (1984)
2.0 mm
3.0 mm
5.0 mm
12. Friedman, N.R., Saleeby, E.R., Rubin, M.G., et al.: Safety parameters for avoiding acute ocular damage from the reflected CO2 (10.6 microns) laser beam. J. Am. Acad. Dermatol. 17, 815–818 (1987) 13. Fulton Jr., J.E.: Complications of laser resurfacing.Methods of prevention and management. Dermatol. Surg. 24, 91–99 (1998) 14. Grossman, A.R., Majidian, A.M., Grossman, P.H.: Thermal injuries as a result of CO2 laser resurfacing. Plast. Reconstr. Surg. 102, 1247–1252 (1998) 15. Hackel, A., Badgwell, J., Binding, R., et al.: Guidelines for the pediatric perioperative anesthesia environment. American Academy of Pediatrics. Section on Anesthesiology. Pediatrics 103, 512–515 (1999) 16. Healy, G.B., Strong, M.S., Shapshay, S., et al.: Complications of CO2 laser surgery of the aerodigestive tract: experience of 4416 cases. Otolaryngol. Head Neck Surg. 92, 13–18 (1984) 17. Holinger, L.D.: Instrumentation, equipement and standardization. In: Holinger, L.D., Lusk, R.P., Green, C.G. (eds.) Pediatric laryngology and bronchoesophagology, p. 75. Lippincott-Raven, Philadelphia; New York (1997) 18. Hunton, J., Oswal, V.H.: Metal tube anaesthesia for ear, nose and throat carbon dioxide laser surgery. Anaesthesia 40, 1210–1212 (1985) 19. Ilgner, J., Falter, F., Westhofen, M.: Long-term follow-up after laser-induced endotracheal fire. J. Laryngol. Otol. 116, 213–215 (2002) 20. Jaquet, Y., Monnier, P., Van Melle, G., et al.: Complications of different ventilation strategies in endoscopic laryngeal surgery: a 10-year review. Anesthesiology 104, 52–59 (2006) 21. Meyers, A.: Complications of CO2 laser surgery of the larynx. Ann. Otol. Rhinol. Laryngol. 90, 132–134 (1981)
References 22. Monnier, P., Ravussin, P., Savary, M., et al.: Percutaneous transtracheal ventilation for laser endoscopic treatment of laryngeal and subglottic lesions. Clin. Otolaryngol. Allied Sci. 13, 209–217 (1988) 23. Ossoff, R.H.: Implementing the ANSI Z 136.3 laser safety standard in the medical environment. Otolaryngol. Head Neck Surg. 94, 525–528 (1986) 24. Ossoff, R.H.: Laser safety in otolaryngology-head and neck surgery: anesthetic and educational considerations for laryngeal surgery. Laryngoscope 99, 1–26 (1989) 25. Oswal, V., Remacle, M.: Principles and Practice of Lasers in Otorhinolaryngology and Head and Neck Surgery. Kugler Publications, The Hague, The Netherlands (2002) 26. Pransky, S.M., Canto, C.: Management of subglottic hemangioma. Curr. Opin. Otolaryngol. Head Neck Surg. 12, 509–512 (2004) 27. Ravussin, P., Freeman, J.: A new transtracheal catheter for ventilation and resuscitation. Can. Anaesth. Soc. J. 32, 60–64 (1985) 28. Ravussin, P., Depierraz, B., Chollet, M., et al.: Transtracheal High Frequency Jet Ventilation in Adults and Children. Operat Tech Otolaryngol Head Neck Surg 8, 136–141 (1997) 29. Sallavanti, R.A.: Protecting your eyes in the laser operating room. Todays OR Nurse 17, 23–26 (1995) 30. Santos, P., Ayuso, A., Luis, M., et al.: Airway ignition during CO2 laser laryngeal surgery and high frequency jet ventilation. Eur. J. Anaesthesiol. 17, 204–207 (2000) 31. Simpson, J.I., Wolf, G.L.: Flammability of esophageal stethoscopes, nasogastric tubes, feeding tubes, and nasopharyngeal
75 airways in oxygen- and nitrous oxide-enriched atmospheres. Anesth. Analg. 67, 1093–1095 (1988) 32. Smith, J.P., Topmiller, J.L., Shulman, S.: Factors affecting emission collection by surgical smoke evacuators. Lasers Surg. Med. 10, 224–233 (1990) 33. Smith, J.P., Moss, C.E., Bryant, C.J., et al.: Evaluation of a smoke evacuator used for laser surgery. Lasers Surg. Med. 9, 276–281 (1989) 34. Snow, J.C., Norton, M.L., Saluja, T.S., et al.: Fire hazard during CO2 laser microsurgery on the larynx and trachea. Anesth. Analg. 55, 146–147 (1976) 35. Sosis, M., Dillon, F.: What is the safest foil tape for endotracheal tube protection during Nd-YAG laser surgery? A comparative study. Anesthesiology 72, 553–555 (1990) 36. Sosis, M.B.: Evaluation of five metallic tapes for protection of endotracheal tubes during CO2 laser surgery. Anesth. Analg. 68, 392–393 (1989) 37. Vauthy, P.A., Reddy, R.: Acute upper airway obstruction in infants and children. Evaluation by the fiberoptic bronchoscope. Ann. Otol. Rhinol. Laryngol. 89, 417–418 (1980) 38. Walker, N.P., Matthews, J., Newsom, S.W.: Possible hazards from irradiation with the carbon dioxide laser. Lasers Surg. Med. 6, 84–86 (1986) 39. Wood, R.E.: Spelunking in the pediatric airways: explorations with the flexible fiberoptic bronchoscope. Pediatr. Clin. North Am. 31, 785–799 (1984) 40. Wood, R.E., Fink, R.J.: Applications of flexible fiberoptic bronchoscopes in infants and children. Chest 73, 737–740 (1978)
5
Endoscopic Assessment of the Compromised Paediatric Airway
Contents Emergency Airway Support for Severe Respiratory Distress............................. 5.1.1 Transnasal Fibre-Optic Laryngoscopy (TNFL)........ 5.1.2 Rigid Bronchoscopy................................................. 5.1.3 Emergency Surgical Airway Access.........................
Core Messages
›› Management
5.1
Noisy Child with or Without Respiratory Distress and Undiagnosed Disease........................ 5.2.1 Anaesthetic Techniques for Endoscopy in Spontaneous Respiration.......................................... 5.2.2 Asleep Transnasal Fibre-Optic Laryngoscopy (TNFL)...................................................................... 5.2.3 Direct Laryngoscopy with the Bare 0° Rod-Lens Telescope...............................
78 79 80 80
››
5.2
5.3 5.3.1 5.3.2 5.3.3 5.3.4 5.4 5.4.1 5.4.2 5.4.3 5.4.4
Tracheotomised Child with Known Airway Obstruction................................................ Transnasal Flexible Laryngoscopy........................... Direct Laryngotracheobronchoscopy with a Rod-Lens Telescope................................................... Suspension Microlaryngoscopy................................ Broncho-oesophagoscopy......................................... Treatment Plan for Laryngotracheal Stenosis.................................................................... Primary Endoscopic Treatment................................ Laryngotracheal Reconstruction with Cartilage Expansion (LTR)....................................... Partial Cricotracheal Resection (PCTR)................... Extended Partial Cricotracheal Resection................
80 81
››
82 84
››
85 85 85 85 90
››
91 92
››
93 93 93
References............................................................................ 93
››
››
of a difficult paediatric airway involves a multidisciplinary approach based on strong mutual trust between anaesthetists, otolaryngologists, and intensive care specialists. Awake transnasal fibre-optic laryngoscopy (TNFL) plays a crucial part in the assessment of vocal cord mobility. Asleep transnasal TNFL is a technique that serves to visualise all extralaryngeal obstruction sites (naso- and oropharynx, supraglottis, and tracheostoma). Direct laryngotracheoscopy using a bare 0° telescope is essential in the assessment of the location, extent, and degree of subglottic stenosis and tracheostoma The length of normal residual trachea located between the tracheostoma and the carina must be measured if a resection-anastomosis is scheduled. Suspension microlaryngoscopy (SML) is performed in cases of vocal fold immobility so as to differentiate between neurogenic paralysis and cricoarytenoid ankylosis. Additional broncho-oesophagoscopy is implemented to rule out congenital mediastinal anomalies, reflux or eosinophilic oesophagitis, and obtain a bacteriological aspirate of the trachea. Choosing the best surgical option as well as the timing of surgery is facilitated by a thorough and detailed preoperative assessment of the stenosis and any other medical problem.
P. Monnier (ed.), Pediatric Airway Surgery, DOI: 10.1007/978-3-642-13535-4_5, © Springer-Verlag Berlin Heidelberg 2011
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5 Endoscopic Assessment of the Compromised Paediatric Airway
›› It is essential that surgeons master both endo-
scopic and open surgical techniques such as laryngotracheal reconstruction (LTR) and partial cricotracheal resection (PCTR) to address all types of airway stenosis adequately.
Thorough and detailed endoscopic assessment is the cornerstone of the evaluation of the compromised airway in infants and children. The three main scenarios encountered in clinical practice include: 1. An infant or child experiencing severe respiratory distress requiring immediate airway support. 2. A noisy infant or child experiencing stable, mild to moderate respiratory distress of unknown origin. 3. An infant or child with a pre-existing tracheostomy for known airway obstruction for which an elective procedure has been scheduled as the definitive treatment. In non-tracheotomised children, periodic airway assessment is required to detect early worsening or improvement of the airway obstruction and plan further management. Improvement in airway symptoms obviates the need for further endoscopic intervention. The identification of infants and children presenting a risk of rapid respiratory deterioration is facilitated by monitoring the following parameters: pulse rate, respiratory rate, oxygen saturation (SpO2), level of carbon dioxide retention (pCO2), use of accessory respiratory muscles and level of consciousness. The ‘worst case scenario’ is when the child becomes progressively unresponsive, with signs of deterioration such as decreased SpO2 levels, increased pCO2, shallow breathing, spells of somnolence and decreased respiratory and cardiac rates. As P. Bull stated [6]: ‘It is vital to intervene early if the clinical condition is getting worse, before crisis becomes disaster’. When the stridor or the general condition of the child worsens, it is imperative to perform an endoscopic evaluation. This evaluation should always be considered before the impending ‘worst case scenario’ arises.
5.1 Emergency Airway Support for Severe Respiratory Distress A child with impending airway obstruction requires urgent endoscopic evaluation by a medical team comprising paediatric anaesthetists and otolaryngologists experienced in difficult airway management. According to the American Society of Anesthesiology (ASA) [1], a difficult airway is defined as a clinical situation where a conventionally trained anaesthesiologist experiences difficulties conducting face mask ventilation of the upper airway or endotracheal intubation. This scenario of ‘cannot intubate, cannot ventilate’ requires urgent skilled airway management and cannot be improvised. It is beyond the scope of this chapter to describe all of the clinical situations involving severely compromised paediatric airways. Correct difficult airway management with appropriate treatment decisions is based on hands-on experience and cannot be learned through textbooks alone. However, a few basic principles need to be em phasised: • With the exception of passive oxygenation of the child’s immediate surroundings, it is mandatory to verify the content of the ‘difficult paediatric airway cart or cupboard’ before starting any anaesthetic manoeuvre [21]. All of the instruments and endoscopes, along with their respective connections, must be carefully checked by the anaesthetist and the otolaryngologist prior to anaesthesia induction. In order to avoid disastrous complications that could occur during endoscopy, it is crucial to anticipate every possible problem and identify the best possible solution. • As a rule, an endoscopic evaluation should always precede intubation or tracheotomy in order to establish the site and cause of the airway obstruction, provided that securing the airway is not considered as an ultimate life-saving measure. Quoting P. Bull again [6]: ‘Once a tube has been passed, the opportunity for diagnosis has been compromised’. A situation of imminent respiratory obstruction occurs rarely in clinical practice and is almost always due to the inadequate handling of the compromised acute airway. It should be noted that passive oxygenation with 100% oxygen and continuous positive airway pressure (CPAP) delivered through a face mask, a nasopharyngeal airway
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5.1 Emergency Airway Support for Severe Respiratory Distress
or a percutaneous cricothyrotomy needle, can save a patient’s life even if the patient cannot be ventilated. Remember that oxygen is life. • When conventional intubation fails in conditions such as space-occupying lesions of the oral cavity, oropharynx (i.e., massive adenotonsillar hyperplasia, quinsy, vascular tumour) or pharyngolarynx (i.e., abscess, cyst, tumour), it is best managed by rigid bronchoscopy. A rigid open-tube bronchoscope can be used to bypass the obstructing lesions and manoeuvre through the field to gain access into the endolarynx. • Intubation in children with cranio-maxillo-facial anomalies is not always straightforward. Anaes thetists and otolaryngologists should use all available techniques when confronted with difficult intubation. In most cases, the main obstruction occurs at the level of the nasal cavity, nasopharynx, oropharynx or pharyngolarynx. Multilevel obstructions are more challenging, particularly when an acute inflammatory obstruction is superimposed on a pre-existing congenital craniofacial anomaly. Anticipating difficult airways is facilitated by the knowledge of the morphological changes associated with distinct syndromic congenital anomalies. For instance, malformed and low-set external ears may be indicative of a difficult laryngeal exposure. The presence of retrognathia, a limited mouth opening or even a trismus should be researched during the physical examination of the child. The role of the otolaryngologist is to secure the airway when managing a child with difficult intubation. Choosing the right technique straight away, instead of resorting to endoscopic manoeuvres after several failed attempts at direct laryngoscopy, is of the utmost importance. Pharyngolaryngeal oedema and bleeding can worsen the initial clinical situation. A few additional anaesthetic methods used in difficult airway management are mentioned below. They include naso- and oropharyngeal airway tubes for mask ventilation, a variety of laryngoscope blades and angulated video-intubation laryngoscopes, lighted stylets and laryngeal mask airways, retrograde intubation. The aim here is not to give a detailed description of these various techniques. The appropriate technique for a given clinical situation should be carefully planned prior to anaesthesia induction. Teamwork and mutual trust between anaesthesiologists and otolaryngologists are essential to ensure a favourable outcome.
5.1.1 Transnasal Fibre-Optic Laryngoscopy (TNFL) The role of TNFL in difficult airway management is well recognized. After placing the pulse oximeter and ECG leads, anaesthesia induction is performed using sevoflurane and 100% oxygen with the child in a sitting position. Assisting spontaneous ventilation with a CPAP of 10 cm H2O helps maintain a patent airway. Prior to laryngoscopy, an intravenous (i.v.) line is placed and atropine is given intravenously. Anaesthesia is maintained under spontaneous respiration, with sevoflurane or i.v. propofol. The procedure begins with the application of a local anaesthetic and decongestant into the nasal cavities. The child under anaesthesia and breathing spontaneously is oxygenated using a transparent face mask and slight positive airway pressure. The centre of the mask is fitted with a plastic ring covered by a silicone membrane; in order to reach the nasopharynx, a soft endotracheal ET tube of appropriate size is then gently pushed inside one nostril. The video-bronchoscope is advanced inside the ET tube under visual control. The images on the monitor provide the entire airway team with the necessary information for proper coordination of the procedure undertaken to secure the airway. A jaw lift performed by the assistant surgeon is useful to elevate the tongue base from the posterior pharyngeal wall, facilitating the visualisation of the pharyngolarynx. Pharyngeal secretions can be cleared using the Yankauer suction device. When the tip of the video-bronchoscope reaches the larynx, deep anaesthesia is required in order to further advance the video-bronchoscope into the trachea without any risk of laryngospasm. Topical application of a local anaesthetic is also possible. The ET tube is then gently slid over the endoscope in a clockwise rotation to avoid any inadvertent injury to the laryngeal ventricle by its bevelled tip. This technique is only possible in older children whose airways are sufficiently large to insert a nasotracheal tube over a slim bronchofibroscope. In infants and small children, nasotracheal intubation is carried out after complete fibre-optic evaluation of the airway. The nasotracheal tube is gently pushed into the pharynx through one nostril and it is guided into the larynx and trachea using a Magill forceps and an ‘anaesthetist laryngoscope’ for laryngeal exposure.
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5.1.2 Rigid Bronchoscopy In situations where access to the pharyngolarynx is obscured by oedema, inflammation or tumours, the role of rigid bronchoscopy is invaluable in securing the airway when conventional, direct laryngoscopy fails. The outer tube of the rigid bronchoscope helps bypass the sites of oropharyngeal or laryngeal obstruction and reach the level of the vocal cords. Gentle pressure applied to the chest may reveal expiratory gas bubbles if the supraglottis is swollen and the vocal cords are not readily visible. With this manoeuvre, the glottic lumen may be identified. Deep anaesthesia is required in order for the patient to tolerate the rigid bronchoscopy, and the endoscopist must ensure that the laryngotracheal airway can be cannulated. Video monitoring of the exact position of the bronchoscope enables the anaesthetist to deepen the level of anaesthesia at the precise moment to avoid potential laryngospasm when the bronchoscope is situated just above the vocal cords. As soon as the bronchoscope is in the trachea and adequate ventilation is restored, the patient is brought back to normal inspired O2 (FiO2) and end-tidal CO2 (ET-CO2) levels. Intubation is then performed over an ET tube exchanger (Cook exchange catheter) introduced through the bronchoscope, which acts as a conduit for intubation. Cook manufactures airway exchange catheters in four different sizes. The 8 Fr size is 45 cm in length and can be used in a 3.4 mm ET tube [22]. If the airway cannot be secured by these measures, then the last resort is to create an emergency surgical airway access.
5.1.3 Emergency Surgical Airway Access According to the ASA difficult airway algorithm [1], emergency tracheotomy, cricothyrotomy and percutaneous needle cricothyrotomy represent the last measures in the ‘cannot ventilate, cannot intubate’ clinical scenario. During these manoeuvres, passive 100% oxygenation is supplied with CPAP through a snugly fit face mask and a naso- or oropharyngeal airway. In children younger than 6 years of age, emergency tracheotomy is the procedure of choice. In older children, percutaneous needle cricothyrotomy can be performed easily
and quickly with kits available from Cook with 3.5–6.0 mm internal diameter (ID) airway catheters. Once the airway is secured, the cricothyrotomy must be changed to a conventional tracheotomy. Transtracheal jet ventilation can be attempted with caution [42]. Jet ventilation below a glottic or subglottic obstruction may result in barotrauma because of the limited egress of air and oxygen [49]. Tension pneumothorax may ensue.
5.2 Noisy Child with or Without Respiratory Distress and Undiagnosed Disease With the exception of airway stenosis secured by a tracheostomy, this clinical situation is commonly encountered during the evaluation of a compromised paediatric airway. In-office examination of the upper airway with awake TNFL is used as the first screening method. It is helpful for assessing vocal cord mobility but is less reliable for documenting pharyngeal obstructions during sleep. Since visualisation of the subglottis is impossible in the awake patient, endoscopy under general anaesthesia is necessary to inspect the entire airway. In this case, the challenge is to perform the diagnostic endoscopy without making the initial condition worse to avoid a tracheostomy. At times, endoscopy alone may be therapeutic and lead to an improved airway. Parental consent must always be obtained for interventional endoscopy, which may follow diagnostic endoscopy. When laryngomalacia is diagnosed during the endoscopy, this can be explained to the parents, and a final consent can then also be obtained for definite therapeutic endoscopy. A standardised airway examination should comprise the following steps: 1. TNFL for dynamic evaluation of the upper and lower airways; 2. Direct laryngotracheoscopy with a bare rod-lens telescope; 3. SML, when deemed necessary; and 4. Broncho-oesophagoscopy, when possible and depending on the type of airway obstruction. Diagnostic laryngeal endoscopy for the assessment of the paediatric airway involves both flexible and rigid endoscopes, and must be done routinely.
5.2 Noisy Child with or Without Respiratory Distress and Undiagnosed Disease
5.2.1 Anaesthetic Techniques for Endoscopy in Spontaneous Respiration Madeleine Chollet-Rivier, MD, Marc-André Bernath, MD, Staff Anaesthesiologists
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Table 5.1 Indications for spontaneous respiration anaesthesia in paediatric airway endoscopy • Dynamic evaluation of the upper airways by TNFL • Predictable difficult intubation • Endoscopic therapeutic procedure requiring a free laryngeal field: −− Endoscopic LTOC repair
General anaesthesia under spontaneous respiration without respiratory support or airway instrumentation is the optimal anaesthetic technique for the ENT endoscopist. When using this technique, the airway is totally free and accessible, though natural movements of the pharyngo-laryngeal structures under spontaneous respiration may cause problems, particularly in the case of delicate interventional procedures using laser techniques. Combining adequate anaesthesia levels, analgesia and oxygenation under spontaneous respiration constitutes, even in experienced hands, a real challenge requiring optimal coordination between the ENT endoscopist and the anaesthesiologist. Main risks include hypoxaemia, gastric regurgitation, laryngospasm as well as the child’s movements, which may compromise the operation [25]. Hy poxaemia may result from both hypoventilation and atelectasis whose incidence and severity increase with prematurity, pre-existing respiratory disease, and long-duration procedures. If treated with intermittent positive inspiratory and expiratory pressure ventilation by mask or via endotracheal intubation, atelectasis does not induce long-term morbidity. Nevertheless, while applying these recruiting manoeuvres, frequent operation interruptions may compromise the surgical results. Gastric regurgitation represents a risk factor if there is no endotracheal tube. Yet, as the oropharynx remains under direct vision during the entire procedure, prompt evacuation of bile may be performed if necessary, thus decreasing the risk of bronchoaspiration. Among anaesthetic drugs, the therapeutic range allowing for spontaneous respiration to occur along with a sufficiently deep anaesthesia level to prevent reflex closure of the vocal cords varies widely [39]. Currently, most anaesthesiologists favour the use of three drugs for these procedures under spontaneous respiration: sevoflurane, propofol and remifentanil [4]. The main indications for anaesthesia under spontaneous respiration for the paediatric age group are shown in Table 5.1.
−− Laryngotracheal stenosis −− Microlaryngeal laser surgery for various indications
5.2.1.1 Dynamic Evaluation of the Upper Airway As upper airway obstruction is often the result of abnormal muscle tone rather than anatomic abnormalities, anaesthetic techniques play a significant role in endoscopic evaluation and diagnosis [48]. Fibre-optic evaluation of upper airway dynamics during various anaesthesia depth levels, which mimic changes occurring during the transition from being awake to being asleep is a good indication for anaesthesia under spontaneous respiration. The observed airway dynamics result from the interplay of the pressure-flow in the airway and the muscle tone holding the airway open [28]. Assessment of vocal cord motion is performed by reflex closure of the vocal cords elicited by lightening the anaesthetic level. To correlate the patient’s symptoms with the endoscopic findings, external manipulations of the head such as flexion, extension, and jaw lifting during endoscopy may provide useful information on airway dynamics under various conditions. The chosen anaesthetic agent must preserve both spontaneous ventilatory drive and laryngeal closure reflex, and allow the anaesthesiologist to quickly modify anaesthetic levels. When assessing the degree of dynamic airway obstruction, lidocaine should not be administered topically as this may induce some degree of muscle relaxation, which may increase the collapsibility of supraglottic laryngeal structures [38]. For the dynamic examination of the paediatric airway, the inhalational anaesthetic sevoflurane is the drug of choice [29], as this agent has been shown to maintain spontaneous respiration under deeper anaesthesia levels while better preserving the laryngeal closure reflex in comparison to propofol [39]. Unlike propofol, sevoflurane has no effect on pharyngeal muscle tone, thereby preventing upper airway collapse and obstruction [14]. To administer anaesthetic gases, an
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Fig. 5.1 Face mask for transnasal fibre-optic laryngoscopy: this device exists in different sizes for use in newborns and older children
endoscopy face mask (VBM Medizintechnik GmbH, Germany) should be used (Fig. 5.1) rather than a simple naso-pharyngeal cannula. This tight facial silicone mask has a small orifice for the fibrescope along with a flexible hose to be connected with the anaesthetic circuit. It allows the surgeon to perform fibroscopy while maintaining oxygenation, inhalational anaesthesia, and positive pressure ventilation if necessary, with less operating room pollution [5]. Sevoflurane’s main disadvantage is the high incidence of emergence delirium, which affects approximately 30% of children during the immediate post-anaesthetic period [27]. In contrast, replacing sevoflurane by propofol as soon as the dynamic supraglottic evaluation has been completed allows for a quiet and safe emergence from anaesthesia [13]. In order to pass the glottis with the fibrescope for examination of the infralaryngeal airway, the anaesthesia must be deepened so as to prevent vocal cord movements, which may cause mucosal trauma. Combining 5–6 mg/kg remifentanil and 3 mg/kg propofol ensures similar intubation conditions as those provided by succinylcholine [23], while preventing deleterious curare effects [19]. In addition, the analgesic properties of remifentanil [23] along with the laryngeal muscle relaxing features of propofol [12], associated with the drugs’ short duration of action, constitute real advantages, even in the premature infant. Bradycardia is the main adverse event when using the propofol-remifentanil association, which
may be prevented by injecting 20 mg/kg of atropine or 10 mg/kg of glycopyrrolate. The anaesthetic techniques for endoscopic airway procedures are described in Sect. 18.1, Chap. 18. Although spontaneous respiration anaesthesia is considered effective and safe for endoscopic procedures [27], airway control is not optimal, and constant vigilance is required to ensure the airway’s patency, particularly in the presence of a partial airway obstruction. Anaesthesia maintenance depends on a carefully balanced mixture of inhaled and intravenously administered agents aimed at anaesthetizing the patient without suppressing spontaneous respiration. In the absence of reliable anaesthesia-level monitoring [30], the respiratory rate and the child’s movements during spontaneous respiration are the best indicators of insufficient hypnosis and may thus be instrumental in reducing the risk of awareness. Optimal cooperation between the anaesthesiologist and the surgeon is essential in order to guarantee both the success and safety of the technique.
5.2.2 Asleep Transnasal Fibre-Optic Laryngoscopy (TNFL) When an infant or child presenting inspiratory stridor and chest retractions is ventilated through a face mask after being put to sleep, the respiratory distress usually improves. Assisting spontaneous inspiration with positive airway pressure delivered through the face mask diminishes the Bernouilli effect and improves the upper airway obstruction. In infants, a 3.5-mm videobronchoscope can usually be passed through the nose under anaesthesia. In small newborns and premature babies, a 2.2-mm slim fibre-optic bronchoscope must be used. However, the absence of a working channel necessitates use of an accessory suction catheter [52]. In older children, a 3.5 or 4.9 mm paediatric videobronchoscope is the instrument of choice. The flexible scope is introduced through a small opening in the silicone membrane covering the centre of the face mask (Fig. 5.2). Inspection of nasal cavities on both sides aims at identifying any pathology, such as vestibular stenosis, pyriform aperture stenosis, deviated septum or turbinate hypertrophy. Special attention should be given to identifying anatomical or functional
5.2 Noisy Child with or Without Respiratory Distress and Undiagnosed Disease
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Fig. 5.2 Transnasal fibre-optic laryngoscopy through face mask in an anaesthetised, spontaneously breathing child: (a) Diagram. (b) External view
Fig. 5.3 Nasal and nasopharyngeal obstructions: (a) Choanal atresia (right nostril). (b) Adenoid hyperplasia (left choana)
narrowings at the choana or nasopharynx (choanal atresia, adenoid hyperplasia or tumour masses) (Fig. 5.3). When the endoscope reaches the junction of the nasopharynx and oropharynx, the anaesthetist is asked to stop supplying positive airway pressure. He/ she should also release the chin lift and allow the child to adopt normal head and recumbent body positions. In cases of obstructive sleep apnoea (OSA), when patients undergo general anaesthesia with spontaneous breathing, their muscle tone decreases, and the level of obstruction should then be identified. If not, potentially significant obstructions created by the negative pressure induced during inspiration may be overlooked. Various causes of dynamic obstruction detectable by fibre-optic endoscopy include retroposition of the soft palate, hypertrophy of tonsils and tongue base and epiglottic and supraglottic prolapse (Fig. 5.4). This assessment is highly relevant, especially in the preoperative
evaluation of subglottic stenosis. All of these potential sites of obstruction may be overlooked by direct inspection of the larynx using the rigid rod-lens optic along with a laryngoscope. This can have an adverse effect on the final outcome of single-stage surgery for subglottic stenosis. When the fibre-optic scope is passed behind the epiglottis and reaches the laryngeal inlet, a detailed and careful assessment of vocal cord mobility should be carried out. This is best performed in the awake patient [7]; it should be noted that large cuneiform cartilages and short aryepiglottic folds can obscure the laryngeal inlet as well as a proper view of the vocal cords. Furthermore, flexible laryngoscopy in the office setting may not be able to document oropharyngolaryngeal obstructions responsible for OSA. Thus, both techniques of awake and asleep TNFL are complementary in the evaluation of a compromised airway.
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Fig. 5.4 Dynamic obstructions of the naso-oro-pharynx and pharyngo-larynx: (a) Functional circumferential narrowing of the nasooropharynx during inspiration. (b) Patent naso-oropharynx during expiration. (c) Epiglottic prolapse and tonsillar hyperplasia
Fig. 5.5 Direct laryngoscopy with a bare rigid telescope: (a) Diagram of endoscopic examination. (b) Grade II subglottic stenosis
Normally, abduction of both vocal cords is observed during each inspiration, counteracting the Bernoulli effect at the level of the narrow glottic chink. In patients with unilateral or bilateral vocal cord immobility, an additional investigation with SML is justified (see Sect. 5.3.3.2). The level of anaesthesia must be slightly increased in order to permit the flexible scope’s passage through the vocal cords without inducing laryngospasm. Dynamic examination of the trachea and bronchi during inspiration, expiration and coughing is indispensable for the diagnosis of localised or diffuse tracheomalacia. Other anatomical narrowings of the lower airways can also be identified. If the level of anaesthesia is too deep, then the surgeon should wait for the child to wake up to obtain a more dynamic view of the lower airways.
5.2.3 Direct Laryngoscopy with the Bare 0° Rod-Lens Telescope In order to assess a possible glottic, subglottic or tracheal stenosis in more detail, the child must be deeply anaesthetised, or fully paralysed. The larynx is exposed using an ‘anaesthetic’ or general-purpose Storz laryngoscope with the blade inserted into the vallecula [2].
A rigid 4-mm-diameter magnifying telescope (adult sinuscope) offers a panoramic, clear view of the endolarynx, subglottis and trachea, all the way down to the carina (Fig. 5.5). In the presence of a subglottic or tracheal stenosis, care is taken not to traumatise the mucosa with the telescope. Indeed, the slightest injury to a small, narrow airway decompensates a stable obstructive dyspnoea, necessitating a tracheostomy. If the 4-mm-diameter endoscope is too large, then a 2.7mm or even 1-mm-diameter (sialendoscopy) scope should be used to assess the length of the stenosis and the integrity of the distal airway. Precise measurements of the stenosis, as described in Sect. 5.3.2 of this chapter, should be taken. In general, an unplanned tracheostomy resulting from diagnostic upper airway endoscopy is to be considered as an unacceptable event. Additional endoscopic measures may be applied depen ding on the diagnosis of the pathological conditions: • Suspension microlaryngoscopy (SML) This measure is implemented for diagnostic purposes to differentiate between bilateral neurogenic vocal cord paralysis and a posterior glottic stenosis (PGS) (see Sect. 5.3). Additionally, the use of a right angled probe allows for the precise assessment of the extent of a laryngotracheo-oesophageal cleft.
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5.3 Tracheotomised Child with Known Airway Obstruction
• Broncho-oesophagoscopy Broncho-oesophagoscopy is performed routinely provided that the passage of a rigid or flexible scope does not worsen the child’s initial condition. This technique aims to rule out associated mediastinal malformations, especially in the case of a congenital laryngeal anomaly (e.g. tracheo-oesophageal fistula, tracheobronchial anomalies, extrinsic vascular compression). Another indication for rigid or flexible oesophagoscopy is to search for gastrooesophageal reflux and eosinophilic oesophagitis.
5.3 Tracheotomised Child with Known Airway Obstruction This represents the typical situation of a known congenital or acquired SGS with a secured airway. Given the unfavourable consequences of a failed primary airway (LTR or PCTR) reconstruction [17], careful attention should be paid to the pre-therapeutic endoscopic work-up. As described in the previous sections, it should comprise a TNFL during spontaneous respiration, direct laryngotracheoscopy in deep general anaesthesia, broncho-oesophagoscopy and SML when indicated. While the presence of a tracheostomy facilitates the anaesthetic and overall airway management, it may add a few constraints as far as the dynamic assessment of the airway is concerned.
5.3.1 Transnasal Flexible Laryngoscopy Basically, this procedure is similar to that performed in the non-tracheostomised infant or child (see Sect. 5.2.2). Anatomical obstructions of the upper airway are readily seen, but the precise evaluation of dynamic narrowings is more difficult. The presence of SGS and tracheostomy modifies the degree of negative pressure transmitted to the pharynx during inspiration. Prior to the surgical correction of the SGS, the true degree of functional upper airway collapse is almost impossible to assess. However, this examination is of great interest after the treatment of SGS in cases where plugging the tracheostomy cannula prior to decannulation fails during the night, even though it is successful during the day. Transnasal flexible laryngoscopy
during general anaesthesia and spontaneous respiration is performed as follows: • Anaesthesia and oxygenation through the tracheostomy tube • Spontaneous respiration • Flexible nasopharyngoscopy • Removal of tracheostomy cannula and temporary occlusion of the tracheostoma by the anaesthetist’s finger • Careful inspection for a dynamic airway collapse in the nasopharynx, oropharynx, pharyngolarynx and trachea Localised malacia at the site of the former tracheostoma is a potential reason for failed decannulation in an otherwise normal airway. If the cannula, acting as a stent at the stoma site, is not temporarily removed during TNFL, then the condition remains undiagnosed, and repeated failures to decannulate may ensue.
5.3.2 Direct Laryngotracheobronchoscopy with a Rod-Lens Telescope In the fully relaxed patient, the larynx is exposed using the ‘anaesthetic’ or general-purpose Storz laryngoscope while the 4-mm-diameter sinuscope is used to assess the exact location of the stenosis with respect to the vocal cords and the tracheostoma. The degree of SGS is measured by passing telescopes or bougies of different given sizes through the stricture. The Myer–Cotton airway grading system is routinely used [36]. When vocal cord immobility is found during TNFL, SML must be implemented.
5.3.3 Suspension Microlaryngoscopy The Benjamin-Lindholm laryngoscope is usually preferred for obtaining a panoramic view of the pharyngolarynx and subglottis [2]. The use of both hands is necessary to manipulate the telescopes and appropriate instruments. Telescopes are used to measure the length of the stenosis in the craniocaudal direction with precision. The Lindholm vocal cord retractor and angulated probes are used to differentiate a bilateral vocal cord paralysis (BVCP) from a PGS, with or without cricoarytenoid joint fixation. Lastly, telescopes and
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tapered bougies of a given size are used to assess the degree of stenosis.
5.3.3.1 Craniocaudal Measurements of Airway Stenoses The rod-lens telescope is inserted through the laryngoscope and further advanced to the level of the vocal cords. The recorded distance is marked on the shaft of the telescope. Repeated measures are taken at the upper and lower margins of the stenosis and tracheostoma, and lastly at the level of the carina (Fig. 5.6). Serial still photographs are taken in cranial to caudal direction (Fig. 5.7). A diagram with all of the measurements is added to the endoscopy report (Fig. 5.8). In order to plan the surgery accurately, especially in the case of a resection and anastomosis, such measurements are indispensable. With complete airway obstruction, CT scanning with 3D reconstructions are very useful. The cricoid ring can also be identified by external palpation, and the distance between the cricoid ring and the tracheostoma can be measured on the skin of the neck, however, with less precision.
5.3.3.2 Bilateral Vocal Cord Paralysis (BVCP) Versus Posterior Glottic Stenosis (PGS) The differentiation of vocal cord immobility due to a neurogenic cause from PGS is usually straightforward and based on the patient’s medical history, when this condition is seen in a newborn with no history of prior
Fig. 5.6 Assessment of the precise location of the SGS craniocaudal extension with respect to the vocal cords and tracheostoma: The bare rod-lens telescope is used for precise measurements that are marked on the shaft of the instrument with an indelible pen
intubation. All infants and children having undergone a short-term endotracheal intubation require precise assessment of the posterior laryngeal commissure and cricoarytenoid joint function using the Lindholm false cord retractor and an angulated probe. • The Lindholm self-retaining false cord retractor This instrument is placed at the level of the ventricular bands and is opened. The interarytenoid distance is restored to its normal size in the case of a neurogenic BVCP. The interarytenoid distance remains narrow, and a stretched band of scar tissue may be seen from posterior commissure scarring (Fig. 5.9). Electromyography (EMG) is not required to differentiate these two conditions. • Arytenoid palpation (Fig. 5.10) This manoeuvre can identify the different types of PGS precisely, according to Bogdasarian’s classification (Fig. 5.11) [3].
Type I: Interarytenoid Adhesion (Fig. 5.11a) Endoscopically, interarytenoid adhesion is easily recognised as a band of scar tissue tethering the vocal cords in the midline. A small residual posterior opening with intact interarytenoid mucosa is the key feature that differentiates this condition from other forms of PGS.
T ype II: Interarytenoid and Posterior Commissure Scarring Adhesion (Fig. 5.11b) In simple PGS, the fibrous tissue fills the posterior glottis without any residual opening. This condition must be differentiated from PGS with cricoarytenoid joint ankylosis (CAA). In SML, lateral mobilisation of a single arytenoid pulls the contralateral arytenoid towards the same side; an identical phenomenon is reproduced in reverse fashion when it is performed on the opposite side in simple PGS (see Fig. 5.10).
T ype III: Posterior Commissure Scarring with Unilateral Cricoarytenoid Joint Fixation (Fig. 5.11c) Mobilisation of the fixed arytenoid is impossible. The contralateral arytenoid can be moved slightly laterally with an angulated probe.
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5.3 Tracheotomised Child with Known Airway Obstruction Fig. 5.7 Serial still photographs of a subglottic stenosis: (a) Intact vocal cords. (b) Subglottic stenosis reaching the under-surface of the left vocal cord. (c) Segment of normal cervical trachea with suprastomal granuloma
position. Dense scar tissue is usually seen at the posterior laryngeal commissure. The Lindholm false cord retractor cannot spread apart the vocal cords.
5.3.3.3 Myer–Cotton Airway Grading System
Fig. 5.8 Diagram of the endoscopy report: the length and precise location of the subglottic stenosis with respect to the vocal cords and tracheostoma, as well as the length of the tracheostoma and residual normal trachea (in centimetres and number of normal tracheal rings) must be recorded
T ype IV: Scarring of Posterior Commissure with Bilateral Cricoarytenoid Joint Ankylosis (Fig. 5.11d) Mobilisation of the arytenoids with a probe is not possible in this condition. Indeed, they are firmly fixed to the cricoid plate, remaining in the median or paramedian
Myer and Cotton established a grading system that incorporates endotracheal tube sizes for the evaluation of the airway’s response to a conservative ‘wait and see’ approach or to LTR with costal cartilage grafts [36]. This modification of the original Cotton airway grading system [8] classifies SGS into four grades (Fig. 5.12). Severe grade III (pinhole residual opening) and grade IV (no residual lumen) SGSs are readily identified without using a gauge, such as a tapered dilator or an endotracheal tube. The latter permits an improved classification of grade I–II and minor grade III SGSs. The largest endotracheal tube that can pass through the narrowest point of the stenosis without encountering any resistance is connected to the anaesthetic circuit while the pressure valve is closed. The tracheostomy cannula is removed, and the anaesthetist uses a finger to temporarily plug the stoma. When observed with a rod-lens telescope placed just above the stenosis, a leak audible at less than 30 cm H2O pressure may be detected or air bubbles may be seen escaping through secretions around the tube; the size of this tube is then recorded and compared to the expected normal size for age on the Myer–Cotton chart [36]. The grade of stenosis is thus measured and attributed to a given patient. However, tube sizes differ significantly from one manufacturer to the next for an identical tube number, and this chart does not reveal which manufacturer’s measurements have been used (see Table 2.1, Chap. 2). This grading system has proven useful in predicting the success or failure rates after LTR for SGS [11, 37, 40]. Since the advent of PCTR for the cure
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Fig. 5.9 Contribution of the Lindholm false vocal cord retractor in bilateral immobility of the vocal cords: (a) The Lindholm self-retaining false vocal cord retractor. (b) Bilateral vocal cord paralysis: the paramedian position of both vocal cords (left) is
easily spread apart with the false vocal cord retractor (right). (c) Scarring of the posterior commissure: the paramedian position of both vocal cords (left) is not improved by the false vocal cord retractor, but a band of scar tissue is conspicuous (right)
Fig. 5.10 Posterior glottic stenosis without cricoarytenoid joint fixation: (a) Endoscopic aspect of a posterior glottic stenosis. (b) Mobilisation of the right arytenoid to the right attracts the left arytenoid towards the right side. The reverse phenomenon is observed on the opposite side
of severe SGS, the limitations of this classification system as a true indicator of decannulation have been revealed. During PCTR, the entire diseased segment of the airway is resected [18]. Thus, PCTR for subglottic stenosis without vocal cord involvement has
similar decannulation rates, irrespective of the initial stenosis grade. Incorporating additional patient and disease characteristics is therefore required for better outcome measurements after PCTR for subglottic stenosis. Prediction of the chances of decannulation
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5.3 Tracheotomised Child with Known Airway Obstruction Fig. 5.11 Bogdasarian’s classification of posterior glottic stenosis [3]: (a) Interarytenoid adhesion: residual normal mucosal bridge between the arytenoids. (b) Interarytenoid and posterior commissure scarring: no residual normal interarytenoid mucosa. (c) Scarring of posterior commissure with unilateral cricoarytenoid joint fixation. (d) Scarring of posterior commissure with bilateral cricoarytenoid joint fixation
or delayed decannulation will be facilitated by these measurements, which will also help in more accurately explaining the prognosis to the child’s parents. However, the introduction of a new grading system is hazardous, because there is a high risk that it will not be used. This shortcoming was previously observed with McCaffrey’s grading system used for adult laryngotracheal stenosis [31]. Although quite helpful in predicting the success or failure after resection and anastomosis, McCaffrey’s grading system is seldom used as it involves memorising too many parameters. When the authors analysed the results of 100 paediatric PCTRs performed at their institution [35], they realised the limitations of considering the initial Myer–Cotton stenosis grade alone as an outcome measure in terms of decannulation. Associated comorbidities or glottic involvement appeared to influence the failure or delay in decannulation significantly. PCTR may be successful in creating a patent airway, but depending on other comorbidities, a patient’s decannulation may still fail.
5.3.3.4 New Grading System This new grading system is based on the original Myer–Cotton airway grading system. Simple and easy to remember, it incorporates three additional parameters only: comorbidities, glottic involvement and the association of both. The comorbidities include severe prematurity with hyaline membrane disease, respiratory insufficiency, cardiac anomalies, neurological conditions, severe gastroesophageal reflux or extralaryngeal airway obstruction, as well as severe syndromic or non-syndromic congenital anomalies. The glottic involvement includes PGS, vocal cord fusion, and bilateral or unilateral vocal cord fixation or paralysis. Mild restriction of vocal cord movement, whether unilateral or bilateral, was not included in this group. This new airway grading system is shown in (Table 5.2). It was applied to 100 PCTRs from a prospectively collected database. All of the patients
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5 Endoscopic Assessment of the Compromised Paediatric Airway Table 5.3 Overall decannulation rates of 100 PCTRs for grades III and IV SGS according to the new airway grading system [35] Types of Nb Overall grade III–IV SGS decannulation (follow-up from 6 months to 21 years) (a)
Isolated SGS
36
97%
(b)
Isolated SGS + comorbidities
31
93%
(c)
SGS + glottic involvement
19
89%
(d)
SGS + comorbidities + glottic 14 involvement
64%
patients from multiple centres using uniform selection criteria.
5.3.4 Broncho-oesophagoscopy The preoperative assessment of the tracheostomised infant and child with SGS is incomplete if the lower airways and oesophagus are not inspected. Fig. 5.12 Myer–Cotton airway grading system [36]
5.3.4.1 Bronchoscopy Below the Tracheostoma Table 5.2 New airway grading system [35] SGS + Myer–Cotton Isolated Isolated glottic grade SGS SGS + involvecomorment bidities
SGS + glottic involvement + comorbidities
(a)
(b)
(c)
(d)
I
0–50%
Ia
Ib
Ic
Id
II
51–70%
II a
II b
II c
II d
III
71–99%
III a
III b
III c
III d
IV
No lumen IV a
IV b
IV c
IV d
belonged to severe grade III or grade IV SGS, based on Myer–Cotton classification. The results of the overall decannulation rates are displayed in (Table 5.3). The association of comorbidities and glottic dysfunctions in SGS are the worst prognosticators in terms of decannulation following PCTR. Validation of this system requires the evaluation of a larger number of
An appropriately-sized bronchoscope is introduced through the tracheostoma under direct vision using a rod-lens telescope. If the distal end of the cannula has induced a narrowing of the lower trachea, then the rigid bronchoscope is not advanced any further into the distal airway in order to avoid bleeding. The inspection of the lower airway is then carried out with a long 0° bare rodlens telescope. If the tracheal wall is not traumatised by the cannula, then all of the rings may be identified. The distance between the lower edge of the tracheostoma and the carina should be measured with precision by placing the tip of the scope at the level of the carina, and by marking the distance on the shaft of the telescope at the tracheostoma site. After the removal of the telescope, the distance is then recorded and noted in the endoscopy report, as well as the number of residual normal tracheal rings. The same measurement may be obtained with a rigid open tube bronchoscope. This information is essential in planning possible resection and anastomosis of the airway. Further examination down to the basal bronchi is performed on both sides.
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Caution should be exercised to avoid bending the telescope. If this were the case, a crescent-shaped shadow superimposed on the normally round endoscopic image would appear on the images displayed on the monitor. Using the same technique, a larger video-bronchoscope with a suction channel can also be used in infants in order to inspect the upper lobes during a short apnoea. Endoscopic biopsies and bronchoalveolar lavage (BAL) should always be performed at the end of the complete bronchoscopic evaluation, as bleeding might compromise any further examination. In the trachea and bronchi, the presence of congenital and acquired lesions, such as tracheo-oesophageal fistula, anomalous tracheal origin of the upper lobe bronchus (bronchus suis), localised or diffuse malacia, extrinsic compressions and anomalous distribution of the bronchial tree is investigated. Acquired lesions may originate from local trauma induced by the tracheostomy cannula (see Sect. 14.4, Chap. 14) as well as suction catheters at the level of the carina or further down the lower airways. The type of bronchial secretions (mucus, muco-purulent) and the quality of bronchial mucosa (i.e., swelling, inflammation and friability) should be documented, along with a precise assessment of their effects on the narrowed segmental bronchi’s ventilation. A bacteriological examination of the aspirate should be conducted systematically. Additional diagnostic biopsies and BAL should be carried out at the end of the procedure. Bronchoalveolar lavage is useful in confirming the diagnosis of chronic aspiration when lipid-laden macrophages are observed on the smear examination. Failure to diagnose infection of the distal airways may adversely affect the postoperative outcome. This may lead to adverse consequences such as anastomotic dehiscence, cartilage graft infection or secondary tracheostomy.
5.3.4.2 Oesophagoscopy With modern slim video-oesophagoscope technology, endoscopy of the upper digestive tract can be performed in infants using flexible or rigid scopes. The technique of rigid oesophagoscopy has been described in detail elsewhere [20, 44]. It should be noted that this technique is much easier to perform in infants and children than in adults. The role of oesophagoscopy in the assessment of SGS is to assess any gastro-oesophageal reflux (GOR) while ruling out eosinophilic oesophagitis.
Although GOR is best diagnosed using 24-h pHmonitoring or impedancemetry, endoscopy is also helpful when it reveals clear signs of erosive oesophagitis [44]. Redness and oedema of the laryngeal mucosa may not be consistent with signs of GOR, and random biopsies have proven ineffective in assessing GOR based on a histological examination. The absence of the angle of His, with the cardia opening leading in a straight line to the gastric pouch, is an anatomical configuration that may be compatible with chronic reflux. A thickened or ringed oesophageal mucosa may be indicative of eosinophilic oesophagitis [45]. Biopsies should be taken on a regular basis to confirm this diagnosis; this condition seems to be more frequent in the USA than in Europe in the paediatric age group.
5.4 Treatment Plan for Laryngotracheal Stenosis Before engaging in any endoscopic or open surgery, a thorough discussion with the child’s parents is essential. The initial condition is most often that of a tracheostomised child with a poor or absent voice, and an obstructed subglottis. Parents expect the outcome to be a normally breathing and speaking child after the surgery, which in most cases is not realistic, especially in terms of the voice. Various patient and disease parameters must be taken into account and integrated in the decision-making process to determine the best surgical option. In particularly difficult cases, input from neonatologists, intensivists and specialty physicians (e.g. pneumology, cardiology, gastroenterology) is essential. Various parameters must be considered: • Site and extent of airway stenosis • Glottic involvement with or without cricoarytenoid ankylosis or vocal cord synechia • Site of tracheostoma, with possible additional tracheal damage • Multilevel pharyngeal, laryngeal and tracheal stenoses • Severe pulmonary, cardiac, neurological or gastrooesophageal comorbidities • Congenital anomalies • A mixture of several aforementioned conditions An identical situation of tracheostomy with aphonia and total airway obstruction may result from either a grade IV SGS with intact mobile vocal cords or a
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5 Endoscopic Assessment of the Compromised Paediatric Airway
severely damaged larynx with barely recognisable anatomical structures (Fig. 5.13). The possible surgical outcomes for each of these two different situations must clearly be explained to the parents, and additional parameters such as comorbidities or congenital anomalies must be incorporated into the decision-making. Videoprints of endoscopic pictures are helpful in providing clear explanations to the parents. The surgery must be tailored to each individual situation. It is essential that surgeons treating laryngotracheal stenosis in infants and children have the ability to choose the best procedure based on their expertise in therapeutic endoscopy and various reconstructive procedures (i.e., LTR, PCTR and extended PCTR). In certain cases, surgery may not be feasible because of the risk of decannulation and should therefore be avoided. An example of such a situation is the treatment of a child with complex glotto-subglottic stenosis (LTS with PGS and bilateral CAA), mental retardation and uncoordinated pharyngolaryngeal function. In this case, surgical reconstruction may restore a patent airway; however, owing to the child’s mental status, incompetent glottic function will result in severe recurrent aspiration pneumonias, and there will be no chance of improvement.
5.4.1 Primary Endoscopic Treatment Congenital subglottic stenosis is not amenable to any primary laser treatment as the stenosis is usually cartilaginous by nature. Cautious carbon-dioxide
Fig. 5.13 Grade IV subglottic stenoses with different potential outcomes after surgery: (a) Grade IV subglottic stenosis clear from normal mobile vocal cords: The postoperative result is likely to be excellent (i.e., normal or subnormal voice with patent airway). (b) Grade IV transglottic stenosis with unrecognisable vocal cords and bilateral cricoarytenoid ankylosis: The best postoperative result is likely to be a patent airway with a breathy voice and some aspiration
(CO2) laser incision combined with dilation may be effective in treating thin web-like cicatricial airway stenoses. The results may be excellent in the case of thin diaphragmatic, subglottic and tracheal stenoses, provided the stenosis does not involve the posterior wall of the airway, especially at the level of the membranous trachea (see Fig. 22.1, Chap. 22). Extensive use of the laser can worsen a pre-existing acquired airway stenosis [34]. The contra-indications set down by Simpson [47] are still valuable today as a basis for the endoscopic treatment of LTS. The CO2 laser should be set to superpulse or ultrapulse mode, and the laser beam should be directed to the target with a microspot manipulator (250-m spot size at 400-mm focal distance) to minimise heat diffusion into the surrounding tissues. Radial incisions in the stenosis are made using the Shapshay technique [46], and gentle dilation is done using tapered bougies or with angioplasty balloons. Then, a cotton swab soaked in a solution of 1–2 mg/mL mitomycinC may be applied topically to the subglottis for 1 or 2 min. Repeated mitomycin-C applications should be avoided because of possible delayed adverse effects [15, 41]. In the case of the recurrence of the stenosis to its initial grade following primary endoscopic treatments (CO2 laser, dilation, stenting), any further endoscopic treatment is strictly contraindicated [34]. Open surgical reconstruction should be considered in this case.
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References
5.4.2 Laryngotracheal Reconstruction with Cartilage Expansion (LTR) This surgery is almost exclusively reserved for mild or moderate grades of paediatric SGS or combined glottosubglottic stenoses. LTR with an anterior graft alone is used as a singlestage operation for the resolution of grade II stenosis [9, 32]. Mild grade III stenosis is likely to require an anterior graft with a posterior cricoid split supported by an endoluminal stent, whereas severe grade III stenosis requires both anterior and posterior grafts with stenting [11, 40]. However, over the last decade, PCTR has emerged as a superior alternative to LTR for the treatment of grades III and IV SGSs [17, 50]. In cases of congenital stenosis, the LTR may be combined with submucosal resection of cartilage to increase the size of a thickened anterior lamina of the cricoid ring. PGS in children presents specific management difficulties. A posterior cartilage graft is necessary, but overexpansion of the posterior commissure should be avoided, as it impairs the resulting voice quality and may induce potential aspiration. Stenting is essential until the glottis and subglottis are completely healed.
In children with multiple congenital anomalies, impaired neurological, cardiac or pulmonary function, a double-stage PCTR (with postoperative maintenance of the tracheostoma) is preferred.
5.4.4 Extended Partial Cricotracheal Resection In the paediatric age group, when SGS is combined with glottic involvement (PGS, cicatricial fusion of the vocal cords) or when the laryngeal framework is distorted because of previously failed LTRs, a PCTR supplemented with a posterior cricoid split and costal cartilage graft (extended PCTR) is recommended. The reconstructed site also requires stenting with an LT-Mold (see Sect. 2.8, Chap. 2) for about 3 weeks until complete healing of the subglottic area is obtained. Closure of the tracheostoma is the next step [33, 43]. As an alternative to extended PCTR, an LTR with anterior and posterior costal cartilage grafts with stenting may be performed [11, 37, 40].
References 5.4.3 Partial Cricotracheal Resection (PCTR) In infants and children, PCTR is the procedure of choice for the treatment of severe (>70% luminal obstruction) SGS of congenital or acquired aetiology. Recent experience with PCTR has shown that it can be safely performed in infants weighing less than 10 kg [16, 24, 26], as opposed to the initial school of thought, which advised waiting for the child to reach 10 kg of bodyweight prior to performing any airway reconstruction [10]. PCTR is performed as a single-stage operation (with concomitant resection of the tracheostoma during the surgery) when the stenosis is purely subglottic, and the child is otherwise healthy. The only exception to this rule is when the tracheostoma is very distal (fifth or sixth tracheal ring), with normal and steady tracheal rings available between the subglottic stenosis and the upper margin of the tracheostoma for anastomosis. Closure of the tracheostoma is the next step.
1. Practice guidelines for management of the difficult airway: an updated report by the American Society of Anes thesiologists Task Force on Management of the Difficult Airway 2003. Anesthesiology 98, 1269–1277 (2003) 2. Benjamin, B.: Pediatric laryngoscopes: design and application. Ann. Otol. Rhinol. Laryngol. 110, 617–623 (2001) 3. Bogdasarian, R.S., Olson, N.R.: Posterior glottic laryngeal stenosis. Otolaryngol. Head Neck Surg. 88, 765–772 (1980) 4. Bonnin, M., Therre, P., Albuisson, E., et al.: Comparison of a propofol target-controlled infusion and inhalational sevoflurane for fibreoptic intubation under spontaneous ventilation. Acta Anaesthesiol. Scand. 51, 54–59 (2007) 5. Bourgain, J.L., Billard, V., Cros, A.M.: Pressure support ventilation during fibreoptic intubation under propofol anaesthesia. Br. J. Anaesth. 98, 136–140 (2007) 6. Bull, P.D.: Evaluation of the pediatric airway by rigid endoscopy. In: Cotton, R.T., Myer III, C.H.M. (eds.) Practical Pediatric Otolaryngology, pp. 477–481. Lippincott-Raven, Philadelphia/New York (1999) 7. Chen, E.Y., Inglis Jr., A.F.: Bilateral vocal cord paralysis in children. Otolaryngol. Clin. North Am. 41, 889–901 (2008) 8. Cotton, R.T., Seid, A.B.: Management of the extubation problem in the premature child. Anterior cricoid split as an alternative to tracheotomy. Ann. Otol. Rhinol. Laryngol. 89, 508–511 (1980)
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9. Cotton, R.T., O’Connor, D.M.: Paediatric laryngotracheal reconstruction: 20 years’ experience. Acta Otorhinolaryngol. Belg. 49, 367–372 (1995) 10. Cotton, R.T., Myer III, C.M.: Practical Pediatric Otolaryngology. Lippincott-Raven, Philadelphia/New York (1999) 11. Cotton, R.T., Gray, S.D., Miller, R.P.: Update of the Cincinnati experience in pediatric laryngotracheal reconstruction. Laryngoscope 99, 1111–1116 (1989) 12. Crawford, M.W., Rohan, D., Macgowan, C.K., et al.: Effect of propofol anesthesia and continuous positive airway pressure on upper airway size and configuration in infants. Anesthesiology 105, 45–50 (2006) 13. Dahmani, S., Stany, I., Brasher, C., et al.: Pharmacological prevention of sevoflurane- and desflurane-related emergence agitation in children: a meta-analysis of published studies. Br. J. Anaesth. 104, 216–223 (2010) 14. Eastwood, P.R., Platt, P.R., Shepherd, K., et al.: Collapsibility of the upper airway at different concentrations of propofol anesthesia. Anesthesiology 103, 470–477 (2005) 15. Eliashar, R., Eliachar, I., Esclamado, R., et al.: Can topical mitomycin prevent laryngotracheal stenosis? Laryngoscope 109, 1594–1600 (1999) 16. Garabedian, E.N., Nicollas, R., Roger, G., et al.: Cricotracheal resection in children weighing less than 10 kg. Arch. Otolaryngol. Head Neck Surg. 131, 505–508 (2005) 17. George, M., Ikonomidis, C., Jaquet, Y., et al.: Partial cricotracheal resection in children: potential pitfalls and avoidance of complications. Otolaryngol. Head Neck Surg. 141, 225–231 (2009) 18. George, M., Jaquet, Y., Ikonomidis, C., et al.: Management of severe pediatric subglottic stenosis with glottic involvement. J. Thorac. Cardiovasc. Surg. 139, 411–417 (2010) 19. Goudsouzian, N.G.: Muscle relaxants in children. In: Cote, C.J., Todres, D., Goudsouzian, N.G., et al. (eds.) A practice of Anesthesia for Infants and Children, pp. 196–215. Saunders, Philadelphia (2001) 20. Green, C.G., Holinger, L.D., Gartlan, M.G.: Technique. In: Holinger, I.D., Lusk, R.P., Green, C.G. (eds.) Paediatric Laryngology and Bronchoesophagology, pp. 106–107. Lippincott-Raven, Philadelphia/New York (1997) 21. Hackel, A., Badgwell, J.M., Binding, R.R., et al.: Guidelines for the pediatric perioperative anesthesia environment. American Academy of Pediatrics. Section on Anesthesiology. Pediatrics 103, 512–515 (1999) 22. Hagberg, C.A.: Special devices and techniques. Anesthesiol. Clin. N Am. 20, 907–932 (2002) 23. Hume-Smith, H., McCormack, J., Montgomery, C., et al.: The effect of age on the dose of remifentanil for tracheal intubation in infants and children. Paediatr. Anaesth. 20, 19–27 (2010) 24. Ikonomidis, C., George, M., Jaquet, Y., et al.: Partial cricotracheal resection in children weighing less than 10 kilograms. Otolaryngol. Head Neck Surg. 142, 41–47 (2010) 25. Jaquet, Y., Monnier, P., Van Melle, G., et al.: Complications of different ventilation strategies in endoscopic laryngeal surgery: a 10-year review. Anesthesiology 104, 52–59 (2006) 26. Johnson, R.F., Rutter, M., Cotton, R.T., et al.: Cricotracheal resection in children 2 years of age and younger. Ann. Otol. Rhinol. Laryngol. 117, 110–112 (2008)
27. Lerman, J., Johr, M.: Inhalational anesthesia vs total intravenous anesthesia (TIVA) for pediatric anesthesia. Paediatr. Anaesth. 19, 521–534 (2009) 28. Litman, R.S., McDonough, J.M., Marcus, C.L., et al.: Upper airway collapsibility in anesthetized children. Anesth. Analg. 102, 750–754 (2006) 29. Machotta, A.: Anaesthetic management for endoscopy of the pediatric airway. Anaesthesist 51, 668–678 (2002) 30. Mani, V., Morton, N.S.: Overview of total intravenous anesthesia in children. Paediatr. Anaesth. 20(3), 211–222 (2009) 31. McCaffrey, T.V.: Classification of laryngotracheal stenosis. Laryngoscope 102, 1335–1340 (1992) 32. McQueen, C.T., Shapiro, N.L., Leighton, S., et al.: Singlestage laryngotracheal reconstruction: the Great Ormond Street experience and guidelines for patient selection. Arch. Otolaryngol. Head Neck Surg. 125, 320–322 (1999) 33. Monnier, P., Lang, F., Savary, M.: Partial cricotracheal resection for pediatric subglottic stenosis: a single institution’s experience in 60 cases. Eur. Arch. Otorhinolaryngol. 260, 295–297 (2003) 34. Monnier, P., George, M., Monod, M.L., et al.: The role of the CO2 laser in the management of laryngotracheal stenosis: a survey of 100 cases. Eur. Arch. Otorhinolaryngol. 262, 602– 608 (2005) 35. Monnier, P., Ikonomidis, C., Jaquet, Y., et al.: Proposal of a new classification for optimising outcome assessment following partial cricotracheal resections in severe pediatric subglottic stenosis. Int. J. Pediatr. Otorhinolaryngol. 73, 1217–1221 (2009) 36. Myer III, C.M., O’Connor, D.M., Cotton, R.T.: Proposed grading system for subglottic stenosis based on endotracheal tube sizes. Ann. Otol. Rhinol. Laryngol. 103, 319–323 (1994) 37. Ndiaye, I., Van de Abbeele, T., Francois, M., et al.: Traitement chirurgical des sténoses laryngées de l’enfant. Ann. Otolaryngol. Chir. Cervicofac. 116, 143–148 (1999) 38. Nielson, D.W., Ku, P.L., Egger, M.: Topical lidocaine exaggerates laryngomalacia during flexible bronchoscopy. Am. J. Respir. Crit. Care Med. 161, 147–151 (2000) 39. Oberer, C., von Ungern-Sternberg, B.S., Frei, F.J., et al.: Respiratory reflex responses of the larynx differ between sevoflurane and propofol in pediatric patients. Anesthesiology 103, 1142–1148 (2005) 40. Ochi, J.W., Evans, J.N., Bailey, C.M.: Pediatric airway reconstruction at Great Ormond Street: a ten-year review. I. Laryngotracheoplasty and laryngotracheal reconstruction. Ann. Otol. Rhinol. Laryngol. 101, 465–468 (1992) 41. Rahbar, R., Shapshay, S.M., Healy, G.B.: Mitomycin: effects on laryngeal and tracheal stenosis, benefits, and complications. Ann. Otol. Rhinol. Laryngol. 110, 1–6 (2001) 42. Ravussin, P., Bayer-Berger, M., Monnier, P., et al.: Percutaneous transtracheal ventilation for laser endoscopic procedures in infants and small children with laryngeal obstruction: report of two cases. Can. J. Anaesth. 34, 83–86 (1987) 43. Rutter, M.J., Hartley, B.E., Cotton, R.T.: Cricotracheal resection in children. Arch. Otolaryngol. Head Neck Surg. 127, 289–292 (2001) 44. Savary, M., Miller, G.: The Esophagus: Handbook and Atlas of Endoscopy. Gassmann Solothurn, Switzerland (1978) 45. Shannon, R.: Eosinophilic esophagitis in children. Gastroenterol. Nurs. 32, 123–125 (2009)
References 46. Shapshay, S.M., Beamis Jr., J.F., Hybels, R.L., et al.: Endoscopic treatment of subglottic and tracheal stenosis by radial laser incision and dilation. Ann. Otol. Rhinol. Laryngol. 96, 661–664 (1987) 47. Simpson, G.T., Strong, M.S., Healy, G.B., et al.: Predictive factors of success or failure in the endoscopic management of laryngeal and tracheal stenosis. Ann. Otol. Rhinol. Laryngol. 91, 384–388 (1982) 48. Sivan, Y., Ben-Ari, J., Soferman, R., et al.: Diagnosis of laryngomalacia by fiberoptic endoscopy: awake compared with anesthesia-aided technique. Chest 130, 1412–1418 (2006)
95 49. Steward, D.J.: Percutaneous transtracheal ventilation for laser endoscopic procedures in infants and small children. Can. J. Anaesth. 34, 429–430 (1987) 50. White, D.R., Cotton, R.T., Bean, J.A., et al.: Pediatric cricotracheal resection: surgical outcomes and risk factor analysis. Arch. Otolaryngol. Head Neck Surg. 131, 896–899 (2005) 51. Wong, E., Bradrick, J.: Surgical approaches to airway management for anesthesia practitioners. In: Hagberg, C.A. (ed.) Handbook of Difficult Airway Management, pp. 209–210. Churchill Livingstone, Philadelphia (2000) 52. Wood, R.E.: Pitfalls in the use of the flexible bronchoscope in pediatric patients. Chest 97, 199–203 (1990)
Part Congenital Anomalies of the Larynx and Trachea
Introduction Congenital anomalies of the larynx include a variety of conditions that cause respiratory distress in the neonate or infant. A number of anomalies are self-limiting while others are life-threatening and require immediate attention. The prevalence of congenital airway anomalies has been estimated to range between 1 in 10,000 and 1 in 50,000 live births, and their relative prevalence is shown in Table 1. Table 1 Prevalence of congenital laryngeal anomalies
This section summarises the main features of congenital airway anomalies and discusses endoscopic and open surgical treatments in detail. For further information, the following textbooks may be consulted [1, 2, 4, 5]. Congenital tracheal anomalies are also examined from an otolaryngologist’s perspective. When dealing with airway problems, the ENT surgeon and endoscopist must have a clear understanding of congenital tracheal and bronchial anomalies. Treatments for these conditions are usually performed by a team working in close cooperation with the thoracic or cardio-thoracic surgeon. The management of primary tracheomalacia and extrinsic airway compressions due to vascular, cardiac or neoplastic conditions is explained in detail, as are congenital tracheo- oesophageal fistulas associated with oesophageal atresia and intrinsic anomalies of the trachea (long segment tracheal stenosis with circular “O” tracheal rings).
References
When surgical treatment is an option, both a structured approach enabling a definitive endoscopic diagnosis (see Sect. 5.4, Chap. 5) and an appropriate decision-making process are needed. Some children may present with more than one airway anomaly [3].
1. Benjamin, B.: Congenital disorders of the larynx. In: Cummings, C.H., Frederickson, J.M. (eds.) Otolaryngol Head Neck Surgery, pp. 1831–1853. Mosby year book, St. Louis/Baltimore (1993) 2. Cotton, R.T., Myer III, C.M.: Practical Pediatric Otolaryngology. Lippincott-Raven, Philadelphia/New York (1999) 3. Dickson, J.M., Richter, G.T., Meinzen-Derr, J., et al.: Secondary airway lesions in infants with laryngomalacia. Ann Otol Rhinol Laryngol 118, 37–43 (2009) 4. Ferlito, A.: Diseases of the Larynx. Arnold/Oxford University Press, New York (2000) 5. Holinger, L.D.: Congenital laryngeal anomalies. In: Holinger, L.D., Lusk, R.P., Green, C.G. (eds.) Pediatric Laryngology and Bronchoesophagology, pp. 139–142. Lippincott-Raven, Philadelphia/New York (1997)
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II
6
Laryngomalacia (LM)
Contents
Core Messages
6.1
Pathogenesis............................................................ 100
››
6.2
Symptoms................................................................ 100
6.3
Patient Assessment.................................................. 100
6.4
Endoscopy Under General Anaesthesia............... 101
6.5
Indications for Surgical Intervention.................... 101
6.6
Supraglottoplasty in Suspension Microlaryngoscopy................................................. 101 6.6.1 Type I Laryngomalacia............................................. 103 6.6.2 Type II Laryngomalacia............................................ 103 6.6.3 Type III Laryngomalacia.......................................... 104 6.7
Postoperative Care.................................................. 104
6.8
Complications and Results..................................... 105
References............................................................................ 105
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Most common (~60%) congenital laryngeal anomaly. Most common source of stridor in newborns. Male to female ratio 2:1. Inward collapse of supraglottic structures on inspiration. High-pitched fluttering inspiratory stridor exacerbated by crying, feeding, agitation and supine position. Self-limiting condition: −− Onset: 2–4 weeks after birth −− Progression: up to 6–8 months after birth −− Resolution: 18 (range: 12–24) months after birth Diagnosis made using awake transnasal flexible laryngoscopy (TNFL): −− Three main types of obstruction Associated gastro-oesophageal reflux in up to 80 % of cases. Severity of the disease: −− Mild to moderate in 80 % of cases −− Severe in 15 % of cases; supraglottoplasty required −− Very severe in 1–3 % of cases; tracheotomy required Prevalence of synchronous airway anomalies varies widely in published literature. Severe stridor, feeding difficulties, failure to thrive, obstructive apnoea, dyspnoea with easy fatigability and severe suprasternal or intercostal retractions warrant a surgical intervention.
P. Monnier (ed.), Pediatric Airway Surgery, DOI: 10.1007/978-3-642-13535-4_6, © Springer-Verlag Berlin Heidelberg 2011
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100
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6 Laryngomalacia (LM)
Chest deformity, pulmonary hypertension and cor pulmonale are signs of chronic obstruction. CO2 laser supraglottoplasty (parameters set to ultrapulse mode, 125 mJoules/cm2, 250 m spot size and 10 Hz repetition rate) is effective in 95 % of Type I and II LMs. The CO2 laser (parameters set to the CW mode, 3 W output power and 500 µ spot size) should be used for Type III LM. Additional epiglottopexy is recommended.
Laryngomalacia (LM) is the most common cause of congenital stridor in infants, accounting for approximately 60% (range 50–75%) of all congenital laryngeal anomalies [8, 16]. Boys are affected twice as often as girls.
6.1 Pathogenesis Laryngomalacia is an enigmatic disease of unknown aetiology. It is believed to be due to a delay in maturation of the supporting laryngeal cartilages, causing an inward collapse of the supraglottic structures on inspiration. Although immaturity of laryngeal cartilages is thought to be a contributing factor [12], this has never been proven histologically [29]. Furthermore, a higher prevalence of LM has not been found in premature newborns compared to full-term newborns [1]. The weak laryngeal tone seen in LM could be more appropriately accounted for by the defective neuromuscular support to the pharyngolaryngeal structures [1]. In 2007, this theory was revisited by DM Thompson [25], who showed that the laryngeal tone and sensorimotor integrative functions were altered in LM, also explaining occasional feeding difficulties encountered in LM [30].
6.2 Symptoms A high-pitched fluttering inspiratory stridor is the hallmark of LM. Typically, the stridor worsens during increased airway demands, such as crying, feeding, or
the child’s being in the supine position. Usually, the course of the disease is self-limiting, with onset around the age of 2–4 weeks, progression to a culminating point at around 6–8 months, and resolution occurring by 2 years of age. Feeding difficulties are related to gastro-oesophageal reflux in up to 80% of cases [7]. Regurgitation, recurrent vomiting, occasional coughing, or choking are seen in moderate to severe cases [13]. Aspiration is often due to uncoordinated breathing and swallowing during deglutition. Hence, this entity has been named discoordinate pharyngolaryngomalacia [6].
6.3 Patient Assessment Mild cases of LM, seen in 80–90% of infants [20], require only diagnostic confirmation conducted in the outpatient clinic by awake transnasal fibreoptic laryngoscopy (TNFL) (see Sect. 3.5.1, Chap. 3). The Holinger classification distinguishes five types of LM [9] and describes the various mechanical anomalies, but is not easily applicable in clinical practice. This may be explained by the similarities between Type I and III LM and the frequent association between Type II and V LM. A modified classification, distinguishing only three LM types, better reflects the endoscopic reality. This three-type classification also appears more appropriate when considering the three different supraglottoplasties used to treat the condition (Fig. 6.1). The three main LM types are identified as follows: Type I: Inward collapse of the aryepiglottic (AE) folds on inspiration Type II: Curled tubular epiglottis with shortened AE folds, which collapses circumferentially on inspiration Type III: An overhanging epiglottis that collapses posteriorly, obstructing the laryngeal inlet on inspiration After diagnostic endoscopy, mild cases of LM do not require surgery. Parents should be reassured about the self-limiting nature of this condition. Additional high-kilovolt plain radiographs of the neck and chest are necessary to rule out any secondary airway lesions (SAL), the incidence of which varies widely in the published literature [5, 11, 21, 23, 28]. Although SAL figures as high as 28.8% in mild cases of LM has been reported [5], the use of endoscopy under general anaesthesia should be decided on a caseby-case basis. In the case of atypical LM with
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6.6 Supraglottoplasty in Suspension Microlaryngoscopy
Fig. 6.1 Types of laryngomalacia: (a) Type I: inward collapse of the aryepiglottic folds. (b) Type II: tubular epiglottis with short aryepiglottic folds. (c) Type III: retroflexed epiglottis with prolapse into the laryngeal inlet
significant worsening of symptoms during the first few months of life, thorough airway endoscopy under general anaesthesia is required.
6.4 Endoscopy Under General Anaesthesia Informed consent must be obtained from the parents before performing diagnostic and therapeutic endoscopies under general anaesthesia. TNFL (see Sect. 5.2.2, Chap. 5) in spontaneous respiration through the face mask facilitates the assessment of the dynamic features of the laryngeal obstruction, permitting, at the same time, the exclusion of synchronous congenital anomalies, such as impaired vocal cord function, subglottic stenosis, and tracheo(broncho)malacia [3, 17, 26]. Airway inspection below the vocal cords using flexible endoscopes is mandatory. Rigid bronchoscopy is then performed to rule out other airway anomalies that may mimic LM symptoms, for example, laryngeal clefts. This technique is more accurate than TNFL for diagnosing minor additional airway lesions. Oesophagoscopy is also performed to detect direct or indirect signs of reflux oesophagitis.
6.5 Indications for Surgical Intervention Indications for supraglottoplasty in the case of LM include severe stridor with compromised airway, feeding difficulties, failure to thrive and obstructive sleep
apnoea [4, 18, 20, 25]. Dyspnoea with severe suprasternal retractions, hypoxaemia and hypercapnoea warrant immediate surgical intervention [22]. Chest deformity, pulmonary hypertension and cor pulmonale are late signs of chronic obstruction [2]. When endoscopic evaluation under general anaesthesia is planned for a child with severe LM (due to an inconclusive TNFL), performing a CO2 laser supraglottoplasty at the same time prevents the need for multiple clinical reassessments. In most cases, a single intervention suffices to relieve the parents’ anxiety.
6.6 Supraglottoplasty in Suspension Microlaryngoscopy Following diagnostic endoscopy and after obtaining the parents’ informed consent, supraglottoplasty in suspension microlaryngoscopy can be performed in a child with severe LM. The Benjamin–Lindholm laryngoscope is the preferred instrument for obtaining wide and full exposure of the pharyngolarynx. Smaller instruments such as Parsons, Karl Storz or Kleinsasser laryngoscopes do not provide the same panoramic view. Although moderate sedation under spontaneous respiration is often used, our approach is to induce deep sedation or full curarization with intermittent apnoeas, enabling us to benefit from a fully immobile larynx during laser work. The child is ventilated through a face mask until the highest possible SpO2 is reached. The suspension laryngoscope, illuminated with a Benjamin–Haves
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6 Laryngomalacia (LM)
light-clip, is positioned during an apnoeic period. To obtain a non-distorted view of the entire larynx, great care should be taken while inserting the blade of the Benjamin–Lindholm laryngoscope into the valleculae. Asymmetric exposure can modify the position of the epiglottis and the AE folds, which may mislead the surgeon as to the amount of mucosa to be resected. The larynx is suspended to allow for the epiglottis to be erect, creating a panoramic view of the supraglottis and glottis. The quality of the endoscopic exposure is the guarantee of a successful intervention. If exposure is not optimal, then an elastic band (Elastoplast®) (see Fig. 4.9, Chap. 4) can be used to exert pressure on the neck to bring the anterior commissure into the field of view. When exposure is optimal, reassessment of the supraglottis, glottis and subglottis with a rigid rod-lens telescope is performed. A careful intubation using a soft Portex Blue Line® tube of the appropriate size is then performed through the laryngoscope under visual control, following which the child is re-ventilated. This technique of intermittent ventilation and apnoea provides ample time to install a microscope equipped with a three-CCD Digital camera and a CO2 laser micromanipulator attached to the articulated arm of the laser console. Set at 400 mm focal length, the microscope provides an unsurpassed stereoscopic view to the surgeon who has to perform a delicate procedure on a small infant larynx.
A debate exists as to which technique of mucosal resection is the most appropriate, that is, cold knife versus carbon dioxide laser. With the superpulse or ultrapulse technology, the CO2 laser is more precise than microscissors to resect the desired amount of tissue without causing any bleeding. Furthermore, depending on the child’s individual situation, the CO2 laser allows for additional vaporisation of tissue to obtain a tailored resection. If proper CO2 laser parameters are used, then a char-free resection with less than 50 m (four to five cells) depth of coagulation necrosis is achieved (see Fig. 4.29, Chap. 4). This technique offers more versatility and precision than a microscissors resection. Bilateral mucosal resection can always be performed during two to four apnoeic periods. Before starting the procedure, proper alignment of the pilot He-Ne laser with the CO2 laser must be checked using a wooden tongue depressor (see Fig. 4.34, Chap. 4). To get the most precise cutting effect of the laser, optimal focussing of the spot size is necessary. In the case of LM Type I or Type II (Fig. 6.2), supraglottoplasty using the CO2 laser is performed with the following parameters:
Fig. 6.2 Extent of mucosal resection during CO2 laser supraglottoplasty: (a) Type I laryngomalacia: the redundant mucosa of the aryepiglottic fold is excised. Enough mucosa should be preserved at the posterior laryngeal commissure. The pharyngo-
epiglottic fold should not be transected (arrows). (b) Type II laryngomalacia: trimming of the lateral edges of the epiglottis and resection of the short aryepiglottic folds. The laser cut must remain medial to the pharyngo-epiglottic fold (arrows)
• CO2 laser set to ultrapulse mode, 125-mJoules/cm2, and 10-Hz repetition rate • Highly focused, 250 m spot size at a 400-mm working distance (focal length)
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6.6 Supraglottoplasty in Suspension Microlaryngoscopy
6.6.1 Type I Laryngomalacia (Fig. 6.2a) The redundant mucosa of the AE is delicately grasped on one side using a Bouchayer heart-shaped microforceps. The mucosa is pulled slightly towards the pharyngeal side, and an incision is made starting at the level of the corniculate cartilage along the AE fold. The upper lateral limit of resection should never transect the pharyngo-epiglottic fold that lies slightly laterally to the lateral edge of the epiglottis. The incised mucosa is then reflected towards the laryngeal inlet, and the CO2 laser section is carried out on the pharyngeal aspect of the AE fold. The interarytenoid mucosa must be fully preserved to avoid supraglottic cicatricial stenosis. Once the mucosa has been removed from the AE fold, additional vaporisation of the cuneiform cartilage and the bed of the laser wound produces a small groove, thereby reapproximating to some extent the endolaryngeal and pharyngeal mucosae. This resection takes approximately 1–2 min, which is within the limits of an apnoeic period. Proper communication with the anaesthetist during the entire procedure is indispensable for a successful outcome. If the SpO2 drops sooner than expected, then laser work must be stopped, and the endotracheal tube must be temporarily re-inserted until the SpO2 reaches a level above 95%. Laser work is completed during another apnoeic period, and the same intervention is then carried out on the opposite side using the same technique of intermittent apnoeas. There is no evidence that performing unilateral supraglottoplasty decreases the incidence of cicatricial supraglottic stenosis. In fact, the wrong laser
settings and inappropriate surgical techniques are the main causes leading to unacceptable complications [10, 19].
6.6.2 Type II Laryngomalacia (Fig. 6.2b) The endoscopic trimming of a severely curled tubular epiglottis is more delicate and potentially more liable to lead to complications than the relatively simpler resection of redundant AE folds seen in Type I LM. Type II LM is also associated with short, high and redundant AE folds. The lines of resection must be carried out using the same CO2 laser parameters as those used for the treatment of Type I LM. It is essential that only a small rim of the epiglottic portion curled over the laryngeal inlet be resected or vaporised. The adjacent mucosa is shielded with laser platforms to avoid unwanted laser strikes on the normal mucosa. The laser cut should not transect the pharyngo-epiglottic fold that lies slightly laterally to the insertion of the epiglottis at this level. This is mandatory in order to avoid potential postoperative aspiration. The laser resection is then carried out along the AE folds as done in the case of Type I LM. The advantage of the CO2 laser over cold knife excision is that it offers the possibility of vaporising additional tissue until the appropriate surface and depth of resection are obtained. This cannot be achieved with the same precision when using cold instruments. The identical procedure is repeated on the opposite side during subsequent apnoeic periods (Fig. 6.3).
Fig. 6.3 Supraglottoplasty for type II laryngomalacia: (a) Preoperative view: curled, tubular epiglottis. (b) Peroperative view: CO2 laser resection with preservation of the pharyngo-epiglottic folds. (c) Postoperative view at 3 months: open laryngeal inlet
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6.6.3 Type III Laryngomalacia (Fig. 6.4) In the case of Type III LM, the following CO2 laser parameters should be used: • CW mode, set at 3–5 W output power • Slightly defocused beam at 400-mm focal length The weaker power density thus obtained using these parameters generates more coagulation necrosis. Absence of bleeding at the tongue base, valleculae and epiglottis with more cicatricial retraction is the desired tissue effect in Type III LM. The infant is intubated transnasally using a 3.0 Portex Blue Line® tube. The blade of the Benjamin– Lindholm laryngoscope is positioned about 1 cm proximally to the valleculae to provide a symmetrical exposure of the lingual aspect of the epiglottis and the posterior third of the tongue base. Wet gauzes are placed on the ET tube to protect it from accidental laser strikes. Using the CO2 laser set at 3 W of output power in the CW mode with a slightly defocused beam of 500 m in diameter (power density ~1,200 W/cm2), an ovalshaped laser wound is thus created, half on the tongue base and half on the epiglottis. The raw surface will evolve into cicatricial retraction during the healing phase, attracting the epiglottis towards the tongue base. This improves access to the laryngeal inlet. However, it
Fig. 6.4 Treatment diagram for type III laryngomalacia: (a) A laser wound is created on the tongue base and lingual aspect of the epiglottis (yellow arrows). (b) An epiglottopexy is performed, using 4.0 vicryl sutures to stitch the epiglottis to the tongue base with an endoscopic needle-holder
6 Laryngomalacia (LM)
is preferable to fix the epiglottis to the tongue base with two 4.0 transfixion Vicryl sutures. A Microfrance endoscopic needle holder is used to place the transepiglottic stitches. The stitches should appear at the level of the valleculae where they are then recaptured before being re-inserted through the tongue base. The knots are tied with the knot pusher on the tongue base. The final result of this epiglottopexy should display open access to the supraglottis and laryngeal inlet (Fig. 6.5). Despite the advances in surgical techniques, a tracheostomy is still necessary for 3% of patients with LM [24], most often as a result of associated comorbidities, such as discoordinate pharyngolaryngeal functions [22] [6].
6.7 Postoperative Care If the child does not present any comorbidity or synchronous airway lesions, then immediate extubation is possible after surgery, along with admission to the PICU for overnight monitoring. In the absence of any comorbidity, children under 1 year of age are likely to respond as well as older children. Corticosteroids must be administered intra-operatively and be continued for a few days after surgery. Due to the small size of the mucosal defects created during the supraglottoplasty,
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6.8 Complications and Results Fig. 6.5 Supraglottoplasty for type III laryngomalacia: (a) Preoperative view: epiglottic prolapse obstructing the laryngeal inlet. (b) Postoperative view: the epiglottis adheres to the tongue base, providing better access to the laryngeal inlet
peri-operative antibiotics are unnecessary for Types I and II LM. A nasogastric tube is not inserted unless a history of aspiration is present. In the case of Type III LM, a 5-day course of antibiotics is given to avoid a superinfection of the wound and a breakdown of the epiglottopexy sutures. Depending on the initial treatment of the infant, proton pump inhibitors (PPI) are administered twice daily. The decision to keep the infant or child intubated overnight is related to the severity of the disease and the associated comorbidities rather than the patient’s age.
6.8 Complications and Results The risk of complications is minimal provided the aforementioned parameters are respected. The 4% risk of supraglottic stenosis reported in a few series [19] may be accounted for by excessive mucosal removal. With the use of modern technology and precise surgical techniques, staged unilateral supraglottoplasty is not indicated [19]. Superinfection may occur and should be anticipated when bronchoscopy reveals an infected lower airway. After taking bacteriological aspirates for culture, antibiotics should be started empirically. In the literature, the reported complication rate is roughly 8% [4]. The reported success rates for supraglottoplasty range from 69% to 94% [4, 13–15, 18–20, 22, 25–27]. Of note is that the results may be influenced by the severity of LM and the presence of associated comorbidities or SAL. In our unpublished series of 45 infants and children without comorbidities, CO2 laser supraglottoplasty resulted in a resolution of symptoms in 96.5% of the cases.
References 1. Belmont, J.R., Grundfast, K.: Congenital laryngeal stridor (laryngomalacia): etiologic factors and associated disorders. Ann. Otol. Rhinol. Laryngol. 93, 430–437 (1984) 2. Benjamin, B.: Congenital disorders of the larynx. In: Cummings, C.H., Frederickson, J.M. (eds.) Otolaryngol Head Neck Surg, pp. 1831–1853. Mosby year book, St. Louis/Baltimore (1993) 3. Cotton, R.T., Prescott, C.A.: Congenital anomalies of the larynx. In: Cotton, R.T., Myer III, C.H.M. (eds.) Practical Pediatric Otolaryngology, pp. 497–514. Lippincott-Raven, Philadelphia/New York (1999) 4. Denoyelle, F., Mondain, M., Gresillon, N., et al.: Failures and complications of supraglottoplasty in children. Arch. Otolaryngol. Head Neck Surg. 129, 1077–1080 (2003) 5. Dickson, J.M., Richter, G.T., Meinzen-Derr, J., et al.: Secondary airway lesions in infants with laryngomalacia. Ann. Otol. Rhinol. Laryngol. 118, 37–43 (2009) 6. Froehlich, P., Seid, A., Denoyelle, F., et al.: Discoordinate pharyngolaryngomalacia. Int. J. Pediatr. Otorhinolaryngol. 39, 9–18 (1997) 7. Giannoni, C., Sulek, M., Friedman, E.M., et al.: Gastroe sophageal reflux association with laryngomalacia: a prospective study. Int. J. Pediatr. Otorhinolaryngol. 43, 11–20 (1998) 8. Holinger, L.D.: Etiology of stridor in the neonate, infant and child. Ann. Otol. Rhinol. Laryngol. 89, 397–400 (1980) 9. Holinger, L.D.: Congenital laryngeal anomalies. In: Holinger, L.D., Lusk, R.P., Green, C.G. (eds.) Pediatric Laryngology and Bronchoesophagology, pp. 139–142. Lippincott-Raven, Philadelphia/New York (1997) 10. Kelly, S.M., Gray, S.D.: Unilateral endoscopic supraglottoplasty for severe laryngomalacia. Arch. Otolaryngol. Head Neck Surg. 121, 1351–1354 (1995) 11. Krashin, E., Ben-Ari, J., Springer, C., et al.: Synchronous airway lesions in laryngomalacia. Int. J. Pediatr. Otorhinolaryngol. 72, 501–507 (2008) 12. Lane, R.W., Weider, D.J., Steinem, C., et al.: Laryngomalacia. A review and case report of surgical treatment with resolution of pectus excavatum. Arch. Otolaryngol. 110, 546–551 (1984)
106 13. Lee, K.S., Chen, B.N., Yang, C.C., et al.: CO2 laser supraglottoplasty for severe laryngomalacia: a study of symptomatic improvement. Int. J. Pediatr. Otorhinolaryngol. 71, 889–895 (2007) 14. Loke, D., Ghosh, S., Panarese, A., et al.: Endoscopic division of the ary-epiglottic folds in severe laryngomalacia. Int. J. Pediatr. Otorhinolaryngol. 60, 59–63 (2001) 15. Martin, J.E., Howarth, K.E., Khodaei, I., et al.: Aryepi glottoplasty for laryngomalacia: the Alder Hey experience. J. Laryngol. Otol. 119, 958–960 (2005) 16. Narcy, P., Bobin, S., Contencin, P., et al.: Laryngeal anomalies in newborn infants. A propos of 687 cases. Ann. Otolaryngol. Chir. Cervicofac. 101, 363–373 (1984) 17. Olney, D.R., Greinwald Jr., J.H., Smith, R.J., et al.: Laryngomalacia and its treatment. Laryngoscope 109, 1770–1775 (1999) 18. Polonovski, J.M., Contencin, P., Francois, M., et al.: Aryepiglottic fold excision for the treatment of severe laryngomalacia. Ann. Otol. Rhinol. Laryngol. 99, 625–627 (1990) 19. Reddy, D.K., Matt, B.H.: Unilateral vs. bilateral supraglottoplasty for severe laryngomalacia in children. Arch. Otolaryngol. Head Neck Surg. 127, 694–699 (2001) 20. Roger, G., Denoyelle, F., Triglia, J.M., et al.: Severe laryngomalacia: surgical indications and results in 115 patients. Laryngoscope 105, 1111–1117 (1995) 21. Sakakura, K., Chikamatsu, K., Toyoda, M., et al.: Congenital laryngeal anomalies presenting as chronic stridor: a retrospective study of 55 patients. Auris Nasus Larynx 35, 527–533 (2008)
6 Laryngomalacia (LM) 22. Senders, C.W., Navarrete, E.G.: Laser supraglottoplasty for laryngomalacia: are specific anatomical defects more influential than associated anomalies on outcome? Int. J. Pediatr. Otorhinolaryngol. 57, 235–244 (2001) 23. Shugar, M.A., Healy, G.B.: Coexistant lesions of the pediatric airway. Int. J. Pediatr. Otorhinolaryngol. 2, 323–327 (1980) 24. Sichel, J.Y., Dangoor, E., Eliashar, R., et al.: Management of congenital laryngeal malformations. Am. J. Otolaryngol. 21, 22–30 (2000) 25. Thompson, D.M.: Abnormal sensorimotor integrative function of the larynx in congenital laryngomalacia: a new theory of etiology. Laryngoscope 117, 1–33 (2007) 26. Toynton, S.C., Saunders, M.W., Bailey, C.M.: Aryepiglottoplasty for laryngomalacia: 100 consecutive cases. J. Laryngol. Otol. 115, 35–38 (2001) 27. Whymark, A.D., Clement, W.A., Kubba, H., et al.: Laser epiglottopexy for laryngomalacia: 10 years’ experience in the west of Scotland. Arch. Otolaryngol. Head Neck Surg. 132, 978–982 (2006) 28. Yuen, H.W., Tan, H.K., Balakrishnan, A.: Synchronous airway lesions and associated anomalies in children with laryngomalacia evaluated with rigid endoscopy. Int. J. Pediatr. Otorhinolaryngol. 70, 1779–1784 (2006) 29. Zalzal, G.H., Anon, J.B., Cotton, R.T.: Epiglottoplasty for the treatment of laryngomalacia. Ann. Otol. Rhinol. Laryngol. 96, 72–76 (1987) 30. Zoumalan, R., Maddalozzo, J., Holinger, L.D.: Etiology of stridor in infants. Ann. Otol. Rhinol. Laryngol. 116, 329–334 (2007)
7
Vocal Cord Paralysis (VCP)
Contents 7.1 Unilateral Vocal Cord Paralysis (UVCP)............. 108 7.1.1 Surgical Intervention................................................. 109 7.2 Bilateral Vocal Cord Paralysis (BVCP)................ 109 7.2.1 Aetiology of BVCP.................................................. 110 7.2.2 Surgical Treatment for BVCP................................... 110 References............................................................................ 116
Core Messages
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most common (15–20%) congenital laryngeal anomaly. With the exception of traumatic sections of the RLN(s), VCP is caused by dysfunctional laryngeal innervations without complete muscular flaccidity or denervations. Associated upper airway pathological conditions are observed in 45% of the cases. Unilateral vocal cord paralysis (UVCP). –– Prevalence: ~48% of all VCPs –– Mild stridor with hoarse, breathy cry and feeding difficulties (aspiration) –– Main aetiology: injury to the peripheral nervous system –– Most frequent causes: cardiovascular (~50%) and oesophageal surgeries for congenital mediastinal anomalies –– Tendency for natural voice improvement –– Watchful follow-up with no invasive treatment –– Tracheotomy rarely needed (~8% of the cases) Bilateral vocal cord paralysis (BVCP): –– Prevalence: ~52% of all VCPs. –– High-pitched stridor with dyspnoea, apnoeic spells and cyanosis but normal voice. –– Main aetiologies: congenital disorders of the central nervous system, traumatic and idiopathic causes. –– Neurogenic BVCP must be differentiated from cicatricial posterior glottic stenosis (PGS). –– Tracheotomy is required in approximately 53% (50–65%) of the cases. –– Forty-six to sixty-four percent of all children affected by BVCP recover spontaneously dur-
P. Monnier (ed.), Pediatric Airway Surgery, DOI: 10.1007/978-3-642-13535-4_7, © Springer-Verlag Berlin Heidelberg 2011
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ing the first 6–12 months of life and up to 10% after the age of 5 years. –– Watchful follow-up until 2 years of age, before any surgical intervention is planned. –– The multitude of surgical options reflect an absence of consensus regarding treatment. –– The least invasive treatment is preferred.
In the paediatric population, BVCP is the second most common congenital laryngeal anomaly, and its prevalence (~10–15%) in newborns is four to six times lower than that of laryngomalacia (~60% of the cases). A mild inspiratory stridor along with a hoarse, breathy cry and feeding difficulties (aspiration) are suggestive of UVCP. In contrast, a high-pitched inspiratory stridor with a normal voice, apnoeic spells and cyanosis are consistent with BVCP. Awake transnasal flexible laryngoscopy (TNFL) is essential to confirm the clinical diagnosis. Yet, interpretation of this test may not be straightforward for the following reasons: global pharyngolaryngeal movements overlying supraglottic structures, retention of secretions and large overhanging arytenoids obscuring the abductive movements of the vocal cords. In BVCP, the absence of complete muscular denervation and the Bernouilli effect may provide a false impression of preserved adduction, resulting in a paradoxical movement of glottic closure during inspiration. In a normally functioning larynx, true abductive movements of the vocal cords should occur with each inspiration, although the use of sedative drugs may affect the mobility of the vocal cords. In UVCP, this abductive movement must be clearly identified on one side. A formal microlaryngoscopy and bronchoscopy under general anaesthesia are essential in the assessment of the entire upper airway. Endoscopy under general anaesthesia is aimed at: • Assessing vocal cord mobility when awake office TNFL has failed • Differentiating BVCP from PGS • Searching for associated lesions of the upper airways
Anaesthesia under spontaneous respiration must be titrated in such a way that it provides adequate sedation without suppressing active abduction of the vocal cords during inspiration (Sect. 5.2.1, Chap. 5). Long sessions of endoscopy video recording under different levels of anaesthesia help achieve this goal. Reassessment of the video recordings is the safest way to achieve the correct diagnosis. To differentiate BVCP from PGS, suspension microlaryngoscopy (see Sect. 5.3.3.2, Chap. 5) is carried out and represents an important part of the endoscopic investigation, especially in the case of prior endotracheal intubation. In all cases of BVCP, a complete broncho-oesophagoscopy is warranted to rule out associated upper airway diseases. In approximately 45% of the cases, BVCP is associated with upper airway diseases, among which the most common are laryngomalacia, tracheo(broncho)malacia and subglottic stenosis [14]. Once UVCP, BVCP or PGS with or without cricoarytenoid joint fixation has been firmly diagnosed, the aetiology of the condition must be investigated and the different treatment options discussed.
7.1 Unilateral Vocal Cord Paralysis (UVCP) Slightly less common in newborns than BVCP, UVCP is characterised by a mild, position-dependent inspiratory stridor with a hoarse, breathy cry and potential feeding difficulties (aspiration) [55]. In newborns, UVCP paralysis mostly results from an injury to the peripheral nervous system [19] during a difficult delivery. In contrast, UVCP paralysis in infants occurs mainly following a surgical iatrogenic injury to the vagus or the recurrent laryngeal nerve (RLN). In 50% of the cases, these injuries are linked to cardiovascular surgery for ligation of patent ductus arteriosus or correction of heart defects and vascular mediastinal anomalies [17, 29, 41], oesophageal surgery for atresia with tracheo-oesophageal fistula [45, 46] or as a sequela of oesophagectomy for caustic injuries later in life [5, 16, 49]. Paediatric UVCP has received less medical attention than BVCP as it does not require any therapy in the majority of cases. A few cases are likely to remain undiagnosed as natural improvement in the voice occurs over time even when the VC mobility does not
7.2 Bilateral Vocal Cord Paralysis (BVCP)
return to normal [10, 19]. Contrary to BVCP, tracheotomy is seldom needed. In the published literature, approximately 8% of UVCP require tracheostomy for intractable aspiration [55]. Watchful follow-up with dietary recommendations is usually sufficient. The infant should be fed on the affected side during meals, and fluids should be thickened with an appropriate powder (Thicken-up®) to allow for adequate nutritional intake and weight gain. During sleep, the same position contributes to decrease the inspiratory stridor.
7.1.1 Surgical Intervention Tracheotomy for UVCP is indicated in the case of dyspnoea or persistent aspiration. Even if vocal cord mobility is not restored, improvement in the voice does occur over time because of compensatory mechanisms [28]. Vocal cord medialisation should be reserved for older children and adolescents when speech therapy has not proved efficient in treating dysphonia. Preference should be given to autologous fat [51] or human-derived (Cymetra® collagen) [12] materials, even though partial resorption has been reported with both substances [11, 31]. Fat must be injected through an 18- or 19-gauge needle, laterally to the thyroarytenoid muscle with a pressurised injection device such as a Brüning syringe. Cymetra® collagen must be injected into the thyroarytenoid muscle [39]. Two to three injection points (one lateral to the arytenoid
Fig. 7.1 Fat and collagen injection sites for vocal cord medialisation: (a) Axial view: three injection sites are needed to obtain homogenous medialisation of the vocal cord. (b) Coronal view: fat is injected deeply, laterally to the thyroarytenoid muscle, and Cymetra collagen is injected into the thyroarytenoid muscle
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cartilage) facilitate a more homogenous medialisation, with minimal residual posterior glottic chink (Fig. 7.1). Non-resorbable materials, such as silicone paste (Vox-implant®) [58], teflon [32] or calcium hydroxylapatite [2], should not be injected into a growing larynx because of their irreversible and unpredictable long-term effects [57]. Conversely, laryngeal framework surgery (thyroplasty Type I), during which a lateral window is created in the ala of the thyroid cartilage, should be reserved for adults; the same applies to the use of silicone, hydroxylapatite, Gore-Tex® [38] or titanium implants [54] for medialisation. Reinnervation procedures are an interesting way of maintaining muscle tone and bulk in a paralysed VC. The ansa hypoglossal-RLN anastomosis [13] and nerve-muscle pedicle implantation into the lateral thyroarytenoid muscle [24] have proven to be effective in restoring a good voice after UVCP [57]. Yet, these techniques are seldom used in clinical practice and are usually limited to specialised centres [37].
7.2 Bilateral Vocal Cord Paralysis (BVCP) BVCP accounts for slightly more than 50% of all paediatric VCPs. Clinically, it is characterised by a highpitched stridor along with a normal or near normal cry. Signs of respiratory distress with suprasternal and chest retractions are present, with exacerbations noted
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during increased airway demands. Indications of airway stabilisation include failure to thrive, spells of apnoea, or cyanotic attacks. Contrary to UVCP, tracheotomy is required to secure the airway in roughly 50% of patients with BVCP [55]. This rate is even higher if one takes into account the newborn or infant with significant comorbidities, that is, neurological disorders, bronchopulmonary dysplasia or severe gastro-oesophageal reflux. Narcy et al. advocated long-term intubation with a periodic reassessment of the VC mobility because with this technique, 53% of their patients recovered within the first 3 months of life [15, 42]. However, this series was biased by the inclusion of UVCP patients in the outcome analysis. Furthermore, owing to prolonged intubation, the advantage of avoiding tracheostomy is offset by the risk of developing PGS. More recently, monitoring in the PICU using nasal CPAP along with enteral feeding has been proposed as an alternative method to buy time until spontaneous recovery of VC function occurs. The main problem with this method is that CPAP and enteral feeding need to be continued for several weeks, representing a prolonged period of discomfort for the child.
7.2.1 Aetiology of BVCP In infants and children, BVCP is mainly due to neurological, traumatic and idiopathic causes [14, 40, 52, 61]. When the cause is neurological, the Arnold–Chiari II malformation accounts for about one-third of the cases. Concomitant hydrocephalus, myelomeningocele, intracerebral haemorrhage or other CNS conditions may stretch or compress the vagus nerve or damage its nuclei. In BVCP patients, magnetic resonance imaging (MRI) is necessary to detect any central nervous system pathology. Birth trauma is the most common cause of traumatic BVCP. In this case, VCP may be unilateral or bilateral [14, 17]. A significant number of BVCPs are idiopathic in origin [14, 17, 52] and recover spontaneously in roughly 50% of the cases within 1 or 2 years [7]. However, Daya et al. [14] reported that in 10% of their patients, recovery took more than 5 years, and in isolated cases reported in literature, recovery even took 9–11 years [23, 43]. Delayed maturation in the vagal
7 Vocal Cord Paralysis (VCP)
nuclei has been proposed as the likely mechanism to explain late vocal cord function recovery [1]. Neck ultrasonography is a reliable tool for assessing the return of vocal cord function, alleviating the need for laryngoscopy during the follow-up period [20, 59].
7.2.2 Surgical Treatment for BVCP Once the diagnosis of BVCP has been established by TNFL, it is confirmed under general anaesthesia. The presence of PGS (see Sect. 5.3.3.2, Chap. 5) and other upper airway anomalies must be ruled out. Based on the aetiology and severity of the condition, various treatment options may be considered. If urgent stabilisation of the airway is required, then the infant should first be intubated, and an emergency MRI should be conducted. A Type II Arnold–Chiari malformation with hydrocephalus can benefit from a shunt as this procedure decreases the high intracranial pressure at the origin of a stretching of the vagus nerve. The subsequent recovery of VC movements alleviates the need for tracheostomy. Despite all of these measures, a tracheostomy must be performed in 50% of all patients diagnosed with BVCP [55]. Since spontaneous recovery has been noted to occur within 12–24 months in idiopathic BVCP cases and in 46–64% of iatrogenic BVCP cases [3], it is reasonable to wait until the child reaches 2 years of age before any surgery is envisaged. Deferring definite treatment until the child reaches adolescence to include her/him in the treatment decision-making process will only prolong the tracheostomy dependence. The advantage of providing possibilities for a spontaneous recovery of VC functions is offset by the social handicap of living with a tracheostomy, even though a cannula with a speaking-valve does not significantly compromise the communication skills in children with BVCP. The optimal time of surgical intervention must be discussed on a case-by-case basis. A poor social environment may require early decannulation, whereas a patient with a supportive family circle may be willing to wait for a longer time before definitive surgery is considered. Among the multiple options that are available to the surgeon, there is no fixed treatment algorithm to solve this problem. The dilemma resides in the fact that any surgery that widens the glottic chink further deteriorates the quality and volume of the voice. Conceptually, the least invasive and damaging procedure for the larynx
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7.2 Bilateral Vocal Cord Paralysis (BVCP)
should be selected in an effort to avoid irreversible sequelae that would compromise a late recovery of VC movements. Over the years, several techniques to enlarge the glottic airway have been developed to achieve decannulation. They fall into two main groups: open and endoscopic surgeries. • Open surgery: –– Arytenoidopexy using the lateral approach [15, 42] –– Arytenoidectomy ± lateralisation through laryngofissure [6] or lateral approach [42] –– Arytenoid separation by posterior cricoid split and cartilage grafting [25, 53] • Endoscopic surgery: –– CO2 laser arytenoidectomy [47] –– CO2 laser posterior cordotomy [18] –– Arytenoidopexy with the Lichtenberger needlecarrier [34] –– Posterior cricoid split with cartilage grafting [30] Chen and Inglis appropriately mentioned in their review on BVCP in children [8]: Evaluation and comparison of the relative merits of individual techniques are hindered by a) a lack of objective outcomes regarding voice and swallowing in children, b) the variety of comorbidities present, c) the differing degrees of underlying airway obstruction present, and d) the relatively small number of affected children within a given institution.
Another factor that could be added to the list is the surgeon’s expertise with a specific surgical technique. Decannulation rate following surgery remains the most common outcome measure in the published literature. Although voice quality following surgery appears to be satisfactory, no data pertaining to this issue is available in the literature. Irrespective of the surgical procedure used, the final result is likely to be a trade-off between airway patency and voice quality.
larynx by reflecting the sternocleidomastoid muscle and great vessels laterally, the inferior constrictor muscle is incised along the posterior edge of the thyroid ala. The mucosa of the piriform fossa is elevated on its lateral and medial portions without opening the pharynx. In children whose thyroid cartilage is soft and pliable, disarticulation of the cricothyroid joint is not necessary. The arytenoid cartilage is exposed by simply pulling the thyroid cartilage anteriorly with a hook. The arytenoid can be either removed (arytenoidectomy) or sutured laterally to the thyroid ala (arytenoidopexy), or a combined procedure (arytenoidectomy with suture lateralization of the vocal process) may be used (Fig. 7.2). Excellent results with this technique have been reported by Narcy [42], Priest [48], and Cohen [9].
Laryngofissure Approach A laryngofissure approach for performing the three abovementioned procedures has also been recommended. A full vertical midline incision of the thyroid cartilage is made, and the arytenoid is removed on one side, either partially [26] or totally [7]. It is recommended that the vocal ligament be lateralised with a suture placed at the former vocal process, as this procedure seems to increase the decannulation rate [26] (Fig. 7.3).
7.2.2.2 Endoscopic Surgical Techniques As early as 1952, endoscopic arytenoidectomy using electrocautery was advocated by Thornell [56]. The
7.2.2.1 Open Surgical Techniques Postero-lateral Approach to the Larynx The first article dealing with an arytenoidectomy through a postero-lateral approach with suture lateralisation of the vocal process was published in 1946 by Woodman [60]. After exposing the lateral aspect of the
Fig. 7.2 External lateral approach for arytenoidectomy with suture lateralisation of the vocal process
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7 Vocal Cord Paralysis (VCP)
Fig. 7.3 Laryngofissure approach for arytenoidectomy, with suture lateralisation of the vocal process: (a) Laryngofissure. (b) Arytenoidectomy and vocal cord lateralisation. (c) End result
Fig. 7.4 Submucosal CO2 laser arytenoidectomy: (a) Mucosal flap design. (b) Medial reflexion of the mucosal flap with exposure of the arytenoid. (c) Posterior reflexion of the mucosal flap into the arytenoidectomy bed
advent of the CO2 laser has widely popularised this technique, first described by Ossoff in 1984 [47]. This technique is extensively used in adults and has been refined over the years in an effort to avoid recurrent scarring of the arytenoidectomy bed, resulting in recurrent airway stenosis. Granulation tissue formation and subsequent scarring appear to occur more often in children in than adults.
CO2 Laser Arytenoidectomy (Fig. 7.4) Usually, the intervention is performed on tracheostomised children as this situation provides a free operative field of the entire larynx. The largest laryngoscope possible to maximise exposure of the posterior glottis is used. The CO2 laser is set to ultrapulse mode, 150
mJoules/cm2, and a 10-Hz repetition rate. The laser spot is sharply focused to 250 m at a 400-mm focal distance. A large curve-shaped mucosal flap, starting at the vocal process of the arytenoid and reaching the aryepiglottic fold on its laryngeal side, is created (Fig. 7.4a). This sharp incision can only be performed when using the aforementioned CO2 laser parameters. The mucosa is gently grasped with heart-shaped Bouchayer forceps and then elevated and reflected medially by submucosal dissection with the CO2 laser (Fig. 7.4b). In children, the arytenoid is never calcified, which allows the surgeon to vaporise the cartilage progressively without causing any bleeding. A thin layer of cartilage should be preserved on the posterior aspect of the arytenoid to avoid inward collapse of the arytenoid mucosa during inspiration after the arytenoidectomy bed has completely healed. Likewise, a small portion of the
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7.2 Bilateral Vocal Cord Paralysis (BVCP)
muscular process of the arytenoid must be preserved in order to avoid bleeding and monopolar coagulation capable of generating granulation tissue formation and rescarring. Anteriorly, the vocal ligament is detached from the vocal process of the arytenoid. Medially, great care must be taken to remove the arytenoid cartilage completely without tearing the mucosal flap. At the cricoarytenoid joint level, additional tissue is vaporised submucosally to identify the cricoid plate. Anteriorly, the mucosal flap is completely cut below the vocal ligament until it is freely mobile except for its medial attachment. The arytenoidectomy bed should be char-free, thereby affirming that minimal thermal damage has been scattered in the surrounding tissues. Following this, mitomycin-C (2 mg/mL) soaked in a cotton-swab is applied topically to the arytenoidectomy bed for 2 min [50]. The mucosal flap is then reflected into the arytenoidectomy bed where it is fixed in place with fibrin-thrombin glue (Tisseel®) (Fig. 7.4c). The efficacy of open versus endoscopic arytenoidectomy in children has been investigated by Bower et al. [6] and by Brigger and Hartnick [7, 26]. In both series, external arytenoidectomy with lateralisation was found to be superior to endoscopic-CO2 laser arytenoidectomy. However, both series originate from the same group, while a recent update is being carried out by Harnick in 2003 [26]. With the use of more sophisticated CO2 laser techniques and more refined surgical techniques, the results of paediatric CO2 laser arytenoidectomy are likely to improve (Fig. 7.5).
Fig. 7.5 Left arytenoidectomy for BVCP in a 14 year-old adolescent: (a) Design of the mucosal flap with the CO2 laser set to ultrapulse mode, 150 mJ/cm2, and 250 m spot-size: the aryepiglottic fold and posterior part of the cuneiform cartilage are preserved to avoid aspiration. (b) Situation after arytenoidectomy: the medially pedicled flap of mucosa is preserved and still
Endoscopic CO2 Laser Posterior Cordotomy This procedure, described by Dennis and Kashima in 1989 [18], is fast and easy to perform. A simple transection from the vocal process of the arytenoid through the vocal ligament, false vocal cord and ventricle is performed, with the thyroid cartilage as a lateral extent (Fig. 7.6). Additional partial vaporisations of the vocal process of the arytenoid and posterior one-third of the vocal ligament may be carried out [21]. The thyroarytenoid muscle is then completely transected and retracted anteriorly, thus creating a wide posterior opening. Some authors have combined this intervention with total arytenoidectomy, with the objective of further increasing the posterior glottic chink [4]. Because of these surgical techniques, decannulation may be achieved in all of the patients. The question, however, will be how much residual voice may be preserved while creating a patent airway.
Endoscopic Vocal Cord Lateralization In this technique proposed by Lichtenberger, endoextralaryngeal suture lateralization of one arytenoid is performed by using the Lichtenberger needle carrier [36], as a reversible method to avoid tracheotomy [33]. The larynx is exposed in suspension microlaryngoscopy. The distal tip of the needle carrier is placed just above the vocal process of one arytenoid, and the
attached to the vocal process of the arytenoid (white arrow). Please note the char-free arytenoidectomy bed. (c) After CO2 laser section of the mucosal flap at the vocal process of the arytenoid, it is reflected laterally into the posterior aspect of the arytenoidectomy bed, thus preventing recurrent obliterating cicatricial stenosis (dotted white line)
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Fig. 7.6 CO2 laser posterior cordotomy: a simple transverse section from the vocal process of the arytenoid to the lateral thyroid cartilage creates a wedge-opening of the glottis with anterior retraction of the thyro-arytenoid muscle (arrow)
7 Vocal Cord Paralysis (VCP)
In the literature, reported experience with this technique pertains mostly to adults [33], with updates on 94 patients published in 2002 and 2003 [34, 35]. A 95% success rate (89 of 94 patients) has been reported, which in several cases was associated with vocal cord function recovery and subsequent removal of sutures. Although an adaptation of the technique to newborns has not yet been published, close attention should be paid to this procedure as a potentially reversible method to enlarge the glottic chink in congenital BVCP. Unpublished results (personal communication) show that the threads progressively cut through the arytenoid cartilage, generating granulation tissue formation. Further experience is needed before any definite conclusions may be drawn.
Endoscopic Posterior Cricoid Split and Rib Grafting
Fig. 7.7 Endoscopic vocal cord lateralisation with the Lichtenberger endo-extra-laryngeal suture technique: a nonresorbable 4.0 prolene suture is placed around the vocal process of the arytenoid and tied on the external aspect of the thyroid cartilage. A second stitch is often used to improve lateralisation
needle is then pushed through the thyroid cartilage and skin of the neck. The second point of entrance in the larynx is situated just below the vocal process of the cord, and the needle is again reintroduced through the thyroid ala and the skin. A second 3.0 prolene suture is placed slightly posteriorly to the first stitch in order to secure the lateralization procedure. A small skin incision is performed between the exit points of the threads. The threads are then recaptured under the skin by skin hooks and tied on the sternohyoid muscle, and the skin is closed. In the case of subsequent recovery of vocal cord motion, the suture may be removed (Fig. 7.7).
This technique consists of a posterior enlargement of the interarytenoid space by CO2 laser division of the cricoid plate and endoscopic interposition of a costal cartilage graft [8, 25, 30, 53]. As described by Chen and Inglis [8], adequate endoscopic exposure of the cricoid plate is a prerequisite to performing this surgery. Minimal suspension of the larynx and anterior lifting of the tracheostomy tube provide better exposure of the cricoid plate, enabling the surgeon to perform the vertical midline incision with the CO2 laser. Spreaders are used to facilitate this manoeuvre until the cricoid plate is fully transected. To achieve optimal cutting properties, the laser must be set to ultrapulse mode with 150 mJ/cm2 and a 10-Hz repetition rate. An endoscopic measuring device (see Fig. 4.11b, Chap. 4) is used for assessing the precise shape and size of the graft. The cricoid plate is then spread open, and a costal cartilage graft, carved to the desired width and length, is snapped into place under microscopic visualisation. Suturing of the graft should not be attempted as this is technically difficult or impossible (Fig. 7.8). In their 10-patient series [30], no cases of graft dislodgment were observed by the authors. Stabilisation of the reconstruction with an endoscopically placed LT-Mold (see Fig. 14.17, Chap. 14) for 2–3 weeks would probably persuade more surgeons to try this appealing technique. Endoscopic posterior rib grafting presents the following advantages over other procedures: the integrity of the vocal cords and arytenoid
7.2 Bilateral Vocal Cord Paralysis (BVCP)
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Fig. 7.8 Endoscopic posterior cricoid split with costal cartilage grafting (Inglis technique [30]): (a) Bilateral vocal cord paralysis. (b) Exposure of the posterior glottis with Lindholm false cord retractor. The arrow shows the extent of the cricoid split. (c) Complete posterior midline cricoid split with the CO2 laser and costal cartilage ready to be placed between the two cricoid laminae. (d) End result: the interarytenoid distance is improved as compared to the initial condition
cartilages is preserved; the anterior laryngeal commissure is not damaged; this minimally invasive approach does not compromise further surgery, if necessary. Lastly, in the case of late VC function recovery [14], no irreversible damage to laryngeal tissues has occurred, provided that the costal cartilage graft has not overexpanded the posterior laryngeal commissure. The risk of aspiration is no higher than that observed following treatment of PGS associated with bilateral cricoarytenoid joint fixation.
einnervation of the Posterior R Cricoarytenoid Muscle Conceptually, reinnervation using the ansa cervicalis nerve-muscle pedicle transfer to the posterior cricoarytenoid muscle is the most appealing technique. Twenty years ago, Tucker reported a 50% decannulation
rate in 9 of 18 tracheostomised children who sustained BVCP [57]. More recently, another group published similar results [44]. However, due to technical difficulties and inconsistent results, these techniques are not routinely used in clinical practice. Further research is required before implementing this procedure into daily practice [22, 27]. When treating a patient with persistent BVCP (without spontaneous recovery), the real challenge is related to the risk of creating irreversible damage to the larynx to achieve decannulation. To date, only decannulation rates have been used as outcome measures for success or failure. In the paediatric age group, there is very little objective data available regarding voice outcome after different enlargement procedures. It should be noted that the balance between airway patency, voice and swallowing may be compromised to some extent after surgical correction of congenital BVCP.
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References 1. Bailey, M.: Congenital disorders of the larynx, trachea and bronchi. In: Graham, J.M., Scadding, G.K., Bull, P.D. (eds.) Pediatric ENT, pp. 189–195. Springer, Berlin/Heidelberg (2008) 2. Belafsky, P.C., Postma, G.N.: Vocal fold augmentation with calcium hydroxylapatite. In: Sulica, L., Blitzer, A. (eds.) Vocal Fold Paralysis, pp. 123–126. Springer, Berlin/ Heidelberg (2006) 3. Berkowitz, R.G.: Natural history of tracheostomy-dependent idiopathic congenital bilateral vocal fold paralysis. Otolaryngol. Head Neck Surg. 136, 649–652 (2007) 4. Bizakis, J.G., Papadakis, C.E., Karatzanis, A.D., et al.: The combined endoscopic CO2 laser posterior cordectomy and total arytenoidectomy for treatment of bilateral vocal cord paralysis. Clin. Otolaryngol. Allied Sci. 29, 51–54 (2004) 5. Borgnon, J., Tounian, P., Auber, F., et al.: Esophageal replacement in children by an isoperistaltic gastric tube: a 12-year experience. Pediatr. Surg. Int. 20, 829–833 (2004) 6. Bower, C.M., Choi, S.S., Cotton, R.T.: Arytenoidectomy in children. Ann. Otol. Rhinol. Laryngol. 103, 271–278 (1994) 7. Brigger, M.T., Hartnick, C.J.: Surgery for pediatric vocal cord paralysis: a meta-analysis. Otolaryngol. Head Neck Surg. 126, 349–355 (2002) 8. Chen, E.Y., Inglis Jr., A.F.: Bilateral vocal cord paralysis in children. Otolaryngol. Clin. North Am. 41, 889–901 (2008) 9. Cohen, S.R.: Arytenoidectomy in children. Laryngoscope 83, 1293–1299 (1973) 10. Cohen, S.R., Geller, K.A., Birns, J.W., et al.: Laryngeal paralysis in children: a long-term retrospective study. Ann. Otol. Rhinol. Laryngol. 91, 417–424 (1982) 11. Courey, M.: Homologous collagen substances for vocal fold augmentation. Laryngoscope 111, 747–758 (2001) 12. Courey, M.S.: Collagen in vocal fold injection. In: Sulica, L., Blitzer, A. (eds.) Vocal Fold Paralysis, pp. 111–116. Springer, Berlin/New York (2006) 13. Crumley, F.G.: Nerve transfer technique as it relates to phonatory surgery. In: Cummings, C. (ed.) Otolaryngology – Head and Neck Surgery, pp. 100–106. Elsevier Mosby, St. Louis (1991) 14. Daya, H., Hosni, A., Bejar-Solar, I., et al.: Pediatric vocal fold paralysis: a long-term retrospective study. Arch. Otolaryngol. Head Neck Surg. 126, 21–25 (2000) 15. De Gaudemar, I., Roudaire, M., Francois, M., et al.: Outcome of laryngeal paralysis in neonates: a long term retrospective study of 113 cases. Int. J. Pediatr. Otorhinolaryngol. 34, 101–110 (1996) 16. de Jong, A.L., Macdonald, R., Ein, S., et al.: Corrosive esophagitis in children: a 30-year review. Int. J. Pediatr. Otorhinolaryngol. 57, 203–211 (2001) 17. Dedo, D.D.: Pediatric vocal cord paralysis. Laryngoscope 89, 1378–1384 (1979) 18. Dennis, D., Kashima, H.: Carbon dioxide laser posterior cordectomy for treatment of bilateral vocal cord paralysis. Ann. Otol. Rhinol. Laryngol. 98, 930–934 (1989) 19. Emery, P.J., Fearon, B.: Vocal cord palsy in pediatric practice: a review of 71 cases. Int. J. Pediatr. Otorhinolaryngol. 8, 147–154 (1984)
7 Vocal Cord Paralysis (VCP) 20. Friedman, E.M.: Role of ultrasound in the assessment of vocal cord function in infants and children. Ann. Otol. Rhinol. Laryngol. 106, 199–209 (1997) 21. Friedman, E.M., de Jong, A.L., Sulek, M.: Pediatric bilateral vocal fold immobility: the role of carbon dioxide laser posterior transverse partial cordectomy. Ann. Otol. Rhinol. Laryngol. 110, 723–728 (2001) 22. Gacek, R.R.: Morphologic correlates for laryngeal reinnervation. Laryngoscope 111, 1871–1877 (2001) 23. Gentile, R.D., Miller, R.H., Woodson, G.E.: Vocal cord paralysis in children 1 year of age and younger. Ann. Otol. Rhinol. Laryngol. 95, 622–625 (1986) 24. Goding Jr., G.S.: Nerve-muscle pedicle reinnervation of the paralyzed vocal cord. Otolaryngol. Clin. North Am. 24, 1239–1252 (1991) 25. Gray, S.D., Kelly, S.M., Dove, H.: Arytenoid separation for impaired pediatric vocal fold mobility. Ann. Otol. Rhinol. Laryngol. 103, 510–515 (1994) 26. Hartnick, C.J., Brigger, M.T., Willging, J.P., et al.: Surgery for pediatric vocal cord paralysis: a retrospective review. Ann. Otol. Rhinol. Laryngol. 112, 1–6 (2003) 27. He, X., Sun, J., Zhang, D., et al.: Experimental study on simultaneous selective reinnervation of the adductors and the abductor muscle for the treatment of the laryngeal paralysis. Rev. Laryngol. Otol. Rhinol. 126, 131–134 (2005) 28. Hirano, M., Kirchner, J., Bless, D.M.: Electromyography for laryngeal paralysis. In: Hirano, M., Kirchner, J., Bless, D.M. (eds.) Neurolaryngology: Recent Advances, pp. 232–248. Little Brown, Boston (1987) 29. Holinger, P.H., Brown, W.T.: Congenital webs, cysts, laryngoceles and other anomalies of the larynx. Ann. Otol. Rhinol. Laryngol. 76, 744–752 (1967) 30. Inglis Jr., A.F., Perkins, J.A., Manning, S.C., et al.: Endoscopic posterior cricoid split and rib grafting in 10 children. Laryngoscope 113, 2004–2009 (2003) 31. Laccourreye, O., Papon, J., Kania, R., et al.: Intracordal injection of autologous fat in patients with unilateral laryngeal nerve paralysis: long-term results from the patient’s perspective. Laryngoscope 113, 541–545 (2003) 32. Levine, B.A., Jacobs, I.N., Wetmore, R.F., et al.: Vocal cord injection in children with unilateral vocal cord paralysis. Arch. Otolaryngol. Head Neck Surg. 121, 116–119 (1995) 33. Lichtenberger, G.: Reversible immediate and definitive lateralization of paralyzed vocal cords. Eur. Arch. Otorhinolaryngol. 256, 407–411 (1999) 34. Lichtenberger, G.: Reversible lateralization of the paralyzed vocal cord without tracheostomy. Ann. Otol. Rhinol. Laryngol. 111, 21–26 (2002) 35. Lichtenberger, G.: Comparison of endoscopic glottis-dilating operations. Eur. Arch. Otorhinolaryngol. 260, 57–61 (2003) 36. Lichtenberger, G., Toohill, R.J.: The endo-extralaryngeal needle carrier. Otolaryngol. Head Neck Surg. 105, 755–756 (1991) 37. Marie, J.P., Dehesdin, D., Ducastelle, T., et al.: Selective reinnervation of the abductor and adductor muscles of the canine larynx after recurrent nerve paralysis. Ann. Otol. Rhinol. Laryngol. 98, 530–536 (1989) 38. McCulloch, T.M., Hoffman, H.T.: Medialization laryngoplasty with Gore-Tex (expanded Polytetrafluoroethylene). In: Sulica, L., Blitzer, A. (eds.) Vocal Fold Paralysis, p. 169. Springer, Berlin/Heidelberg (175)
References 39. Merati, A.L.: Treatment of glottal insufficiency using micronized human acellular dermis (cymetra). In: Sulica, L., Blitzer, A. (eds.) Vocal Fold Paralysis, pp. 117–121. Springer, Berlin/Heidelberg (2006) 40. Miyamoto, R.C., Parikh, S.R., Gellad, W., et al.: Bilateral congenital vocal cord paralysis: a 16-year institutional review. Otolaryngol. Head Neck Surg. 133, 241–245 (2005) 41. Murty, G.E., Shinkwin, C., Gibbin, K.P.: Bilateral vocal fold paralysis in infants: tracheostomy or not? J. Laryngol. Otol. 108, 329–331 (1994) 42. Narcy, P., Contencin, P., Viala, P.: Surgical treatment for laryngeal paralysis in infants and children. Ann. Otol. Rhinol. Laryngol. 99, 124–128 (1990) 43. Narcy, P., Manac’h, Y., Bobin, S., et al.: Treatment of laryngeal paralysis in the new born (author’s transl). Ann. Otolaryngol. Chir. Cervicofac. 98, 405–410 (1981) 44. Nunez, D.A., Hanson, D.R.: Laryngeal reinnervation in children: the Leeds experience. Ear Nose Throat J. 72, 542–543 (1993) 45. Oestreicher-Kedem, Y., DeRowe, A., Nagar, H., et al.: Vocal fold paralysis in infants with tracheoesophageal fistula. Ann. Otol. Rhinol. Laryngol. 117, 896–901 (2008) 46. Okamoto, T., Takamizawa, S., Arai, H., et al.: Esophageal atresia: prognostic classification revisited. Surgery 145, 675–681 (2009) 47. Ossoff, R.H., Sisson, G.A., Duncavage, J.A., et al.: Endoscopic laser arytenoidectomy for the treatment of bilateral vocal cord paralysis. Laryngoscope 94, 1293–1297 (1984) 48. Priest, R.E., Ulvestad, H.S., Van De Water, F.: Arytenoidectomy in children. Trans. Am. Laryngol. Assoc. 81, 192–206 (1960) 49. Riffat, F., Cheng, A.: Pediatric caustic ingestion: 50 consecutive cases and a review of the literature. Dis. Esophagus 22, 89–94 (2009)
117 50. Roh, J.L., Lee, Y.W., Park, C.I.: Can mitomycin C really prevent airway stenosis? Laryngoscope 116, 440–445 (2006) 51. Rosen, C.A.: Autologous fat for vocal fold injection. In: Sulica, L., Blitzer, A. (eds.) Vocal Fold Paralysis, pp. 105– 110. Springer, Berlin/Heidelberg (2006) 52. Rosin, D.F., Handler, S.D., Potsic, W.P., et al.: Vocal cord paralysis in children. Laryngoscope 100, 1174–1179 (1990) 53. Rutter, M.J., Cotton, R.T.: The use of posterior cricoid grafting in managing isolated posterior glottic stenosis in children. Am. Med. Assoc. 130, 737–739 (2004) 54. Schneider, B.: Titanium medialization implant. In: Sulica, L., Blitzer, A. (eds.) Vocal Fold Paralysis, pp. 165–168. Springer, Berlin/Heidelberg (2006) 55. Smith, M.E.: Vocal fold paralysis in children. In: Sulica, L., Blitzer, A. (eds.) Vocal Fold Paralysis, pp. 225–235. Springer, Berlin/Heidelberg (2006) 56. Thornell, W.C.: Intralaryngeal arytenoidectomy for bilateral abductor vocal cord paralysis. Ann. Otol. Rhinol. Laryngol. 61, 601–608 (1952) 57. Tucker, H.M.: Vocal cord paralysis in small children: principles in management. Ann. Otol. Rhinol. Laryngol. 95, 618–621 (1986) 58. Turner, F., Duflo, S., Michel, J., et al.: Endoscopic medialization with Vox implant: our experience. Rev. Laryngol. Otol. Rhinol. 127, 339–343 (2006) 59. Vats, A., Worley, G.A., de Bruyn, R., et al.: Laryngeal ultrasound to assess vocal fold paralysis in children. J. Laryngol. Otol. 118, 429–431 (2004) 60. Woodman, D.: A modification of the extralaryngeal approach in arytenoidectomy for bilateral abductor palsy. Arch. Otolaryngol. 48, 63–65 (1946) 61. Zbar, R.I., Smith, R.J.: Vocal fold paralysis in infants twelve months of age and younger. Otolaryngol. Head Neck Surg. 114, 18–21 (1996)
8
Congenital Subglottic Stenosis (C-SGS)
Contents
Core Messages
8.1 Pathogenesis and Classification............................. 120
›› Third
8.2 Symptoms................................................................ 121 8.3
Endoscopic Assessment.......................................... 121
8.4 Indications for Surgery.......................................... 122 8.4.1 Soft Tissue Versus Cartilaginous C-SGS.................. 122 8.4.2 Isolated C-SGS Versus Glotto-Subglottic Stenosis........................................ 122 8.4.3 Mild Versus Severe Grade C-SGS............................ 122 8.4.4 Congenital Versus Acquired on Congenital SGS..... 123 8.5 Surgery for C-SGS.................................................. 124 References............................................................................ 124
›› ›› ›› ›› ›› ››
››
most common (10–15%) congenital laryngeal anomaly. Most common laryngeal anomaly requiring tracheotomy in children under 1 year of age. Defined as subglottic diameter less than 4.0 mm in a full-term neonate and 3.0 mm in a premature baby. Results from incomplete recanalisation of the laryngeal lumen during the tenth week of gestation. Belongs to the spectrum of laryngeal webs and atresia. The true prevalence is difficult to determine, as many cases are aggravated by ET intubation. Histopathology: −− Cartilaginous stenosis is congenital in nature. −− Soft-tissue stenosis is usually acquired. −− The mixed type (‘acquired on congenital’) results from ET intubation on an abnormally shaped cricoid ring. Symptoms: −− Manifest when subglottic stenosis (SGS) shows more than a 50% luminal diameter restriction. −− Primary biphasic stridor. −− Recurrent or prolonged croup, barking cough. −− Obstructive dyspnoea with suprasternal and chest retractions.
P. Monnier (ed.), Pediatric Airway Surgery, DOI: 10.1007/978-3-642-13535-4_8, © Springer-Verlag Berlin Heidelberg 2011
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120
8 Congenital Subglottic Stenosis (C-SGS)
›› Endoscopic examination should assess:
››
››
−− Extent and nature of SGS −− Vocal cord mobility −− Size of the residual lumen −− Associated airway anomalies Therapy rationale is based upon: −− Nature of SGS: cartilaginous versus softtissue −− Extent: isolated SGS versus glotto-subglottic stenosis −− Type: purely congenital versus acquired on congenital −− General condition of the patient Surgical options: −− No endoscopic CO2 laser treatment or dilatation for cartilaginous SGS −− Customised treatment for each patient −− Conservative treatment for Grade I SGS −− Single-stage LTR for Grade II and mild Grade III SGS −− Single-stage LTR or PCTR for severe Grade III SGS
Congenital subglottic stenosis (C-SGS) is defined as a restriction of the subglottic diameter to less than 4.0 mm in a full-term neonate and 3.0 mm in a premature baby [16]. It is the third most common congenital anomaly of the larynx [13] after laryngomalacia and vocal cord paralysis, and the most common laryngeal anomaly necessitating tracheotomy in children under 1 year of age [15]. Its true prevalence is difficult to determine, as many cases are aggravated by an emergency ET intubation leading to the so-called acquired on congenital or mixed SGS [3].
subglottic component seen in extensive glottic webs and the complete obliteration of the atretic larynx [1]. The histopathological classification of SGS, established by P.H. Holinger more than 30 years ago, is still widely used [7] (Table 8.1). Congenital SGSs are usually cartilaginous in nature, which is of major therapeutic significance as endoscopic laser resection or incisions and dilatation will be ineffective because of troublesome granulation tissue formation, with subsequent severe restenosis. Very few C-SGSs are composed of soft tissue only; in other cases C-SGSs are associated with a cricoid cartilage deformity (Fig. 8.1). The most frequent forms of cartilaginous SGS are composed of a thick anterior lamina, and a generalised thickening of the cricoid ring or an elliptical cricoid (Fig. 8.2). First described by Tucker in 1979 [15], the elliptical cricoid is the most frequent abnormal shape seen in C-SGS (Fig. 8.3). It can be associated with a posterior submucosal cleft, and less frequently, with a true laryngeal cleft [5]. As an elliptical-shaped cricoid cannot accommodate a round-shaped ET tube, an emergency tracheostomy is necessary in this case to secure the airway. If the child is healthy, presenting no associated comorbidities, an immediate single-stage
Table 8.1 Histopathologic classification of subglottic stenosis (Adapted with permission from Holinger [6]) Cartilaginous stenosis (usually congenital) • Cricoid cartilage deformity − Normal shape, small size − Abnormal shape − Elliptical − Cleft (partial, submucosal) − Flattened − Generalized thickening
8.1 Pathogenesis and Classification Congenital SGS results from failure of the laryngeal lumen to recanalise completely during the tenth week of gestation [10]. Failures at different stages of recanalisation of the epithelial lamina [11] lead to various degrees of SGS. This entity is closely related to laryngeal webs and atresia, which also result from a laryngeal recanalisation failure [14]. This accounts for the frequent cartilaginous
• Trapped first tracheal ring Soft-tissue stenosis (usually acquired) • Submucosal gland hyperplasia • Ductal cysts • Submucosal fibrosis ±Distorted cartilage ±Cricoid ossification • Granulation tissue
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1 year of age, these symptoms are always suggestive of C-SGS. Later in life, mild C-SGS (which does not compromise more than 50% of the subglottic size) may become symptomatic during an upper airway infection only. Therefore, recurrent or prolonged croup should alert the paediatrician, who should then rule out a C-SGS. Depending on the degree of the C-SGS, other signs of respiratory distress, such as severe dyspnoea with suprasternal or chest retractions, warrant prompt endoscopic investigation. The endoscopic appearance of SGS may be disproportionate with regard to the clinical presentation as infants are remarkably tolerant to airway compromise. Fig. 8.1 Flattened cricoid with hyperplasia of the submucosal glands: association of a cricoid ring deformity with increased soft tissue within the lumen (Reproduced with the permission of Holinger [4])
LTR or PCTR without tracheotomy may solve the problem, even in newborns [2, 8, 9]. The trapped first-tracheal ring, a less frequent cause of C-SGS, is usually associated with the so-called flattened cricoid ring (see Fig. 8.1).
8.2 Symptoms A cartilaginous C-SGS causes biphasic stridor. An additional mucosal component (submucosal gland hyperplasia or mucosal oedema, for instance) generates biphasic stridor with a more prominent inspiratory phase. The condition is characterised by recurrent episodes of croup with a barking cough. In children under
Fig. 8.2 Endoscopic views of congenital cartilaginous SGSs: (a) Thick anterior lamina of the cricoid ring: asymptomatic <50% SGS. (b) Generalised thickening of the cricoid ring: mild
8.3 Endoscopic Assessment This examination is carried out as described in Sect. 5.2, Chap. 5. It starts with a TNFL using face mask ventilation to assess the mobility of the vocal cords and detect other potential sites of extralaryngeal obstruction. Associated anomalies are observed in more than 50% of the cases [3]. A rigid laryngo-tracheo-bronchoscopy is performed in order to assess the craniocaudal extension of the stenosis and gauge the size of its residual lumen. Tapered bougies, less traumatic than ET tubes, are preferred. In order to assess the diameter of the stenotic segment, the bougies should pass freely without any resistance. They must not be used to dilate the stricture. Additional palpation of the C-SGS in suspension microlaryngoscopy (SML) helps determine its nature,
grade III C-SGS requiring surgery. (c) Elliptical cricoid: grade III C-SGS requiring surgery
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the initial condition by creating a wound with exposed cartilage, and healing by secondary intention is likely to lead to granulation tissue formation, scarring, and restenosis. Open surgery is therefore the sole treatment option and must be selected carefully.
8.4.2 Isolated C-SGS Versus Glotto-Subglottic Stenosis
Fig. 8.3 Elliptical cricoid: This abnormally shaped cricoid does not accommodate any of the ET tubes without severe mucosal damage. Once diagnosed, tracheostomy or immediate singlestage laryngeal reconstruction with postoperative intubation must be performed (Reproduced with the permission of Holinger [4])
that is, cartilaginous versus soft-tissue SGS. Lastly, depending on the severity of the symptoms, a decision is made to secure the airway. If possible, a tracheotomy should be performed without endotracheal intubation, or intubation should be carried out with the smallest possible ET tube that provides adequate ventilation for a short procedure. Intubation with a large ET tube must be avoided as it can traumatise the SG mucosa and worsen the initial condition.
8.4 Indications for Surgery Selection of treatment for C-SGS should be based on the nature, extent, degree, and type of stenosis, as well as the patient’s general condition: 1. Soft tissue versus cartilaginous C-SGS 2. Isolated C-SGS versus glotto-subglottic stenosis 3. Mild versus severe C-SGS grade 4. Congenital versus acquired SGS
8.4.1 Soft Tissue Versus Cartilaginous C-SGS As most C-SGSs are cartilaginous, endoscopic treatment is not indicated [12]. Laser and dilation worsen
Enlargement LTR with costal cartilage grafts is important in ‘virgin’, isolated C-SGSs. The presence of normal mucosa between the anterior, posterior, or combined costal cartilage grafts facilitates rapid reepithelialisation of the costal cartilage graft. The elliptical cricoid is particularly suited for this type of surgery (Fig. 8.4). On the contrary, a flattened cricoid with mucosal gland hyperplasia represents an excellent indication for PCTR. The cricoid plate is flat and easily accommodates the tracheal stump for subglottic reconstruction; the abnormally thickened mucosa is completely removed with the resected specimen (Fig. 8.5). Glotto-subglottic stenoses with a cartilaginous SG component are part of congenital webs and atresia of the larynx, in close relationship with C-SGS. The two main surgical options include LTR with anterior and posterior costal cartilage grafts and extended PCTR. Both reconstructions require stenting, and the design and quality of the stent are key factors in obtaining optimal final results in terms of airway and voice quality. In this respect, the LT-Mold (see Sect. 2.8.6, Chap. 2) has yielded very satisfactory results.
8.4.3 Mild Versus Severe Grade C-SGS If treated using LTR, a generalised thickening of the cricoid cartilage (Grade III SGS) leaves very little residual normal mucosa at the stenotic level, even if submucosal resection of cartilage is performed (see Fig. 8.2b). Due to the lack of residual mucosa, the reepithelialisation process over the cartilage inserts is compromised as in the case of a cicatricial Grade III SGS. Severe Grade III C-SGS should thus be treated by PCTR, as should acquired SGS.
8.4 Indications for Surgery
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Fig. 8.4 Diagram of LTR for elliptical cricoid cartilage stenosis: (a) Severe SGS with normal anteroposterior distance and preserved mucosa. Dotted arrows show anterior and posterior midline cricoidotomies. (b) Situation after subglottic enlargement with posterior and anterior costal cartilage grafting. The normal mucosa on the divided portions of the elliptical cricoid facilitates rapid reepithelialisation of the graft’s periosteum
Fig. 8.5 Diagram of PCTR for flattened cricoid ring with mucosal hyperplasia and fibrosis (axial views of the subglottis): (a) Initial situation requiring entire removal of the abnormally thick subglottic mucosa. (b) During PCTR, the anterior arch of
the cricoid ring is completely removed with the thick abnormal mucosa. The flattened cricoid ring, with its wide cricoid plate, represents a favourable situation for this type of surgery. (c) Reconstruction of the subglottis with a normal tracheal ring
8.4.4 Congenital Versus Acquired on Congenital SGS
post-intubation laryngotracheal stenosis, regardless of the initial C-SGS type. As normal mucosa may be lacking at the SG level, it does not play any significant role in the reepithelialisation process. Only Grade II and mild Grade III SGSs may benefit from LTR. For severe Grade III or IV SGS, PCTR is the preferred treatment.
The treatment of C-SGS is described above. Congenital subglottic stenosis with mixed aetiology ‘acquired on congenital’ should be treated in the same manner as
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8.5 Surgery for C-SGS Basically, the techniques used for C-SGS are similar to those for acquired SGS. They will be described in detail in Chaps. 19 and 20 with information concerning expected results for LTR and PCTR surgeries.
References 1. Ferguson, C.F.: Congenital abnormalities of the infant larynx. Otolaryngol. Clin. North Am. 3, 185–200 (1970) 2. Garabedian, E.N., Nicollas, R., Roger, G., et al.: Cricotracheal resection in children weighing less than 10 kg. Arch. Otolaryngol. Head Neck Surg. 131, 505–508 (2005) 3. George, M., Ikonomidis, C., Jaquet, Y., et al.: Partial cricotracheal resection for congenital subglottic stenosis in children: the effect of concomitant anomalies. Int. J. Pediatr. Otorhinolaryngol. 73, 981–985 (2009) 4. Holinger, L., Lusk, R., Green, C.: Pediatric laryngology and bronchoesophagology. Lippincott-Raven, Philadelphia (1997) 5. Holinger, L.D.: Histopathology of congenital subglottic stenosis. Ann. Otol. Rhinol. Laryngol. 108, 101–111 (1999) 6. Holinger, L.D.: Congenital laryngeal anomalies. In: Holinger, L.D., Lusk, R.P., Green, C.G. (eds.) Pediatric Laryngology and Bronchoesophagology, p. 154. LippincottRaven, Philadelphia/New York (1997)
8 Congenital Subglottic Stenosis (C-SGS) 7. Holinger, P.H., Kutnick, S.L., Schild, J.A., et al.: Subglottic stenosis in infants and children. Ann. Otol. Rhinol. Laryngol. 85, 591–599 (1976) 8. Ikonomidis, C., George, M., Jaquet, Y., et al.: Partial cricotracheal resection in children weighing less than 10 kg: assessment of safety, efficacy and longterm outcome. Int. J. Pediatr. Otorhinolaryngol. 142, 41–47(2010) 9. Johnson, R.F., Rutter, M., Cotton, R.T., et al.: Cricotracheal resection in children 2 years of age and younger. Ann. Otol. Rhinol. Laryngol. 117, 110–112 (2008) 10. McGill, T.J.: Congenital anomalies of the larynx. In: Ferlito, A. (ed.) Diseases of the larynx, pp. 207–215. Arnold/Oxford University Press, New York (2000) 11. Milczuk, H., Smith, J., Everts, E.: Congenital laryngeal webs: surgical management and clinical embryology. Int. J. Pediatr. Otorhinolaryngol. 52, 1–9 (2000) 12. Monnier, P., George, M., Monod, M.L., et al.: The role of the CO2 laser in the management of laryngotracheal stenosis: a survey of 100 cases. Eur. Arch. Otorhinolaryngol. 262, 602–608 (2005) 13. Narcy, P., Bobin, S., Contencin, P., et al.: Laryngeal anomalies in newborn infants. A propos of 687 cases. Ann. Otolaryngol. Chir. Cervicofac. 101, 363–373 (1984) 14. Nicollas, R., Triglia, J.M.: The anterior laryngeal webs. Otolaryngol. Clin. North Am. 41, 877–888 (2008) 15. Tucker, G.F., Ossoff, R.H., Newman, A.N., et al.: Histopathology of congenital subglottic stenosis. Laryngoscope 89, 866–877 (1979) 16. Willing, J.: Subglottic stenosis in the pediatric patient. In: Myer, C.M., Cotton, R.T., Shott, S.R. (eds.) The Pediatric Airway – An Interdisciplinar Approach, pp. 111–132. JB Lippincott, Philadelphia (1995)
9
Laryngeal Web and Atresia
Contents 9.1 Patient Assessment.................................................. 126 9.1.1 Symptoms................................................................. 126 9.1.2 Endoscopic Assessment............................................ 126 9.1.3 Additional Examinations.......................................... 127 9.2 Management of Laryngeal Webs........................... 127 9.2.1 Type I Web (<35% of Glottic Length)...................... 128 9.2.2 Type II Web (35–50% of Glottic Length)................. 128 9.2.3 Type III Web (50–75% of Glottic Length)............... 130 9.2.4 Type IV Web (75–90% of Glottic Length)............... 131 References............................................................................ 131
Core Messages
›› Uncommon (~5%) congenital anomaly result›› ›› ››
››
››
››
ing from an incomplete recanalisation of the primitive larynx Similar embryological mechanism as seen in C-SGS, but involving the glottic level with frequent subglottic extensions Association with microdeletion of chromosome 22q11 (velo-cardio-facial syndrome) in some cases Four grades of glottic webbing according to Cohen’s classification: longer webs are always thicker than shorter webs and present a subglottic cartilaginous component The four degrees of severity according to Cohen’s classification reflect the time at which laryngeal recanalisation ended during the embryological period Symptoms depend highly on the web’s severity: –– Mild hoarseness to aphonia. –– Absent to severe obstructive dyspnoea. –– Without an emergency tracheostomy or an EXIT procedure, complete atresia is incompatible with life. Diagnosis: –– TNFL to assess vocal cord mobility –– Rigid rod-lens laryngoscopy to define the degree of SG extension and the size of the SG lumen –– SML to palpate the web for a cartilaginous component or a submucosal cleft –– Lateral high-kilovolt neck films or fine-cut CT scans to assess the craniocaudal extension of the web –– Genetic consultation and counselling
P. Monnier (ed.), Pediatric Airway Surgery, DOI: 10.1007/978-3-642-13535-4_9, © Springer-Verlag Berlin Heidelberg 2011
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›› Cohen’s classification of laryngeal webs:
››
››
–– Type I: Thin anterior web: <35% of glottic length –– Type II: Moderately thick anterior web: 35–50% of glottic length –– Type III: Thick anterior web: Potentially cartilaginous SG component 50–75% of glottic length –– Type IV: Uniformly thick web: Cartilaginous SG component 75–90% of glottic length Treatment according to Cohen’s classification: –– Type I: Observation or CO2 laser division with mucosal flap –– Type II: CO2 laser division with endoscopic keel –– Type III: CO2 laser division with endoscopic keel or open surgery if a cartilaginous component is present –– Type IV: Tracheotomy; two-stage PCTR or LTR with temporary stenting Terminology: –– The term web is restricted to congenital membranous stenosis. –– The term synechia is used for acquired cicatricial fusion of two adjacent structures, such as the vocal cords or ventricular bands.
Anterior laryngeal webs are uncommon (~5%) congenital anomalies resulting from a recanalisation failure of the primitive larynx during the eighth and tenth week of embryological development. In fact, they share the same pathogenesis as C-SGS and may be considered as a subgroup of this entity. This explains why the most severe types of glottic webs are associated with a cartilaginous SGS. If the process of recanalisation of the epithelial lamina [5] stops at an early stage of embryogenesis, a complete laryngeal atresia ensues. This situation is incompatible with life unless an emergency tracheotomy or an ex-utero intrapartum treatment (EXIT) procedure [6] is carried out in the delivery room. Some newborns survive longer if their laryngeal atresia is associated with an oesophageal atresia and a tracheooesophageal fistula (TOF). The ET tube inserted
into the proximal oesophagus ensures ventilation of the infant through the TOF. This condition is also associated with some degree of tracheal agenesis [3]. Since recanalisation of the larynx proceeds from caudal to cranial, the web’s extent and its cartilaginous SG component are directly related to the time at which this recanalisation process ceased. Cohen’s classification [1], a useful clinical illustration of this embryological process, divides glottic webs into four types (Fig. 9.1): • Type I (Fig. 9.1a) –– Thin anterior web with less than 35% of glottic involvement –– Mild hoarseness, no airway symptoms • Type II (Fig. 9.1b) –– Thin to moderately thick web with 35–50% of glottic involvement –– Weak husky cry, mild airway symptoms • Type III (Fig. 9.1c) –– Thick web with anterior, potentially cartilaginous subglottic extension involving 50–75% of glottic length –– Very weak voice, moderate airway symptoms • Type IV (Fig. 9.1d) –– Uniformly thick web involving 75–90% of the glottic length with a cartilaginous subglottic extension –– Aphonia, severe airway symptoms; need for tracheotomy
9.1 Patient Assessment 9.1.1 Symptoms All patients present some degree of dysphonia, from mild hoarseness to aphonia. Airway symptoms increase with the extension of the web, the most severe cases warranting a tracheotomy to secure the airway.
9.1.2 Endoscopic Assessment A standardised endoscopic examination should comprise a TNFL in order to assess arytenoid mobility,
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9.2 Management of Laryngeal Webs
Fig. 9.1 Cohen’s classification of glottic webs: endoscopic views and sagittal diagrams: (a) Type I: <35% of glottic length, no subglottic extension. (b) Type II: 35–50% of glottic length, minimal subglottic extension. (c) Type III: 50–75% of glottic
length, significant anterior subglottic extension, possibly with cartilaginous component. (d) Type IV: 75–90% of glottic length, severe subglottic extension with cartilaginous component
possible extralaryngeal sites of airway obstruction and submucosal palatal or laryngeal clefts. Direct laryngoscopy with a rod-lens telescope is used to assess precisely the subglottic extension of the web and the size of the residual subglottic lumen. Lastly, in Types III and IV, suspension microlaryngoscopy is implemented to palpate the web for the presence of a possible cartilaginous component.
Genetic consultation with karyotyping for microdeletion of chromosome 22q11 should be envisaged, especially if the patient shows discrete signs of velo-cardio-facial syndrome. This syndromic malformation, also known as Shprintzen or DiGeorge syndrome, encompasses a wide variety of potential anomalies with different combinations. No less than 185 different anomalies affecting almost any system have been reported. The list is available at the following address: www.vcfsef.org. Cleft lip and cleft palate account for about 8% of the malformations while cardiovascular anomalies account for 30% [2, 4].
9.1.3 Additional Examinations Lateral high-kilovolt neck X-rays or thin-cut helical CT scan images offer additional information as to the length of the SG extension, particularly in severe SGS where inspection through the stenosis with the slim telescope does not provide the adequate information (see Fig. 3.5, Chap. 3).
9.2 Management of Laryngeal Webs Given the wide range of vocal cord webs, many surgical options exist. They should be carefully selected for each type of web.
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9.2.1 Type I Web (<35% of Glottic Length) Minor anterior vocal cord webs with minimal voice problems do not require treatment. For longer membranous webs with no airway compromise, endoscopic repair may be delayed until pre-school age. In suspension microlaryngoscopy (SML), a Parsons laryngoscope is used to expose the entire length of the vocal cords. External pressure can be exerted on the neck to improve the exposure of the anterior laryngeal commissure (see Fig. 4.9, Chap. 4). On one side of the anterior web, a submucosal injection (0.5 mL of 1:100,000 adrenalin-saline solution) is performed. Using the CO2 laser set to ultrapulse mode, 100–125 mJoules/cm2, 10 Hz repetition rate and 250 m microspot, a mucosal flap is created; it should be made large enough laterally towards the ventricle. Exposure at this level is improved when using a Lindholm self-retaining false cord retractor. The flap is then elevated towards the midline as shown in Fig. 9.2. The membranous web is sectioned, and the flap is reflected on the homolateral vocal cord, preventing the presence of two opposite raw surfaces, which may induce recurrent synechia during the healing phase. The flap can be sutured to the subglottis using a 6.0 Vicryl suture, but this difficult procedure may lead to a tearing of the flap. It is recommended that a drop of fibrin-glue (Tisseel®) be used to maintain the flap in place.
9 Laryngeal Web and Atresia
9.2.2 Type II Web (35–50% of Glottic Length) (Fig. 9.3) The web is not extensive enough to provoke a clinical airway compromise. Late repair is preferable as a silicone keel is not well tolerated in an infant larynx without a tracheotomy. By the age of 4 years, surgical correction is easier as the larynx is larger. In SML, the CO2 laser is set to ultrapulse mode, 150 mJoules/cm2 and a 10-Hz repetition rate with a sharp spot size of 250 m. A midline division of the web is performed. A Lindholm false cord retractor placed on the ventricular bands helps spread out the web between the vocal ligaments. Submucosal injection should not be made to avoid obscuring the slight projection of the vocal cords (Fig. 9.3a). The technique described for Type I webs is not used in Type II webs because the anteriorly based subglottic extension is too long. Laser section between the vocal cords requires an endoscopic keel for the healing phase. Open-keel placement is no longer the preferred method as it requires a full laryngofissure, a procedure that is far too invasive for the treatment of membranous webs. The keel is custom-made: a very thin silicone sheet 0.05-mm thick, cut approximately to a 2.5 × 2.5cm surface, is wrapped around a very thin catheter usually used for IV injections in premature babies. The purpose of the catheter is to prevent progressive transection of the silicone sheet during the period of
Fig. 9.2 Diagram of endoscopic treatment for type I membranous web of the vocal cords: (a) Flap design. (b) Elevation of flap and web section. (c) Reflexion of mucosal flap on the homolateral vocal cord
9.2 Management of Laryngeal Webs
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Fig. 9.3 Endoscopic treatment of Type II–III vocal cord webs: (a) CO2 laser incision (ultrapulse mode). (b) Design of the keel
Fig. 9.4 Diagram of endoscopic placement of the silicone keel: (a) A first inside-out stitch using the Lichtenberger needle-carrier is made in the subglottic region. (b) A second inside-out
stitch is made above the anterior laryngeal commissure, and the knots are tied under the skin to hold the silicone keel in place at the anterior laryngeal commissure
endolaryngeal splinting. Silicone glue (Nusil silicone technology, Carpinteria, CA, USA) serves to seal the two reflected silicone sheets together. With the IV catheter as its pole, the design of a flag is so created (Fig. 9.3b). It can be cut to any appropriate size and should not abut the posterior laryngeal commissure. Several attempts are made until an adequate fitting in the craniocaudal and anteroposterior axes is obtained. Using a Lichtenberger needle-carrier (see Fig. 4.11e, Chap. 4), a subglottic endo-extralaryngeal 3.0 prolene stitch is then placed just below the lowermost section of the web. One end of the stitch is recovered on the outer surface of the skin of the neck, and the other end is inserted through the shaft of the IV catheter. The silicone keel is slid down into the larynx, and the second inside-out supraglottic stitch is passed through the epiglottis using the Lichtenberger needle-carrier. The cranial distance from the anterior commissure should be at least 5 mm to avoid granulation tissue formation at
this level. The thread is recaptured on the outer skin. A 1-cm horizontal skin incision is made midway between the two exit points of the threads on the neck. A blunt subcutaneous dissection with a curved haemostat is carried out cranially and caudally until the threads are identified. They are then recaptured with skin hooks and tied under the skin to tack the keel at the exact point of the anterior laryngeal commissure (Fig. 9.4). The skin is closed with a resorbable intradermal running suture. The silicone keel is left in place for about 4 weeks and then removed in SML by cutting the 3.0 prolene thread with microscissors. The silicone keel is easily removed as is the thread, by pulling strongly on one of its extremities, while a biopsy forceps is used to remove the granulation tissue that is always present at the entrance points of the stitches. The older technique of open-keel placement is now obsolete in the case of webs without a cartilaginous subglottic component (Fig. 9.5).
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Fig. 9.5 Treatment result of a type II web after endoscopic splinting with a keel: (a) Preoperative view: Type II web. (b) Postoperative view: sharp anterior laryngeal commissure
9.2.3 Type III Web (50–75% of Glottic Length) Timing for repair must be based on respiratory symptoms. If tracheotomy is necessary to secure the airway, then endoscopic or open surgical repair can be performed early, during the first 2 years of life. The type of surgery essentially depends upon the degree of subglottic extension. In rare cases where a Type III web is purely membranous and limited to the glottic level, the same endoscopic treatment as for Type II webs is applied. Most often, Type III webs present a thick anteriorly based subglottic involvement, requiring open surgery for successful repair. An LTR with anterior costal cartilage graft and stenting by means of an adequate laryngeal stent is indispensable for restoring a satisfactory anterior commissure and reepithelialisation of the vocal cords. In Type III webs, the interarytenoid distance is usually preserved; hence, posterior grafting is not always necessary. The LTR method is similar to that for acquired glotto-subglottic stenosis, except for submucosal resection of a possible cartilaginous subglottic component. The full laryngofissure should be carried out under visual control by incising the epiglottis above the thyroid notch and by opening the supraglottic larynx with skin hooks. Separation of the vocal cords is then performed by progressively extending the cartilaginous excision caudally and spreading the thyroid cartilage apart until the glottis level is clearly visible. A midline section is thus achieved and continued caudally to the second tracheal ring. In the subglottis, fibrous tissue can be cored out below the vocal cords to restore the dome
shape of the elastic cone. Usually, the thyroarytenoid muscle can be identified and preserved. In congenital webs, the mucosa of the floor of the ventricle is mobilised to redrape the free border of the vocal cords and is sutured with a 6.0 Vicryl suture to the under surface of the vocal cords. Provided this manoeuvre is successful (with no mucosal tear), a stent may be avoided. Usually, an LT-Mold stent (Sect. 2.8.6, Chap. 2) with a size appropriate for splinting the reconstruction is used in our centre. The stent is selected by measuring the exact length of the neo-glottis, and it is fixed in place by two transversal 3.0 prolene sutures through the ventricular bands at the supraglottic level first and then at the cervical tracheal level above the tracheostomy (see Sect. 20.4, Chap. 20). A resorbable 5.0 Vicryl suture is placed at the anterior laryngeal commissure through the LT-Mold in order to fix it precisely at the correct level. This thread will be resorbed spontaneously before the stent is removed. When closing the laryngofissure, great care should be exercised to reapproximate the vocal cords at the same level. Furthermore, a pexy of the epiglottic petiole using mattress sutures is performed through the thyroid cartilage to avoid posterior displacement of the epiglottis. The subglottic portion of the laryngofissure is usually distended by the stent in an oval-shaped manner. This anterior defect is filled with a boat-shaped costal cartilage graft, the perichondrium facing the lumen. If the defect is small, then a small piece of cartilage is harvested from the upper rim of one thyroid ala in order to avoid donor-site morbidity. The prosthesis is left in place for 3–4 weeks, giving both vocal cords time for a full reepithelialisation, and then removed endoscopically as explained in Fig. 20.41, Chap. 20.
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References Fig. 9.6 A 5-month-old child presenting with velo-cardiofacial syndrome: (a) Cohen’s Type IV webbing of the vocal cords with Grade III congenital cartilaginous subglottic stenosis. (b) Result at 3 months after extended partial cricotracheal resection and 2 weeks after LT-Mold removal: patent glotto-subglottic airway with sharp anterior commissure
9.2.4 Type IV Web (75–90% of Glottic Length) Severe webs, similar at times to complete laryngeal atresia, are always combined with a cartilaginous subglottic stenosis. The interarytenoid distance is markedly narrowed because of the cricoid deformity. The infant’s airway has already been secured by a tracheostomy. This condition most likely requires an LTR with anterior and posterior costal cartilage grafts and submucosal coring out of the cricoid ring’s excess cartilage. In the absence of any residual mucosa at the glotto-subglottic level, long-term stenting is required, and healing by secondary intention may produce a suboptimal final result. In a situation such as this, the author by far prefers to perform an extended PCTR (see Sect. 20.4, Chap. 20), which fully restores a mucosalised airway. Stenting with an LT-Mold is still necessary to minimise blunting at the anterior laryngeal commissure and facilitate reepithelialisation of the under surface of both vocal cords (Fig. 9.6). A detailed description of LTR and PCTR is provided in Chaps. 19 and 20.
References 1. Cohen, S.R.: Congenital glottic webs in children. A retrospective review of 51 patients. Ann. Otol. Rhinol. Laryngol. Suppl. 121, 2–16 (1985) 2. Dyce, O., McDonald-McGinn, D., Kirschner, R.E., et al.: Otolaryngologic manifestations of the 22q11.2 deletion syndrome. Arch. Otolaryngol. Head Neck Surg. 128, 1408–1412 (2002) 3. Holinger, L.D., Volk, M.S., Tucker Jr., G.F.: Congenital laryngeal anomalies associated with tracheal agenesis. Ann. Otol. Rhinol. Laryngol. 96, 505–508 (1987) 4. McElhinney, D.B., Jacobs, I., McDonald-McGinn, D.M., et al.: Chromosomal and cardiovascular anomalies associated with congenital laryngeal web. Int. J. Pediatr. Otorhinolaryngol. 66, 23–27 (2002) 5. McGill, T.J.: Congenital anomalies of the larynx. In: Ferlito, A. (ed.) Diseases of the Larynx, pp. 207–215. Arnold/Oxford University Press, New York (2000) 6. Morrison, G.: Exit-antenatal (pre-natal) diagnoses and management. In: Graham, J.M., Scadding, G.K., Bull, P.D. (eds.) Pediatric ENT, pp. 73–81. Springer, Berlin/Heidelberg (2008)
Subglottic Haemangioma (SGH)
Contents 10.1
Clinical Course........................................................ 134
10.2
Patient Assessment.................................................. 135
10.3 10.3.1 10.3.2 10.3.3
Management of SGH.............................................. 135 Medical Treatment.................................................... 135 Endoscopic Treatment.............................................. 136 Open Surgery............................................................ 137
References............................................................................ 139
10
Core Messages
›› Rare (~1.5%) congenital laryngeal anomaly ›› Benign vascular tumour characterised by ›› ›› ››
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hyperplasia of endothelial cells, pericytes, mast cells, fibroblasts and macrophages Associated in 50% of the cases with cutaneous haemangiomas, most frequently with a ‘beared’ distribution (chin, lower lip, and anterior neck) Female predominance (2–3:1) Typical evolution: –– Rapid proliferative phase between 4–6 weeks and 4–10 months of life –– Stabilisation as of 10–12 months of life –– Slow involution phase between 10–12 months and 5–10 years of age Clinical course: –– No symptoms during the first weeks of life –– Beginning of symptoms between 2 and 4 months of age –– All infants are symptomatic by 6 months of age –– Progressive resolution between 12 and 18 months of age –– Complete resolution by 5–12 years of age Symptoms: –– Biphasic, predominantly inspiratory stridor –– Barking cough –– Recurrent or prolonged ‘croup’ –– Voice altered to varying degrees Diagnosis: –– Rigid endoscopy (after exclusion of laryngomalacia and vocal cord paralysis using TNFL)
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10 Subglottic Haemangioma (SGH)
–– Anteroposterior neck X-ray films –– MRI to assess the mediastinal involvement, if necessary Conservative management: –– Observation: Children with mild symptoms in the involution phase –– Systemic steroids: Rarely curative (25% of the cases) As adjuvant therapy –– Interferon a-2a: Abandoned owing to severe side effects –– Propanolol: Rapid onset of symptom relief Might replace all other treatment modalities in the future Endoscopic management –– Intralesional steroids: Serial injections and ET-intubations required Intubations increase risks and costs Success rate ~75% –– CO2 laser resection: Appropriate for slow-growing tumours CW/chopped mode, 3 W output power, slightly defocused beam at 400 mm focal distance (power density ~1,200 W/cm2) and laser strikes of 70–100 ms Treatment restricted to 30–50% of subglottic circumference –– Microdebrider submucosal dissection: Still in a nascent stage Open surgery: –– Tracheotomy: Morbidity/mortality related to prolonged tracheostomy High (> 90 %) success rate with spontaneous evolution –– Excision through laryngofissure: Preferred indication for fast-growing tumours Primary procedure for bilateral or circumferential lesions Best success rates, albeit more invasive procedure
Approximately 60% of infantile haemangiomas are located in the head and neck regions [10], where they represent the most common tumours in paediatric patients. In contrast, subglottic haemangiomas (SGH) are rare benign tumours of the airway, accounting for only 1.5% of all congenital laryngeal anomalies [11]. When airway symptoms suggestive of a laryngeal pathology are associated with cutaneous haemangiomas found in a ‘beard’ distribution (chin, anterior neck and lower lip), SGH is a likely diagnosis. In fact, coexisting pathologies are observed in 50% of the cases. SGH are more common in female than in male patients with a ratio of 2–3:1 and are potentially lifethreatening in the absence of treatment. They are benign tumours associated with hyperplasia of the endothelial cells, mast cells, pericytes, fibroblasts and macrophages. In contrast, vascular malformations display a normal cell turnover rate [16].
10.1 Clinical Course Similarly to cutaneous haemangiomas, SGH are unique in their mode of presentation and evolution. They undergo a rapid proliferative phase lasting a few months, followed by a period of stabilisation, and finally, a slow involution phase of several years. Understanding these three phases is essential in making a decision about the best treatment option. According to Bruckner [3], complete resolution occurs in 50% of the cases by the age of 5 years, 70% by the age of 7 years and 100% by the age of 10–12 years (Fig. 10.1). Due to this typical evolution pattern, the clinical course is often stereotyped even if there are wide
Fig. 10.1 Evolution pattern of subglottic haemangioma: a typical three-phase evolution is observed in all patients, that is growth, stabilisation and involution phase
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10.3 Management of SGH
Fig. 10.2 Endoscopic views of typical aspects of subglottic haemangiomas: (a) Left posterolateral subglottic haemangioma. (b) Posterior subglottic haemangioma. (c) Bilateral subglottic haemangioma
variations in rate, degree and duration of the disease. During the first weeks of life, the infant is asymptomatic. Usually, symptoms of inspiratory stridor followed by biphasic stridor with barking cough and slight hoarseness start at around 2–4 months, becoming manifest in all infants by the age of 6 months. Recurrent or prolonged episodes of croup should always alert the physician to a likely congenital anomaly. Symptoms of respiratory distress with suprasternal and chest retractions, feeding difficulties and failure to thrive depend on the severity of the airway obstruction. If symptoms worsen at an early stage, then early intervention is indicated more strongly. The progression of symptoms reaches a plateau between the ages of 10 and 12 months, and the symptoms then decrease slowly and finally disappear around the age of 2 years, although complete resolution of the tumour may take as long as 5–10 years.
10.2 Patient Assessment In a noisy infant with mild to moderate respiratory distress, an anteroposterior high-kilovolt neck X-ray may reveal asymmetric subglottic narrowing. Based on the clinical history and examination, this presentation must be differentiated from a subglottic cyst, stenosis or papilloma. However, the mainstay of the diagnosis is rigid endoscopy under general anaesthesia after laryngomalacia and vocal cord paralysis have been ruled out by TNFL. An extensive or therapy-resistant large haemangioma warrants a contrast-enhanced MRI or CT scan to identify potential extension into the upper mediastinum.
The SGH appears as a reddish smooth mass, mostly located in the left posterolateral subglottis and extending cranially to the under surface of the vocal cord. Right-sided, posterior and bilateral SGH are also frequently seen (Fig. 10.2). The tumour mass is spongy and compressible, allowing for easy intubation with an ET tube with no risk of major haemorrhage. A therapeutic endoscopic procedure is thereby made more secure as the tube can be used to control the bleeding source by a mere compression of the SGH.
10.3 Management of SGH Knowing that SGH is a self-limiting disease with spontaneous resolution, treatment must be aimed at maintaining the airway without tracheotomy, while avoiding any long-term sequelae. Over the years, many treatment modalities have been tried, attesting to the difficulty of finding the optimal treatment for a given patient. These modalities include medical measures, endoscopic resections, and open surgical resections. Of note, the least invasive treatments are not always the most innocuous.
10.3.1 Medical Treatment 10.3.1.1 Observation This measure is appropriate for children with mild symptoms as well as children older than 1 year having
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reached the phase of spontaneous tumour regression. Close monitoring is sufficient because the children will eventually grow out of the problem.
10.3.1.2 Systemic Steroids Systemic steroids should be used as adjuvant therapy or as curative treatment only for a short period of time. Only 25% of the SGH resolve completely when this treatment is administered alone [19]. The Cincinnati [20] and Boston protocols [19] do not recommend systemic steroid treatment for longer than 3 weeks if the symptoms do not markedly improve. Potential long-term side effects such as failure to thrive, osteoporosis, adrenal suppression and Cushing syndrome should not be underestimated.
10 Subglottic Haemangioma (SGH)
whom had also failed treatment with vincristine [8], responded spectacularly to 2–3 mg/kg/day of propanolol. To the best of my knowledge, this was the first report of a successful treatment of SGH with propanolol, and likely the first of a long series [12], as this approach might well supersede all other current treatment modalities. However, CO2 laser may still have a role in treating small unilateral haemangiomas, as cardiovascular side effects potentially preclude the use of propanolol in certain patients. Unknown issues need further investigation, such as responsiveness of all haemangiomas to propanolol, duration of treatment and risk of rebound after stopping treatment. Results from several other medical groups are pending.
10.3.1.3 Interferon a-2a
10.3.2 Endoscopic Treatment
Although commonly used in the past, interferon a-2a has been abandoned owing to its severe side effects, suboptimal efficacy and the adoption of other treatment modalities.
10.3.2.1 Intralesional Steroid Injections
10.3.1.4 Propanolol An interesting article, published in the New England Journal of Medicine in 2008, highlighted the potential advantages of using propanolol, a non-selective betablocker, for treating infantile capillary haemangiomas of the head and neck [14]. After 24 h of treatment with propanolol (at 2 mg/kg of bodyweight per day), corticosteroid treatment could be discontinued because of the fast and sustained improvement of all head and neck haemangiomas in their study group. The authors did not mention any case of subglottic haemangioma in their series. Possible explanations for the therapeutic effects of propanolol include vasoconstriction, decreased expression of VEGF and bFGF genes via the downregulation of the RAF-mitogen-activated protein kinase pathways [6], as well as the triggering of apoptosis of capillary endothelial cells [21]. Since this first publication on the successful treatment of cutaneous haemangiomas with propanolol, a first report on the efficacy of this drug to alleviate respiratory symptoms due to SGH was published in May 2009 [7]. Two infants who had failed several previous treatment regimens with corticosteroids, one of
With success rates exceeding 75%, this treatment modality is much more efficacious than systemic steroids. However, repeated injections, temporary ET-intubations and postoperative PICU stays increase intubationrelated risks as well as treatment costs. The author’s preference is to use this modality only as an adjuvant treatment to CO2 laser resection. 10.3.2.2 Laser Resection This treatment modality is appropriate for slow-growing tumours that become symptomatic at the age of 4–6 months. The CO2 laser should be used in the CW/chopped mode, at an output power of 3 W, with a slightly defocused beam at 400 mm focal distance, along with a 70–100 ms duration of the laser strikes. These parameters permit the blanching of the tumour, followed by vaporisation with no significant carbonisation, hence little heat diffusion into the surrounding tissues. In SML, the use of the Lindholm self-retaining false cord retractor offers excellent access to the SGH. Forty to maximally fifty per cent of the subglottic circumference must be vaporised when treating a laterally situated SGH (Fig. 10.3). The reported risks of cicatricial SGS complicating CO2 laser resection [2, 4, 19] merely reflect the
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10.3 Management of SGH
Fig. 10.3 CO2 laser vaporisation of a left subglottic haemangioma: (a) Left-sided subglottic haemangioma. (b) CO2 laser vaporisation with minimal charring. (c) Immediate postoperative result
inappropriate use of laser parameters for extensive, almost circumferential subglottic resections. Using the aforementioned laser parameters and given that vaporisation of the SGS circumference to more than 40% is avoided, no cicatricial SGS has been observed in the unpublished 20-case series treated at our institution. The need for multiple reoperations may be accounted for by the use of the CO2 laser during the active proliferation phase, which is far from being the best indication for this treatment modality. As its laser light is strongly absorbed by haemoglobin, the KTP laser is theoretically an optimal tool for treating vascular tumours, but it is more difficult to use than the CO2 laser. As the power density is intimately related to the distance between the fibre tip and the target tissue, specific laser parameters cannot be set up. An output power of 10–15 W allows for tumour blanching, which is followed by vaporisation while shortening the ‘fibre-tip to target’ distance. In comparison with the CO2 laser, control of deep thermal damage is more difficult to achieve with the KTP laser. In a sensitive area such as the infant glottis, the CO2 laser is thus preferred over the KTP laser in the treatment of SGH. 10.3.2.3 Microdebrider Submucosal Resection Introduced by Pransky et al. in 2004 [18], this treatment technique aims at preserving the mucosa and perichondrium by inserting the microdebrider probe through a small mucosal opening. Although this is certainly a viable option, further assessment of the technique is still needed to ascertain its value. The author has no experience with this treatment modality to date.
10.3.3 Open Surgery Surgical options include tracheostomy and open excision of SGH through a laryngofissure.
10.3.3.1 Tracheostomy Tracheostomy, once considered the standard treatment for SGH, has the great advantage of leaving the subglottis untouched. In the case of SGH, the high percentage of spontaneous involution (90%) [9] is offset by the 1–3% mortality rate related to prolonged tracheostomy in proximally obstructed airways [13]. However, it is still a viable option in centres where sophisticated techniques for treatment are unavailable.
10.3.3.2 Open Excision of SGH Through a Laryngofissure Over the last decade, this technique has gained wide popularity for the treatment of large, fast-growing SGH in the proliferative phase [22] or when involution has not occurred by the age of 2 years [20]. It is best used as a primary treatment rather than as salvage surgery after several failed laser treatments. Indeed, due to the cicatricial adhesion between the recurrent SGH and the mucosa, submucosal resection is rendered more difficult in salvage cases. In the case of bilateral or circumferential SGH, open excision is more appropriate than endoscopic treatment. Surgery starts with a transnasal intubation of the patient, and the tube may be maintained during the
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postoperative period. A horizontal skin incision is made at the level of the cricoid ring, and the strap muscles are reflected laterally in order to expose the thyroid cartilage and upper trachea after dividing the thyroid isthmus in the midline. After performing a horizontal intercartilaginous incision through the fourth and fifth tracheal rings, an RAE-tube is inserted into the inferior portion of the airway for ventilation. Using an accurate midline laryngofissure approach to avoid damage to the anterior laryngeal commissure, the airway is opened, and the nasotracheal tube is secured with a 3.0-Vicryl suture placed at its bevelled tip. The anaesthetist retrieves the tube cranially until a free operative field is obtained. A Lone Star retractor system (Lone Star medical products, TX, USA) may then be used to provide excellent exposure of the endolarynx and the subglottis by placing a few elastic stays on the laryngotracheofissure’s edges. With increased experience, some centres [15, 20] have limited the thyroid midline split to the subglottis to avoid violation of the anterior laryngeal commissure. Though less optimal, this exposure appears to be sufficient. With the help of magnifying glasses, the neighbouring mucosa is first infiltrated with an adrenalin solution, and a submucosal flap is then elevated. The haemangioma is dissected off the mucosa and perichondrium, and pledgets of Gelfoam soaked in adrenalin can be placed in the resulting submucosal pocket for 1–2 min. After the Gelfoam is removed, a drop of fibrin glue (Tisseel®) is used to reapproximate the mucosa on the perichondrium. The nasotracheal Portex Blue-Line® tube is gently pulled back with the 3.0 Vicryl thread into the larynx and pushed distally into the trachea. This serves as a temporary stent. The RAE-tube is then removed, and the transverse incision of the trachea is closed using 5.0 Vicryl sutures. If a full laryngofissure has been performed, then great care should be exercised to reapproximate both vocal cords exactly at the same level. If required, a small piece of cartilage, harvested on one side from the upper aspect of the thyroid ala, is used to increase the subglottic lumen below the anterior laryngeal commissure. The graft should never rise above this level to preserve the voice postoperatively. The graft is sutured in place using 5.0 Vicryl sutures. Non-resorbable sutures should never be used in laryngotracheal surgery, except for the fixation of stents. The patient is kept intubated for 24–48 h. Direct laryngoscopy to check the integrity of the mucosa on the resected side is performed prior to extubation. Although ET tube calibration may show an adequate
10 Subglottic Haemangioma (SGH)
subglottic airway lumen, oedema of the vocal cords must be appropriately assessed. Extubation and close monitoring in the PICU are indispensable until the child can be safely transferred to a regular in-patient room. Postoperative intubation time has been reported to range between 2 days and 1 week [1, 2, 17]. In a meta-analysis, Bitar et al. [2] evaluated the success rates and complications of different treatment modalities (Table 10.1). Open surgery was found to be the most efficient treatment, albeit with potential complications. It is mostly suitable for fast-growing tumours or bilateral tumours. With a success rate of 89%, CO2 laser is a viable option for slow-growing tumours or symptomatic infants having reached the quiescent period at the age of 10–12 months. If a proper technique and optimal laser parameters are used, then cicatricial SGS (~1.5%) should not occur. However, CO2 laser resection may require two to three endoscopic sessions to maintain a safe airway. From a theoretical point of view, intralesional steroid injections are the least invasive technique, but serial injections and ET-intubations are required to achieve a satisfactory result. Intubation-related complications such as pneumonia or pneumothorax have been reported. Systemic corticosteroids should be used only for a short trial with curative intent or as adjuvant postoperative therapy. Finally, tracheostomy was once considered the standard treatment for infants with SGH but has become obsolete in modern otolaryngology practice [5]. The morbidity and mortality risk (~1–3%) [13] along with the delay in speech and language acquisition make this modality a less attractive treatment option. However, in some difficult cases, tracheostomy may still be required, Table 10.1 Results and complications of different treatment modalities for SG haemangiomas [2] Type of Success rate Complications treatment Open surgery
49/50 ~ 98%
5/50 ~ 10.0%
CO2 laser
124/139 ~ 89%
SGS ~ 1.5%
19/21 ~ 90%
1/21 ~ 5.6%
25/102 ~ 25%
13/102 ~ 13.0%
ILCSI
a
Systemic CS
b
ILCSI, Intralesional corticosteroid injection b CS, Corticosteroids Tracheostomy as a sole or adjunctive measure was done in 128 cases The mortality rate was 1/128 ~ 0.8% a
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Fig. 10.4 Left posterolateral subglottic haemangioma treated with propanolol (2 mg/kg/day): (a) Initial condition: The SGH obstructs the subglottic space by 70%, causing rest dyspnoea and inspiratory stridor. (b) Situation 2 months after propanolol treatment: significant regression of the SGH. Symptom-free patient
and it remains a viable option in centres where modern equipment and expertise are lacking. In the future, propanolol might well supersede all other treatment modalities for children who do not have a contra-indication to the prescription of b-blocking agents (Fig. 10.4). At the time of this book’s publishing, experience is still very limited and needs further appraisal [7, 12, 14].
References 1. Bajaj, Y., Hartley, B.E., Wyatt, M.E., et al.: Subglottic haemangioma in children: experience with open surgical excision. J. Laryngol. Otol. 120, 1033–1037 (2006) 2. Bitar, M.A., Moukarbel, R.V., Zalzal, G.H.: Management of congenital subglottic hemangioma: trends and success over the past 17 years. Otolaryngol. Head Neck Surg. 132, 226– 231 (2005) 3. Bruckner, A.L., Frieden, I.J.: Infantile hemangiomas. J. Am. Acad. Dermatol. 55, 671–682 (2006) 4. Cotton, R.T., Tewfik, T.L.: Laryngeal stenosis following carbon dioxide laser in subglottic hemangioma. Report of three cases. Ann. Otol. Rhinol. Laryngol. 94, 494–497 (1985) 5. Cotton, R.T., Prescott, C.A.J.: Congenital anomalies of the larynx. In: Cotton, R.T., Myer III, C.M. (eds.) Practical Pediatric Otolaryngology, p. 511. Linpincott-Raven, Philadelphia/New York (1999) 6. D’Angelo, G., Lee, H., Weiner, R.I.: cAMP-dependent protein kinase inhibits the mitogenic action of vascular endothelial growth factor and fibroblast growth factor in capillary endothelial cells by blocking Raf activation. J. Cell. Biochem. 67, 353–366 (1997) 7. Denoyelle, F., Leboulanger, N., Enjolras, O., et al.: Role of propranolol in the therapeutic strategy of infantile laryngotracheal hemangioma. Int. J. Pediatr. Otorhinolaryngol. 73, 1168–1172 (2009) 8. Enjolras, O., Breviere, G.M., Roger, G., et al.: Vincristine treatment for function- and life-threatening infantile hemangioma. Arch. Pediatr. 11, 99–107 (2004)
9. Feuerstein, S.S.: Subglottic hemangioma in infants. Laryngoscope 83, 466–475 (1973) 10. Fishman, S.J., Mulliken, J.B.: Hemangiomas and vascular malformations of infancy and childhood. Pediatr. Clin. North Am. 40, 1177–1200 (1993) 11. Holinger, P.H., Brown, W.T.: Congenital webs, cysts, laryngoceles and other anomalies of the larynx. Ann. Otol. Rhinol. Laryngol. 76, 744–752 (1967) 12. Jephson, C.G., Manunza, F., Syed, S., et al.: Successful treatment of isolated subglottic haemangioma with propranolol alone. Int. J. Pediatr. Otorhinolaryngol. 73, 1821–1823 (2009) 13. Kremer, B., Botos-Kremer, A.I., Eckel, H.E., et al.: Indications, complications, and surgical techniques for pediatric tracheostomies – an update. J. Pediatr. Surg. 37, 1556–1562 (2002) 14. Leaute-Labreze, C., de la Roque, D.: Propranolol for severe hemangiomas of infancy. N. Engl. J. Med. 358, 2649–2651 (2008) 15. Messner, A.: Subglottic hemangioma. Otolaryngol. Clin. North Am. 41, 903–911 (2008) 16. Mulliken, J.B., Glowacki, J.: Hemangiomas and vascular malformations in infants and children: a classification based on endothelial characteristics. Plast. Reconstr. Surg. 69, 412–422 (1982) 17. O-Lee, T., Messner, A.: Subglottic hemangioma. Otolaryngol. Clin. North Am. 41, 903–911 (2008) 18. Pransky, S.M., Canto, C.: Management of subglottic hemangioma. Curr. Opin. Otolaryngol. Head Neck Surg. 12, 509–512 (2004) 19. Rahbar, R., Nicollas, R., Roger, G., et al.: The biology and management of subglottic hemangioma: past, present, future. Laryngoscope 114, 1880–1891 (2004) 20. Rutter, M.J.: Laryngeal webs and subglottic hemangiomas. In: Graham, J.M., Scadding, G.K., Bull, P.D. (eds.) Pediatric ENT, pp. 211–222. Springer, Berlin/Heidelberg (2008) 21. Sommers Smith, S., Smith, D.: Beta blockade induces apoptosis in cultured capillary endothelial cells. In Vitro Cell. Dev. Biol. Anim. 38, 298–304 (2002) 22. Vijayasekaran, S., White, D.R., Hartley, B.E., et al.: Open excision of subglottic hemangiomas to avoid tracheostomy. Arch. Otolaryngol. Head Neck Surg. 132, 159–163 (2006)
Ductal Cysts, Saccular Cysts and Laryngoceles
Contents
Core Messages
11.1
Ductal Cysts............................................................. 142
›› Ductal cysts:
11.2
Saccular Cysts......................................................... 142
11.3
Laryngoceles............................................................ 142
11.4
Treatment of Ductal Cysts, Saccular Cysts and Laryngoceles.................................................... 144
References............................................................................ 145
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11
−− Most frequent cysts in the pharyngolaryngeal region −− Mucus retention cysts secondary to the obstruction of the gland’s excretory duct −− Unrelated to the laryngeal saccule Saccular cysts and laryngoceles are rare (~2%) congenital lesions Saccular cysts are much more common than laryngoceles (85% versus 15%) Both correspond to an abnormal dilatation of the saccule, saccular cysts being mucus-filled and laryngoceles air-filled Symptoms: −− Present at birth −− Inspiratory stridor with respiratory com promise −− Muffled cry −− Position-dependent owing to asymmetric laryngeal obstruction −− Increased during agitation Diagnosis: −− Posteroanterior high-kilovolt X-rays −− Direct laryngotracheoscopy under general anaesthesia Anterior cyst: fullness of ventricular band Lateral cyst: fullness of ventricular band and aryepiglottic fold Treatment: −− Emergency needle aspiration −− CO2 laser excision in SML −− Rarely, open surgical excision
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11.1 Ductal Cysts Ductal cysts are the most common cysts found in the pharyngolaryngeal region. They result from the retention of mucus due to obstruction of the mucus gland duct, leading to a mucus retention cyst [9, 12, 13]. Depending on their location (subglottis or pharyngolarynx), ductal cysts may provoke upper airway obstruction [1] (Fig.11.1) and generate symptoms that are similar to saccular cysts or laryngoceles. Saccular cysts and laryngoceles exhibit anatomical similarities. They both result from abnormal dilatation or herniation of the saccule, which is mucus-filled in the case of saccular cysts and air-filled in the case of laryngoceles. In saccular cysts, there is no opening to the ventricle, whereas in laryngoceles, there is a residual opening that communicates with the ventricle.
11.2 Saccular Cysts Although more frequent than laryngoceles in the newborn, saccular cysts are rare (~1.5%) congenital lesions of the larynx [4, 8]. Diagnosis can often be made almost immediately after birth and is based on symptoms of laryngeal obstruction. Due to the unilateral nature of the lesion, the inspiratory stridor with respiratory distress is slightly position-dependent [10, 15]. Symptoms worsen with agitation, and the infant’s cry is often abnormal and typically muffled. Diagnosis may be established using posteroanterior high-kilovolt neck films, revealing a supraglottic
Fig. 11.1 Mucus retention cyst of the vallecula: (a) Preoperative view: the cyst causes a posterior prolapse of the epiglottis into the laryngeal inlet. (b) Postoperative view: after endoscopic CO2 laser resection, the epiglottis resumes its normal position
11 Ductal Cysts, Saccular Cysts and Laryngoceles
unilateral mass. The mainstay in diagnosis, however, is direct laryngoscopy under general anaesthesia. Two types of saccular cysts exist: anterior and lateral [5]. The anterior saccular cyst is characterised by a submucosal mass of the false vocal cord protruding through the anterior opening of the ventricle (Fig. 11.2). The lateral saccular cyst, which is the most common, presents as a fullness of the ventricular band. Typically, it extends posterosuperiorly into the pharynx underneath the mucosa of the aryepiglottic fold, and the latter may become enormously distended [3, 6]. When they become infected, these cystic lesions are referred to as mucopyoceles.
11.3 Laryngoceles These air-filled dilatations of the laryngeal saccule are extremely rare in newborns. Usually, they occur in older children or adolescents who play wind instruments, resulting in increased pressure on the laryngeal lumen [11]. In newborns, a laryngocele is by definition a congenital anomaly. When it remains confined within the endolarynx, it is called an internal laryngocele, and when the air-filled pouch herniates through the thyrohyoid membrane, it becomes an external laryngocele [2]. Both air-filled pouches may coexist, resulting in a combined laryngocele (Fig. 11.3). Due to obstruction of the saccular orifice, laryngoceles may become filled with mucus. In this case, they are indistinguishable from saccular cysts. Whether they contain air or fluid, treatment is similar for both entities.
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11.3 Laryngoceles
Fig. 11.2 Diagram of saccular cysts of the larynx: (a) Anterior saccular cyst (b) Lateral saccular cyst (Adapted from Holinger [7]. With permission)
a
b
c
Fig. 11.3 Diagram of laryngoceles: (a) Internal laryngocele (b) External laryngocele (c) Combined laryngocele (Adapted from Holinger [7]. With permission)
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11 Ductal Cysts, Saccular Cysts and Laryngoceles
11.4 Treatment of Ductal Cysts, Saccular Cysts and Laryngoceles Although the same basic principles apply to all of the lesions, only mucus-filled cysts are responsible for acute respiratory distress at birth [14]. If intubation proves difficult, then an emergency needle aspiration may be performed by the neonatologist or anaesthetist before the otolaryngologist is called for help. Diagnosis and treatment are conducted during the same session. Direct visualisation of the pharyngolarynx with a rod-lens telescope easily identifies the pathology, which is confirmed by diagnostic puncture. The larynx is exposed using a Benjamin–Lindholm laryngoscope, the anterior blade of which is placed in the vallecula. A quick inspection of the endolarynx and subglottis is made with a rigid rod-lens telescope, and the larynx is intubated with a 3.5 Portex BlueLine® tube through the laryngoscope. General anaesthesia with intermittent apnoeas or spontaneous respiration, when possible, provides good working
a
Fig. 11.4 Left lateral saccular cyst excised using the CO2 laser: (a) Preoperative view: the cyst greatly distends the aryepiglottic fold. (b) Peroperative view: situation immediately after resection of the cyst. (c) Postoperative view at 3 months: cicatricial tissue is seen on the pharyngo-epiglottic and aryepiglottic folds. Patency of the larynx is restored
c
conditions, enabling the complete excision of the cyst with a CO2 laser set to 3 W output power, CW/chopped mode and 250 m spot size at 400 mm working distance. Since the mucosa of the pharyngolaryngeal region contains larger capillaries, the CW mode achieves a better coagulating effect. Even though this procedure may induce some postoperative scarring, it is usually devoid of consequences on the voice and airway patency. The cyst must be completely removed because simple marsupialisation has proven ineffective in many cases (Fig. 11.4). The anterolateral cervical approach is indicated only in the case of an external laryngocele, but some authors also recommend the external approach for recurrent saccular cysts [16]. As for adults, the airfilled pouch can be resected without removing the upper aspect of the thyroid ala. For combined (external and internal) laryngoceles, the cyst is dissected through the thyrohyoid membrane and then removed after closing its laryngeal opening between the true and false vocal cords using interrupted 5.0 Vicryl sutures.
b
References
References 1. Ahrens, B., Lammert, I., Schmitt, M., et al.: Life-threatening vallecular cyst in a 3-month-old infant: case report and literature review. Clin. Pediatr. (Phila) 43, 287–290 (2004) 2. Barnett, R.J., Ceasar, S.C., Wisdom, G.S.: Laryngoceles and saccular cyst. J. La. State Med. Soc. 153, 170–173 (2001) 3. Bielamowicz, S., Bhabu, P.: Saccular cyst. Ear Nose Throat J. 81, 761 (2002) 4. Civantos, F.J., Holinger, L.D.: Laryngoceles and saccular cysts in infants and children. Arch. Otolaryngol. Head Neck Surg. 118, 296–300 (1992) 5. DeSanto, L.W., Devine, K.D., Weiland, L.H.: Cysts of the larynx–classification. Laryngoscope 80, 145–176 (1970) 6. Evans, D.A.: Saccular cyst of the larynx. Otolaryngol. Head Neck Surg. 128, 303–304 (2003) 7. Holinger, L.D.: Congenital laryngeal anomalies. In: Holinger, L.D., Lusk, R.P., Green, C.G. (eds.) Pediatric Laryngology and Bronchoesophagology, pp. 139–142. Lippincott-Raven, Philadelphia/New York (1997) 8. Holinger, L.D., Barnes, D.R., Smid, L.J., et al.: Laryngocele and saccular cysts. Ann. Otol. Rhinol. Laryngol. 87, 675–685 (1978)
145 9. Hsieh, W.S., Yang, P.H., Wong, K.S., et al.: Vallecular cyst: an uncommon cause of stridor in newborn infants. Eur. J. Pediatr. 159, 79–81 (2000) 10. Kastowsky, T.K., Stevenson, M.P., Duflou, J.A.: Sudden death from saccular laryngeal cyst. J. Forensic Sci. 51, 1144–1146 (2006) 11. MacFie, D.D.: Asymptomatic laryngoceles in wind-instrument Bandsmen. Arch. Otolaryngol. 83, 270–275 (1966) 12. Nishimura, B., Tabuchi, K., Aoyagi, Y., et al.: Epiglottic cyst in an infant. Auris Nasus Larynx 35, 282–284 (2008) 13. Pak, M.W., Woo, J.K., van Hasselt, C.A.: Congenital laryngeal cysts: current approach to management. J. Laryngol. Otol. 110, 854–856 (1996) 14. Thabet, M.H., Kotob, H.: Lateral saccular cysts of the larynx. aetiology, diagnosis and management. J. Laryngol. Otol. 115, 293–297 (2001) 15. Tosun, F., Soken, H., Ozkaptan, Y.: Saccular cyst in an infant: an unusual cause of life-threatening stridor and its surgical treatment. Turk. J. Pediatr. 48, 178–180 (2006) 16. Ward, R.F., Jones, J., Arnold, J.A.: Surgical management of congenital saccular cysts of the larynx. Ann. Otol. Rhinol. Laryngol. 104, 707–710 (1995)
Laryngeal and Tracheal Clefts
Contents 12.1 Pathogenesis and Definition................................... 148 12.1.1 Four Syndromes Are Encountered with LTOC........ 148 12.2 Classification........................................................... 148 12.3
Symptoms................................................................ 149
12.4
Diagnosis.................................................................. 149
12.5 Management............................................................ 150 12.5.1 Airway Control......................................................... 150 12.5.2 Control of Aspiration and Lung Infection................ 151 12.5.3 Endoscopic Repair.................................................... 151 12.5.4 Open Surgical Repair................................................ 153 References............................................................................ 156
12
Core Messages
›› Very ››
›› ››
›› ›› ››
››
uncommon pathology accounting for 0.5–1.5% of all congenital laryngeal anomalies Defined as a craniocaudal slit-defect of the “party wall” between the laryngotracheal airway and the upper digestive tract (pharynx, oesophagus) High prevalence (~60%) of associated (gastrointestinal, genitourinary, cardiac and craniofacial) anomalies Tracheo-oesophageal fistula (± atresia), gastro-oesophageal reflux and tracheo (broncho) malacia are the most common associated anomalies in non-syndromic patients Syndromic associations: Opitz-Frias (G) and Pallister–Hall syndromes, and VACTERL and CHARGE associations Classification into four types based on the craniocaudal extent of the cleft Symptoms: −− Correlated to the extent of the cleft −− Combined feeding–respiratory difficulties with coughing, choking and cyanotic attacks during feeding −− Recurrent aspiration pneumonia Diagnosis: −− Chest X-ray: non-specific signs of aspiration pneumonia are possible −− Oesophagram with water-soluble contrast: spillover into larynx and trachea −− Direct rigid laryngo-tracheo-bronchoscopy and SML in general anaesthesia: probing of posterior cleft
P. Monnier (ed.), Pediatric Airway Surgery, DOI: 10.1007/978-3-642-13535-4_12, © Springer-Verlag Berlin Heidelberg 2011
147
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›› Treatment:
››
››
−− Highly dependent on the extent of the cleft and the associated anomalies −− Airway support and protection from aspiration −− Control of gastro-oesophageal reflux −− Endoscopic repair for Type I, II and III clefts −− Open surgery for certain Type III and IV clefts or for relapses after failed primary endoscopic repair Management problems: −− Breakdown of repair site (11–15%) −− Residual tracheo(broncho)malacia −− Associated syndromic or non-syndromic anomalies Mortality: −− Related to associated anomalies (>60% of cases) −− Significant (~14% overall) −− Range: 6–50% depending on the extent of the cleft
A posterior laryngeal cleft (LC) may be limited to the interarytenoid region or involve the cricoid lamina. When the cleft is more extensive and reaches the cervical or intrathoracic trachea, it is termed a laryngotracheo-oesophageal cleft (LTOC). This condition is very uncommon, accounting for only 0.5–1.5% of all congenital laryngeal anomalies [8, 10]. When taking into account the minor cases that are frequently overlooked and undiagnosed, the actual figures are likely to be higher. More recent studies by Parsons [12] and Chien [2] reveal prevalence rates of 6.2% and 7.6%, respectively. These variations in prevalence figures may also reflect referral bias.
12.1 Pathogenesis and Definition The embryological development of LTOC is controversial and elusive [6, 11]. Whatever the exact mechanism may be, a failure of complete formation of the tracheooesophageal septum best explains the formation of tracheo-oesophageal fistulas/LTOCs. An LC is defined as a craniocaudal slit of the ‘party wall’ between the
larynx and pharynx, and in the case of an extension to the cervicothoracic trachea and oesophagus, it is defined as an LTOC. A slight male predominance is present [9]. The majority of cases are sporadic, with only few families presenting multiple cases [15]. There is a high prevalence of associated anomalies, particularly tracheo(broncho)malacia, gastro-oesophageal reflux and tracheo-oesophageal fistulae (~30% of cases) with or without oesophageal atresia. Yet other malformations of the gastrointestinal and genitourinary tracts, cardiovascular system or cervicofacial region may be part of the non-syndromic or syndromic associations.
12.1.1 Four Syndromes Are Encountered with LTOC • G (Opitz-Frias) syndrome, which includes other defects of the median line: cleft lip, cleft palate and hypospadias, with abnormal implantation of the external ears and hypertelorism. • The Pallister–Hall syndrome comprises CNS anomalies (hypothalamic hamartoma, hypopituitarism) along with imperforate anus, cardiac, pulmonary and renal malformations as well as distal extremity anomalies (syndactyly and postaxial polydactyly). • VACTERL (Vertebral anomalies, anal Atresia, Cardiac anomalies, Tracheo-oesophageal fistula, Ear anomalies, Rhinal anomalies and Limb anomalies) and CHARGE (Coloboma, Heart disease, choanal Atresia, Growth and mental Retardation, Genital anomalies and Ear anomalies) associations.
12.2 Classification The proposed classifications over the past 50 years [1, 4, 9, 13, 20] rely on the extent of the cleft, which correlates with the severity of symptoms, therapeutic challenges and prognosis. The Benjamin and Inglis classification, established in 1989, is the most widely used [1]. Four types of clefts can be distinguished: • Type I: supraglottic interarytenoid cleft extending down to the level of the vocal cords • Type II: partial cricoid cleft extending beyond the level of the vocal cords
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12.4 Diagnosis
Fig. 12.1 Modified Benjamin–Inglis classification of laryngotracheo-oesophageal clefts (LTOC): The subdivision of type III into type IIIa and IIIb allows the surgeon to better define the limits of endoscopic repair: Type 0: submucosal cleft, Type I:
interarytenoid cleft, Type II: partial cricoid cleft, Type IIIa: total cricoid cleft, Type IIIb: LTOC extending into the extrathoracic portion of the trachea, Type IVa: LTOC extending to the carina Type IVb: LTOC extending into one main-stem bronchus
• Type III: LTOC extending down into the cervical, extrathoracic trachea • Type IV: LTOC extending into the thoracic trachea and occasionally into one main-stem bronchus
and recurrent pneumonia are the rule. The degree of inspiratory stridor is linked to the amount of redundant mucosa that collapses into the laryngotracheal lumen during inspiration, whereas expiratory stridor may be indicative of tracheomalacia (Fig. 12.2). Depending on the severity of dyspnoea, the infant requires intubation or bilevel positive airway pressure (BiPAP) ventilation through a face mask. Type IV clefts show signs of early respiratory distress, such as coughing, choking and apnoeic and cyanotic spells. This condition requires immediate repair if possible.
With the advent of endoscopic repairs for extrathoracic clefts extending into the cervical trachea, the author has introduced a further subdivision of Type III into Type IIIa (complete cleft of the cricoid plate) and Type IIIb (cleft extending into the extrathoracic trachea) in order to better assess the limits of endoscopic repair in the future (Fig. 12.1).
12.3 Symptoms
12.4 Diagnosis
The severity of symptoms is directly related to the extent of the cleft. Although this is not pathognomonic of LTOCs, a combination of feeding and respiratory difficulties should always alert the physician to the diagnosis. Laryngomalacia, discoordinate pharyngolaryngeal function, severe gastro-oesophageal reflux disease and central neurological disorders are the differential diagnoses as these conditions may present similar symptoms. Certain Type I clefts are almost asymptomatic, except for some aspiration during feeding [17]. Other cases may present stridor, a hoarse cry and episodes of choking and coughing during feeding. Type II and III clefts display the same symptoms, albeit more frequent and more pronounced. Aspiration
As medical history and symptoms are non-specific, radiological studies and endoscopic investigations are mandatory. A chest X-ray may reveal non-specific signs of aspiration pneumonia. If an oesophagram with watersoluble contrast (Gastrograffin®) is performed, then spillover into the larynx and trachea may be seen. However, this sign is not pathognomonic as it may also result from functional swallowing disorders observed in some cases of laryngomalacia, unilateral vocal cord paralysis or discoordinate pharyngolaryngeal function. The mainstay of diagnosis is endoscopy. Transnasal flexible laryngoscopy, during spontaneous respiration with a face mask, is conducted to assess vocal cord function and to rule out laryngomalacia, signs of
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Fig. 12.2 Endoscopic view of a type III LTOC with redundant posterior mucosa herniated into the laryngeal lumen: (a)Endoscopic view (b)Corresponding histology (Reproduced from Holinger [5]. With permission)
pharyngolaryngeal aspiration, tracheomalacia and extrinsic tracheal compressions. The cleft can easily be diagnosed using rigid laryngotracheo-bronchoscopy, alternatively passing from the laryngotracheal to the pharyngo-oesophageal lumen. A handheld Benjamin–Holinger anterior commissure laryngoscope may be used to splay open the posterior commissure, rendering the cleft conspicuous. In the SML procedure, a right-angled probe is inserted through the posterior laryngeal commissure to assess the extent of the cleft. The length of the cleft must be measured precisely to select the most appropriate repair technique. The ENT surgeon should bear this rare condition in mind, otherwise a failure in probing the posterior commissure of the larynx may lead to misdiagnosis. Considering the high percentage of associated nonsyndromic or syndromic anomalies, a systematic evaluation of the child must be done; this should include a genetic consultation with karyotyping if deemed necessary, cardiac and renal ultrasounds, spine radiographs and thoraco-abdominal CT scans.
Table 12.1 Laryngo-tracheo-oesophageal clefts: indications for endoscopic and open surgical repairs
12.5 Management
12.5.1 Airway Control
The treatment approach is completely dependent on the length of the cleft [17]. Over the past decade, the indications for endoscopic repair have broadened. This minimally invasive surgical approach was initially reserved for certain Type I and minor Type II laryngeal clefts. With improvements in anaesthesia and endoscopic techniques, Type IIIa and even IIIb LTOCs can now be treated by this approach, provided that there are no severe concomitant congenital
In Types I, II and IIIa clefts, the degree of airway obstruction is linked to the extent of pharyngeal mucosa herniation. This phenomenon appears to protect against aspiration to some extent. If possible, non-invasive ventilation with CPAP or BiPAP through a face mask is the preferred treatment. Endotracheal intubation may induce an inflammatory reaction of the laryngotracheal mucosa, thereby increasing the risk of wound breakdown after endoscopic or open surgical repair.
Type of cleft
Type of surgical repair
I II
Endoscopic repair
IIIa IIIb
Open surgical repair
IV
anomalies. Immediate one-stage open surgical repair is indicated in the rare cases of intrathoracic extension of LTOCs (<20%), and in certain Type III clefts (Table 12.1). Prior to surgery, it is important to stabilise the airway, prevent lung infections and diminish aspiration. These measures may show a certain degree of efficacy in Types I to IIIa clefts, but often remain insufficient for longer clefts, which hence require immediate surgical repair.
12.5 Management
In Type IIIb clefts associated with significant tracheomalacia, a tracheotomy should be done below the caudal end of the cleft, thus retaining optimal conditions for subsequent endoscopic or surgical repairs. In Type IV clefts, deep intubation into the tracheo-oesophageal slit is usually sufficient to provide respiratory support until open surgical repair can be conducted.
12.5.2 Control of Aspiration and Lung Infection Thickening of fluids, prescription of PPI and daily pulmonary physiotherapy have proven useful in infants with minor clefts who do not undergo surgery within the first 24–48 h. Possible aspiration pneumonia must be treated at an early stage with antibiotics. More extensive clefts may require a small and soft naso-gastric tube before early surgical repair is conducted. Finally, Type IV clefts must be managed on a case-bycase basis, with treatment decisions depending on the severity of symptoms and associated comorbidities. In many cases, medical measures are ineffective. In addition to surgical repair of the cleft, the surgeon must take measures to control severe reflux where present.
12.5.3 Endoscopic Repair Treatment may not be required in Type I clefts with no aspiration. For symptomatic Type I–III clefts without significant comorbidities, an endoscopic repair should be attempted. If possible, endoscopic repair should be carried out without tracheotomy or with a low tracheotomy, if necessary, to facilitate the procedure. Open surgery is indicated only in cases where partial breakdown of the repair site occurs. The arguments in favour of an endoscopic repair without postoperative intubation are as follows: • A nasotracheal or tracheostomy tube exerting pressure on the posterior suture line increases the risk of superinfection of the reconstruction site, along with an increased risk of wound breakdown.
151
• Using an external open approach, the anterior midline incision of the larynx and trachea may have a negative impact on the reconstructed airway’s stability. • Finally, during the reconstruction, only the endoscopic approach provides an axial view of the airway and digestive tract. Hence it is easier to reconstruct an adequately sized airway without any excess or lack of intraluminal mucosa, both of which may result in laryngotracheal stenosis. The endoscopic repair is done under general anaesthesia in spontaneous respiration. A side-slotted Parsons laryngoscope is introduced distally to the vocal cords to spread apart the LTOC and gain access to its caudal extremity. The largest laryngoscope that fits into the cleft should be employed. Using the CO2 laser set to ultrapulse mode, 150 mJ/cm2, 10 Hz repetition rae, and 250 m microspot, a sharp incision of the mucosa at the lateral edges of the cleft is made from the distal end to the level of the cuneiform cartilages. With the same CO2 laser parameters, a precise incision of the mucosa, 3–5 mm in depth, is created to adequately separate the tracheal and pharyngo-oesophageal mucosal layers. At the lower end of the cleft, this procedure allows for optimal placement of stitches to avoid the risk of a recurrent fistula. Closure of the cleft occurs in two layers (Fig. 12.3). First, the tracheolaryngeal closure is performed in the distal to proximal direction by placing inverted stitches through the mucosa of the posterior membranous trachea, with the knots tied on the pharyngo-oesophageal side of the cleft repair. A 70-cm long, 5.0 Vicryl thread with a small TF plus needle is used with either a Storz or a MicroFrance needle holder. When tying the knots, a Pilling pusher is routinely employed (see Fig. 4.12c, Chap. 4). Sutures are tied to obtain meticulous mucosal approximation, with the cut surfaces facing inward. The second layer of suturing is placed in a similar fashion in the distal to proximal direction, with the knots tied on the mucosal surface of the pharyngo-oesophageal repair. The redundant pharyngeal mucosa plays a key role in sealing off. The upper limit of the cleft repair is situated just below the level of the cuneiform cartilages (Fig. 12.4). Once a certain degree of expertise in endoscopic suturing is attained, reconstruction of Type I–IIIa clefts becomes straightforward. For clefts extending into the cervical trachea (Type IIIb), the endoscopic procedure is more demanding. A full reconstruction
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Fig. 12.3 Diagram of laryngo-tracheo-oesophageal repair: In the case of long type IIIb clefts, the CO2 laser incisions and the two-layer closure are made in a step-wise fashion from caudal to cranial. This diagram shows the principle of endoscopic surgery:
Fig. 12.4 Endoscopic views of a type IIIb laryngeal cleft repair: (a)Endoscopic exposure: the Parsons laryngoscope is inserted below the vocal cords to splay the posterior cleft. (b) CO2 laser incisions with proper parameters: char-free incision, little bleeding. (c) End of LTOC repair. (d) Postoperative view at 2 years
(a) CO2 laser incision (red line). (b) Suturing of the tracheal layer with the knots tied on the pharyngeal side. (c) Suturing of the pharyngeal layer
a
b
c
d
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may take up to 2 h. To prevent apnoeas or the infant’s waking up, close cooperation with an experienced anaesthesiology team is necessary. In the case of apnoeas, a temporary intubation through the laryngoscope with a Portex Blue Line® tube is performed to reoxygenate the patient before continuing the endoscopic repair. For a very long cleft, the reconstruction is usually done in small stages using endoscopic suturing to avoid several reinstallations of the laryngoscope. Three rows of two-layer stitches are placed; then the laryngoscope is retrieved cranially for further cranial extension of the laser cuts; thereafter, a new series of three rows of double-layer stitches is performed. This procedure is repeated until the level of the cuneiform cartilages is reached. At times, when following this procedure, up to 20 stitches may be necessary. Meticulous care should be taken when placing the stitches to avoid partial breakdown of the repair site, which may lead to a small residual fistula. The infant is gradually woken up, without the need for a temporary intubation or tracheotomy. Positive inspiratory and expiratory pressure is supplied using a BiPAP system installed immediately during the wakeup phase following the anaesthesia. The infant is then transferred to the intensive care unit for surveillance. Towards the end of the operation, a small soft nasogastric tube (Fresenius®) is routinely placed, except in cases of Type I–II clefts where the infant resumes normal feeding the following day. Antibiotics are given routinely, whereas corticosteroids are only used in cases of slight laryngeal obstruction resulting from postoperative oedema. The most feared complication is a residual fistula resulting from partial breakdown of the suture line. Respiratory symptoms can always be improved by a low tracheostomy that must be placed distally to the lowest extremity of the cleft repair. However, when a residual fistula occurs in the cervical trachea, there is no laryngoscopic approach that can provide the necessary exposure. As the cleft is closed proximally, the insertion of a Parsons laryngoscope to gain access to the fistula is not possible. Furthermore, access from the pharynx below the cricoid is also impossible. At this stage, salvage surgery must be carried out through a laryngotracheal fissure, along with a low tracheostomy to facilitate the procedure.
12.5.4 Open Surgical Repair An open surgical approach is reserved for certain Type IIIb clefts, all Type IV LTOCs and as salvage surgery after failed primary endoscopic repair.
12.5.4.1 Extrathoracic LTOC A low tracheostomy and percutaneous endoscopic gastrostomy are established at the beginning of the surgery. An extended laryngo-tracheofissure covering the entire length of the cleft is carried out above the tracheostomy. Care must be taken to divide the anterior laryngeal commissure exactly in the midline. A Lone Star retractor system (Lone Star medical products, TX, USA) is used to keep the laryngotracheal fissure splayed open by elastic stays. On both sides of the cleft, two stay-retracting sutures are placed at the upper- and lowermost extremities of the mucosal slit, thus putting the edges under tension. Using a Beaver-knife, the mucosa is incised slightly off-side of the mucosal ridge, on one side more in the pharyngeal, and on the other side more in the tracheal aspect of the mucosa. A 4–5 mm deep groove is thus created on either side of the cleft between the tracheal and oesophageal mucosae. Haemostasis is achieved using a fine bipolar coagulation forceps or via topical application of adrenaline-soaked pledgets. Thereafter, the anterior oesophageal wall is closed with 5.0 Vicryl interrupted and inverted sutures up to the level of the posterior laryngeal commissure. A costal cartilage graft is harvested and carved to the appropriate rectangular size, as for conventional LTR with posterior grafting (see Fig. 19.5, Chap. 19). The PCCG is fixed into position using 4.0 Vicryl stitches to the clefted cricoid, and a tibial periosteum graft or a strip of perichondrium is interposed between the tracheal and oesophageal mucosal layers. The reconstruction is secured on both sides by four mastress sutures placed at the postero-lateral angle of the trachea, followed by submucosal injection of one or two fibrin glue (Tisseel®) drops. This procedure ensures optimal sealing of the reconstruction while preventing early superinfection. A running 5.0 Vicryl suture is then used to close the tracheal mucosa. A tracheal repair should be left without stenting, for any foreign body (ET tube, naso-gastric tube) may adversely
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affect the healing process. However, to calibrate the endolaryngeal reconstruction, a short LT-Mold may be used provided that it does not reach beyond the inferior edge of the cricoid ring. The advantage of having a stent to calibrate the reconstruction is offset by a higher risk of wound breakdown [14]. Yet, if the LT-Mold is snugly fixed to the anterior portion of the subglottis, then excessive pressure on the posterior reconstruction is avoided.
12.5.4.2 Intrathoracic LTOC Type IV clefts are more surgically challenging, but represent less than 20% of the already rare LTOCs. As a result, no single centre has extensive experience in their management. Type IV cleft is an emergency situation for the following reasons: Tracheotomy is unlikely to improve ventilation to the lungs, as the distal end of the cleft may reach the carina or one main-stem bronchus. Due to the risk of early lung infections, intubation straddling the trachea and oesophagus cannot be maintained for long. Finally, control of severe reflux must also be achieved. Repair of the thoracic tracheo-oesophageal ‘party wall’ is best achieved through an anterior cervicothoracic approach. Once the entire length of the trachea has been prepared, a transtracheal stitch may be used to fix the lower extremity of the ET tube, just above the carina for the rest of the procedure. However, repair on extracorporal membrane oxygenation (ECMO) is recommended as it facilitates surgery during the open phase of tracheal reconstruction. The tracheo-oesophageal common cavity is opened longitudinally along the right postero-lateral angle of the trachea (Fig. 12.5). A sufficiently large ET tube facilitates the calibration of the airway during the reconstruction. The posterior membranous trachea is then reconstructed by using a craniocaudal strip of the oesophageal wall, which is sutured to the right postero-lateral angle of the trachea. The remaining oesophagus is resutured longitudinally on itself. Due to the longitudinal suture line, a loss in circumferential calibre of the oesophagus has no negative impact on swallowing. Interposition of a muscular layer between the trachea and oesophagus has been recommended in order to reduce the risk of fistula formation. Usually, the left sternohyoid muscle is sectioned from its hyoid bone attachment and reflected into the thorax where it is secured between the trachea and oesophagus (Fig. 12.6). For the cervical portion of the cleft repair, the right hemithyroid gland and the right RLN are reflected laterally by carrying out the dissection on the outer surface
Fig. 12.5 Open surgical repair of Type IV LTOC through a combined right cervico-thoracic approach: longitudinal incision along the right tracheo-oesophageal groove from the origin of the right main-stem bronchus up to the level of the cricoid cartilage. Avoiding a long anterior tracheofissure helps maintaining a better tracheal framework
Fig. 12.6 Open surgical repair of Type IV LTOC through a combined right cervico-thoracic approach/posterior view of the tracheal repair: the oesophageal wall is pulled to the right postero-lateral angle of the trachea, where it can be adjusted so as to restore a correct tracheal arch around the ET tube. About onethird of the oesophageal circumference is used for reconstructing the posterior trachea. It is sutured longitudinally to the right postero-lateral angle of the trachea up to the level of the cricoid ring. As the oesophagus is closed longitudinally on itself, this does not create any oesophageal stenosis
of the tracheal rings. At this stage, if necessary, a tracheotomy is performed between the sixth–seventh tracheal rings in the lower neck. The tracheal reconstruction may be carried out up to the inferior border of the cricoid ring
12.5 Management
155
with the same technique as that used for repairing the intrathoracic portion. At the level of the larynx, a transverse section between the cricoid and the first tracheal ring is performed, along with a full laryngofissure. This provides optimal exposure for reconstructing the laryngeal and upper tracheal components of the cleft, without risking injuring the right RLN which is kept laterally to the tracheal dissection. The technique of laryngeal cleft reconstruction is identical to that described for extrathoracic LTOC repair. In continuity with the tracheo-oesophageal repair, the mucosa is incised on either side of the laryngeal cleft up to the level of the posterior laryngeal commissure. The redundant pharyngeal mucosa is first sutured using inverted stitches. Next, a rectangular costal cartilage graft is sutured to the clefted cricoid in order to restore an adequate interarytenoid space. The right sternohyoid muscle is then mobilised from its hyoid attachment and slit between the cervical portion of the trachea and oesophagus where it is secured with fibrin glue (Tisseel®). Next, the tracheal mucosa is closed with a running 5.0 Vicryl suture, and a short LT-Mold is chosen to fit the reconstructed subglottic airway, as done in extrathoracic LTOC repair (Fig. 12.7). The prosthesis is fixed with a 4.0 nonresorbable Prolene suture through the cervical trachea. Finally, the laryngofissure and the anterior cricotracheal opening are closed using interrupted 4.0 Vicryl stitches.
This technique used for Type IV LTOC repair provides several advantages. First, by avoiding an extensive anterior tracheofissure, it preserves the steadiness of the tracheal framework. Second, by recreating a steady cricoid plate with a PCCG, it restores an adequate interarytenoid space. Furthermore, there is no risk of injuring the right RLN and by interposing a vascularised muscular layer between the reconstructed trachea and oesophagus, the risk of recurrent fistula is also reduced. Lastly, the LT-Mold ensures proper sizing of the glotto-subglottic space. Lastly, to address gastro-oesophageal reflux, a Nissen or a Toupet fundoplication may be required. In cases of uncontrollable acid reflux, a gastric division with proximal drainage and distal gastrostomy may be indicated. It should be stressed that these challenging cases must be dealt with by a multidisciplinary team including thoracic and digestive surgeons, in addition to a highly competent anae sthesiology team. In the literature, rates of revision surgery for failed primary repair range from 11% [18] to 50% [16] for shorter clefts. For Type IV clefts, the 93% mortality rate reported in 1983 [19] dropped to 50% in 1996 [21]. In the case of shorter clefts, recent series have reported lower mortality rates averaging 14%, with a range from 6% [7] to 25% [3].
Fig. 12.7 Open surgical repair of Type IV LTOC through a combined right cervico-thoracic approach/cervical repair of LTOC: (a) through a laryngofissure, the reconstruction is made in three layers as for the repair of extrathoracic LTOC, with interposition of a costal cartilage graft to restore an adequate interarytenoid distance. The tracheal mucosa is closed with a
running 5.0 Vicryl suture. If the child does not require a tracheotomy, the ventilating ET tube is kept until a first extubation attempt is envisaged. Should the child require a tracheotomy, a short LT-Mold prosthesis that does not extend below the reconstructed cricoid plate must be used to optimise the final subglottic space. (b) final result after completion of the reconstruction
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References 1. Benjamin, B., Inglis, A.: Minor congenital laryngeal clefts: diagnosis and classification. Ann. Otol. Rhinol. Laryngol. 98, 417–420 (1989) 2. Chien, W., Ashland, J., Haver, K., et al.: Type I laryngeal cleft: establishing a functional diagnostic and management algorithm. Int. J. Pediatr. Otorhinolaryngol. 70, 2073–2079 (2006) 3. Eriksen, C., Zwillenberg, D., Robinson, N.: Diagnosis and management of cleft larynx. Literature review and case report. Ann. Otol. Rhinol. Laryngol. 99, 703–708 (1990) 4. Evans, J.N.: Management of the cleft larynx and tracheoesophageal clefts. Ann. Otol. Rhinol. Laryngol. 94, 627–630 (1985) 5. Holinger, L.D.: Congenital laryngeal anomalies. In: Holinger, L.D., Lusk, R.P., Green, C.G. (eds.) Pediatric Laryngology and Bronchoesophagology, pp. 139–142. Lippincott-Raven, Philadelphia/New York (1997) 6. Kluth, D., Steding, G., Seidl, W.: The embryology of foregut malformations. J. Pediatr. Surg. 22, 389–393 (1987) 7. Kubba, H., Gibson, D., Bailey, M., et al.: Techniques and outcomes of laryngeal cleft repair: an update to the Great Ormond street hospital series. Ann. Otol. Rhinol. Laryngol. 114, 309–313 (2005) 8. Moungthong, G., Holinger, L.D.: Laryngotracheoesophageal clefts. Ann. Otol. Rhinol. Laryngol. 106, 1002–1011 (1997) 9. Myer III, C.M., Cotton, R.T., Holmes, D.K., et al.: Laryngeal and laryngotracheoesophageal clefts: role of early surgical repair. Ann. Otol. Rhinol. Laryngol. 99, 98–104 (1990) 10. Narcy, P., Bobin, S., Contencin, P., et al.: Laryngeal anomalies in newborn infants. A propos of 687 cases. Ann. Otolaryngol. Chir. Cervicofac. 101, 363–373 (1984) 11. O’Rahilly, R., Muller, F.: Chevalier Jackson lecture. Respiratory and alimentary relations in staged human embryos.
12 Laryngeal and Tracheal Clefts New embryological data and congenital anomalies. Ann. Otol. Rhinol. Laryngol. 93, 421–429 (1984) 12. Parsons, D.S., Stivers, F.E., Giovanetto, D.R., et al.: Type I posterior laryngeal clefts. Laryngoscope 108, 403–410 (1998) 13. Pettersson, G.: Inhibited separation of larynx and the upper part of trachea from oesophagus in a newborn; report of a case successfully operated upon. Acta Chir. Scand. 110, 250–254 (1955) 14. Pezzettigotta, S.M., Leboulanger, N., Roger, G., et al.: Laryngeal cleft. Otolaryngol. Clin. North Am. 41, 913–933 (2008) 15. Phelan, P.D., Stocks, J.G., Williams, H.E., et al.: Familial occurrence of congenital laryngeal clefts. Arch. Dis. Child. 48, 275–278 (1973) 16. Rahbar, R., Rouillon, I., Roger, G., et al.: The presentation and management of laryngeal cleft: a 10-year experience. Arch. Otolaryngol. Head Neck Surg. 132, 1335–1341 (2006) 17. Rahbar, R., Chen, J.L., Rosen, R.L., et al.: Endoscopic repair of laryngeal cleft type I and type II: when and why? Laryngoscope 119, 1797–1802 (2009) 18. Robie, D.K., Pearl, R.H., Gonsales, C., et al.: Operative strategy for recurrent laryngeal cleft: a case report and review of the literature. J. Pediatr. Surg. 26, 971–973 (1991) 19. Roth, B., Rose, K.G., Benz-Bohm, G., et al.: Laryngotracheo-oesophageal cleft. Clinical features, diagnosis and therapy. Eur. J. Pediatr. 140, 41–46 (1983) 20. Sandu, K., Monnier, P.: Endoscopic laryngotracheal cleft repair without tracheotomy or intubation. Laryngoscope 116, 630–634 (2006) 21. Simpson, B.B., Ryan, D.P., Donahoe, P.K., et al.: Type IV laryngotracheoesophageal clefts: surgical management for long-term survival. J. Pediatr. Surg. 31, 1128–1133 (1996)
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Contents 13.1 Tracheomalacia....................................................... 159 13.1.1 Primary Diffuse TM or Posterior Membranous Dyskinesia.......................................... 159 13.1.2 Secondary Localised Tracheomalacia...................... 160 13.1.3 Oesophageal Atresia with Tracheo-Oesophageal Fistula................................... 165 13.2 Intrinsic Anomalies of the Trachea....................... 167 13.2.1 Congenital Tracheal Stenosis.................................... 167 13.2.2 Tracheal Agenesis and Atresia................................. 175 References............................................................................ 177
13
Core Messages
›› Incidence of congenital tracheal anomalies: ›› ››
›› ››
››
−− 1:60,000 live births −− 0.3–1% of all laryngotracheal stenoses An embryological model explaining congenital tracheal anomalies remains elusive The intimate embryological development of the trachea, oesophagus and cardiovascular system accounts for the frequency of associated mediastinal anomalies Congenital tracheal stenosis may result from: −− Extrinsic mediastinal anomalies −− Structural anomalies of the trachea itself Mediastinal anomalies include: −− Extrinsic tracheal compressions −− Vascular anomalies −− Cardiac anomalies −− Masses: cysts, neoplasms etc. −− Oesophageal atresia with tracheo-oesophageal fistula −− Laryngotracheo-oesophageal clefts Structural anomalies of the trachea include: −− Primary diffuse tracheomalacia −− Tracheal webs −− Tracheal stenosis with ‘O’ rings of cartilage −− Tracheal agenesis and atresia
Congenital tracheal anomalies are rare entities, accounting for 0.3–1% of all laryngotracheal stenoses [75], with an incidence estimated to be approximately 1:60,000 live births [42]. Experience managing these anomalies is consequently limited and widely dispersed. P. Monnier (ed.), Pediatric Airway Surgery, DOI: 10.1007/978-3-642-13535-4_13, © Springer-Verlag Berlin Heidelberg 2011
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Although embryological malformations of the aortic arch complex are fairly well understood [17, 30, 79], a unified model explaining the various structural anomalies of the trachea remains elusive [77]. Tracheal anomalies are often associated with other mediastinal anomalies of the cardiovascular system [10, 27, 29, 37, 53, 82] and oesophagus [9, 11, 93]. Mediastinal anomalies may impinge on the trachea via extrinsic compressions due to cardiovascular anomalies or masses, such as bronchogenic cysts or neoplasms [92]; alternately, the trachea may be impinged on by simultaneous abnormal development of the ‘party wall’ between the trachea and the oesophagus, namely, oesophageal atresia with tracheo-oesophageal fistula (TOF) [45] or laryngotracheo-oesophageal clefts (LTOC) (see Chap. 12). Structural anomalies of the trachea comprise primary diffuse tracheomalacia, tracheal webs, tracheal stenosis with circular ‘O’ rings of cartilage, and the exceedingly rare tracheal atresia or agenesis.
Symptoms Clinical symptoms of tracheal and mediastinal anomalies appear when the tracheal lumen is compromised by more than 50% or in the case of a TOF or an LTOC. Symptoms depend on the location, length and severity of the airway obstruction, as well as on the type and size of the oesophageal anomalies (oesophageal atresia with TOF and LTOC). Symptoms, which vary in intensity, include: biphasic stridor with a predominantly expiratory wheeze, brassy seal-barking cough, washing machine breathing, respiratory distress with chest retractions, cyanosis and apnoeic spells, hyperextension of the neck and recurrent pulmonary infections. Episodic dyspnoea may occur, and intubation difficulties may at times lead to the diagnosis. As none of the aforementioned symptoms are truly specific, imaging studies and endoscopic investigations are indispensable for correct diagnosis.
Patient assessment A lower airway infection with respiratory deterioration in a child can lead to the discovery of a previously unknown tracheal anomaly. If respiratory distress requires urgent airway stabilisation, then endoscopy should always precede intubation or tracheotomy.
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For the diagnostic approach, simple imaging studies, beginning with anteroposterior and lateral chest X-rays, and an oesophagram using water-soluble contrast medium may be performed. Chest X-ray films can reveal a variety of anomalies, such as pneumonia, atelectasis from mucostasis or obstructing emphysema, tracheobronchial aspiration, trachea-oesophageal fistula, as well as extrinsic airway compression, notably from a double aortic arch or a right retrooesophageal subclavian artery (arteria lusoria). However, fast acquisition helical CT scan and MRI with digital subtraction have superseded conventional radiologic studies [26, 93]. Anomalies of the cardiovascular system, seen in approximately 50% of all cases of congenital tracheal stenosis [1], as well as complete tracheal rings are often diagnosed accurately thanks to these techniques, which, however, do not allow to assess the dynamic nature of tracheo(broncho) malacia. Cine-computer tomography, a recently developed ultrafast imaging technique [54, 55], has proved efficient in determining the site, extent, severity and dynamics of airway collapse in the tracheobronchial tree. Cine-MRI allows for accurate detection of dynamic airway compression, as seen in primary or secondary tracheomalacia [25, 26]. In spite of this, the length of image acquisition limits the use of cine-MRI in clinical practice. The combined use of flexible and rigid bronchooesophagoscopy under general anaesthesia with spontaneous respiration is considered the gold standard method for determining the correct diagnosis, with additional use of modern imaging studies, especially in the case of extrinsic tracheobronchial compressions due to cardiovascular anomalies. Transnasal flexible laryngoscopy (TNFL), using face mask ventilation, allows not only to rule out potential concomitant upper airway anomalies, but also permits detection of diffuse primary tracheomalacia, vascular pulsatile compressions of the airway, intrinsic tracheal stenosis or TOF. To evaluate primary diffuse tracheomalacia, good teamwork with the anaesthetist is mandatory. The child must be examined in spontaneous respiration under general anaesthesia to detect a significant (more than 50%) bulging of the membranous trachea during coughing or during the expiratory phase of the respiratory cycle. A widening of the posterior membranous wall with a crescentshaped lumen of the trachea should alert the endoscopist to the possibility of primary tracheomalacia.
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Rigid bronchoscopy is then carried out to enable an in-depth evaluation of the suspected lesion. In case of tracheobronchomalacia, the rigid scope should not be inserted below the subglottis, in order to avoid splinting of the malacic airway, which can result in a missed diagnosis of tracheomalacia [71]. In our centre, endoscopic examination is performed according to the following standardised protocol: To assess the distal airway, a 2.2 mm bronchofibroscope or a long, rigid 2.7 mm telescope is inserted via a short (20-cm long) rigid ventilating bronchoscope placed in the subglottic area. The bronchofibroscope cannot always be passed beyond a long-segment tracheal stenosis with circular ‘O’ rings of cartilage without causing trauma to the underlying mucosa. Bronchoscopes should never be advanced forcefully through a congenital cartilaginous stenosis, nor should any attempt be made at dilating the stenosis. Alternatively, if the stenosis is too tight, a 1-mm (16-cm long) sialendoscope can be used in suspension microlaryngoscopy in order to assess the entire length of the long-segment tracheal stenosis. This procedure can also enable the detection of a tracheal bronchus distal to the stenosis (i.e., ‘bronchus suis’, an anomalous right upper lobe bronchus originating from the trachea), frequently associated with this condition [1]. If bronchoscopy is unsuccessful, a virtual endoscopy using helical CT scan reconstructions can reveal a long-segment tracheal stenosis that does not accommodate even a slim telescope [47]. Although accuracy rates of 95% have been reported with virtual endoscopy, the surgeon should attend to potential artefacts due to mucus retention distal to the obstruction. Furthermore, this technique provides no information on the quality of the tracheal mucosa. Less tight stenoses, such as those resulting from extrinsic vascular compressions, can easily be bypassed with a rigid ventilating bronchoscope of appropriate size. Tracheo-oesophageal fistulas are more conspicuous on the posterior membranous trachea than in the oesophagus. A Fogarty or thin angioplasty catheter can be passed through the fistula into the oesophagus. Inflation of the balloon facilitates localisation of the fistula during open surgery. As a last step, rigid oesophagoscopy is routinely carried out to assess extrinsic vascular compressions, signs of gastrooesophageal reflux or the level of a blind pouch in the case of oesophageal atresia.
Once a precise diagnosis has been established, a multidisciplinary team approach is mandatory in providing the best treatment possible.
13.1 Tracheomalacia Tracheomalacia (TM), defined as more than 50% collapsibility of the tracheal lumen during expiration, accounts for 50% of all congenital anomalies of the trachea [44]. The disease is classified into primary diffuse TM, which is relatively rare [72], and secondary localised TM.
13.1.1 Primary Diffuse TM or Posterior Membranous Dyskinesia Primary diffuse TM describes a weak and abnormally shaped long segment of tracheal framework. This condition results from the failure of the tracheal rings to reach their full maturity. The subsequent flaccidity of the tracheal vault engenders a widening of the posterior membranous wall, leading to abnormal development and hypotonia of the transverse tracheal muscle, responsible for posterior membranous dyskinesia. In severe cases, the normal cartilage-to-membranous wall ratio of 4–5:1 can decrease to 2:1 (Fig. 13.1). This condition can occasionally be seen in full-term newborns but is more frequent in premature babies, and may be associated with laryngomalacia [8]. Stridor is often insidious during the first few weeks of life. In 60% of the cases, symptoms appear before the age of 3 months, whereas in the remaining cases, the symptoms appear by 1 year of age. The hallmarks of this condition are: prolonged expiratory phase with wheezing, harsh barking cough, attacks of cyanosis, apnoeic spells and recurrent airway infections. Another characteristic of this dynamic condition is variability in both the symptoms and their intensity. Cyanosis and apnoeic spells often occur during feeding, coughing and crying. They are typically interspersed with normal periods of quiet sleep. Careful observation of the infant, however, reveals an expiratory wheeze even during the quiet period. The baby frequently assumes a position of neck hyperextension to straighten the
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Fig. 13.1 Normal versus malacic trachea: (a) Normal trachea during inspiration: The cartilaginous trachea to posterior membranous trachea ratio is 4–5:1. (b) Normal trachea during expiration: The slight bulging of the posterior membranous trachea does not cause any significant narrowing of the airway. (c) Primary tracheomalacia during inspiration: The anteroposterior distance is much shorter than the transverse diameter. The cartilaginous trachea to posterior membranous trachea ratio is 2:1. (d) Primary tracheomalacia during expiration: The intraluminal collapse of the posterior membranous wall causes severe (>50%) airway obstruction. This is the so-called membranous dyskinesia
trachea. As a rule, the infant should be left in the position he/she has adopted to alleviate the symptoms. This condition usually improves spontaneously during the first 2 years of life [76]. In the absence of concomitant mediastinal anomalies, treatment of primary diffuse TM consists of pulmonary physiotherapy, as well as prevention and treatment of both gastro-oesophageal reflux and respiratory infections. In moderate cases, bi-level positive airway pressure (BiPAP) is delivered through a face mask during periods of exacerbation. Although this treatment should not be pursued for very long periods of time and requires constant medical support, it can ‘buy time’ at home [24]. In very severe cases, a low tracheotomy enables stenting of the distal trachea with a long tracheostomy cannula, bypassing the upper airway, and thus significantly diminishing the dead space. Alternatively, if the obstruction is predominantly distal, an aortopexy can be performed [72]. Because this condition is self-limiting, and recovery generally occurs within 2 years of age, a temporary tracheostomy is both less invasive and more straightforward. Invasive procedures should be avoided if possible, since the complications associated with such procedures can be more problematic than the disease
itself [2]. Furthermore, airway stenting should be avoided in primary diffuse tracheomalacia until more experience has been gained with biodegradable stents [88]. Due to their increased thickness, Y-shaped silicone stents are not suitable for infant tracheae. Though immediate results using self-expandable metallic stents in the paediatric airway [31, 64] have been impressive, the longterm results of this procedure appear to be catastrophic. Severe complications have been reported, such as granulation tissue formation with subsequent cicatricial stenosis as well as fatal haemorrhages due to mediastinal migration of the stent [14, 97]. In the end, self-expandable uncoated metallic stents, which progressively integrate into the tracheal wall, can be extremely difficult or even impossible to remove. In addition, they prevent the normal growth of the stented airway segment [50].
13.1.2 Secondary Localised Tracheomalacia Secondary TM is characterised by a localised weakness of the trachea associated with mediastinal anomalies,
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such as extrinsic cardiovascular compressions, masses (e.g., cysts, tumours) or oesophageal malformations (atresia with TOF and LTOC) (Table 13.1). In general, symptoms of secondary TM are identical to those of primary TM, except for defects in the tracheooesophageal ‘party wall’ that increase tracheal secretions, producing ‘washer machine’ breathing. Only endoscopy and sophisticated imaging techniques such as MRI with digital subtraction angiography permit a precise assessment of the extrinsic tracheobronchial compression. A variety of abnormal developments of the aortic arch complex, subdivided into complete and incomplete vascular rings [10], may be encountered.
Aberrant Innominate Artery (Fig. 13.2) Symptoms are similar to those caused by extrinsic compressions of the trachea except for a potential decrease in stridor severity in the prone position. On endoscopic examination, the condition is easily recognised by a right anterolateral pulsatile compression of the mid-trachea. The endoscopic diagnosis is confirmed by compressing the vessel with the rigid bronchoscope tip and simultaneously palpating the right brachial or radial pulse, the intensity of which is likely to decrease. As the condition is self-limiting, surgical intervention is rarely necessary. However, innominate arteriopexy is indicated when apnoeic spells occur frequently or exertional dyspnoea becomes bothersome later in life.
13.1.2.1 Incomplete Vascular Rings Among the incomplete rings, accounting for slightly more than 50% of all cardiovascular anomalies, the innominate artery compression is the most common. Table 13.1 Secondary causes of tracheobronchomalacia 1. Extrinsic compression: • Vascular causes – Incomplete rings ~56% ° aberrant innominate artery ~36% ° aberrant right subclavian artery ~17% ° anomalous left pulmonary artery sling ~3% – Complete rings ~38% ° double aortic arch ° right aortic arch • Cardiac causes – Enlarged left atrium
berrant Right Subclavian A Artery (Fig. 13.3) Aberrant right subclavian artery, accounting for approximately 17% of all extrinsic vascular compressions, does not cause any symptoms as it does not significantly impinge on the posterior membranous trachea. This aberrant vessel originates from the descending part of the aortic arch on the left, runs posteriorly to the trachea and oesophagus in an oblique fashion then reaches the right lower neck. Interestingly, dysphagia may occur late in life, when the vessel becomes rigid from arteriosclerosis, obstructing the progression of the food bolus in the oesophageal duct. This condition is called dysphagia lusoria in the elderly [63].
nomalous Left Pulmonary A Artery Sling (Fig. 13.4)
– Enlarged pulmonary arteries • Mediastinal masses – Cysts ° bronchogenic, thymic ° lymphatic malformation – Neoplasms ° teratoma, lymphoma, neuroblastoma 2. Oesophageal atresia (OA) with tracheo-oesophageal fistula (TOF) 3. Prolonged intubation
This anomaly accounts for 3% of all extrinsic vascular compressions of the trachea. In such cases, the left pulmonary artery originates from the proximal portion of the right pulmonary artery and proceeds between the trachea and oesophagus before reaching the left lung. This anomaly is frequently associated with complete circular tracheal rings of cartilage that extend cranially beyond the stenotic segment of the pulmonary artery sling. In the absence of intrinsic tracheal stenosis, the vascular compression generates a localised malacic segment that must be addressed after rerouting the
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Fig. 13.2 Innominate artery compression of the right anterolateral aspect of the trachea: (a) Diagram: The anterior extrinsic compression is oblique from right to left and from cranial to caudal. (b) Transverse section: The trachea is compressed ante-
Fig. 13.3 Aberrant right subclavian artery: Diagram: The artery originates from the aortic arch on the left and passes behind the oesophagus, where it is recognised endoscopically by a pulsating extrinsic compression of the posterior wall RS, LS = Right and left subclavian arteries; RCC, LCC = Right and left common carotid arteries
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riorly by the innominate artery. (c) Endoscopic view: 15-yearold adolescent with persistent airway symptoms. Please note the right anterior extrinsic compression and the denuded cartilage resulting from intubation trauma
Fig. 13.4 Anomalous left pulmonary artery sling: It originates from the right pulmonary artery, encircles the lower trachea, and passes between the trachea and oesophagus. PA = Pulmonary artery; LPA = Left pulmonary artery; A = Aorta; V = Vagus nerve; BC = Brachiocephalic trunk; LCC = Left common carotid artery; LS = Left subclavian artery
13.1 Tracheomalacia
aberrant left pulmonary artery sling. Symptoms of respiratory distress are progressive, mostly occurring during an episode of lower airway infection.
13.1.2.2 Complete Vascular Rings (Fig. 13.5) These developmental abnormalities of the aortic arch complex, accounting for 38% of vessel-related airway compressions, are classified in three types [91]:
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not specific to the condition, as they are also observed in patients with other extrinsic tracheal compressions. Later in life, slight dysphagia to solid food may occur, reflecting significant oesophageal compressions (Fig. 13.6). The diagnosis is established using MRI with digital subtraction, which provides a clear assessment of the abnormal anatomical presentation. Comprehensive operative planning is thereby possible.
1. Double aortic arch with dominant right arch (~57% of cases) (Fig. 13.5a) 2. Right aortic arch with retro-oesophageal left subclavian artery and left ligamentum arteriosum (~25% of cases) (Fig. 13.5b) 3. Right aortic arch with mirror-image branching and left ligamentum arteriosum (~18% of cases) (Fig. 13.5c). Additional subtypes exist. As they are of less clinical relevance, they are not treated in this chapter [91]. In the case of complete vascular rings, symptoms are present at birth in the majority of patients [89], such as biphasic stridor with predominant wheezing, respiratory distress, recurrent lower airway infections, and cyanotic episodes. However, these symptoms are
Fig. 13.5 Main vascular rings responsible for extrinsic compression of the trachea: (a) Double aortic arch: It encircles both the trachea and oesophagus. The right arch is usually predominant. (b) Right aortic arch with retro-oesophageal left subclavian artery and left ligamentum arteriosum. (c) Right aortic arch
Fig. 13.6 Oesophagoscopic view of a right aortic arch with left aberrant subclavian artery. Significant dysphagia was noted at the age of 37 years
with the mirror-image branching and left ligamentum arteriosum. OE = Oesophagus; RS, LS = Right and left subclavian arteries; RCC, LCC = Right and left common carotid arteries; A = Aorta; LA = Ligamentum arteriosum
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13.1.2.3 Cardiac Anomalies Extrinsic airway compressions due to cardiac anomalies are mainly located in the left main stem bronchus, and very rarely, in the intermediate and right middle lobe bronchi. The sequence of events leading to these extrinsic bronchial compressions may be summarised as follows: A ventricular septal defect (including tetralogy of Fallot) with subsequent left-to-right shunts increases blood flow, and thus, the size of the pulmonary arteries, resulting in an indentation of the bronchial walls. As the airway compression is located distally to the carina, symptoms of expiratory wheezing and pulmonary manifestations such as unilateral air-trapping, recurrent or persistent atelectasis and pneumonia are prevalent. This diagnosis may become suspected during endoscopy, depending on the level, side, and shape of the intraluminal compression. Moreover, during endoscopic examination, other anomalies such as aberrant innominate artery, typical double aortic arch, pulmonary artery sling, and distended left pulmonary artery may be suspected, though this task can prove difficult in the case of complex vascular rings (Fig. 13.7).
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13.1.2.4 Tracheal Compression due to Mediastinal Masses A wide variety of congenital benign and malignant tumours may compromise the airway, resulting in a secondary localised tracheomalacia. The range of symptoms depends on the type of tumour. At birth, teratomas are already present, resulting in symptoms of airway distress. In contrast, lymphatic malformations and neuroblastomas grow in size during the first 2 years of life. Generally, bronchogenic cysts and other malignant tumours (lymphomas and rhabdomyosarcomas) occur and become symptomatic at a later stage during childhood. Computerised tomography scan and MRI are the diagnostic tools of first choice to assess the location and degree of airway compression, as well as the mediastinal extent of the mass. On rigid tracheobronchoscopy, a non-pulsating extrinsic compression indents the airway silhouette anteriorly in the case of teratomas, posteriorly in the case of neuroblastomas and frequently in the middle mediastinum in the case of bronchogenic cysts. A transtracheal needle aspiration should be attempted to obtain histological confirmation of the diagnosis.
13.1.2.5 Treatment of Extrinsic Vascular and Tumoural Compressions of the Tracheobronchial Tree
Fig. 13.7 Sites of extrinsic vascular compressions resulting from various congenital cardiovascular anomalies (Adapted and reproduced from Holinger [45]. With permission)
Severe airway compressions require early cardiothoracic intervention. In contrast, less severe indentations of the trachea by an aberrant innominate artery compression may not necessitate any surgery, as the condition is selflimiting, resolving spontaneously within the first 2 years of life. If symptoms of severe exertional dyspnoea persist, open surgery may be required later on in life to relieve the symptoms (see Fig. 13.2). Because these extrinsic vascular compressions are associated with localised malacia in most cases, the efficacy of the cardiovascular correction must always be assessed by intraoperative endoscopy, this being rather the exception than the rule in many centres. Yet, if left untreated, a malacic airway segment may cause persistence of airway symptoms. Before closing the thoracotomy or sternotomy, the ET tube is removed, and a rigid ventilating bronchoscope is inserted just above the level of the vascular repair. If a localised malacia is palpated
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by the cardiothoracic surgeon or visualised by the endoscopist, all efforts must be made to properly splint the airway during the same operative session. To this end, a costal cartilage can be harvested from the operative field to reinforce the malacic tracheal wall; it is then fixed into position with non-resorbable mattress sutures. Endoscopy must be used to assure that the tracheal wall is adequately stiffened. To avoid direct contact with the pulsating vessel, additional sheets of Vicryl meshes glued over the cartilage graft are used as a cushion. This external reinforcement of the airway, which takes only a few additional minutes, should be done systematically if access to the malacic segment is adequate. Using this procedure, the delicate problem of residual malacia with persistent airway symptoms is avoided. Resorbable (Vicryl plates) and non-resorbable materials are not recommended, as both are likely to provoke severe complications. In one of our own cases, a Vicryl plate was used to rigidify a severe localised malacia after an innominate arteriopexy, and this material caused erosion of the tracheal wall, requiring revision surgery. In another case, a Gortex muff was used to rigidify the distal trachea after correcting a left pulmonary artery sling, and it prevented normal tracheal growth from occurring. Endoscopic evaluation conducted 16 years later revealed a distal tracheal stenosis, which had been the source of the patient’s exertional dyspnoea. Taking the time and making the effort to accomplish a perfect primary repair with autologous material
will avoid difficult and often unsuccessful revisional surgeries. Though the incidence of secondary interventions is not high, there are individual reports of dramatic consequences. Good intraoperative teamwork is key to avoiding incomplete repairs.
13.1.3 Oesophageal Atresia with Tracheo-Oesophageal Fistula Oesophageal atresia with tracheo-oesophageal fistula (OA with TOF) occurs in approximately 1:5,000 live births [9, 11, 93]. It is associated with localised or more diffuse tracheomalacia in about 60% of the cases. The malacic segment is usually adjacent to the fistula. At this level, abnormal development of the posterior transverse tracheal muscle accounts for the localised weakness of the ‘party wall’ between the trachea and oesophagus. If not addressed during the primary fistula repair, the resulting posterior membranous dyskinesia may be troublesome. Posterior dyskinesia cannot be solely explained by overdistension of the blind proximal pouch of the oesophagus, since this condition is not observed in OA without TOF. There are five distinct Types of OA, with or without TOF, for which several different classifications exist (Fig. 13.8). The most common OA type comprises a
Fig. 13.8 Diagram of oesophageal atresia and tracheo-oesophageal fistula: The type III with a blind proximal oesophageal pouch and a distal fistula is by far the most common (Reproduced from Holinger [45]. With permission)
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Fig. 13.9 Examples of tracheo-oesophageal fistulae (TOF) with and without oesophageal atresia (OA): (a) Type III OA with TOF: The supracarinal fistula is large. (b) H-fistula without OA (type V): The small fistula is located higher in the mid-trachea
blind proximal oesophageal pouch along with a distal tracheo-oesophageal fistula into the distal oesophagus. The H-Type fistula without concomitant OA, generally of small diameter, is often found at a higher level of the trachea (Fig. 13.9).
13.1.3.1 Symptoms In all cases, symptoms of OA and TOF occur immediately after birth, except for H-Type fistula without OA. Due to the absence of dysphagia and only minor tracheal aspiration caused by a small oblique (from cranial trachea to caudal oesophagus) TOF, the diagnosis of this latter anomaly is often made late, sometimes not before adulthood. In all other types of OA and TOF, feeding problems with persistent aspiration as well as ‘washer machine’ breathing are suggestive of the condition. Failure to pass a nasogastric tube into the stomach and the presence of air in the gastric cavity add further clues to the clinical suspicion of OA with TOF. Fifty percent of the infants also present other congenital anomalies of the digestive, genitourinary or cardiovascular system [22, 32, 62]. These comorbidities generally dictate the overall prognosis, which is otherwise good following primary repair of OA and TOF, with estimated survival rates exceeding 90% [7].
evaluation. An oesophagram is reserved for cases where a small H-fistula or an additional fistula (as seen in Type IV of OA + TOF) might have been overlooked during the first endoscopy. If performed correctly, then rigid tracheobronchoscopy should enable the detection of a TOF. In order to avoid any bleeding that might obscure further inspection, atraumatic suction of excess mucus in the trachea is first performed. The posterior membranous trachea is then carefully examined for a TOF. In most cases, the fistula tract is easily visible on the smooth posterior tracheal wall. When immediate surgical repair is planned, a Fogarty or angioplasty catheter is passed through the fistula, and the balloon is inflated in the oesophagus. This procedure is instrumental in identifying the exact location of the fistula during a thoracotomy or cervicotomy for a proximal H-fistula. The child is then intubated, and rigid oesophagoscopy is conducted in order to determine the level of the blind upper pouch. In the oesophagus, an H-fistula or a proximal Type IV OA with double TOF (a rare entity) may be easily overlooked as the redundant oesophageal mucosa sometimes conceals the oesophageal orifice of the fistula. Additional anomalies, such as a cleft larynx, subglottic stenosis, or second fistula (seen in Type IV OA + TOF), must be sought in order to avoid incomplete surgical repair and re-interventions with subsequent recovery difficulties [46].
13.1.3.2 Patient Assessment 13.1.3.3 Management If there is a high degree of suspicion for OA with TOF based on the clinical presentation, immediate bronchooesophagoscopy is warranted for the preoperative
It is essential that an in-depth preoperative discussion takes place between the endoscopist and the paediatric
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surgeon in charge of the primary extrapleural or thoracoscopic OA repair [81, 84]. If a malacic segment is seen adjacent to the TOF, simple division and closing of the fistula will not suffice. Additionally, restoration of oesophageal continuity by single-layer end-to-end anastomosis and reinforcement of the posterior tracheal wall are indispensable in preventing residual malacia with persisting respiratory symptoms. A patch of tibial periosteum is best suited to rigidify the posterior membranous wall of the trachea with mattress sutures, whereas cartilage is less appropriate. Indeed, the stiffness of the cartilage may provoke an indentation on the posterior membranous wall. Based on the preoperative endoscopic findings, it is possible to anticipate the need for tracheal wall reinforcement, and in this case the procedure should be discussed prior to the intervention. If severe posterior tracheal dyskinesia is associated with the fistula, thoracoscopic repair is contra-indicated as the membranous wall cannot be reinforced with a patch of periosteum using this technique.
13.1.3.4 Postoperative Endoscopic Management In spite of a water-tight closure, the oblique course of a large TOF, as seen in Type III OA, may persist after repair and contribute to the retention of secretions resulting in a persistent disabling cough. Superficial KTP or CO2 laser vaporisation of the mucosa covering the inside of the funnel-shaped diverticulum and additional submucosal injection of Ethibloc® (a fast hardening aminoacid solution) have proven effective in creating a cicatricial closure of the diverticulum with immediate symptom relief (personal unreported experience). Treatment of residual malacia is more complicated and similar to that of primary TM (see Sect. 13.1.1). Due to the high risk of severe complications [14, 64, 97, 98], self-expandable metallic stents should not be used. In the future, biodegradable stents may possibly be used, provided they have proven safe and are easily available [88]. Finally, oesophageal strictures may occur at the site of an end-to-end anastomosis, especially when the two oesophageal stumps had initially been at some distance from each other. Anastomosis under tension predisposes the structures to leakage with subsequent stricture formation [81]. Sessions of endoscopic dilatation with Savary–Gilliard bougies are safe and effective in most cases [85]. The
bougies are passed over a pilot metallic thread inserted into the stomach under endoscopic and fluoroscopic control. In cases of oesophageal strictures, the need and rate for endoscopic sessions of dilation should be dictated by swallowing abilities rather than contrast studies or endoscopic findings. Gastro-oesophageal reflux is another potential complication of the surgery. Cranial mobilisation of the distal oesophagus for the end-to-end anastomosis may increase the incompetence of the lower oesophageal sphincter, thus worsening gastro-oesophageal reflux. The reflux favours the development of erosive oesophagitis and peptic strictures. For this reason, the administration of long-term perioperative proton pump inhibitors (PPI) is necessary. If fundoplication is envisaged, a less than 360° wrap of the gastric fundus around the lower oesophagus must be performed to prevent severe dysphagia due to the lack of efficient peristaltic waves in the abnormal oesophagus.
13.2 Intrinsic Anomalies of the Trachea Intrinsic structural anomalies affecting the trachea are extremely rare [3, 13, 39, 65]. Included in this group are diffuse primary tracheomalacia (described in Sect. 13.1.1), tracheal webs, tracheal stenosis with circular ‘O’ rings of cartilage as well as tracheal agenesis and atresia.
13.2.1 Congenital Tracheal Stenosis Tracheal webs are exceedingly rare. They may lead to significant narrowing of the airway, a source of biphasic stridor with predominant wheezing. At endoscopy, they manifest as thin intrinsic membranes with intact cartilaginous rings. Tracheal webs can easily be treated by simple dilation, and recurrence is rarely observed. In contrast to tracheal webs, congenital tracheal stenoses (CTS) are true developmental abnormalities of the trachea’s cartilaginous skeleton. Varying in location, severity and length, they are all characterised by the presence of complete, circular ‘O’ rings of cartilage. Roughly 50% of CTS are associated with an anomalous left pulmonary artery sling, while in another 50%, a tracheal origin of the right upper lobe bronchus
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(bronchus suis) is observed. Multiple other cardiovascular and digestive anomalies are encountered with varying frequencies [3, 6, 18, 39].
13.2.1.1 Symptoms and Patient Assessment In general, the onset of symptoms starts a few months after birth when the baby’s activities lead to an increase in respiratory demands. The length is less critical than the degree of the stenosis in producing symptoms. In fact, airway resistance is linearly proportional to the length of the stenosis, whereas resistance increases fourfold as the luminal diameter decreases [87]. Biphasic stridor with predominant wheezing, chest retractions, cyanotic attacks and recurrent pneumonia are likely to occur during the first respiratory illness. Although abnormalities on an anteroposterior chest X-ray may be suggestive of the diagnosis, a CT scan with 3D reconstructions and an MRI with digital subtraction are the examinations of first choice for achieving an accurate diagnosis (Fig. 13.10). These tools permit a clear assessment of the relationship between the airway and mediastinal cardiovascular anomalies if present (see Fig. 3.6, Chap. 3). If the diagnosis is not suspected and a bronchoscopy is performed, then when the condition is recognised, the endoscopist must be careful to prevent trauma during
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the examination. In fact, the slightest mucosal injury is likely to decompensate the compromised airway, provoking an acute airway crisis as a tracheotomy will be of no benefit with a long-segment congenital stenosis. In the absence of infection, tracheal cartilages are readily visible during endoscopy and must be precisely counted. Normal rings are easily distinguished from circular rings. When planning further surgical reconstruction, the utility of endoscopic assessment should not be underestimated.
13.2.1.2 Classification of CTS The stenotic segment is most often composed of complete circular ‘O’ rings of cartilage, but disorganised plates of cartilage or even a complete cartilaginous sleeve may occasionally be encountered [45]. Congenital tracheal stenoses are classified into four main types according to Grillo [34] (Fig. 13.11): • Type I: generalised tracheal hypoplasia Almost the entire trachea is stenotic while only the first to third cranial rings are normal. • Type II: funnel-shaped tracheal narrowing The abnormal tracheal segment varies by location and length, but always has a funnel configuration that is shaped from the cranial to caudal direction. • Type III: segmental tracheal stenosis This type is characterised by a short-segment stenosis located at different levels of the trachea, at times below an anomalous right upper lobe bronchus. • Type IV: bridge bronchus stenosis In this variant of Type III, the anomalous right upper lobe bronchus is in the proximity of the carina, and via horizontally branching bronchi, the stenotic bridge bronchus connects the proximal trachea to the rest of the lungs.
13.2.1.3 Management
Fig. 13.10 3D CT-scan reconstruction of a long-segment congenital tracheal stenosis (LSCTS) with circular ‘O’ rings of cartilage and right bronchus suis (postero-anterior view): Please note the narrowness of the trachea and the tracheal origin of the right upper lobe bronchus (white arrow)
The surgical management of CTS is dependent on the presence of circular ‘O’ tracheal rings of cartilage and the length of the stenosis. Single-stage surgery is always preferential and should include an intervention for concomitant cardiovascular anomalies as needed. Although proposed by some authors [69, 83], balloon dilatation associated with posterior longitudinal
13.2 Intrinsic Anomalies of the Trachea
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Fig. 13.11 Classification of congenital tracheal stenoses with circular ‘O’ rings according to Grillo [34]: Type I: long-segment stenosis involving almost the entire trachea Type II: funnelshaped trachea of various locations and variable lengths Type III: short-segment stenosis with or without anomalous right
upper lobe bronchus Type IV: bridge bronchus originating from a pseudo-carina created by the tracheal origin of the right upper lobe bronchus and connecting the trachea via horizontally branching bronchi to the rest of the lungs.Location of the left pulmonary artery sling is indicated when present
division of the circular cartilaginous rings is dangerous as it requires stenting of a small airway, which carries potential complications. The use of self-expandable metallic stents as proposed by Maeda et al. [69] is unacceptable in these circumstances. A minimally invasive approach does not necessarily translate into a minimally invasive procedure for the patient! In accordance with Grillo [34] and other colleagues [60], the author affirms that dilation and stenting are of no value in the treatment of CTS with circular tracheal rings, considering the current success rates of open surgical procedures [73]. Five main open surgical approaches have been used:
experience [78] as well as that of others [49] has shown that longer resections of trachea are possible, slide tracheoplasty is still much safer in a long-segment congenital tracheal stenosis, and should be used instead. The technique of primary resection with end-to-end anastomosis is straightforward and similar to that applied for acquired stenoses (see Sect. 22.1.1, Chap. 22). When the stenosis is located in the distal trachea or associated with concomitant cardiovascular anomalies, a sternotomy with cardiopulmonary bypass offers the best operating conditions. Surgery starts with a horizontal suprasternal cervicotomy. The strap muscles, the thyroid isthmus and the thymus are divided in the midline and reflected laterally. The use of a retractor ring (Lone Star medical products, TX, USA) with elastic stay hooks is very useful in small infants, as it provides excellent exposure. Additionally, the retractor ring facilitates the lifting of the trachea towards the surface of the operative field (see Fig. 20.4, chap. 20). The dissection of the trachea is limited to its anterior and lateral portions, with careful preservation of the vascular supply originating on both sides from the tracheo-oesophageal grooves. Dissection down to the carina is performed by staying in close contact with the cartilaginous rings and passing underneath the great vessels. In the absence of associated cardiovascular anomalies, a mid-tracheal stenosis can be resected
• • • • •
Resection with end-to-end anastomosis Enlargement patch tracheoplasties Tracheal autograft technique Slide tracheoplasty Tracheoplasty with cadaveric tracheal homografts
rimary Resection with P End-to-End Anastomosis This technique is reserved for short stenoses not exceeding one-third of the tracheal length. Although our own
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using a cervical approach as the infant larynx is located high in the neck. For intrathoracic stenoses, a partial sternotomy may be necessary. The length of the stenotic segment is easily appreciated from the outside. A second sterile ventilation circuit connected to an RAE tube is prepared and installed in the operative field. Stay sutures (4.0 Vicryl) are placed distally to the stenotic segment to keep the distal trachea in the operating field. The caudal transverse section between the tracheal rings is conducted first, keeping the posterior membranous trachea temporarily intact. At this stage, the distal trachea stump can be intubated with an RAE tube and connected to the second ventilation circuit. A transfixion stitch is used to temporarily secure the tube at the distal tracheal stump. The proximal transverse section of the trachea, including the posterior membranous wall, is made without prior separation from the oesophageal wall. This procedure allows for full preservation of the adjacent blood supply to the trachea. Dissection in the tracheo-oesophageal plane is only carried out over the stenotic segment down to the distal tracheal stump, and the membranous trachea is sectioned transversally. Anastomosis is performed with inverted 5.0 Vicryl sutures that are placed first at the posterolateral angle of the trachea. A running suture can be used on the posterior membranous trachea to obtain a perfect approximation of the mucosa. Following this, stay sutures are placed under tension to approximate both tracheal stumps, and posterolateral stitches are tied on the outside to secure the membranous reconstruction. The RAE tube is then removed, and the proximal ET tube is advanced distally into the tracheal stump. All anterior and lateral 5.0 Vicryl stitches are placed before being tied on the outside. On both sides of the anastomosis, the stitches are placed alternately around the first tracheal ring and through the second tracheal ring in order to avoid traction on the same suture line (Fig. 13.12). Air tightness is verified using saline immersion, and 0.5 cc of fibrin glue is applied at the anastomosis to achieve a perfect seal. Proper drainage and closure are done in an ordinary fashion. For more details regarding the cricotracheal or tracheal resections, the reader is referred to chaps. 20 and 22.
Anterior Patch Tracheoplasty This technique applies to paediatric patients presenting with a long-segment congenital tracheal stenosis
13 Congenital Tracheal Anomalies
Fig. 13.12 Segmental tracheal resection with end-to-end anastomosis: (a) Section of the trachea is made between two normal tracheal rings cranially and caudally. (b) Anastomosis with 5.0 Vicryl suture. Please note the alternate position of the stitches to avoid tension on the same suture line
(LSCTS) who cannot benefit from simple resection and anastomosis. Twenty-five years ago [6, 48, 52, 56, 96], the treatment of LSCTS consisted of an anterior longitudinal incision of the stenotic segment, with insertion of a patch to widen the lumen. In 1982, costal cartilage patch tracheoplasty was first described by Kimura et al. [56]. Two years later, Idriss et al. [48] modified the procedure by using a pericardial patch that required postoperative splinting with an ET tube (as in cartilage patch tracheoplasty), as well as suture suspension of the pliable pericardial patch and tracheal margins to the mediastinal structures [6, 21, 48, 52]. Innominate arteriopexy was also added to the procedure in some cases. The surgical procedure starts with a median sternotomy. The aortic arch and the great vessels are retracted, and an anterior midline vertical incision is made over the entire length of the stenosis. Control of the airway is facilitated by simply pushing the ET tube, initially placed in the subglottis, through the open airway down
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13.2 Intrinsic Anomalies of the Trachea
to the carina where it is temporarily secured by a transfixion stitch to avoid displacement during the reconstruction. The ET tube, acting as a stent, provides a simple way of estimating the width and length of the graft to be used for the reconstruction. Costal cartilage grafts are harvested from the lower part of the sternotomy. They are carved into appropriate shape to avoid bulging into the lumen and are sutured in situ by 5.0 interrupted Vicryl sutures, with the perichondrium facing the lumen. A pericardial patch is readily available, especially if an additional correction of cardiovascular anomalies is carried out during the same procedure. The patch is trimmed to the appropriate size and fixed with two running sutures around the expanded airway stented by the ET tube. As previously mentioned, additional suspension sutures are necessary to avoid luminal prolapse of the graft after removal of the ET tube 7–10 days after the operation (Fig. 13.13). Several reports in the literature [4, 6, 21, 48, 52, 55, 56, 96] describe the considerable difficulties encountered with granulation tissue formation. In these cases, and especially for grafts extending distally [48], multiple postoperative bronchoscopies were necessary. Additionally, in almost 30% of the cases, tracheotomies for airway stenting [21] were required.
Currently, these patch tracheoplasty techniques have largely been superseded by slide tracheoplasty.
Tracheal Autografts In 2001, one group (Backer, Chicago) introduced the concept of reconstruction with tracheal autografts [5] to decrease the rate of postoperative complications encountered with pericardial or costal cartilage patch tracheoplasties. The extensive circumferential tracheal mobilisation required for this technique is detrimental to the preservation of the tracheal vascular supply. The procedure starts with a vertical anterior midline incision through the entire stenotic segment, as performed during patch tracheoplasty. The narrowest central portion of the stenosis is resected, and to avoid excessive tension at the anastomosis, no more than 30% of the trachea should be removed. The excised mid-portion of the posterior trachea is used as a free tracheal autograft. The two anteriorly divided tracheal stumps are anastomosed posteriorly using interrupted sutures tied on the outside of the tracheal wall. Then, the free graft is sculptured to the appropriate lower configuration of the opened trachea. It is sutured in situ and if necessary, any residual proximal anterior
Fig. 13.13 Patch tracheoplasties for long-segment congenital tracheal stenosis: (a) Long-segment stenosis involving the entire length of the trachea. (b) Cartilage graft tracheoplasty. (c) Pericardial patch tracheoplasty. (d) Homograft tracheoplasty
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13 Congenital Tracheal Anomalies
Fig. 13.14 Tracheal autograft [5]: (a) Longitudinal anterior splitting of the stenotic segment. (b) Resection of the mid-portion of the stenotic segment (about one-third of the tracheal
length). (c) Posterior end-to-end anastomosis. (d) Anterior cartilage (±pericardial) patch tracheoplasty for coverage of the anterior tracheal defect
opening is closed over the ET tube with a pericardial patch. Generally, the free tracheal autografts are not large enough to completely fill the anterior tracheal opening (Fig. 13.14). Although this procedure achieves a more stable and better mucosalised reconstruction than pericardial patch tracheoplasty, the technique is significantly more complicated than simple slide tracheoplasty. It should be noted, however, that the author has had no hands-on experience with this reconstruction.
its midpoint, slitting the upper and lower stenotic segments anteriorly and posteriorly, respectively, and then sliding the two segments over one another [95]. In the case of extensive hypoplasia, the length of the trachea is shortened by half, its circumference is doubled and its cross-sectional area is quadrupled. According to Poiseuille’s law, the resistance to airflow is proportioned to the fourth power of the diameter [67]. It can, therefore, be easily understood that this surgical approach is highly appropriate for alleviating the symptoms of airway obstruction (Fig. 13.15). In over 50% of LSCTS cases, cardiovascular anomalies require intervention during the same operative session, necessitating a full median sternotomy and cardiopulmonary bypass. The surgery is performed as follows (Fig. 13.16): Through a small collar incision, the upper trachea is prepared from the cricoid ring down to the carina, by successively dividing the strap muscles, thyroid isthmus and thymic lobes in the midline. The trachea is prepared anteriorly and laterally, with careful preservation of the posterolateral vascular supply. A median sternotomy is made, and lower dissection is carried out down to both main stem bronchi. Prior to initiating a cardiovascular bypass with cannulae placed in the atrium and aorta, the stenotic segment’s length needs to be precisely measured and its midpoint marked with an intramural stitch. The first part of the intervention is
Slide Tracheoplasty Among the previously described surgical techniques for LSCTS [6, 21, 48, 52, 55, 56, 95, 96], slide tracheoplasty fulfils the basic requirements for adequate airway reconstruction, that is steady cartilaginous support and a fully mucosalised inner lumen. Needless to say, over the last decade, this technique has emerged as the best surgical option in LSCTS treatment [23, 57– 59, 61, 73, 86]. When comparing this technique, initially proposed by Tsang and Goldstraw in 1989 [95], to other techniques, superior results have been consistently reported. The basic principle consists of doubling the tracheal circumference at the level of the stenotic segment. This is achieved by transecting the stenosis horizontally at
13.2 Intrinsic Anomalies of the Trachea
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Fig. 13.15 Slide tracheoplasty: (a) The stenotic segment is transected exactly at its midpoint. (b) The stenotic segment is longitudinally slit anteriorly on its caudal segment and posteriorly on its cranial segment. (c) By gentle traction, the upper and
lower segments are slid over one another. (d) An oval-shaped, oblique from posterior to anterior anastomosis is made, thereby shortening the trachea by half and increasing its cross-sectional area by four
Fig. 13.16 Peroperative views of slide tracheoplasty: (a) Section through the midpoint of the stenotic segment reveals circular ‘O’ shaped rings. (b) Anterior longitudinal slit on the lower
trachea and posterior longitudinal slit on the upper trachea. (c) Reconstructed trachea with oval-shaped anastomosis
done under ventilation anaesthesia to minimise bypass time. Cardiac and vascular anomalies, consisting mostly of an anomalous left pulmonary artery sling, are first corrected by the cardiac surgeon. Airway reconstruction can then be initiated while the patient is still on cardiopulmonary bypass. The second part of the
airway surgery takes approximately one-half hour. The trachea is fully transected horizontally at its midpoint, which has previously been marked using a stitch. Great care should be taken to preserve the vascular supply to the inferior tracheal stump. The proximal stump is freed circumferentially until the posterior membranous
174
trachea of the first one or two normal tracheal rings is identified. The distal segment is slit longitudinally on its anterior aspect down to its lowermost extremity, usually the carina. The proximal segment is then divided longitudinally along its posterior wall until the last circular ring is cut. The membranous trachea of the first one or two normal tracheal rings must be clearly identified. The end of both segments is spatulated, and the two tracheal stumps are approximated slowly by sliding one over the other with traction on the stay sutures. The first stitch is placed posteriorly from the apex of the distal cartilaginous stump to the proximal membranous trachea. In most cases, interrupted 5.0 or 6.0 Vicryl sutures are used when performing the ovalshaped posterior-to-anterior anastomosis. At the proximal extremity, enough of the distal cartilaginous stump must be sutured posteriorly and laterally to expand the tracheal lumen as much as possible. Trimming of the lateral cartilage edges should thus be limited. Once the uppermost part of the anastomosis is accomplished, the ET tube is pushed and guided in the groove created by the distal tracheal stump. To avoid a figure-eight deformity of the reconstructed airway, a slight overlapping of the two tracheal edges is created, and the mattress stitches are passed through the full thickness of both cartilages, the knots being tied on the outside. The anterior tracheal segment is thus slightly intussuscepted onto the posterior tracheal segment (Fig. 13.17) on the longitudinal aspect of the anastomosis, and
Fig. 13.17 Technical detail of slide tracheoplasty anastomosis: (a) When both tracheal stumps are sutured side-to-side, a figureeight deformity of the trachea ensues. (b) Overlap of the lateral tracheal walls with transfixing mattress sutures prevents the figure-eight deformity from occurring
13 Congenital Tracheal Anomalies
the distal anterior end is sutured flush to the anterior wall of the carina. The integrity of the tracheoplasty is tested using saline immersion, and additional fibrin glue is applied onto the suture line. The thymic lobes are resutured over the anastomosis to provide a second layer of closure. The mediastinal drain is installed, and closure is performed in the usual fashion. The infant is extubated 24 or 48 h after surgery (Fig. 13.18). Slide tracheoplasty has emerged as the procedure of choice for LSCTS. Endoluminal granulations pose only a minor problem after slide tracheoplasty, requiring fewer postoperative endoscopic procedures (mean 2, range 0–3) compared to other interventions such as enlargement tracheoplasty (mean 13, range 3.8–16.8) [6, 18, 21]. In reviewing published data, it was found that no open surgical revisions were needed in the slide tracheoplasty series when compared to the large number in the enlargement tracheoplasty series (5 of 15 [3]; 3 of 12 [6]; 7 of 28 [4]). Surgical revisions were mainly due to luminal obstruction, graft rupture or recurrence of stenosis. Slide tracheoplasty did not result in recurrent nerve injuries or tracheal devascularisation [18, 23, 33, 73, 94, 95]. The functional midterm results following a slide tracheoplasty appear to be better than those with enlargement tracheoplasty. None of the slide tracheoplasty survivors have been recannulated or have shown respiratory problems [59]. After enlargement tracheoplasty, 2 of 23 patients [21] had a long-term tracheostomy, and 60% of the patients [3] experienced persistent dyspnoea [6] or required a stent for adequate respiration. Children with LSCTS and complex cardiac anomalies are thought to carry a higher risk of morbidity and mortality. Due to poor haemodynamics and the obstruction of small dimensional airways with increased mucosal reactivity, compensatory mechanisms are rendered inadequate, especially during respiratory tract infections [66]. When cardiac lesion surgery is conducted first, the patient often experiences severe and sometimes fatal respiratory compromise in the postoperative period. In contrast, when the tracheal lesion is repaired first, there is an increased postoperative risk of wound dehiscence and infection owing to impaired micro-circulation, hypoxia or malnutrition. To improve the postoperative outcome, it is crucial to surgically correct both disease entities concomitantly and effectively. The reasons for laryngotracheal growth after various surgeries have now been elucidated. Growth of tracheal
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13.2 Intrinsic Anomalies of the Trachea
Fig. 13.18 Late endoscopic results of slide tracheoplasty: (a) Preoperative view: long-segment tracheal stenosis with circular ‘O’ tracheal rings. (b) Postoperative view after slide tracheoplasty: Please note the figure-eight deformity of the reconstruc-
tion. (c) Postoperative result with overlap of the tracheal walls and mattress sutures: The reconstructed airway shows a more round-shaped lumen
cartilage tends to occur continuously over the convex side of a ring, with resorption taking place on the concave side, without identifiable growth centres [12]. Serial bronchoscopic observations of unoperated congenital stenoses have shown that the stenotic segment grows proportionally to the normal trachea. Manson et al. [74] have documented this growth using radiological studies. Macchiarini et al. [68] observed growth in an experimental model approximating slide tracheoplasty for long-segment congenital stenosis. Such growth has now been confirmed clinically by Grillo et al. [36, 70]. The slide tracheoplasty technique can also be used to treat a stenotic bridge bronchus. When very narrow and short, it can be resected with a side-to-side anastomosis between the proximal pseudo-carina (anomalous right upper lobe bronchus and bridge bronchus) and the true distal carina, as described by Grillo [35].
A silicone stent is placed inside the lumen, with the ET tube inserted slightly into its proximal extremity for ventilation. The stent is fixed on the tracheal wall, and the chemically preserved tracheal homograft is trimmed so as to reflect the defect of the anterior and lateral trachea. The homograft is sutured in place with horizontal-mattress resorbable sutures joining the allograft to the posterior tracheal remnants (see Fig. 13.13d). With long-term stenting, the allograft is revascularised progressively from the tracheal remnants and mediastinal structures. The worldwide experience reported in 1999 with this technique [51] shows a 16% mortality rate, with 1 out of 26 survivors needing a permanent tracheostomy.
T racheoplasty with Cadaveric Tracheal Homografts Following the work of Herberhold on chemical preservation of cadaveric trachea [40, 41], this technique has essentially been used for recurrent tracheal stenoses after failed primary patch tracheoplasties, but it is not indicated for primary repair of LSCTS. The principle is fairly similar to that of patch tracheoplasty. The anterior wall of the stenotic segment is opened, and slits in the posterior remnant of the stenosis are created in order to splay out the posterior wall.
13.2.2 Tracheal Agenesis and Atresia Tracheal agenesis is a rare congenital anomaly that is not compatible with prolonged life despite the current advances in medical technology. Its incidence is reported to be less than 1:50,000 live births, with a male predominance [16]. Associated anomalies, notably of the larynx, are found in over 90% of the cases. Prematurity is also a common associated (~50%) feature of this severe malformation [38]. The diagnosis can be made at birth if the neonate presents profound respiratory distress, is unable to produce an audible cry despite obvious physical efforts and cannot be intubated, showing improvement when ventilated by a face mask. Attempts at intubation are
176
generally unsuccessful, but an accidental oesophageal intubation may temporarily improve the respiratory condition if a tracheo-oesophageal fistula (TOF) coexists. In 1962, Floyd [28] proposed an anatomic classification of this malformation (Fig. 13.19). In Type I, accounting for approximately 20% of the malformations, there is atresia of part of the trachea with a normal but short distal trachea, normal bronchi and a tracheo-oesophageal fistula (TOF). Sixty percent of the reported cases are of Type II, where there is complete tracheal atresia along with normal bifurcation and bronchi. Type III, accounting for 20% of cases, presents no trachea, and the bronchi arise directly from the oesophagus. Prenatal ultrasonography may show bilateral uniform hyperechoic lungs and ascites if the trachea or larynx is obstructed completely. The inspissated lung secretions cause overdistension of the lungs. Contiguous compression of the foetal heart leads to low-output cardiac failure. In the presence of an oesophageal fistula, the lungs do not become enlarged as the fluid escapes through the fistula into the gastro-
13 Congenital Tracheal Anomalies
intestinal tract. An EXIT procedure [80] or ECMO must be performed expeditiously upon delivery. A systematic surgical approach to these anomalies does not exist, which may be accounted for by the rarity, variability and complexity of the defect [20]. Hiyama et al. have successfully treated one of two infant patients with the following procedures: gas trostomy and abdominal oesophageal banding, transoesophageal ventilation by endotracheal tube, tracheotomy and then T-tube, pharyngeal sump drainage followed by cervical oesophagostomy, and lastly, oesophageal reconstruction by colonic interposition at the age of 3 years [43]. Other reported patients have survived up to 6 years, with varying qualities of life [15, 90]. The use of the oesophagus as an air conduit can only be a temporary measure. The greatest challenge is to recreate a steady trachea by using the oesophagus and re-establish digestive continuity with a colon interposition. Thanks to research in tracheal allotransplantation [19] and to advances in tissue-bioengineering, the outcome for infants who present no other major congenital anomalies could improve in the future.
Fig. 13.19 Floyd’s classification of tracheal agenesis [28]: Type II is by far the most frequent, accounting for approximately 60% of all cases
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179 86. Rafay, M.A., Hajjar, W.M., Essa, M.A., et al.: Slide tracheoplasty for congenital tracheal stenosis with glottic stenosis. Asian Cardiovasc. Thorac. Ann. 12, 190–192 (2004) 87. Sandu, K., Monnier, P.: Congenital tracheal anomalies. Otolaryngol. Clin. North Am. 40, 193–217 (2007) 88. Sewall, G.K., Warner, T., Connor, N.P., et al.: Comparison of resorbable poly-L-lactic acid-polyglycolic acid and internal Palmaz stents for the surgical correction of severe tracheomalacia. Ann. Otol. Rhinol. Laryngol. 112, 515–521 (2003) 89. Smith, R.J., Smith, M.C., Glossop, L.P., et al.: Congenital vascular anomalies causing tracheoesophageal compression. Arch. Otolaryngol. 110, 82–87 (1984) 90. Soh, H., Kawahawa, H., Imura, K., et al.: Tracheal agenesis in a child who survived for 6 years. J. Pediatr. Surg. 34, 1541–1543 (1999) 91. Stewart, J., Kincaid, O., Edwards, J.: An Atlas of Vascular Rings and Related Malformations of the Aortic Arch System. Charles C. Thomas, Sprinfield (1964) 92. Triglia, J.M.: Tracheomalacia in children. In: Graham, J.M., Scadding, J.K., Bull, P.D. (eds.) Pediatric ENT, p. 244. Springer, Berlin/Heidelberg (2008) 93. Triglia, J.M., Guys, J.M., Louis-Borrione, C.: Tracheomalacia caused by arterial compression in esophageal atresia. Ann. Otol. Rhinol. Laryngol. 103, 516–521 (1994) 94. Tsang, V., Goldstraw, P.: Tracheal approach to pulmonary artery sling associated with funnel-shaped tracheal stenosis. Cardiovasc. Surg. 1, 300–302 (1993) 95. Tsang, V., Murday, A., Gillbe, C., et al.: Slide tracheoplasty for congenital funnel-shaped tracheal stenosis. Ann. Thorac. Surg. 48, 632–635 (1989) 96. Tsugawa, C., Kimura, K., Muraji, T., et al.: Congenital stenosis involving a long segment of the trachea: further experience in reconstructive surgery. J. Pediatr. Surg. 23, 471–475 (1988) 97. Urschel, J.D.: Delayed massive hemoptysis after expandable bronchial stent placement. J. Laparoendosc. Adv. Surg. Tech. A 9, 155–158 (1999) 98. Zakaluzny, S.A., Lane, J.D., Mair, E.A.: Complications of tracheobronchial airway stents. Otolaryngol. Head Neck Surg. 128, 478–488 (2003)
Part Acquired Laryngeal and Tracheal Stenoses
Acquired subglottic stenosis (A-SGS) represents one aspect of the multiple facets of intubation-related lesions that may damage the larynx. The term laryngotracheal stenosis (LTS) better reflects the glottic component of such lesions and should thus be used instead [1]. Ninety percent of all acquired LTSs result from post-intubation injuries [6, 10, 15, 24]. Since the introduction of long-term intubation for mechanical ventilatory support to newborns suffering from respiratory failure [2, 17], the incidence of LTS has declined from 8.3% in the 1980s to less than 2% in 2000 [8, 25]. Good tolerance of infant larynges to long-term ET intubation is attributed to the soft and pliable cartilaginous framework of the cricoid ring. This is due to the high fluid content of its cellular matrix [12]. With growth, the laryngeal framework becomes more rigid and partially ossifies at adulthood or after chronic injuries caused by ET tubes. Other less frequent causes of laryngeal stenosis include iatrogenic complications resulting from endoscopic laryngeal interventions (such as inappropriate use of lasers and dilation) [7, 14, 18, 22], benign tumours [13, 26], external blunt or penetrating trauma [5, 11], caustic or thermal injuries [9, 20, 21, 23], chronic inflammatory disorders [4, 16] and idiopathic causes [3, 19].
References 1. Albert, D.: Post-intubation laryngotracheal stenosis. In: Graham, J.M., Scadding, J.K., Bull, P.D. (eds.) Pediatric ENT, p. 224. Springer, Berlin/Heidelberg (2008) 2. Allen, T.H., Steven, I.M.: Prolonged endotracheal intubation in infants and children. Br J Anaesth 37, 566–573 (1965) 3. Bodart, E., Remacle, M., Lawson, G., et al.: Idiopathic subglottic stenosis in a nine-year-old boy: diagnosis and management. Pediatr Pulmonol 25, 136–138 (1998)
4. Cohen, S.R., Landing, B.H., King, B.K., et al.: Wegener’s granulomatosis causing laryngeal and tracheobronchial obstruction in an adolescent girl. Ann Otol Rhinol Laryngol Suppl 87, 15–19 (1978) 5. Cooper, A., Barlow, B., Niemirska, M., et al.: Fifteen years’ experience with penetrating trauma to the head and neck in children. J Pediatr Surg 22, 24–27 (1987) 6. Cotton, R.T., Evans, J.N.: Laryngotracheal reconstruction in children. Five-year follow-up. Ann Otol Rhinol Laryngol 90, 516–520 (1981) 7. Crockett, D.M., McCabe, B.F., Shive, C.J.: Complications of laser surgery for recurrent respiratory papillomatosis. Ann Otol Rhinol Laryngol 96, 639–644 (1987) 8. da Silva, O., Stevens, D.: Complications of airway management in very-low-birth-weight infants. Biol Neonate 75, 40–45 (1999) 9. Einav, S., Braverman, I., Yatsiv, I., et al.: Airway burns and atelectasis in an adolescent following aspiration of molten wax. Ann Otol Rhinol Laryngol 109, 687–689 (2000) 10. Fearon, B., Cotton, R.: Subglottic stenosis in infants and children: the clinical problem and experimental surgical correction. Can J Otolaryngol 1, 281–289 (1972) 11. Ford, H.R., Gardner, M.J., Lynch, J.M.: Laryngotracheal disruption from blunt pediatric neck injuries: impact of early recognition and intervention on outcome. J Pediatr Surg 30, 331–335 (1995) 12. Hawkins, D.B.: Hyaline membrane disease of the neonate prolonged intubation in management: effects on the larynx. Laryngoscope 88, 201–224 (1978) 13. Healy, G.B.: Neoplasia of the pediatric larynx. Otolaryngol Clin North Am 17, 69–74 (1984) 14. Healy, G.B., Strong, M.S., Shapshay, S., et al.: Complications of CO2 laser surgery of the aerodigestive tract: experience of 4416 cases. Otolaryngol Head Neck Surg 92, 13–18 (1984) 15. Holinger, P.H., Kutnick, S.L., Schild, J.A., et al.: Subglottic stenosis in infants and children. Ann Otol Rhinol Laryngol 85, 591–599 (1976) 16. Lebovics, R.S., Hoffman, G.S., Leavitt, R.Y., et al.: The management of subglottic stenosis in patients with Wegener’s granulomatosis. Laryngoscope 102, 1341–1345 (1992) 17. McDonald, I.H., Stocks, J.G.: Prolonged nasotracheal intubation. A review of its development in a paediatric hospital. Br J Anaesth 37, 161–173 (1965) 18. Meyers, A.: Complications of CO2 laser surgery of the larynx. Ann Otol Rhinol Laryngol 90, 132–134 (1981)
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182 19. Modgil, G., Havas, T., Mellis, C.: Idiopathic subglottic stenosis and the relationship to menses in a 12-year-old girl. J Paediatr Child Health 41, 374–376 (2005) 20. Rafeey, M., Shoaran, M.: Clinical characteristics and complications in oral caustic ingestion in children. Pak J Biol Sci 11, 2351–2355 (2008) 21. Riffat, F., Cheng, A.: Pediatric caustic ingestion: 50 consecutive cases and a review of the literature. Dis Esophagus 22, 89–94 (2009) 22. Rinne, J., Grahne, B., Sovijarvi, A.R.: Laryngeal stenosis following papillomatosis – a report of three severe cases. Int J Pediatr Otorhinolaryngol 5, 309–316 (1983)
Part III Acquired Laryngeal and Tracheal Stenoses 23. Rosen, D., Avishai-Eliner, S., Borenstein, A., et al.: Lifethreatening laryngeal burns in toddlers following hot liquid aspiration. Acta Paediatr 89, 1018–1020 (2000) 24. Shah, R.K., Lander, L., Choi, S.S., et al.: Resource utilization in the management of subglottic stenosis. Otolaryngol Head Neck Surg 138, 233–241 (2008) 25. Walner, D.L., Loewen, M.S., Kimura, R.E.: Neonatal subglottic stenosis-incidence and trends. Laryngoscope 111, 48–51 (2001) 26. Ward, R.F.: Neoplasia of the pediatric larynx. In: Fried, M.P. (ed.) The Larynx, pp. 171–177. Mosby-Yearbook, St. Louis (1996)
Acquired Post-Intubation and Tracheostomy-Related Stenoses
Contents
Core Messages
14.1
›› Ninety percent of all laryngotracheal stenoses
14.2
Acute Lesions and Cicatricial Intubation Sequelae................................................ 185 Prevention of Acute Intubation Lesions............... 186
14.3 Treatment of Acute Intubation Lesions................ 189 14.3.1 Treatment of Soft-Tissue Stenosis without Mucosal Necrosis........................................ 189 14.3.2 Anterior Cricoid Split (ACS).................................... 190 14.3.3 Treatment of Obstructive Granulation Tissue........... 191 14.3.4 Correct Tracheostomy Placement in case of Impending Laryngotracheal Stenosis................... 194
›› ››
14.4 Acquired Tracheal Stenosis.................................... 195 14.4.1 Tracheal Incision-Related Stenosis........................... 196 14.4.2 Cannula-Related Stenosis......................................... 197 References............................................................................ 198
›› ››
›› ›› ›› ››
14
are due to post-intubation injuries The incidence of post-intubation stenosis ranged from 0.9% to 3% in 2000 Predisposing factors of post-intubation stenosis include: –– Patient: age, laryngeal size and shape, systemic diseases or gastro- oesophageal reflux –– ET tube: oversized, excessive hardness or poor biocompatibility –– Intubation: traumatic and multiple intubations, emergency intubation followed by tracheotomy –– Nursing: poor patient sedation, excessive ET tube motion, nasogastric tube or traumatic ET suctions The duration of intubation is only one predisposing factor to post-intubation stenosis Failed extubation or dysphonia persisting beyond 3 days after extubation requires direct laryngoscopy in order to assess the degree of acute post-intubation injuries In premature babies and full-term newborns, the anterior cricoid split may render the need for tracheotomy after extubation failures unnecessary An asymptomatic congenital subglottic stenosis (C-SGS) must be suspected in the case of a difficult intubation Acute obstructive lesions due to intubation must be promptly treated, even if tracheostomy appears unavoidable to secure the airway Acquired tracheal stenosis is primarily a sequela of tracheostomy
P. Monnier (ed.), Pediatric Airway Surgery, DOI: 10.1007/978-3-642-13535-4_14, © Springer-Verlag Berlin Heidelberg 2011
183
184
14 Acquired Post-Intubation and Tracheostomy-Related Stenoses
Intubation trauma and pressure-induced ET tube injuries have been identified as the main local factors contributing to post-intubation stenosis. A traumatic intubation may be due to anatomical differences or a lack of experience on the part of the anaesthesiologist. Other possible factors include an oversized ET tube, an insufficiently anaesthetised patient, the presence of undiagnosed congenital airway narrowing, as well as faulty intubation techniques. As a rule, when there is even the slightest resistance, an ET tube must never be forcibly inserted into the larynx. Whilst the tube size may have been appropriately chosen for the infant’s age, the patient may have an unsuspected congenital narrowing of the larynx and trachea (e.g., Down’s syndrome, cardiovascular congenital anomaly). In other instances, a faulty technique
Fig. 14.1 Faulty technique of intubation: (a) Diagram: a rotating motion should never be imparted to the anaesthesiology laryngoscope. In infants, this manoeuvre exposes the epiglottic petiole in a frontal plane, thereby preventing easy insertion of the endotracheal tube into the subglottis. (b) Endoscopic view: acute traumatic lesion at the anterior laryngeal commissure resulting from a faulty intubation technique
Fig. 14.2 Diagram of the potential sites of pressureinduced endotracheal tube injuries in the larynx: (a) Maximum pressure is exerted on the medial aspect of the arytenoid cartilages (arrows). (b) Other sites of predilection for pressure-induced necrosis include the posterior laryngeal commissure, and the posterolateral and circumferential subglottis (arrows)
may lead to frontal exposure of the epiglottic petiole where the tip of the ET tube thrusts against the anterior laryngeal commissure during intubation, thereby causing severe mucosal injuries (Fig. 14.1). Even after a short period of intubation, the presence of mucosal tears, haematomas and arytenoid luxation can lead to a failed extubation. Although a traumatic intubation may not always lead to the development of severe endolaryngeal lesions, in the case of prolonged intubation, it can aggravate ET tube injuries. The ET tube always lies in the posterior glottis because of its oro-pharyngeal curvature in the sagittal plane, thus it exerts its maximal brunt on the mucosa of the surrounding structures. When the pressure of the ET tube exceeds the capillary mucosal perfusion pressure (~20–40 mmHg), ischemic necrosis ensues (Fig. 14.2).
14.1 Acute Lesions and Cicatricial Intubation Sequelae
Oedema, erosions and ulcerations with exposed perichondrium and cartilage are the main features of this evolving process. Contrary to published reports [24], the degree of ischemic necrosis is more significant than the actual duration of intubation. Major changes are still possible within 48–72 h of intubation [9]. Superinfection due to prolonged intubation, however, increases the severity of perichondritis and cartilaginous necrosis. Tracheotomy performed at this stage worsens the condition by increasing the bacteriologic contamination of the airway [18]. The process of repair begins slowly, with granulation tissue formation creeping from the edges of the denuded cartilage, thus providing a vascularised bed for reepithelialisation. As granulation tissue grows significantly faster than the epithelium, it often leads to excess tissue that may cause airway obstruction and subsequent scarring. In 2008, Benjamin and Holinger [6] updated their previous work on this topic [4] with outstanding illustrations of acute intubation lesions and their cicatricial counterparts.
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In the absence of intubation trauma, supraglottic injuries are infrequent and mostly minor. They show nonspecific erythema or oedematous swelling of the ventricular bands without necessarily leading to future sequelae. Oedema of the vocal cords and subglottis
without exposed cartilage may cause acute airway obstruction that usually resolves thanks to conservative medical therapy (see Fig. 14.9). More severe and typical intubation lesions are associated with ischemic erosions and ulcers of the glottosubglottic region. The most vulnerable structures are the medial aspect of the arytenoids where the cartilage is protected only by the mucoperichondrium. Pressure necrosis from the indwelling ET tube produces ulcerated troughs, with flanges of granulation tissue at the vocal process of the arytenoids (Fig. 14.3). In more severe cases, the excess granulation tissue may completely fill the posterior glottis, thereby significantly restricting the glottic lumen (see Fig. 14.12). Other lesions may occur in the cranial portion of the V-shaped infant cricoid where the round-shaped ET tube exerts maximum pressure on the posterolateral side, which can lead to ulceration of the exposed perichondrium and cartilage (Fig. 14.4). The ET tube may exert its maximal pressure against a small cricoid ring, leading to concentric subglottic ulcerations, or against the posterior laryngeal commissure where annular ulcerations may occur. Acute post-intubation injuries of the larynx are summarised in Table 14.1. In the absence of treatment, acute intubation lesions may evolve into stenotic [1] or non-stenotic cicatricial laryngeal sequelae that significantly impact on the patient’s quality of life. Non-stenotic laryngeal sequelae of an ET tube include: scarring at the posterior glottis, cicatricial furrows at the medial aspect of the arytenoids and fibroepithelial polyps at the vocal process of the arytenoids
Fig. 14.3 Acute lesions of intubation at the posterior glottis: (a) Granulation tissue at the vocal processes of the arytenoids in response to pressure necrosis due to the endotracheal tube.
(b) Exposed cartilage at the medial aspect of both arytenoid cartilages. (c) Corresponding histology for the same type of lesions (Reproduced from Holinger [14]. With permission)
14.1 Acute Lesions and Cicatricial Intubation Sequelae
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Fig. 14.4 Posterolateral ulcers in the V-shaped upper portion of the cricoid cartilage: (a) Deep ulceration with exposed cartilage (arrow). (b) Corresponding histological picture: The arrow points at the denuded cricoid cartilage (Reproduced from Holinger [14]. With permission)
Table 14.1 Acute post-intubation injuries of the larynx • Supraglottis
14.2 Prevention of Acute Intubation Lesions
– Absent to minor lesions – Oedematous protrusion of ventricular mucosa – Erythema or oedematous swelling of the ventricular bands • Glottis – Non-specific swelling in Reinke’s space of the vocal cords – Pressure-induced ischemic necrosis : ° Ulcers at the medial aspect of the arytenoids with flanges of granulation tissue at vocal processes ° Medial exposure of the cricoarytenoid joint ° Posterior interarytenoid ulcer • Subglottis – Non-specific oedematous swelling – Posterolateral cricoid ulcers – Concentric subglottic ulceration
(Fig. 14.5). All of these lesions can cause severe dysphonia. Stenotic laryngeal sequelae include interarytenoid adhesions at the posterior laryngeal commissure or subglottic level, posterior glottic stenosis (PGS) with or without cricoarytenoid joint fixation, concentric subglottic cicatricial narrowing (Fig. 14.6) and lastly mucous retention cysts (see Fig. 18.5, Chap. 18). Combined glottic and subglottic stenoses are the most challenging to treat [10]; they are encountered in very severe cases or when prolonged intubation has been preceded by a trauma (Fig. 14.7).
A good understanding of the factors involved in the development of laryngotracheal stenosis (LTS) is a prerequisite for appropriate prevention. The various factors accounting for the development of acute intubation lesions relate to the patient, ET tube, intubation technique and nursing care in the paediatric intensive care unit (PICU) (Table 14.2). Systemic factors causing hypoperfusion of the mucosa (such as systemic shock, hypotension, anaemia and sepsis), gastro-oesophageal reflux or infections aggravating mucosal damage must be actively treated in order to prevent exacerbation of ET tube trauma. Keys to avoiding intubation complications are the use of an appropriately sized ET tube and an atraumatic intubation. Although infants are more tolerant to intubation than older children, an abnormally narrow larynx must always be suspected in the presence of congenital syndromic/non-syndromic anomalies or when resistance is felt while passing the ET tube through the vocal cords. Prior to securing the airway, a quick inspection of the larynx using a 0° direct telescope clarifies the situation in cases of unexpected difficult intubation. The smallest tube that will adequately ventilate the infant or child must always be chosen. The duration of intubation, once recognised as a significant factor [24], must now be integrated with the other factors predisposing the infant’s larynx to the development of post-intubation stenosis. In modern neonatology and paediatric intensive care units (PICU),
14.2 Prevention of Acute Intubation Lesions
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Fig. 14.5 Non-stenotic cicatricial sequelae due to prolonged endotracheal tube intubation: (a) Diagram of bilateral arytenoid erosions or ulcers with an intact median strip of mucosa
(b) Cicatricial endotracheal tube imprint (c) Cicatricial healed furrows (d) Fibro-epithelial polyp
long-term intubation can often be safely maintained over weeks, without major laryngeal sequelae, provided that systemic diseases are controlled. However, beyond 4 weeks of intubation, the risk of LTS increases [8, 19]. No consensus has been reached within the medical community as to the safe upper limit for the duration of intubation. All aforementioned factors are intermingled and play a major role, though ET tube size appears to be the most significant. When oversized, the tube induces localised ischemic pressure necrosis at distinct sites of the laryngeal mucosa. This mechanism is reinforced by capillary hypoperfusion of the mucosa, frequently associated with the severe systemic diseases that led to the patient’s intubation in the first place. In addition, optimal nursing in the PICU,
which includes maintaining adequate sedation and proper suspension of the ET tube connector to the ventilator’s tube, diminishes the risk of ET tube motion. Atraumatic pharyngeal or endotracheal tube suctions are also critical in minimising the mucosal lesions. In infants and young children, acute lesions caused by intubation may manifest as failed extubations. In older children or adolescents, as post-intubation dysphonia may be the only symptom, it must be investigated further. As a rule, failed extubation or dysphonia persisting beyond 3 days after extubation are strict indications for endoscopic inspection of the larynx and subglottis. This prevents the development of unexpected and late post-intubation stenosis, occurring 3–6 weeks after extubation. Examples are shown in Fig. 14.8.
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Fig. 14.6 Stenotic cicatricial sequelae due to prolonged endotracheal tube intubation: (a) Diagram of ulcerated troughs with an intact median strip of mucosa (b) Interarytenoid adhesion (c) Diagram of annular posterior ulceration with no residual mucosal
Fig. 14.7 Combined glotto-subglottic stenoses due to prolonged intubation: (a) Posterior glottic stenosis associated with subglottic stenosis. (b) Severe vocal cord synechia associated with subglottic stenosis
strip (d) Posterior glottic stenosis, with or without cricoarytenoid joint fixation (e) Concentric subglottic ulceration (f) Cicatricial subglottic stenosis
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14.3 Treatment of Acute Intubation Lesions Table 14.2 Predisposing factors of acquired laryngotracheal stenosis • Patient – Age: infant < adolescent – Larynx: small size, abnormal shape, infection – Abnormal wound healing (keloid formation) – Systemic diseases: GOR, shock (infectious, cardiogenic), immuno-suppression, diabetes, anaemia, hypotension, bronchopulmonary dysplasia • ET tube – Oversized – Excessive hardness
14.3 Treatment of Acute Intubation Lesions In many centres, a failed extubation attempt is considered to be an indication for subsequent tracheostomy. Ulcers and granulation tissue inevitably lead to contracting scars and stenosis as the larynx is left unstented. In clinical practice, two situations may occur: (a) swelling of the lax glotto-subglottic mucosa without ischemic necrosis, and (b) ulcers with fibrin and granulation tissue resulting from ischemic necrosis of the glottic and subglottic mucosa.
– Poor biocompatibility • Intubation – Traumatic
14.3.1 Treatment of Soft-Tissue Stenosis without Mucosal Necrosis
– Multiple – Prolonged – Followed by tracheotomy • Nursing – Inadequate patient’s sedation – Traumatic and repeated suctions – Presence of nasogastric tube – Ventilator-driven tube motion
Fig. 14.8 Acute intubation lesions with different symptoms and outcomes: (a) Prominent oedematous protrusion of ventricular mucosa. Post-extubation dyspnoea, with complete resolution following medical treatment alone. (b) Ulcerated troughs with exuberant granulation tissue filling the posterior glottis. Post- extu-
Airway obstruction manifests itself within a few minutes or up to a few hours of extubation. Direct inspection of the larynx often reveals glotto-subglottic oedema with airway compromise. Premature babies are more prone than older children to develop this condition [17]. Treatment consists of re-intubation with a one-size smaller ET tube, topical application of an endolaryngeal plug of Gentamycin-corticosteroid ointment (Diprogenta®), systemic antibiotics depending
bation dyspnoea, with complete resolution following combined e ndoscopic and medical treatments. (c) Annular interarytenoid ulceration with exposed cartilage but no granulation tissue in an immuno-compromised adolescent. Post-extubation dysphonia but no dyspnoea. Progression to posterior glottic stenosis
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Fig. 14.9 Post-intubation soft-tissue stenosis in a newborn baby: (a) Diffuse submucosal swelling of the glottis and subglottis, narrowing the lumen to 70%. (b) Re-intubation with a
one-size smaller soft Portex Blue Line® tube and topical application of a gentamicin-corticosteroid ointment (Diprogenta®) plug. (c) Subnormal airway at extubation 4 days later
on the tracheal aspirate culture, as well as systemic corticosteroids. Most patients can be extubated after a mean re-intubation period of 2–4 days (Fig.14.9). Adrenalin aerosols (50 mg/kg in 4 ml of NaCl 0.9%), iv Dexamethason (2 mg/kg), continuous positive airway pressure (CPAP), and heliox delivered through a face mask are instrumental in overcoming this difficult post-extubation period. If these manoeuvres fail, an anterior cricoid split combined with a thyroid cartilage graft may be performed in order to avoid the need for tracheostomy.
ring allows the cartilage to spring open, as demonstrated in animal experiments [2, 3]. Furthermore, mucosal section causes leakage of submucosal oedema fluid through the wound. Through a small horizontal skin incision made at the level of the cricoid, the strap muscles and the thyroid isthmus are reflected laterally, thus exposing the anterior larynx and upper trachea. A vertical midline incision is performed through the lower one-third of the thyroid cartilage, anterior arch of the cricoid ring, and first two tracheal rings. The airway should then open, at least partially, allowing for transtubation with an appropriately sized tube for the patient’s age. To preserve voice quality, it is imperative that cranial transection of the anterior laryngeal commissure be avoided. To prevent superinfection of the wound and diminish subcutaneous emphysema in the presence of adequate drainage, ACS has been modified to a single-stage laryngotracheal reconstruction (LTR) with anterior cartilage grafting (Fig. 14.10). The cartilage is harvested on one side from the upper alar portion of the thyroid cartilage. The graft is boat-shaped and sewn into position using 5.0 or 6.0 Vicryl sutures. Fibrin glue (Tisseel® or Tissucol®) is applied on the suture line in order to prevent any air leakage. This surgery takes only a few extra minutes and results in a more stable reconstruction than simple ACS (Fig. 14.11). Intubation with adequate sedation is maintained for 5–7 days after the intervention. Paralysing agents must be avoided where possible. At extubation, the medical treatment that is used for soft-tissue stenosis not requiring ACS is applied (see Sect. 14.3.1). If several
14.3.2 Anterior Cricoid Split (ACS) This operation was introduced by Cotton in 1980 [7] to avoid doing a tracheostomy in premature babies following several failed extubation attempts. It is indicated in the presence of adequate pulmonary reserve provided that no other upper or lower airway obstruction exists. Strict criteria for proper indications have been established [20] and include: at least two extubation failures secondary to a subglottic laryngeal pathology, weight greater than 1,500 g, off ventilator support for at least 10 days, supplemental oxygen requirement below 30%, non-congestive heart failure for at least 1 month, no acute respiratory tract infection and no hypertensive medication intake for at least 10 days prior to the procedure [21]. Anterior cricoid split is based on the principle that an anterior vertical midline transection of the cricoid
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14.3 Treatment of Acute Intubation Lesions Fig. 14.10 Anterior cricoid split modified into an anterior laryngotracheal reconstruction: (a) Anterior laryngotracheal incision: the cricoid ring springs partially open. Harvesting of the thyroid cartilage from the upper alar portion. (b) Suturing the thyroid cartilage graft into position
Fig. 14.11 Anterior cricoid split with thyroid cartilage graft in a premature baby intubated for 1 month: (a) The anterior cricoid split extends from the lower third of the thyroid cartilage to the second tracheal ring. The white dashed line shows the site of harvesting of the left upper thyroid ala. (b) The oval-shaped thyroid cartilage graft is sutured in position
extubation attempts fail despite endoscopic removal of granulation tissue and temporary re-intubations, then a tracheostomy is performed but the larynx should not be left unstented. An LT-Mold of the appropriate size is inserted endoscopically and fixed to the trachea using a non-resorbable suture placed through the cervical opening made for the tracheostomy. The correct positioning of the LT-Mold is verified endoscopically. In a large multicentre survey involving 138 patients undergoing ACS for soft-tissue SGS, Holinger
reported a successful decannulation rate of 77% following ACS [11].
14.3.3 Treatment of Obstructive Granulation Tissue Failed extubations may be due to clusters of granulation tissue obstructing the posterior glottis (Fig. 14.12),
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Fig. 14.12 Exuberant granulation tissue filling the posterior glottis after endotracheal tube removal: (a) Severe dyspnoea resulting from airway obstruction of the posterior glottis. (b) Status 5 days after endoscopic treatment with removal of granulation tissue and topical application of mitomycin C. Uneventful extubation
Fig. 14.13 Severe acute lesions from intubation: (a) Right vocal cord haematoma due to traumatic intubation and cluster of fibrin at the posterior laryngeal commissure. Patient transferred already having undergone tracheotomy. (b) Spreading of the glottis with Lindholm false cord retractor displays a bridge of fibrin suspended between the two arytenoids. (c) Status immediately after endoscopic removal of fibrinous tissue. (d) Minor laryngeal sequelae at 1 month. The absence of endoscopic treatment would have led to an interarytenoid cicatricial adhesion as shown in Fig. 14.6b
bilateral ulceration of the medial aspect of the arytenoids with interarytenoid fibrin bridge (Fig. 14.13) (i.e. a true precursor of fibrous interarytenoid adhesion), and circumferential subglottic ulceration with granulation tissue and oedema (Fig. 14.14).
At this stage, performing a tracheostomy and leaving the larynx unstented only worsens the laryngeal condition. Infected granulations evolve over time into contracting scars, leading to severe cicatricial sequelae, as described in Sect. 14.1. In the author’s opinion,
14.3 Treatment of Acute Intubation Lesions
Fig. 14.14 Circumferential acute subglottic lesions from intubation
most if not all post-intubation cicatricial sequelae of the larynx are preventable with adequate treatment administered at the acute stage.
14.3.3.1 Treatment Is as Follows 1. Careful endoscopic removal of exophytic granulation tissue using a biopsy forceps in suspension microlaryngoscopy. Haemostasis is easily achieved with pledgets soaked in adrenaline. Use of the CO2 laser is contraindicated as it is likely to carbonise the highly vascularised granulation tissue, thereby generating heat diffusion into the surrounding tissues, with subsequent scarring.
Fig. 14.15 Severe acute posterior glottic lesions from intubation: (a) After endotracheal tube removal, the posterior glottis is totally obstructed by exuberant granulation tissue. (b) Status immediately after endoscopic removal of granulation tissue and
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2. Mitomycin C (1–2 mg/ml for 2 min) is administered topically. The cotton swab soaked in the Mitomycin C solution is applied onto granulation tissue but never on the denuded cartilage, as this delays the reepithelialisation process and promotes necrosis by long-standing exposure of the cartilage in the subglottic lumen. 3. Atraumatic re-intubation is carried out with a onesize smaller soft Portex® ET tube smeared with a Gentamycin-corticosteroid ointment (Diprogenta®). 4. Endolaryngeal topical application of a plug of Diprogenta® is conducted as shown in Fig. 14.9. The ointment is applied using a syringe through a large-sized cannula placed around the ET tube. 5. Systemic corticosteroids (2 mg/kg dexamethasone) are administered along with antibiotics, the choice of which is dependent on the cultures obtained from bacteriologic aspirates over several days. 6. Another attempt at extubation is made 4 days later, once a direct laryngoscopy with removal of the ET tube has been conducted assessing the airway patency from the larynx to the bronchi. If extubation fails again, the same treatment is repeated while the child remains intubated for a 4-day period before a further extubation attempt is made (Fig. 14.15). In the author’s unpublished series of patients with acute obstructing intubation lesions, tracheostomy was successfully avoided in 34 of the 35 cases (~97%). As to the long-term results, exertional dyspnoea occurred in two cases (~6%) and mild-to-moderate dysphonia in five cases (~17.5%).
topical application of mitomycin C (2 mg/ml for 2 min). (c) Late result at 1 month: thickened mucosa at the medial aspect of the arytenoids with normal airway
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If a tracheotomy cannot be avoided despite adequate endoscopic treatment, two important precepts must be observed, namely, laryngeal stenting and proper tracheostomy tube placement. Until recently, laryngeal stenting was not recommended at this stage, owing to poorly designed laryngeal prostheses, which were either too hard or could not accommodate the inner laryngeal contours (see Sect 2.8 Chap. 2). Designed as a soft silicone endolaryngeal stent, the LT-Mold offers anatomical support to the larynx and promotes healing without further traumatic lesions [16]. Conceptually, a perfectly adequate stent for splinting a laryngeal reconstruction may also prevent the development of post-intubation stenosis following acute intubation lesions. Even in infants, the LT-Mold can be endoscopically inserted in SML and fixed to the trachea using a Lichtenberger needle-carrier. 14.3.3.2 The Procedure Is Performed as Follows Using metallic LT-Mold gauges designed for endoscopic use (Fig. 14.16), an appropriate LT-Mold size (length and diameter) is chosen, and a 3.0 or 4.0 (70-cm long) prolene stitch is placed through the anterior wall of the silicone prosthesis in the longitudinal axis. In SML, the prosthesis is fixed with endo-extralaryngeal stitches using the Lichtenberger needle-carrier. The first stitch is placed distally and recaptured on the outer neck skin, while the second stitch is placed proximally below the anterior laryngeal commissure (Fig. 14.17a). The prosthesis is guided through the vocal cords using a large grasping forceps, while the assistant gently pulls on both threads from the outside. Once the prosthesis is correctly placed, a small 1-cm-long horizontal skin incision is made at a mid-distance from the exit points of the threads. The submucosal tissue is dissected bluntly using a curved haemostat, and the threads are recaptured with skin hooks placed under the skin and then tied to the strap muscles. Lastly, the skin is closed using resorbable subcutaneous sutures (Fig. 14.17b).
14.3.4 Correct Tracheostomy Placement in case of Impending Laryngotracheal Stenosis Acute post-intubation lesions with incipient LTS requiring tracheostomy warrant special mention.
Fig. 14.16 Metallic LT-Mold gauges for endoscopic use: in suspension microlaryngoscopy, different LT-Mold gauges are inserted into the larynx to select the proper size LT-Mold prosthesis. Identical LT-Mold gauges exist for intra-operative use (see Chap. 19, Fig. 19.8)
Fig. 14.17 Endoscopic placement of an LT-Mold prosthesis in suspension microlaryngoscopy: (a) In suspension microlaryngoscopy, placement of the endo-extralaryngeal fixation stitches with a Lichtenberger needle-carrier. (b) LT-Mold in place and snugly fixed to the tracheal wall
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14.4 Acquired Tracheal Stenosis
Contrary to the current rule stating that the tracheostomy site be placed at the second or third tracheal ring, in the case where the trachea needs to be maximally preserved for further airway reconstruction, the stoma must be placed either immediately below the cricoid ring or very low at the sixth, seventh or eighth tracheal ring (Fig. 14.18). The rationale behind this is either to spare a maximum of normal trachea when placing the stoma just below the cricoid ring or to keep at least five or six normal tracheal rings between the SGS and the upper pole of the tracheostomy site. In the first instance, a singlestage cricotracheal resection necessitates only a short resection, with a reduced risk of anastomotic dehiscence. In the second instance, good quality tracheal rings are preserved for performing the thyrotracheal anastomosis after resection of a short airway segment, namely the anterior arch of the cricoid ring. This prevents anastomotic dehiscence from occurring. The same principles apply to single-stage and double-stage LTRs.
Fig. 14.18 Correct placement of tracheostomy with impending laryngotracheal stenosis: (a) Tracheostoma situated immediately below the cricoid ring to maximally preserve normal trachea. (b) Tracheostoma situated at the sixth–seventh or eighth tracheal ring to spare sufficient length of normal trachea between the stenosis and the tracheostomy
If the cervical trachea has been damaged by endotracheal intubation or a previous tracheostomy, the new tracheostomy must always be placed through the tracheal stenosis. A low substernal cuff stenosis is highly unlikely in children intubated with uncuffed ET tubes. Should such a situation occur, the tracheostomy must be performed in the lower neck just above the stenosis, using a tube that is sufficiently long to extend through the distal stenosis (Fig. 14.19). The same basic principle applies to all situations: when performing a tracheostomy for an impending subglottic or tracheal stenosis, the residual normal trachea must be maximally preserved.
14.4 Acquired Tracheal Stenosis The vast majority of acquired tracheal stenoses are due to complications caused by the tracheostomy cannula above, at or below the stoma level,
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Fig. 14.19 Correct placement of tracheostomy when subglottic stenosis is associated with tracheal stenosis: (a) Cervical cuff or post-tracheostomy stenosis: the new tracheotomy must be placed in the stenotic segment. (b) Substernal cuff or cannula tip stenosis: the new tracheotomy must be placed just above the stenosis, which is stented by the tracheostomy cannula
whereas other aetiologies are uncommon. Over the years, tracheal stenoses due to ET tube lesions have almost disappeared, whereas laryngeal stenoses remain a challenging problem. Several improvements may account for this: ET tubes are now softer, their biocompatibility has improved and their highvolume, low-pressure cuff no longer induces ischemic annular necrosis of the tracheal wall [13, 23]. Furthermore, the use of uncuffed ET tubes in children below 8 years [6] has become standard practice. Further rare aetiologies of acquired tracheal stenosis include caustic and burn injuries, recurrent infections, bronchoscopy-induced trauma and reflux of gastric contents [22]. In recent years, the frequency of iatrogenic complications associated with airway stenting has greatly increased [12]. The aetiopathogenic mechanisms underlying tracheostomy-related stenoses involve two main factors: the required tracheal incision itself and the presence of the tracheostomy cannula.
14.4.1 Tracheal Incision-Related Stenosis Irrespective of the surgical technique used (vertical or horizontal incision with a Björk flap), the roman arch of the tracheal vault is interrupted following a tracheostomy, which may lead to a cicatricial A-shape deformity after decannulation (Fig. 14.20). For short-term tracheostomies, this risk is minimal unless a faulty technique has been used. As a rule, a vertical incision should never transect more than two tracheal rings, and a Björk flap should never extend over more than one tracheal ring. The only measure that provides partial protection is the suturing of neck skin around the tracheostomy edge, following the removal of subcutaneous fat. The cannula should calibrate the tracheal opening to its own size. After prolonged tracheostomy, it is often no longer possible to recognise what technique had been used; moreover, complication rates are roughly similar, regardless of the technique [15].
14.4 Acquired Tracheal Stenosis
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Fig. 14.20 Potential A-frame deformity at the tracheostomy site after decannulation: (a) Tracheal opening due to long-standing tracheostomy cannula. (b) A-frame deformity of the tracheal lumen at the former tracheostomy site. To avoid this complication, surgical closure is recommended
14.4.2 Cannula-Related Stenosis The adequate positioning of the cannula in the trachea must be confirmed using flexible endoscopy. The tip of the cannula should not abut on the anterior or posterior tracheal wall, resting at least 1 cm above the carina. The rigidity of the tracheostomy cannula accounts for the subsequent development of lesions (Fig. 14.21). During coughing, the curved-shaped tracheostomy tube thrusts repeatedly against the upper
Fig. 14.21 Acquired tracheal stenoses due to the tracheostomy cannula: (a) Suprastomal collapse and granuloma. (b) Circumferential cuff lesion, potentially leading to stenosis or tracheo-oesophageal fistula. (c) Cannula tip lesion with possible innominate artery fistula
edge of the stoma and crushes down the anterior wall of the trachea, leading to suprastomal collapse and granuloma formation (Fig. 14.21a). This complication is more frequent in children who require prolonged intubation [5]. In the rare cases where a cuff must be used for mechanical ventilation or airway protection from aspiration, cuff overinflation may induce annular ischemic necrosis, followed by subsequent tracheal stenosis or even tracheo-oesophageal fistula (TOF) (Fig. 14.21b). The tip or the back of the misplaced uncuffed cannula may, at times, exert localised pressure on the posterior tracheal wall, thereby causing erosion, ulceration and TOF (see Fig. 21.4, Chap. 21). Granulomas induced by the cannula tip in the distal trachea are potentially life-threatening and must be removed immediately (Fig. 14.21c). They always result from inadequate cannula length and placement, hence the importance of ensuring proper positioning of a paediatric tracheostomy tube using a flexible scope. A pulsating motion of the cannula as well as slight tracheal bleeding may be early signs of an incipient innominate artery fistula, which requires immediate tracheoscopy before the condition worsens. However, this event is very rare in children unless an extrinsic vascular compression such as an aberrant innominate artery has been overlooked (see Sect. 21.3.2, Chap. 21).
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References 1. Adriaansen, F.C., Verwoerd-Verhoef, H.L., van der Heul, R.O., et al.: Differential effects of endolaryngeal trauma upon the growth of the subglottis. Int. J. Pediatr. Otorhinolaryngol. 15, 163–171 (1988) 2. Adriaansen, F.C., Verwoerd-Verhoef, H.L., van der Heul, R.O., et al.: Morphometric study of the growth of the subglottis after interruption of the circular structure of the cricoid. ORL J. Otorhinolaryngol. Relat. Spec. 50, 54–66 (1988) 3. Babyak, J.W., Passamani, P.P., Sullivan, M.J.: The anterior cricoid split in puppies. Int. J. Pediatr. Otorhinolaryngol. 13, 191–204 (1987) 4. Benjamin, B.: Prolonged intubation injuries of the larynx: endoscopic diagnosis, classification, and treatment. Ann. Otol. Rhinol. Laryngol. Suppl 160, 1–15 (1993) 5. Benjamin, B., Curley, J.W.: Infant tracheotomy-endoscopy and decannulation. Int. J. Pediatr. Otorhinolaryngol. 20, 113–121 (1990) 6. Benjamin, B., Holinger, L.D.: Laryngeal complications of endotracheal intubation. Ann. Otol. Rhinol. Laryngol. 117(suppl 200), 2–20 (2008) 7. Cotton, R.T., Seid, A.B.: Management of the extubation problem in the premature child. Anterior cricoid split as an alternative to tracheotomy. Ann. Otol. Rhinol. Laryngol. 89, 508–511 (1980) 8. Dankle, S.K., Schuller, D.E., McClead, R.E.: Risk factors for neonatal acquired subglottic stenosis. Ann. Otol. Rhinol. Laryngol. 95, 626–630 (1986) 9. Gaynor, E.B., Greenberg, S.B.: Untoward sequelae of prolonged intubation. Laryngoscope 95, 1461–1467 (1985) 10. George, M., Jaquet, Y., Ikonomidis, C., et al.: Management of severe pediatric subglottic stenosis with glottic involvement. J. Thorac. Cardiovasc. Surg. 139, 411–417 (2010) 11. Holinger, L.D., Stankiewicz, J.A., Livingston, G.L.: Anterior cricoid split: the Chicago experience with an alternative to tracheotomy. Laryngoscope 97, 19–24 (1987)
12. Lim, L.H., Cotton, R.T., Azizkhan, R.G., et al.: Complications of metallic stents in the pediatric airway. Otolaryngol. Head Neck Surg. 131, 355–361 (2004) 13. Lindholm, C.E.: Prolonged endotracheal intubation. Acta Anaesthesiol. Scand. Supp l33, 1–131 (1970) 14. Lusk, R.P., Woolley, A.L., Holinger, L.D.: Laryngotracheal stenosis. In: Holinger, L.D., Lusk, R.P., Green, C.G. (eds.) Pediatric Laryngology and Bronchoesophagology, pp. 165– 186. Lippincott-Raven, Philadelphia/New York (1997) 15. MacRae, D.L., Rae, R.E., Heeneman, H.: Pediatric tracheotomy. J. Otolaryngol. 13, 309–311 (1984) 16. Monnier, P.: Airway stenting with the LT-Mold™: Experience in 30 pediatric cases. Int. J. Pediatr. Otorhinolaryngol. 71, 1351–1359 (2007) 17. Pereira, K.D., Smith, S.L., Henry, M.: Failed extubation in the neonatal intensive care unit. Int. J. Pediatr. Otorhinolaryngol. 71, 1763–1766 (2007) 18. Sasaki, C.T., Horiuchi, M., Koss, N.: Tracheostomy-related subglottic stenosis: bacteriologic pathogenesis. Laryngoscope 89, 857–865 (1979) 19. Sherman, J.M., Lowitt, S., Stephenson, C., et al.: Factors influencing acquired subgottic stenosis in infants. J. Pediatr. 109, 322–327 (1986) 20. Silver, F.M., Myer 3rd, C.M., Cotton, R.T.: Anterior cricoid split. Update 1991. Am. J. Otolaryngol. 12, 343–346 (1991) 21. Walner, D.L., Cotton, R.T.: Acquired anomalies of the larynx and trachea. In: Cotton, R.T., Myer III, C.M. (eds.) Practical Pediatric Otolaryngology, p. pp 524. LippincottRaven, Philadelphia/New York (1999) 22. Weber, T.R., Connors, R.H., Tracy Jr., T.F.: Acquired tracheal stenosis in infants and children. J. Thorac. Cardiovasc. Surg. 102, 29–34 (1991) 23. Weiss, M., Dullenkopf, A., Gerber, A.: Der Microcuff Pädia trietubus. ein neuer endotrachealtubus mit hochvolumen-niederdruck-cuff für kinder. Anaesthesist 53, 73–79 (2004) 24. Whited, R.E.: A prospective study of laryngotracheal sequelae in long-term intubation. Laryngoscope 94, 367–377 (1984)
External Laryngeal Trauma
Contents 15.1 15.1.1 15.1.2 15.1.3 15.1.4 15.1.5
Blunt and Penetrating Laryngeal Injuries........... 200 Mechanisms of Injury............................................... 200 Traumatic Lesion Sites............................................. 201 Clinical Presentation and Diagnosis......................... 203 Radiological Evaluation............................................ 205 Management............................................................. 205
15.2
Inhalation Injuries.................................................. 209
15.3 15.3.1 15.3.2 15.3.3 15.3.4
Caustic Ingestion..................................................... 209 Patient Assessment................................................... 210 Endoscopic Assessment............................................ 210 Management............................................................. 211 Late Cicatricial Sequelae.......................................... 212
15
Core Messages
›› Laryngeal trauma
References............................................................................ 214
››
››
−− Laryngeal fractures resulting from blunt trauma are very rare in the paediatric age group −− Due to its high position in the neck, the paediatric larynx is well protected by the mandible from blunt traumatic injuries −− Sporting and play activities are the main causes of injury in children −− Severe laryngeal injuries result in mucosal lacerations and airway disruptions without true fractures of the pliable cartilages −− Endoscopic assessment must precede intubation or tracheotomy −− Early surgical repair yields the best functional results in cases of mucosal lacerations and laryngeal framework disruptions Inhalation injuries −− Steam burns must be differentiated from flame burns in inhalation injuries −− Flame burns in inhalation injuries require endoscopic cleansing of soot debris by tracheobronchial lavages −− Cicatricial sequelae evolve over a long period of time −− The principle of endoscopic and open surgical managements are identical to those of postintubation stenosis Caustic injuries −− Caustic ingestion is typically accidental in children −− Toddlers of developing countries are exposed to dangerous chemicals stored unsafely in softdrink bottles −− Strong acid and alkali induce deep penetrating pharyngo-oesophageal injuries −− Broncho-oesophagoscopy under general anaes-
P. Monnier (ed.), Pediatric Airway Surgery, DOI: 10.1007/978-3-642-13535-4_15, © Springer-Verlag Berlin Heidelberg 2011
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200
15 External Laryngeal Trauma
thesia is the mainstay of the diagnosis −− Type, extent and depth of injuries are best assessed within 24–48 h after the accidental ingestion −− Short (<2–3 cm) oesophageal stenoses respond well to dilation −− Long, multiple or complete pharyngo-oesophageal stenoses require surgical intervention − Severe and even total pharyngolaryngeal stenoses are amenable to full rehabilitation with CO2 laser reopening of the phary ngolarynx and colon transplant to the pharynx
External traumas to the paediatric larynx include blunt and penetrating injuries, inhalation injuries and injuries from caustic ingestion. They are classified depending on the site [3, 21, 22], severity [23] and type of tissue injuries [28].
15.1 Blunt and Penetrating Laryngeal Injuries Due to the rarity of the condition, true prevalence figures for children are missing in the literature. In the adult population, external laryngeal traumas account for one of 30,000 emergency room visits [33], one of 650 maxillo-facial fractures [7] and two to five cases per year in major trauma centres [36]. In the paediatric age group, these figures are likely to be lower. The high-neck position of the paediatric larynx accounts for the natural shields afforded anteriorly by the mandible, posteriorly by the cervical spine and laterally by the sternocleidomastoid muscles. Contrary to adults where motor vehicle accidents, assaults, suicide attempts and occupational accidents are responsible for the majority of external laryngeal traumas, sporting and play activities (e.g. bicycling, falls, accidental hanging) are the predominant causes in the paediatric age group. Car-related injuries increase with age in older children, outweighing all other causes in adolescents [5, 13]. Blunt traumas account for over 80–90% of all external laryngeal injuries.
15.1.1 Mechanisms of Injury In children and adolescents, blunt laryngeal trauma generally occurs when the neck is hyperextended. Owing to the pliability of the laryngeal cartilages, fractures are uncommon but shearing forces to the mucosa may cause significant oedema, haematomas or lacerations with life-threatening respiratory distress. Indeed, the pliant laryngeal framework absorbs the anterior neck impact, then springs back into position. This phenomenon may lead to dislocation of the arytenoid cartilages or rupture of the vocal ligaments. The anterior convex surface of the vertebral bodies acts like a wedge that forces the thyroid alae apart when the thyroid cartilage is driven against it. The cricoid plate is displaced anteriorly by the impact on the spine, releasing tension on the vocal ligaments. Due to its elasticity, the thyroid cartilage springs back, abruptly increasing tension on the vocal ligaments. Three main lesions may ensue: rupture of the membranous vocal cord at the anterior laryngeal commissure, anterior arytenoid dislocation and rupture of the thyro-epiglottic ligament with posterior displacement of the epiglottic petiole (Fig. 15.1). Fractures of the thyroid cartilage may be seen in adolescents. Striking the neck at high speed on a tightly stretched wire (the so-called clothes line injury) during bicycle or motorcycle riding exerts high pressure on a very small area. Depending on the impact point, crushing of the larynx, cricothyroid separation or cricotracheal disruption may occur along with a possible unilateral or bilateral recurrent laryngeal nerve (RLN) injury. A less common mechanism of airway trauma consists of severe thoracic compression leading to increased intratracheal pressure against a closed glottis, with subsequent disruption of the intercartilaginous tracheal membranes. Penetrating injuries of the paediatric larynx, exceedingly rare in peacetime, are usually due to accidental home injuries with hunting weapons or cutting instruments; they may also result from assault with knives and guns. While low velocity handguns have only a moderate blast effect on soft tissue, the bullet may be deviated by a harder structure such as laryngeal cartilages and thus follow an erratic course into soft tissues. With knife wounds and gunshots, the course of the injury can be estimated based on the entrance and exit wounds. In both instances, deep-lying vascular or neurological lesions must be actively sought as they are more likely to occur than with blunt trauma [6, 19, 34].
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15.1 Blunt and Penetrating Laryngeal Injuries
Fig. 15.1 Blunt trauma to the paediatric larynx: (a) Larynx in normal position. (b) The anterior impact applied to the thyroid cartilage spreads apart the thyroid alae, thereby lacerating the
pharyngeal mucosa. (c) Due to its elasticity, the thyroid cartilage springs back, overextending the vocal cords. Arytenoid dislocation or rupture of the vocal ligament may occur (red circles)
15.1.2 Traumatic Lesion Sites (Fig. 15.2)
young adults where the thyroid cartilage is less pliant, a vertical paramedian fracture may ensue. This type of fracture is the most common injury of the adult larynx. Computerised tomography scan may miss this fracture in adolescents (Fig.15.3). Late and persistent dysphonia occurring after resolution of vocal cord haematoma or oedema is a strong indicator of vocal cord instability, possibly due to an undetected thyroid cartilage fracture [9]. Open surgical repair is necessary to stabilise the thyroid cartilage and restore good voice quality.
Blunt injuries to the larynx occur at three distinct levels. They may be combined in the case of massive blunt trauma.
15.1.2.1 Impact on the Thyrohyoid Membrane (Fig. 15.2a) Blunt injury at this level causes rupture of the thyrohyoid and thyro-epiglottic ligaments, with avulsion and posterior displacement of the epiglottic petiole, supraglottic lacerations through the ventricular bands and possible pharyngeal tears. This type of injury requires immediate open surgery for reconstruction of the supraglottis to avoid late cicatricial sequelae that are extremely challenging to treat (see Fig. 15.12). Hyoid bone fractures are seldom observed, and then only in adolescents or adults.
15.1.2.2 Impact on the Thyroid Cartilage (Fig. 15.2b) Damage to the thyroid cartilage depends on its degree of calcification. Children may sustain severe impacts without fractures, while vocal cord or arytenoid avulsion may occur, as previously described. In adolescents and
15.1.2.3 Impact on the Cricoid Cartilage (Fig. 15.2c) An isolated fracture of the cricoid is a rare event in older children and adolescents unless it results from massive blunt trauma associated with thyroid cartilage fracture. The clothes line-type injury often leads to cricothyroid or cricotracheal disruptions, with potentially severe airway restriction and haemoptysis. Due to the close proximity of the anatomical structures, the incidence of concomitant RLN paralysis and oesophageal injuries is high (Fig.15.4). 15.1.2.4 Impact on the Thorax (Fig. 15.5) Tracheal cartilages are pliable, tolerating direct impacts fairly well. Tracheal disruption usually results from
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Fig. 15.2 Types of laryngeal injuries in relation to the level of impact: (a) Impact at the thyrohyoid membrane level (yellow arrow): disruption of the thyro-epiglottic ligament, with posterior displacement of the epiglottis and lacerations of the ventricular bands. (b) Impact at the thyroid cartilage level (yellow arrow): The pliant thyroid cartilage resists fracture,
although arytenoid dislocation, rupture of the vocal cord or massive supraglottic disruption may ensue. Thyroid cartilage fractures are seen in adolescents only. (c) Impact at the cricoid ring level (yellow arrow): Cricothyroid or cricotracheal disruption may be associated with recurrent laryngeal nerve and oesophageal injuries. Cricoid fractures may be observed in adolescents
Fig. 15.3 Vertical paramedian fracture of the thyroid cartilage in a 14-year-old boy: (a) CT scan shows a swelling of the right vocal cord due to a haematoma. The anterior fracture was not visible on any of the serial axial CT scan sections. (b) Direct
laryngoscopy reveals a right vocal cord haematoma extending onto the anterior one-third of the ventricular band (c) During surgery, the vertical fracture is conspicuous and must be stabilised to restore good voice quality
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15.1 Blunt and Penetrating Laryngeal Injuries
examination, a patient in severe respiratory distress who requires urgent airway assessment and stabilisation and, lastly, a patient who is already intubated or tracheostomised.
15.1.3.1 Conscious Patient with Minor to Moderate Laryngeal Trauma
Fig. 15.4 Cricotracheal disruption with avulsion of the mucosa from the cricoid plate and traumatic section of the right recurrent laryngeal nerve (artificially shown in yellow). Reconstruction by cricotracheal resection and thyrotracheal anastomosis
severe thoracic compression with a significant increase in intratracheal pressure against a closed glottis. Disruption of the intercartilaginous tracheal membrane may ensue in children (Fig.15.5).
15.1.3 Clinical Presentation and Diagnosis
Older children and adolescents can provide precise information as to the circumstances of the neck injury. Witnesses are helpful in the case of younger children. Symptoms may range from mild dysphonia to hoarseness and aphonia. Dyspnoea may become apparent only after several hours. Overnight surveillance is thus advocated unless the initial clinical examination does not reveal any sign of laryngeal haematoma or oedema. In the case of minor trauma, only transnasal fibreoptic laryngoscopy (TNFL) is necessary to assess the airway. Vocal cord mobility, oedema and minor haematomas are recorded. A CT scan (see Fig. 15.3) may fail to demonstrate a fracture of the thyroid cartilage; therefore, follow-up of the patient until complete resolution of symptoms (including restoration of a normal voice) is mandatory.
Early diagnosis and treatment of blunt and penetrating laryngeal trauma is crucial in order to avoid significant late cicatricial sequelae. The physician may be confronted with three distinct situations: a conscious child or adolescent who is cooperative during laryngeal
15.1.3.2 Conscious Patient with Moderate to Severe Laryngeal Trauma
Fig. 15.5 Severe thoracic compression in an 8-year-old child, run over by a tractor wheel: (a) Intact neck immediately after surgical exploration. (b) Peroperative view: tracheal separation
between the 11th and 12th tracheal ring at the thoracic inlet. (c) Surgical repair at the 5th postoperative day
The medical history often reveals a significant neck trauma due to a high velocity impact. Within a few
204
hours, minor symptoms may evolve into respiratory distress, masking serious underlying injuries. Neck bruising and tenderness, as well as odynodysphagia with drooling, subcutaneous crepitus, dyspnoea and haemoptysis are hallmarks of potentially severe traumas. In this case, complete endoscopic investigation with TNFL, direct laryngotracheoscopy and bronchooesophagoscopy under general anaesthesia are necessary (Fig. 15.6). Should a cervical spine injury be suspected, TNFL is the sole required examination to assess airway integrity, with maintenance of cervical spine immobilisation. If the airway needs securing, fibrescope-guided intubation or intubation via a tracheotomy should be performed immediately. In all other cases, rigid bronchoscopy is combined with TNFL. After assessing vocal cord mobility, a precise examination under general anaesthesia is performed, with the aim of detecting oedema, haematomas, mucosal tears, exposed cartilage, dislocated or avulsed arytenoid cartilages and supraglottic or incomplete laryngotracheal disruption. With modern endoscopic techniques, airway inspection should always precede tracheotomy. The risk of losing the distal airway is in fact minimal. The rigid bronchoscope is inserted through the vocal cords, down to the carina. The tip of the telescope is set 1 cm back from the tip of the outer tube to avoid blood contaminating the optical lens. An ET tube exchanger is used for intubation (see Sect. 5.1.2, Chap. 5). Immediate airway reconstruction
15 External Laryngeal Trauma
through a cervical necklace incision is carried out. If a tracheostomy is indicated, it should ideally be placed at the appropriate site through the opened neck. This is preferable to an emergency tracheostomy under local anaesthesia, which is difficult to perform on children. Once the airway is secured, rigid oesophagoscopy is performed to assess potential pharyngeal and upper oesophageal tears that may be missed using a flexible scope. Pharyngeal lacerations result from the impact of the thyroid alae on the vertebral bodies. These lacerations present as vertical tears with potentially severe subcutaneous emphysema, which can occur when positive airway pressure has been delivered to the patient via a face mask (Fig. 15.7).
15.1.3.3 Intubated or Tracheostomised Patient In polytraumatised patients, on the slightest suspicion of neck injury, an immediate and thorough endoscopic assessment of the pharyngolarynx and trachea is required. In intubated patients, a direct laryngoscopy is performed after a cervical spine injury has been ruled out. Examination of the supraglottic structures may reveal oedemas, haematomas and lacerations. Under visual control, the ET tube is retrieved and the supraglottis, glottis and subglottis are thoroughly inspected for severe traumatic lesions using the rigid bronchoscope (Fig. 15.8). Re-intubation is achieved through an ET tube exchanger, and a decision as to the appropriate surgical treatment is made immediately. Tracheostomy, if deemed necessary, is usually performed during the open neck surgery. Leaving serious laryngeal or subglottic lesions untreated inevitably leads to severe late cicatricial sequelae, whereas early surgical repair may restore nearly normal laryngeal function, depending on the severity of the initial trauma. In cases of severe laryngotracheal trauma with mucosal lacerations and exposed cartilage structures, the same basic strategy used for open limb fractures should be applied, namely immediate surgical repair.
15.1.3.4 Penetrating Trauma Fig. 15.6 Cervical bruises in a female adolescent who was involved in a car accident while not wearing a seat belt: The neck was swollen, and palpation revealed crepitus. Moderate dyspnoea was observed (same case as in Fig. 15.11)
Clinical signs and symptoms include subcutaneous crepitus, dyspnoea, shock or haemorrhage, expanding neck haematoma, haemoptysis, haematemesis and
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15.1 Blunt and Penetrating Laryngeal Injuries
Fig. 15.7 Vertical pharyngeal laceration with subcutaneous emphysema as the sole aero-digestive lesion after blunt laryngeal trauma: (a) Posterior pharyngeal laceration. (b) Severe sub-
cutaneous emphysema due to positive-pressure face mask ventilation. (c) Immediate endoscopic suturing in suspension micropharyngoscopy
Fig. 15.8 Severe supraglottic lacerations due to a severe impact at the thyrohyoid membrane level: (a) Immediate transfer to a tertiary hospital and early management. Restoration of normal laryngeal functions. (b) Late transfer to a tertiary hospital.
Lacerations with infected fibrin, posterior displacement of the epiglottic petiole and non-visible vocal cords. Surgical management required debridement and difficult reconstruction with suboptimal final results
neurological deficits [6, 17, 18, 34]. An upper aerodigestive tract endoscopy and CT scan facilitate the detection of underlying laryngeal or pharyngeal injuries. The neck can be explored through the cervical wound, following the path made by the cutting instrument or projectile. For each patient, the treatment must be tailored to the severity of the injury, which may require cooperation with vascular surgeons.
tomography scans are usually reserved for evaluating subtle anomalies, thus avoiding unnecessary open surgical procedures. Because of the rarity of fractures and the absence of calcification of the paediatric larynx, a CT scan yields little additional information beyond the preoperative endoscopy workup results. However, in polytraumatised children, CT scans may be very useful for assessing cervical spine and chest injuries.
15.1.4 Radiological Evaluation
15.1.5 Management
In agreement with Schaefer [32], the author believes that a CT scan of the larynx should only be performed when the results of the radiological examination are likely to influence treatment. Computerised
The absence of fractures of the laryngeal framework does not exclude potentially severe injuries such as arytenoid luxation, vocal cord or supraglottic disruption and partial laryngotracheal separation.
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15.1.5.1 Arytenoid Dislocation Early diagnosis facilitates treatment and reduction within 3 weeks of injury and is often associated with good functional results. In suspension microlaryngoscopy (SML) under general anaesthesia, a large and smooth right-angled probe is inserted into the ventricle, where it can be easily anchored between the vocal cord and the ventricular band. Traction on the probe effectively pulls the arytenoid back into its original position (Fig. 15.9). Placing the instrument underneath the vocal cord and arytenoid should not be attempted. Traction at this level is not effective, and there is a risk of lacerating the mucosa. If the arytenoid remains dislocated for an extended period of time, fibrotic ankylosis of the joint can occur, preventing its reposition. However, it is difficult to predict the upper time limit within which reduction can be attempted. Successful late reductions have been reported even after a 1-year delay. In a series of 26 patients reported by Sataloff et al. [31], patients with good results had an average time interval of 10 weeks between injury and surgical reduction, whereas the time interval for the group of patients with residual alteration was 29 weeks. Should reduction be unsuccessful, delayed endoscopic procedures may be required. These include partial arytenoidectomy in the case of a compromised airway or intracordal fat or collagen injection in the case of glottic incompetence. An open reduction through a laryngofissure app roach is indicated only if surgical revision for laryngeal fractures or supraglottic disruption is necessary. Complete arytenoid avulsion (Fig. 15.10) leads to loss of vocal cord function and a frozen larynx. In the
Fig. 15.9 Right anterior arytenoid luxation: (a) The right vocal cord is shortened and lax due to the anterior tilting of the arytenoid. A small haematoma is visible on the medial aspect of the right piriform fossa (b) A large and smooth right-angled probe is inserted into the ventricle, where it is anchored to pull the arytenoid back into position
15 External Laryngeal Trauma
acute phase, the arytenoids are frequently lost and cannot be reimplanted. To avoid superinfection, the mucosal defect can be covered using the retrocricoid mucosa.
15.1.5.2 Supraglottic Disruption This severe laryngeal injury may occur without any fracture of the laryngeal framework (see Sect. 15.1.2), as the impact of the blow is situated at the level of the thyrohyoid membrane. A complete supraglottic disruption can ensue, with lacerations of the ventricular bands and avulsion of the epiglottic petiole, but with preservation of intact vocal cords. Immediate open surgical reconstruction under tracheostomy cover is required. Exploration of the supraglottic area is made through the thyrohyoid membrane, which is usually widely torn open. Checking for proper arytenoid position and function is done first, followed by suturing of the ventricular band lacerations. An anterior pexy of the epiglottic petiole is best achieved by placing mattress sutures through the thyroid cartilage and suspending the epiglottis to the hyoid bone. In some cases, a horizontal supraglottic laryngectomy is instrumental in achieving excellent results (Fig. 15.11). Any delay in surgical repair invariably leads to superinfection, with potentially severe late cicatricial sequelae (Fig. 15.12). As a rule, any patient presenting laryngeal trauma that requires a tracheostomy to secure the airway should be promptly transferred to a tertiary hospital for proper investigation and management. Securing the
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15.1 Blunt and Penetrating Laryngeal Injuries
importance of the fractures in a noncalcified laryngeal cartilage. In adolescents, simple paramedian fractures can be fixed using 3.0 or 4.0 Vicryl sutures, although resorbable miniplates provide better stabilisation since they are fixed with permanent sutures in nonossified cartilages and do not restrict skeletal growth [30].
15.1.5.4 Laryngotracheal Disruption
Fractures of the laryngeal framework, uncommon in children, may be seen in adolescents whose cartilages are less pliable. Minimally displaced or nondisplaced thyroid cartilage fractures have an excellent prognosis with conservative management, but unstable voice restoration after 10–15 days requires surgical exploration for stabilisation of the thyroid cartilage alae. The CT scan can fail to demonstrate or minimise the
Laryngotracheal disruption, with or without cricoid fractures, is a serious but rare injury. Emergency intubation at the scene of the accident may be successful in cases of incomplete laryngotracheal separation. If the patient is brought to a tertiary hospital in acute respiratory distress, the medical team must perform an emergency tracheostomy. In children, this surgery should not be attempted under local anaesthesia. Instead, the patient should be sedated, and rigid bronchoscopy performed to secure the airway. The tip of the telescope should be set 1 cm back from the tip of the rigid outer tube to avoid blood soiling the optical lens. An ET tube exchanger is used to intubate the patient, unless complete airway disruption renders this manoeuvre too risky. An immediate cervical exploration should be performed while the patient is still ventilated using the rigid bronchoscope. Should instability of the cervical spine be suspected, immediate tracheostomy to secure the airway is recommended. Flexible bronchoscopy is unlikely to be effective in a blood-contaminated field. Cervical exposure is ensured through a collar incision made 2–3 cm above the sternal notch. The strapmuscles are separated from the midline, and the
Fig. 15.11 Severe supraglottic disruption: (a) Laryngeal exposure using the intubation laryngoscope reveals deep lacerations of the ventricular bands and disruption of the epiglottic petiole.
(b) Final result 3 months after immediate repair with a horizontal supraglottic laryngectomy technique: normal laryngeal functions
Fig. 15.10 Bilateral arytenoid avulsion following a sport accident in an adolescent: Fibrinous deposits are seen at the level of the former arytenoids, with conspicuous vocal cord haematomas
airway through a tracheostomy and waiting for spontaneous symptom resolution is unacceptable. Failed decannulation is often the result of severe cicatricial airway narrowings, which could have been prevented had primary surgical repair been conducted in a timely manner.
15.1.5.3 Thyroid Cartilage Fracture
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Fig. 15.12 Examples of late cicatricial sequelae of untreated supraglottic disruptions: (a) Subtotal supraglottic obstruction with severe posterior displacement of the epiglottic petiole (arrow) and scarring of the ventricular bands (b) Cicatricial
fusion of the ventricular bands, posterior dislocation of both arytenoids and posterior displacement of the epiglottis. Both conditions are extremely challenging to treat, whereas an immediate repair would have restored almost normal laryngeal functions
Fig. 15.13 Severe damage of the cricoid and upper trachea in an adolescent who sustained a motorcycle accident: (a) Displaced fractures of the cricoid and upper tracheal rings but without
recurrent laryngeal nerve injury. (b) Reconstruction of the upper airway around an LT-Mold prosthesis. (c) Final reconstruction: meticulous reapproximation of all cartilage fragments
anterior wall of the trachea is exposed. The site of injury is identified, and meticulous debridement of both proximal and distal stumps is carried out before performing a cricotracheal or thyrotracheal anastomosis (see Chap. 20). Associated injuries of the pharynx, oesophagus and RLNs can be adequately explored through the airway dehiscence. As identification of the RLNs is difficult in swollen tissues, this may further damage a potentially intact nerve in an already tracheostomised patient, especially if nothing is known about vocal cord mobility. For this reason, exploration of a hypothetically injured RLN is not recommended. If the integrity of the cartilage is preserved, a circumferential primary anastomosis with absorbable
sutures should be performed. In case of extensive laryngotracheal damage, a variety of laryngotracheal reconstructions can be applied, depending on the extent of local damage and the surgeon’s preference. Internal stabilisation with a soft LT-Mold may be necessary in extensive damage of the laryngotracheal framework. When torn pieces of cartilage reach the cricoid or thyroid cartilages, the use of an LT-Mold prosthesis is preferable to that of a Montgomery T-tube, which cannot accommodate the inner complex contours of the larynx (Fig. 15.13). If airway repair is performed early, within the first 24 h after the injury, 10–15 days of stenting are sufficient (Fig. 15.14).
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15.3 Caustic Ingestion Fig. 15.14 Severe damage of the cricoid and upper trachea in an adolescent who sustained a motorcycle accident (same case as Fig. 15.13). Endoscopic result 3 months after surgery, with full rehabilitation of laryngeal functions and good stability of the upper tracheal reconstruction: (a) Normal glottis. (b) Normal-sized subglottis and trachea. Anterior granuloma at former tracheostomy site
15.2 Inhalation Injuries Steam burns must be differentiated from flame burns in inhalation injuries. The former induce upper airway oedema with possible mucosal eschars and submucosal petechiae, whereas the latter cause necrotising laryngotracheobronchitis and intra-alveolar haemorrhagic oedema with soot deposits. In both cases, emergency endoscopy prior to intubation or tracheotomy is recommended, before laryngeal oedema progresses to severe respiratory distress. Laryngotracheobronchoscopy should be conducted to assess the location and severity of burns, classified into three grades, as with skin burns: 1. Erythema and oedema 2. Eschars and submucosal petechiae 3. Deep burn with submucosal necrosis and mucosal sloughing In case of flame burn injuries, cleansing of soot debris by repeated abundant tracheobronchial lavages diminishes the inflammatory reaction of the tracheobronchial tree. It also provides a bacteriological aspirate to select proper antibiotics based on cultures and sensitivities. Corticosteroids and antibiotics are routinely prescribed, and the patient is transferred to the PICU for management and follow-up. Depending on the severity of burns, tracheotomy is preferred over intubation to secure the airway. Difficulties may arise when anterior neck burns are associated with extensive airway burns. Despite the higher long-term risk for the larynx, nasotracheal intubation may be the only initial way to secure the airway, owing to severe neck burns. When neck oedema has
subsided, tracheotomy should be performed. Longer intubation periods are likely to increase the rate of synechia and local complications. Careful multidisciplinary planning with a burn management team is mandatory. Sequelae of intubation or tracheotomy increase up to 30% when tracheobronchial burns are associated with laryngeal burns [20]. However, tracheal sequelae are easier to treat than posterior glottic stenosis or other cicatricial laryngeal narrowings. The management of laryngeal trauma by inhalation differs from that of post-intubation stenosis, due to the long-term evolution of the lesions. Incipient laryngeal stenosis should be treated by stenting with an LT-Mold to avoid cicatricial contractions, even though phonation is temporarily compromised. This handicap will, however, be of shorter duration than that of an airway reconstruction in case of severe cicatricial sequelae. If the larynx is left unstented, then severe burns are likely to evolve into supraglottic stenosis, PGS or SGS. To avoid the risk of recurrences, surgery should only be used to treat fully mature cicatricial sequelae. The surgical principles are identical to those described in Chap. 20.
15.3 Caustic Ingestion Over the last decades, the incidence of caustic injuries in children has dropped to less than five cases per 100,000 inhabitants per year in occidental countries, thanks to preventive measures and legislation on hazardous products [14]. The child-proofing and content labelling of household cleaner containers account for this remarkable
210
change, whereas in developing countries, children are still exposed to dangerous chemicals, often stored unsafely in soft-drink bottles. In contrast to adults in whom corrosive injuries mainly result from suicide attempts through the ingestion of caustics, such ingestions are typically accidental in children, except in cases of child abuse. Often, only one mouthful of the noxious agent is ingested by toddlers, accounting for 80% of all paediatric cases [1]. Consequently, the stomach is rarely involved, and the risk of perforation is lower than in adults. However, severe burns may be observed in the oral cavity, pharyngolarynx or oesophagus. The type of agent ingested is decisive: Weak corrosive agents, such as bleaches and ammonia (NH4OH), cause only superficial mucosal injuries, whereas strong acids and alkali induce deep penetrating injuries due to coagulation and liquefaction necrosis, respectively [10]. The severity of the lesions is dependent on the pH, type of substance ingested (solid versus liquid), duration of exposure and quantity of corrosive chemicals ingested. Lye (NaOH, KOH), found in drain cleaners and electric dishwasher soaps, is an alkaline agent. Other noxious substances include acids, such as industrial-strength bleach (5% HCL) and pool or battery acids. Any suspicion of corrosive ingestion in a child must be taken seriously.
15.3.1 Patient Assessment Interrogation of the child and potential witnesses should try to determine the nature, quantity and brand name of the noxious agent ingested. Prior to a thorough physical examination, the “toxicology centre” must be called to obtain information on the potential local and systemic toxic effects of the corrosive agent. This will facilitate the detection of systemic side effects that might otherwise be overlooked. Symptoms of respiratory distress, such as stridor, hot potato voice, dysphagia, odynophagia, drooling and substernal pain, are indicative of severe injuries. In children, abdominal pain is uncommon in accidental corrosive injuries, owing to the small amount of chemicals ingested. After a suicide attempt, abdominal pain is suggestive of severe gastric injury requiring immediate management. Before focusing on the upper aero-digestive tract, a physical examination of the face and extremities in search of signs of hypoperfusion or systemic toxic
15 External Laryngeal Trauma
effects must be carried out. In toddlers, only the mouth and oro-pharynx are accessible to inspection while the child is awake. Intra-oral and peri-oral burns should be carefully noted. The absence of oral lesions does not preclude severe pharyngo-oesophageal burns. In a large series of 378 cases, 8–20% of patients without oropharyngeal lesions exhibited oesophageal burns upon endoscopy [4]. On the contrary, oro-pharyngeal burns may occur without associated oesophageal lesions [8]. Up to 20% of children are paucisymptomatic upon first examination. Even in the absence of symptoms, these children must be placed under careful observation, as symptoms of airway obstruction may become conspicuous only after several hours. In case of impending respiratory distress, early broncho-oesophagoscopy is mandatory to assess the pharyngolaryngeal region and secure the airway as necessary. If the child remains stable and does not present any sign of dyspnoea or abdominal pain, broncho-oesophagoscopy can be delayed until the delineation of burn lesions has occurred, typically 24–48 h after accidental ingestion [11]. It is unsafe to discharge the child without first performing bronchooesophagoscopy to assess the exact extent and severity of the lesions. Patient management typically comprises hospital admission, control of potential electrolyte imbalances, nil per oral (NPO) with total parenteral nutrition, broad-spectrum antibiotics and proton pump inhibitors (PPI), until endoscopic evaluation dictates further measures. Battery ingestion deserves special attention when the battery is retained at the upper oesophageal sphincter, the aortic arch in the oesophagus, or in the stomach. Local leakage of NaOH, KOH or Hg may cause deep mucosal damage and even perforation after a few hours. Urgent (within 8–12 h) post-ingestion endoscopic removal is mandatory before transmural necrosis occurs [16].
15.3.2 Endoscopic Assessment Broncho-oesophagoscopy under general anaesthesia is the mainstay of the diagnosis, since signs and symptoms do not accurately predict the presence or severity of caustic injuries. After induction of anaesthesia through face mask ventilation, direct laryngotracheoscopy during an apnoeic period using a bare 0-degree 4 mm-diameter sinuscope facilitates inspection of the oral cavity,
211
15.3 Caustic Ingestion
pharyngolarynx and trachea down to the carina, without worsening airway patency in the presence of oedematous swelling of the supraglottis. When there are significant pharyngolaryngeal burns compromising the airway, early tracheotomy is indicated, since severe inflammatory reactions induced by lye burns may take weeks or months to resolve. If the rim of the pharyngolaryngeal junction is circumferentially burned, an LT-Mold stent should be placed endoscopically in order to avoid late cicatricial stenosis of the supraglottis. Oesophagoscopy is first carried out under general anaesthesia using a paediatric rigid scope to carefully inspect the hypopharynx and upper oesophageal sphincter under low-pressure inflation. Next, a slim 6-mm video-gastroscope is inserted under visual control in the upper oesophagus, and passed slowly down to the stomach with minimal inflation. If this examination is performed by a well-trained endoscopist, then the risk of accidental perforation is almost nonexistent, even in grade 3 lesions (see below). The type, extent and depth of injuries are best assessed within 24–48 h after the accidental ingestion, when 3rd degree burns are already fully delineated [12, 37]. Acute lesions may be classified into three grades (Fig. 15.15) [15]: • Grade 1: Erythema and oedema of the mucosa • Grade 2: Epithelial exfoliation with erosions resulting in a papyrus appearance of the pharyngeal or oesophageal mucosa • Grade 3: Deep coagulation or liquefaction necrosis with haemorrhagic and darkened mucosa
Inspection of the stomach is a crucial part of the examination, especially after a suicide attempt, where large quantities of corrosive chemicals may have caused a liquefaction necrosis of the entire gastric pouch. This severe injury may require subsequent (oesophago-) gastrectomy.
15.3.3 Management Appropriate management can only be determined after careful endoscopic assessment of the extent and degree of oesophagogastric burns. First- and secondgrade burns are seen in approximately 60% of the cases, mild non-circumferential third-grade burns in approximately 26% of the cases and severe circumferential third-grade burns (more likely to cause strictures than linear injuries) in approximately 16% of the cases [2]. First-grade burns require no treatment, except for a soft diet over a couple of days. In the case of secondgrade burns, which do not reach beyond the muscularis mucosae of the oesophagus, late cicatricial stenoses are unlikely. The patient is hospitalised and treated with broad-spectrum antibiotics along with PPIs to avoid acid reflux, which may aggravate oesophageal lesions. A thin and supple nasogastric tube of the Fresenius® type is inserted. At this stage, the use of corticosteroids remains controversial although these drugs appear to be of benefit in the case of moderately severe grade 2 or 3 lye burns. Doses of 4 mg/kg of methylprednisolone have been recommended.
Fig. 15.15 Grading of acute caustic injuries: (a) Grade 1: Erythema and oedema (oesophagus). (b) Grade 2: Epithelial exfoliation and erosion (epiglottis). (c) Grade 3: Deep haemorrhagic necrosis (oesophagus)
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In third-grade burns with an intact stomach, supportive measures are initiated, and broad-spectrum antibiotics along with high-dose PPIs are administered. Corticosteroids are contra-indicated in severe burns as they are likely to increase the risk of perforation, without real long-term benefits. Several options for diminishing the risk of oesophageal strictures have been proposed: • Early gastrostomy with placement of a string through the oesophagus to perform safe dilation using Rehbein dilators, starting 3–6 weeks after accidental ingestion, depending on the severity and extent of lesions [29] • Nasogastric tubing with a sausage-like tube of a given diameter to keep the oesophagus expanded while the mucosa regenerates [27, 35] In massive third-grade oesophagogastric burns following a serious suicide attempt, oesophago-gastrectomy may be envisaged. Severe pharyngolaryngeal burns typically spare the vocal cords and ventricular bands, primarily due to the vigorous reflex laryngospasm that contracts the supraglottic structures during accidental ingestion. If the supraglottis remains unstented, subtotal or total cicatricial stenosis may occur. At this stage, a soft LT-Mold prosthesis should be placed endoscopically [24].
15.3.4 Late Cicatricial Sequelae In general, short (<2–3 cm long) oesophageal stenoses respond well to several sessions of dilation using tapered Savary–Gilliard bougies.
Fig. 15.16 Grading of cicatricial pharyngolaryngeal stenoses due to ingestion of corrosive chemicals: (a) Normal larynx with cicatricial stenosis of both piriform fossae. (b) Small residual
15 External Laryngeal Trauma
Frequent ineffective dilations, undilatable strictures, complete oesophageal obliteration, subtotal or total pharyngolaryngeal stenosis and cicatricial stenosis of the oral cavity require surgical intervention. According to the author’s experience, patients with stenotic lesions longer than 3 cm or multiple oesophageal stenoses respond poorly to serial dilation. Oesophageal replacement must be seriously considered in such cases. The description of surgical management will be limited to severe pharyngolaryngeal stenoses requiring a multi disciplinary approach with the paediatric gastroenterology surgeon [20]. Pharyngo-oesophageal stenoses are classified into three grades (Fig. 15.16): • Grade 1: –– Upper oesophageal sphincter –– One or two piriform fossa(e) –– Intact laryngeal rim • Grade 2: –– Upper oesophageal sphincter –– Both piriform fossae –– Incomplete laryngeal obstruction • Grade 3: –– Upper oesophageal sphincter –– Both piriform fossae –– Laryngeal stenosis with complete obliteration The operation should be delayed for several months to 1 or 2 years to allow resolution of the inflammatory processes, improvement of the nutritional status and optimisation of the pulmonary condition. Although challenging, this type of pharyngolaryngeal surgery is highly rewarding, owing to the child’s rehabilitation capacities as far as deglutition is concerned. At initial presentation, the child
opening of the supraglottic larynx. (c) Complete pharyngolaryngeal obstruction
15.3 Caustic Ingestion
is tracheostomy-dependent and fed via percutaneous endoscopic gastrostomy (PEG) tube, without voice, unable to swallow and constantly spitting out saliva. After surgery and intensive rehabilitation, the child may live an almost normal life [26]. The procedure consists of a transhiatal oesophagectomy with isoperistaltic colon interposition in the bed of the native oesophagus, along with a pharyngocolic anastomosis at the level of the arytenoids (Fig. 15.17). The role of the head and neck surgeon is twofold [25]: • Reopening the pharyngolarynx with the CO2 laser • Performing the pharyngocolic anastomosis with the help of the visceral surgeon Prior to abdominal and thoracic surgery, the pharynx is exposed and suspended with the largest possible Lindholm laryngoscope. Retrograde assessment of vocal cord integrity and function is performed by passing a flexible videobronchoscope through the tracheostoma. The vocal cords and ventricular bands are
Fig. 15.17 Diagram of colon transplant into the pharynx for complete pharyngolaryngeal stenosis due to caustic injury: The pharyngolarynx is reopened with the CO2-laser, and the colon transplant is anastomosed to the retro-arytenoid and pharyngeal mucosae
213
often intact, as they have been protected by a severe reflex laryngospasm occurring at the time of the corrosive injury. The CO2 laser, set to ultrapulse mode, 150 mJ/cm2, 250 m spot size at 400 mm working distance and 10 Hz repetition rate, is used to reopen the larynx and circumferentially delineate the line of pharyngeal anastomosis. This landmark will be very helpful when the pharynx is approached from below through a left cervicotomy. Trans-illumination from the subglottis using the flexible scope is used to reopen the supraglottic larynx at the right place, then extend the limits of further resection along the pharyngo-epiglottic folds to the posterior pharyngeal wall. Initial endoscopic surgery is immediately followed by the abdominal preparation of the colon transplant and the transhiatal oesophagectomy. The gastrocolic anastomosis is first carried out, after which resection and replacement of the oesophagus is made through a left cervicotomy by ascending the colon transplant up to the neck. The pharynx is opened along the vertical and superior rims of the left thyroid cartilage alae. The larynx is rotated to the right, providing a wide access to the pharynx from the upper oesophageal sphincter to the uppermost limit of the posterior pharyngeal incision made using the CO2 laser. By staying on the midline posterior to the upper oesophageal sphincter, the left RLN is easily preserved. The pharyngocolic anastomosis is made using a 4.0 Vicryl suture, starting at the anterior portion of the right piriform fossa and continuing along the arytenoid mucosa in the retrocricoid area as well as along the line of the CO2 laser resection on the lateral and posterior pharyngeal walls until a complete circumferential anastomosis is achieved. Preparing the pharyngolarynx with the CO2 laser prior to its opening through the cervical approach helps delineate the exact level at which the colon transplant must be sutured in the pharynx (Fig. 15.18). An LT-Mold stent is useful to calibrate the supraglottic reconstruction, thereby preventing restenosis. Although postoperative rehabilitation is often long, and dilation sessions with additional endoscopic CO2 laser treatments may be required in almost half of the cases, the final 5-year postoperative outcome in all of the 13 children who have undergone this type of surgery at the author’s institution has shown complete restoration of airway, voice and deglutition. Tracheostomy and gastrostomy closure were achieved after a mean rehabilitation period of 46 and 80 days, respectively [25].
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15 External Laryngeal Trauma
Fig. 15.18 Repair of cicatricial pharyngolaryngeal obstruction due to severe caustic injury in a 5-year-old boy: (a) Preoperative view: total cicatricial stenosis of the pharyngolarynx; the rest of the epiglottis is fused with the posterior pharyngeal wall. (b) Peroperative view: With the CO2 laser, the pharyngolarynx is reopened, and the cicatricial mucosa of the pharynx is excised,
leaving only the deep muscular layer in place. Please note the absence of charring on the laser wound. (c) Postoperative view: pharyngolarynx with a horizontal supraglottic laryngectomy. The colon transplant is widely patent. The vocal cords are visible through a slightly narrowed laryngeal inlet. Restoration of normal voice and breathing, but subnormal deglutition
References
11. Holinger, L.D.: Caustic ingestion, esophageal injury and stricture. In: Holinger, L.D., Lusk, R.P., Green, C.G. (eds.) Pediatric Laryngology and Bronchoesophagology, pp. 295– 303. Lippincott-Raven, Philadelphia/New York (1997) 12. Holinger, L.D.: Caustic ingestion, esophageal injury and stricture. In: Holinger, L.D., Lusk, R.P., Green, C.G. (eds.) Pediatric Laryngology and Bronchoesophagology, p. 297. Lippincott-Raven, Philadelphia/New York (1997) 13. Holinger, P.H., Schild, J.A.: Pharyngeal, laryngeal and tracheal injuries in the pediatric age group. Ann. Otol. Rhinol. Laryngol. 81, 538–545 (1972) 14. Irshad, K.: Caustic injuries to the esophagus. In: Patterson, J.A., Cooper, J.D., Deslauriers, J. (eds.) Pearson’s Thoracic and Esophageal Surgery, pp. 759–766. Churchill Livingstone, Philadelphia (2007) 15. Kirsh, M.M., Peterson, A., Brown, J.W., et al.: Treatment of caustic injuries of the esophagus: a ten year experience. Ann. Surg. 188, 675–678 (1978) 16. Maves, M.D., Carithers, J.S., Birck, H.G.: Esophageal burns secondary to disc battery ingestion. Ann. Otol. Rhinol. Laryngol. 93, 364–369 (1984) 17. McConnell, D.B., Trunkey, D.D.: Management of penetrating trauma to the neck. Adv. Surg. 27, 97–127 (1994) 18. Miller, R.H., Duplechain, J.K.: Penetrating wounds of the neck. Otolaryngol. Clin. North Am. 24, 15–29 (1991) 19. Minard, G., Kudsk, K.A., Croce, M.A., et al.: Laryngotracheal trauma. Am. Surg. 58, 181–187 (1992) 20. Nottet, J.B., Duruisseau, O., Herve, S , et al.: Inhalation burns: apropos of 198 cases. Incidence of laryngotracheal involvement. Ann. Otolaryngol. Chir. Cervicofac. 114, 220–225 (1997) 21. Ogura, J.: Management of traumatic injuries of the larynx and trachea including stenosis. J. Laryngol. Otol. 85, 1259– 1261 (1971)
1. Anderson, K.D.: Corrosive injury. In: Pearson, F.G., Cooper, J.D., Deslauriers, J. (eds.) Esophageal Surgery, pp. 577–589. Churchill Livingstone, New York/Edinburgh/London/ Philadelphia (2002) 2. Anderson, K.D., Rouse, T.M., Randolph, J.G.: A controlled trial of corticosteroids in children with corrosive injury of the esophagus. N Engl J. Med. 323, 637–640 (1990) 3. Bryce, D.P.: The surgical management of laryngotracheal injury. J. Laryngol. Otol. 86, 547–587 (1972) 4. Gaudreault, P., Parent, M., McGuigan, M.A., et al.: Predictability of esophageal injury from signs and symptoms: a study of caustic ingestion in 378 children. Pediatrics 71, 767–770 (1983) 5. Gold, S.M., Gerber, M.E., Shott, S.R., et al.: Blunt laryngotracheal trauma in children. Arch. Otolaryngol. Head Neck Surg. 123, 83–87 (1997) 6. Grewal, H., Rao, P.M., Mukerji, S., et al.: Management of penetrating laryngotracheal injuries. Head Neck 17, 494– 502 (1995) 7. Haug, R.H., Giles, D.L.: Laryngeal cartilage fracture: report of a case. J. Oral Maxillofac. Surg. 50, 528–530 (1992) 8. Hawkins, D.B., Demeter, M.J., Barnett, T.E.: Caustic ingestion: controversies in management. A review of 214 cases. Laryngoscope 90, 98–109 (1980) 9. Hirano, M., Kurita, S., Terasawa, R.: Difficulty in highpitched phonation by laryngeal trauma. Arch. Otolaryngol. 111, 59–61 (1985) 10. Holinger, L.D.: Caustic ingestion. In: Cotton, R.T., Myer, C.M.I. (eds.) Practical Pediatric Otolaryngology, pp. 595– 602. Lippincott-Raven, Philadelphia/New York (1999)
References 22. Ogura, J.H., Biller, H.F.: Reconstruction of the larynx following blunt trauma. Ann. Otol. Rhinol. Laryngol. 80, 492– 506 (1971) 23. Olson, N.R.: Wound healing by primary intention in the larynx. Otolaryngol. Clin. North Am. 12, 735–740 (1979) 24. Pasche, P., Lang, F., Monnier, P.: Laryngeal trauma. In: Pearson, F.G., Cooper, J.D., Deslauriers, J. (eds.) Pearson’s Thoracic and Esophageal Surgery, pp. 1738–1754. Churchill Livingstone, Philadelphia (2008) 25. Pasche, P., Reinberg, O., Lang, F., et al.: Traitement des séquelles graves de sténoses caustiques pharyngo-oesophagiennes et laryngées chez l’enfant. Schweiz. Med. Forum Suppl. 29(6), 69–72 (2006) 26. Reinberg, O., Genton, N.: Esophageal replacement in children: evaluation of the one-stage procedure with colic transplants. Eur. J. Pediatr. Surg. 7, 216–220 (1997) 27. Reyes, H.M., Hill, J.L.: Modification of the experimental stent technique for esophageal burns. J. Surg. Res. 20, 65–70 (1976) 28. Richardson, M.A.: Laryngeal anatomy and mechanisms of trauma. Ear Nose Throat J. 60, 346–351 (1981) 29. Saetti, R., Silvestrini, M., Cutrone, C., et al.: Endoscopic treatment of upper airway and digestive tract lesions caused by caustic agents. Ann. Otol. Rhinol. Laryngol. 112, 29–36 (2003)
215 30. Sasaki, C.T., Marotta, J.C., Lowlicht, R.A., et al.: Efficacy of resorbable plates for reduction and stabilization of laryngeal fractures. Ann. Otol. Rhinol. Laryngol. 112, 745–750 (2003) 31. Sataloff, R.T., Bough Jr., I.D., Spiegel, J.R.: Arytenoid dislocation: diagnosis and treatment. Laryngoscope 104, 1353– 1361 (1994) 32. Schaefer, S.: Use of CT scanning in the management of the acutely injured larynx. Otolaryngol. Clin. North Am. 24, 31 (1991) 33. Schaefer, S.D., Close, L.G.: Acute management of laryngeal trauma. Update. Ann. Otol. Rhinol. Laryngol. 98, 98–104 (1989) 34. Vassiliu, P., Baker, J., Henderson, S., et al.: Aerodigestive injuries of the neck. Am. Surg. 67, 75–79 (2001) 35. Wijburg, F.A., Heymans, H.S., Urbanus, N.A.: Caustic esophageal lesions in childhood: prevention of stricture formation. J. Pediatr. Surg. 24, 171–173 (1989) 36. Yen, P.T., Lee, H.Y., Tsai, M.H., et al.: Clinical analysis of external laryngeal trauma. J. Laryngol. Otol. 108, 221–225 (1994) 37. Zargar, S.A., Kochhar, R., Mehta, S., et al.: The role of fiberoptic endoscopy in the management of corrosive ingestion and modified endoscopic classification of burns. Gastrointest. Endosc. 37, 165–169 (1991)
Neoplastic Lesions of the Larynx and Trachea
Contents 16.1 16.1.1 16.1.2 16.1.3 16.1.4
Recurrent Respiratory Papillomatosis (RRP)...... 220 Epidemiology and Pathogenesis............................... 220 Clinical Course......................................................... 221 Management............................................................. 222 Adjuvant Medical Therapy....................................... 225
References............................................................................ 227
16
Core Messages
›› Rare ›› ›› ›› ›› ›› ›› ›› ››
››
entities accounting for only 2% of all paediatric laryngeal anomalies. Benign tumours account for 98% of all paediatric airway neoplasms. Recurrent respiratory papillomatosis and subglottic haemangiomas are the most frequent benign tumours of the paediatric larynx. Symptoms are similar to those of other upper airway stenoses, albeit with a progressive relentless course. MRI is superior to CT scan for assessing tumour extension into surrounding soft tissue structures. TNFL and rigid bronchoscopy are the mainstay of diagnosis. Endoscopic CO2 or KTP laser resections are appropriate means for removing certain benign tumours of the larynx and trachea. The open surgical approach is reserved for tumours that cannot be fully resected by endoscopic means. Exceedingly rare malignant tumours should be discussed at a multidisciplinary tumour board conference in order to select the most appropriate treatment modality. Recurrent respiratory papillomatosis. –– Most common benign laryngeal neoplasm in children –– Second most frequent cause (after vocal cord nodules) of childhood hoarseness –– Unpredictable course with tendency to recur and spread after removal –– Estimated incidence of 4:100,000 children per year
P. Monnier (ed.), Pediatric Airway Surgery, DOI: 10.1007/978-3-642-13535-4_16, © Springer-Verlag Berlin Heidelberg 2011
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218
16 Neoplastic Lesions of the Larynx and Trachea
–– High-risk triad: –– Young primigravid mother –– Vaginal delivery –– First-born child (~75% of RRP affected children) –– Aetiology: –– Human papilloma virus (HPV) –– Types: HPV6, HPV11, HPV16 and HPV18 (rarely) –– Association with latent genital HPV infection or condyloma acuminata in the mother –– Childhood onset: –– 75% before the age of 5 years –– 25% during infancy
Benign and malignant neoplasms of the larynx and trachea are rare entities, accounting for only 2% of the pathologies reported by PH Holinger in a large series of 846 paediatric laryngeal anomalies [8]. Although benign tumours largely outweigh their malignant counterparts by a ratio of 98% to 2%, they can be very challenging for the otolaryngologist. Among benign tumours, the most frequent are recurrent respiratory papillomatosis (RRP) and subglottic haemangiomas (SGH). Other vascular or lymphatic malformations and neurogenic tumours are among the top five diagnoses of paediatric benign airway tumours. Virtually any kind of connective tissue tumour may be encountered (lipomas, rhabdomyomas, chondromas and fibromas) and in the group of epithelial tumours, monomorphic and pleomorphic adenomas are seen only exceptionally in comparison with squamous papillomas. The extremely uncommon malignant tumours mostly belong to the sarcoma group, although anecdotal reports of malignant epithelial tumours have been reported in the literature [10]. The mode of presentation depends on the location of the space-occupying lesion, but symptoms of extraor intra-thoracic airway obstruction prevail. In the larynx, tumours may cause dysphonia or aphonia and inspiratory stridor. In the trachea, expiratory wheeze is the typical hallmark (see Sect. 3.2.3, Chap. 3). In fact, symptoms do not differ from those caused by other
more frequent upper airway obstructions, except for their slow progressive and relentless course. Transnasal fibreoptic laryngoscopy (TNFL) and direct laryngotracheo-bronchoscopy under general anaesthesia (see Sect. 5.2.2 and 5.2.3, Chap. 5) in spontaneous respiration or intermittent apnoeas provide the best conditions for assessing the entire airway, while taking biopsy specimens for histopathological evaluation. In some cases, a pedunculated round-shaped mass can be removed using the CO2 laser and micromanipulator for the larynx, and the OmniGuide fibre for the trachea. This procedure immediately alleviates symptoms and yields a large specimen for precise histological assessment, before definitive treatment is proposed. In rare pathologies, very small biopsy specimens may render histological assessment difficult and imprecise. To determine the exact extension of laryngeal and tracheal tumours, MRI is better suited than CT scan in infants and children. The cartilages of the paediatric larynx are poorly visible on CT scan images, and tumour extension beyond the laryngeal or tracheal air column is thus difficult to delineate. Computerized tomography scan is used as the first diagnostic tool prior to endoscopy, as it is readily available and does not require sedation. If the information provided by the CT scan is insufficient, MRI is implemented to detect tumour extension into surrounding soft tissue structures. With the exception of RRPs, SGHs and certain vascular or lymphatic malformations that can be only partially resected and may benefit from adjuvant therapies, all other benign airway tumours must be fully resected either by endoscopic removal or by open surgery when a large sessile implantation of the tumour precludes complete endoscopic removal (Fig. 16.1). Subglottic haemangiomas have been dealt with in Chap. 10, which was devoted to congenital laryngeal anomalies, and RRPs will be discussed in more detail in Sect. 16.1. For all other benign airway tumours, complete removal is the basic precept, although the way to achieve this goal differs widely, depending on the location, type and extent of the lesion. The key to success lies in the quality of endoscopic exposure and the appropriate choice of anaesthesiologic technique. The principle should be working in a free operative field, either under conditions of spontaneous respiration if the degree of obstruction is not too severe or with intermittent apnoeas (see Sect. 18.1.1 and 18.1.2,
16 Neoplastic Lesions of the Larynx and Trachea
219
Fig. 16.1 Fibrous histocytoma of the trachea with large sessile implantation: (a) Round tumour implanted on the right tracheal wall, subtotally obstructing the airway (b) Final result after simple resection and anastomosis with complete resection of the lesion
Chap. 18). For laryngeal and pharyngolaryngeal tumours, several laryngoscopes should be tried until the best exposure is obtained. For subglottic lesions, a Lindholm self-retaining false cord retractor facilitates exposure, providing a significantly larger view than that obtained with the subglottiscope. Pedunculated lesions can be fully resected with the CO2 laser. Proper parameters must be chosen depending on the vascularity of the lesion. Highly vascularised tumours may need initial blanching of the pedicle of implantation using the same parameters as for SGHs (CW chopped mode, 3 watts output power, slightly defocused beam at 400 mm focal length, and 100 ms impacts), before converting to a more precise cutting effect in the ultrapulse mode. Providing precise laser parameters for all situations is almost impossible, but poorly vascularised tumours (lipomas, chondromas and some fibromas) can be resected with a sharply focused laser beam of 250 m spot size in the CW chopped mode, with laser strikes of 30 ms. If the lesion is adherent to the vocal cord, this part of the tumour must be resected in the ultrapulse mode 125 mJ/cm2, 250 m spot size and 10 Hz repetition rate. Delicate structures such as the vocal cords must always be wellpreserved by using the best cutting properties of the CO2 laser, whereas supraglottic tumours may be resected without adverse effects using the CO2 laser or KTP laser in a continuous working mode. For tracheal tumours, the CO2 or KTP laser can be used with appropriate laser fibres. The KTP laser is preferred for highly vascularised tumours (see Fig. 4.17, Chap. 4), whereas the CO2 laser is favoured for poorly vascularised tumours. The same principles as those used for laryngeal tumours are applied: first, blanching
of the tumour pedicle, and then, resection with a more pronounced cutting effect. With the laser fibres, this can be achieved by changing the distance from the fibre tip to the target (see Sect. 4.6.4.3, Chap. 4) while keeping the same laser parameters. The divergence of the laser beam at the fibre tip is responsible for significant changes in the power density delivered onto tissues, in relation to the distance separating the fibre tip to the target. Prior to laser work, the desired power density must be tested on a wooden tongue depressor by setting fixed laser parameters and observing the tissue effects in relation to the distance from the fibre tip. When using flexible laser fibres, the output laser power is set between 10 and 15 watts for the KTP laser and between 10 and 18 watts for the CO2 laser. Due to the co-axial CO2 airstream that is used to cool down the OmniGuide CO2 laser fibre, treating lesions distally to the carina is dangerous as this may generate significant air embolism in the heart and systemic circulation. Tumours located in the main stem bronchi must be treated using bare KTP laser fibres without co-axial airstream. Malignant tumours of the paediatric larynx, mostly rhabdomyosarcomas [7], require a multidisciplinary discussion at a tumour board conference before adequate specific treatment can be proposed. Despite improved survival rates following chemoradiation therapy for several malignant tumours, late severe sequelae pertaining to laryngeal growth as well as the risk of inducing metachronous second primary tumours must not be underestimated. In the case of malignant tumours, surgery should be seriously considered, particularly when a conservative partial laryngectomy is possible.
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16.1 Recurrent Respiratory Papillomatosis (RRP) First described in the mid-nineteenth century, RRP is a viral disease affecting both paediatric and adult populations with varying degrees of aggressiveness. In children, RRP is the most common benign neoplasm of the larynx [15] and the second most frequent cause (after vocal cord nodules) of childhood hoarseness. Its natural course is unpredictable, with a high propensity to recur and spread. Despite being an infectious disease caused by human papilloma viruses (mainly HPV 6 and 11), the condition behaves like a tumour, with a particular tropism for squamous epithelial tissues. This accounts for the preferential development of exophytic growths at the squamociliary junctions of the upper airways (Fig. 16.2). Contamination of newborns occurs at birth from HPV-infected mothers, most of whom (~ 60% of cases)
Fig. 16.2 Prevalence of human papillomavirus exophytic growth at the squamo-ciliary junctions of the upper airways: 1. Limen vestibuli nasi. 2. Naso-pharyngeal surface of soft palate. 3. Supraglottis 4. Vocal cords. 5. Areas of squamous metaplasia due to chronic trauma (e.g., tracheostoma, cannula tract in the trachea, carina and bronchial spurs)
16 Neoplastic Lesions of the Larynx and Trachea
present condylomata acuminata of the genital tract. In the most severe cases, RRP exhibits a natural propensity to recur relentlessly, requiring a tracheotomy to secure the airway, thereby increasing papilloma dissemination to the distal trachea and bronchi. On rare occasions, lung parenchyma involvement and malignant degeneration have been reported in long-standing cases [5], especially with HPV 11 and 16 subtypes.
16.1.1 Epidemiology and Pathogenesis In western countries, the incidence of RRP is estimated at 4:100,000 children per year [3, 4]. Higher incidence figures may be found in countries with low socio-economic backgrounds, with a high prevalence of sexually transmitted HPV infections in certain subgroups. Although up to 25% of women of childbearing age may be afflicted by latent or active HPV genital tract infections, only a small portion of the children contaminated at birth develop RRP. Abnormal host T-cell functions, prolonged vaginal delivery and a high virus content in genital condylomata play a significant role in the development of juvenile onset RRP (JORRP) [1]. The exact mode of HPV transmission remains unclear, but several features are clinically relevant: • The same HPV 6 and 11 subtypes (rarely 16 and 18) are found in children’s respiratory papillomas and in mothers’ genital warts. • Although up to 30–50% of aerodigestive tract swabs of infants born to mothers with cervical HPV disease are HPV positive, only 7 out of 1,000 children develop JORRP. • However, a history of vaginal condylomata is reported in around 50% of the mothers who gave birth to children with JORRP [6]. • The risk of HPV transmission is higher in infants born through vaginal delivery (one RRP case/400 infected mothers) than by caesarean section [15]. In fact, only 1% of all RRP children are estimated to be born by caesarean section [13], attesting to possible blood transmission through the umbilical cord [15]. • Lastly, a high-risk triad has been identified, consisting of teenaged primigravid mothers, vaginal delivery and first-born children (~75% of all cases). The likely mechanism is related to a prolonged contact of the newborn’s upper airways with the genital tract of the HPV-infected mother during delivery.
16.1 Recurrent Respiratory Papillomatosis (RRP)
16.1.2 Clinical Course For some unknown reason, the upper age limit of JORRP has been set at 12 years but 75% of children with RRP develop the disease before the age of 5 years. Three main clinical courses have been identified: • Low aggressiveness of JORRP, defined as the need for less than five therapeutic procedures over a lifetime, occurs in 25% of the cases. • High aggressiveness of JORRP is seen in around 20% of the patients. It is defined by the following features: onset in the neonatal period or before the age of 2–3 years, need for more than 40 lifetime procedures, need for tracheostomy (~14% of all JORRP cases) and finally likelihood for mortality. Human papilloma virus subtype 11 has been shown to be more aggressive than subtype 6, with higher severity scores at diagnosis, need for more frequent surgical interventions, for adjuvant therapy and higher likelihood to develop distal airway disease (~8% in the trachea, 3% in the bronchi and 3% in the lungs). • Malignant transformation is infrequent but has been reported to occur after more than 15 years of evolution from disease onset in the most severe cases [5]. • The intermediate group of aggressiveness represents more than 50% of all JORRP cases and shows various modes of progression falling between the two extremes. Patients will require more than five therapeutic procedures over their lifetime, but the disease aggressiveness is easily controlled. Papillomas may spontaneously regress and recur several years later, or they tend to remain more or less quiescent with a low proliferative rate that does not warrant regular endoscopic interventions. Colonisation of the normal laryngeal mucosa with HPV DNA explains the propensity for recurrence to some extent, even after several years of apparent remission of the disease. Except in infantile onset where JORRP becomes manifest by obstructive dyspnoea, a slowly progressive hoarseness is the key symptom that warrants investigation in toddlers and older children. With disease progression, signs of obstructive dyspnoea may occur. Children with vocal cord nodules have other voice behavioural habits and are usually easily differentiated from those with JORRP, who show progressive dysphonia to aphonia over a prolonged period of time.
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A slight concomitant airway compromise (not seen with vocal cord nodules) is an additional clue for the clinical diagnosis of JORRP. Since the disease is infrequent (~4:100,000 cases per year), paediatricians tend to forget this possible diagnosis, and referrals may be delayed until respiratory problems become apparent. In-office TNFL is the examination of choice. The papillary nature of the lesion is not always obvious. Mucosal secretions may blur the delicate cauliflower surface of the papillomas and give the false impression of a smooth surface lesion. Direct laryngotracheoscopy under general anaesthesia is the mainstay for assessing the correct diagnosis and the actual extent of the disease. Anaesthesia is induced through face mask ventilation. In spontaneous respiration, the larynx is exposed using a Lindholm laryngoscope placed in the vallecula to provide a free operative field of the supraglottis, glottis and subglottis (see Sect. 5.3.3, Chap. 5). Since papillomas are highly vascularised, the slightest trauma, caused by the laryngoscope blade or a suction catheter, may induce bleeding, thereby compromising precise assessment of the disease process. Delicate intervention is essential, especially in the presence of obstructive papillomas. Rigid rod-lens telescopes of various angulations are used to assess the macroscopic features of the papillomas (Fig. 16.3) as well as their site, type and extent of implantation (Fig. 16.4). A long, bare, rigid rod-lens telescope is inserted beyond the vocal cords to look for any subglottic or tracheal extension. Rigid ventilating bronchoscopes should not be used as they may traumatise and scrape off the papillomas, thereby contributing to potential dissemination of the disease to the lower airways (Fig. 16.5). In an attempt to better assess the disease’s evolution, several endoscopic scoring systems have been developed over time [3, 9, 15]. They are all rather complicated and not easy to use for comparisons across different institutions. With the availability of 3-CCD digital cameras now routinely used in endoscopy suites, precise documentation of the extent of papillomas at each session gives an adequate overall assessment of progression or regression of the disease process. Endoscopic images stored in the computerised patient’s chart provide more accurate figures than a staging sheet, and these images are particularly useful for the patient’s follow-up. Prior to any therapeutic measure, a small biopsy should be taken with cup forceps for histological assessment and HPV subtyping. Haemostasis is achieved using adrenaline-soaked pledgets.
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Fig. 16.3 Macroscopic features of juvenile-onset recurrent respiratory papillomatosis: (a) Sessile implantation of papillomas on the left vocal cord. Prior to suction of the secretions, the papillary nature of the lesion is not conspicuous. (b) Irregular
16 Neoplastic Lesions of the Larynx and Trachea
exophytic clusters of papillomas with multiple implantation sites. (c) Pedunculated papillomas of the right supraglottis and retrocricoid region
synechia or laryngotracheal stenosis, which can be more of a problem than the primary disease itself (Fig. 16.6). Depending on the natural course and aggressiveness of the disease, the treatment plan must be tailored to each specific patient. The ear-nose-throat (ENT) surgeon in charge of the treatment must consider the following questions:
Fig. 16.4 Yield of angulated telescopes to assess the full extent of juvenile-onset recurrent respiratory papillomatosis: With the 70°-angle rod-lens telescope, papillomas are detected in both laryngeal ventricles and the anterior subglottis. None of these lesions were easily visible with the 0° telescope
16.1.3 Management The management of JORRP should pursue three main goals: • Improve voice quality • Provide an adequate airway • Facilitate disease remission Total eradication of all papillomas by an overly aggressive treatment should not be the main goal in the management of this unpredictable disease. Over time, this may lead to cicatricial sequelae, such as vocal cord
1. Is dysphonia the main symptom, and if so, can it be reasonably improved? 2. Is there impending respiratory distress, and can a tracheostomy be avoided? 3. Is a tracheotomy unavoidable due to aggressiveness of the disease, and can the patient’s condition be improved without major late cicatricial sequelae?
16.1.3.1 Voice Improvement for Limited Laryngeal Disease (Fig. 16.7) The main symptom is hoarseness without dyspnoea. The disease may spread from a single exophytic vocal cord mass to multiple laryngeal papillomas (Fig. 16.7a). The main question regarding treatment strategy is whether or not there are anterior and posterior commissure involvements. The treatment of a single papillomatous lesion is straightforward. The procedure is carried out under total intravenous anaesthesia (TIVA) with spontaneous respiration or intermittent apnoeas (see Sect. 18.1.1 and 18.1.2, Chap. 18) in order to provide a free
16.1 Recurrent Respiratory Papillomatosis (RRP)
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Fig. 16.5 Aggressive airway papillomatosis in a 2-year-old child (same patient as in Fig. 16.9): (a) Tracheal involvement at the distal tip of the tracheostomy cannula: Squamous cell metaplasia is probably responsible for implantation of papillomas at this level. (b) Subtotal obstruction of the right intermediate bronchus by a pedunculated papilloma
Fig. 16.6 Unacceptable cicatricial sequelae of treatment for juvenile-onset recurrent respiratory papillomatosis: (a) Severe glottic synechia. (b) Complete transglottic stenosis with residual
clusters of papillomas. (c) Severe pharyngeal and laryngotracheal stenoses with pharyngotracheal fistula
Fig. 16.7 Juvenile-onset recurrent respiratory papillomatosis – limited laryngeal disease: (a) Single papilloma at the free border of the left vocal cord. (b) Multiple sites of papillomatosis on
both vocal cords. (c) More spreading disease involving the anterior and posterior laryngeal commissures
224
operative field to the surgeon. The larynx is suspended using a Holinger laryngoscope. A submucosal injection of 0.5 ml of adrenaline–saline solution (40 mg/ml adrenaline) is administered into Reinke’s space with a Zeitels needle to separate the lesion from the vocal ligament. The CO2 laser set to ultrapulse mode, 100 mJ/cm2 and 10 Hz repetition rate is used to resect (not vaporise) the papilloma, thereby preserving the vocal ligament and normal mucosa at the anterior and posterior laryngeal commissures. A more widespread and multifocal disease, as shown in Fig. 16.7b, is best treated with a microdebrider (see Sect. 4.8.2, Chap. 4) set at the oscillating mode and a speed of 800–1,500 rotations per minute. A dedicated laryngeal probe with a 3-mm diameter side-hole is necessary to avoid damaging the delicate vocal cords. Care should be taken to preserve the mucosa at the anterior commissure in order to prevent the formation of vocal cord synechia. When the disease is more diffuse, involving the anterior or posterior laryngeal commissure as shown in Fig. 16.7c, the microdebrider is used to remove all papillomas except for those at the anterior and posterior laryngeal commissures (see Sect. 16.1.4). A dose of 7.5 mg/ml of cidofovir is injected using a Zeitels needle into the residual papillomas, and the anterior and posterior laryngeal commissures are purposefully left intact. This procedure prevents the formation of anterior vocal cord synechia or PGS. A maximum dose of 2 mg/kg and a total dose of 25 mg per session are recommended. Five sessions of cidofovir injections at intervals of 2–3 weeks often decrease the size of papillomas, allowing additional unilateral resection of residual papillomas. The ultimate goal is to prevent synechia formation. If normal voice restoration cannot be achieved, complete removal of papillomas in areas such as the anterior commissure should not be attempted as this may lead to cicatricial sequelae. As already stated by Crocketts and Reynolds in 1990 [2], ‘Gross total removal of all visible papillomas at each operation may not be in the interest of the patient in terms of future phonatory function’. Disastrous results, as shown in Fig. 16.6, must be avoided at all costs. Considering the unpredictable course of the disease and the possible improvement at the time of puberty, limiting the number of debulking sessions and carefully removing papillomas is essential for preventing late sequelae. In limited laryngeal disease, optimal voice quality, rather than total eradication of all papillomas, should be the desired outcome.
16 Neoplastic Lesions of the Larynx and Trachea
16.1.3.2 Prevention of Tracheostomy for Moderately Invasive Laryngeal Disease The typical clinical scenario involves a child with severe dysphonia and respiratory distress (see Fig. 16.3 b and c). Upon laryngeal examination, sub-obstructive clusters of papillomas obscuring the vocal cords are often found. To confirm the papilloma implantation sites, a precise endoscopic assessment using a bare 0° telescope is necessary prior to the removal of papillomas. Anaesthesia in spontaneous respiration is frequently impossible, because of complete airway obstruction during the inspiratory phase of the respiratory cycle. The larynx is exposed in SML during an apnoeic period, and a Cook ventilating catheter for jet ventilation is passed, under visual control, beyond the clusters of papillomas into the subglottis. If the child underwent the preoperative phase without needing a tracheostomy, egress of air will always be possible, even if the papillomas seem to fully obstruct the larynx upon visual inspection (Fig. 16.8). An alternative solution is to place a Ravussin percutaneous transtracheal catheter using visual control [11]. This technique, although more dangerous, has the advantage of providing a free operative field to safely remove the papillomas with the microdebrider. With modern endoscopic techniques, performing a temporary tracheotomy for such treatments is not justified. Reopening the airway is extremely rapid with the microdebrider, and can be done during an apnoeic period prior to using an intermittent apnoea technique. The ultimate choice of anaesthesiology technique depends on concomitant tracheal disease. To this end, optimal communication with the anaesthesiology team is indispensable.
16.1.3.3 Need for Tracheotomy due to Recurrent Aggressive Disease Early onset papillomatosis during the first months of life, extensive airway involvement at first endoscopy, and frequent recurrence after treatment, are all predictors of an aggressive disease with poor long-term prognosis. A first attempt at debulking the papillomas using concurrent cidofovir injections must be made in order to avoid tracheostomy. If this goal cannot be achieved due to early recurrence of dyspnoea, securing the airway with a tracheostomy is necessary. At this
225
16.1 Recurrent Respiratory Papillomatosis (RRP) Fig. 16.8 Obstructive clusters of papillomas obscuring the glottis: (a) Preoperative view: no visible residual lumen upon endoscopy. No tracheotomy. (b) Immediate postoperative view: complete superficial removal of supraglottic papillomas, and preserved vocal cords and subglottis. The transtracheal catheter for jet ventilation is seen in the cervical trachea
stage, it is essential to maintain a safe lower airway and control disease progression using adjuvant therapies, such as cidofovir injections (7.5 mg/ml), indol-3carbinol (100–200 mg/day, orally) dietary supplement and possibly subcutaneous injections of a-2A interferon (5 million IU/m2 thrice weekly). It is unwise to schedule repeated sessions of papilloma removal in the larynx and subglottis, as the risk of cicatricial sequelae is higher than the patient’s benefits from the treatment itself. Unless adjuvant therapies provide slight airway or voice improvements, the endoscopic surgical debridement of symptomatic lesions should be limited to the tracheostomy site and lower airways. In suspension microlaryngoscopy, a 0°-rod-lens telescope is passed through the glottis to visualise the subglottis and trachea. The tracheostomy cannula is removed intermittently, and the microdebrider probe is passed through the stoma to remove tracheal papillomas at the tracheostomy site, and then further down the lower airways within easy reach of the carina and main stem bronchi. The technique is faster than using CO2 or KTP vaporisations with flexible laser fibres, and less risky in terms of cicatricial stenosis. A trial of five to six sessions of cidofovir injections into the larynx and the lower airways, repeated every 2 weeks, can be done to test the responsiveness of the disease to the treatment. Cidofovir injections are more effective in ‘virgin papillomas’ than in recurrent papillomas embedded in cicatricial tissue, where the injected solution tends to leak out of the dense scar tissue, instead of diffusing inside the mucosa. To date, this phenomenon has not been reported as a potential cause of ineffective cidofovir treatment. This is another argument against the repeated removal of papillomas with a laser or
microdebrider, if no significant symptomatic improvements (airway, voice) can be achieved (Fig. 16.9).
16.1.4 Adjuvant Medical Therapy Despite constant improvements in the surgical removal of JORRP, approximately 25% of all affected children need adjuvant medical therapy due to the aggressiveness of the disease. These figures are on the rise with the use of cidofovir injections for the treatment of papillomas in more delicate laryngeal areas. The other indications for adjuvant therapy are as follows: • Disease onset before 2 years of age • More than three surgical procedures required per year • Need for tracheostomy • Spread of disease to the lower airways • Rapid regrowth of papillomas • Papillomas situated at the anterior or posterior laryngeal commissure The last case does not necessarily represent a very aggressive disease, but the use of repeated cidofovir injections has improved the outcome in terms of cicatricial sequelae (vocal cord synechia and PGS). Over time, many adjuvant therapies have been tried with varying success. Currently, only indol-3-carbinol, a2A interferon and cidofovir are routinely used in clinical practice. More hope lies in the quadrivalent HPV vaccine (subtypes 6, 11, 16 and 18), which may decrease the prevalence of HPV diseases in teenagers, if injected
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16 Neoplastic Lesions of the Larynx and Trachea
Fig. 16.9 Aggressive airway papillomatosis in a 2-year-old child: (a) Total laryngeal obstruction by multifocal clusters of papillomas. Debulking was not attempted because of disease severity. (b) Laryngeal aspect after 3 months of alpha-2A interferon and indol-3-carbinol therapy without any debulking: slight change in the aspect of papillomas without significant mass reduction. (c) Final results several years after cidofovir injection,
and only two sessions of debulking in the larynx and lower airways. Patient decannulated with a small anterior synechia of the vocal cords. This example does not mean that success is achieved in the majority of cases. It illustrates, however, that refraining from over-aggressive treatment is beneficial, provided that the disease evolves favourably with the help of adjuvant ‘non-damaging’ airway treatments
before the first sexual intercourse. Vaccination campaigns would ideally target females and males of around 12 years of age. Based on the current knowledge of HPV replication in the squamous epithelium, HPV vaccination may not benefit JORRP patients, although anecdotal positive results have been reported.
results have been reported, with response rates ranging from 30–60%. Close monitoring of hepatic enzymes and renal function is mandatory. According to Wiatrak BJ, [14], a-2A interferon produced by recombinant DNA techniques provided fewer side effects associated with improved treatment efficacy.
16.1.4.1 Indol-3-carbinol (I3C)
16.1.4.3 Cidofovir
Derived from cauliflower, broccoli and cabbage, I3C has shown efficacy in some cases. Given as an oral dietary supplement, at a dose of 100–200 mg/day, this compound may slow disease progression but cannot completely cure JORRP.
Cidofovir is a cytosine nucleoside analog with potent anti-viral activity, which induces apoptosis in HPVpositive cells. Initially used for the treatment of cytomegalovirus retinitis, the drug has also shown efficacy in the treatment of condylomata acuminata. Due to its nephrotoxicity, the compound cannot be administered intravenously; it must thus be injected locally into the laryngeal papillomas in SML under general anaesthesia, at intervals of 2–3 weeks. The maximum recommended dose is 2 mg/kg at a concentration of 7.5 mg/ ml, with a maximum dose of 25 mg per session, regardless of the bodyweight of older children. In an American web-based survey published in 2004 [12], its efficacy was estimated to be approximately 61% in 72 patients, with a mean of 14 (range 8–30) lifetime RRP debulking procedures prior to inclusion in the study. However, 35% of the patients showed no improvement, while 4% worsened. It is assumed that most patients had
16.1.4.2 Alpha-2A Interferon This glycoprotein is used to stimulate the patient’s immunologic response, thus preventing HPV viral replication and penetration into host cells. The compound is initially administered by subcutaneous injections (5 million IU/m2 body surface/day), twice a day for 1 month and then three times a week for 6 months. Alpha-2A interferon is not tolerated by small children because of the need for repeated shots and their flu-like side effects. In the scientific literature, conflicting
References
cicatricial laryngeal sequelae, rendering the efficacy of injections suboptimal. As the larynges of infants and small children can only tolerate small amounts of injected fluid, at our institution, we first inject papillomas with cidofovir, and then debulk papillomas with the microdebrider, except for risky areas and lastly reinject cidofovir at the end of the procedure. Injecting residual papillomas after debulking leads to much leakage and thus less effective intralesional injections. The normal mucosa surrounding the sites of initial papilloma implantations is also injected with cidofovir in order to reduce the viral load.
References 1. Buchinsky, F.J., Derkay, C.S., Leal, S.M., et al.: Multicenter initiative seeking critical genes in respiratory papillomatosis. Laryngoscope 114, 349–357 (2004) 2. Crockett, D.M., Reynolds, B.N.: Laryngeal laser surgery. Otolaryngol. Clin. North Am. 23, 49–66 (1990) 3. Derkay, C.S., Malis, D.J., Zalzal, G., et al.: A staging system for assessing severity of disease and response to therapy in recurrent respiratory papillomatosis. Laryngoscope 108, 935–937 (1998) 4. Derkay, C.S., Smith, R.J., McClay, J., et al.: HspE7 treatment of pediatric recurrent respiratory papillomatosis: final results of an open-label trial. Ann. Otol. Rhinol. Laryngol. 114, 730–737 (2005) 5. Guillou, L., Sahli, R., Chaubert, P., et al.: Squamous cell carcinoma of the lung in a nonsmoking, nonirradiated patient with juvenile laryngotracheal papillomatosis. Evidence of
227 human papillomavirus-11 DNA in both carcinoma and papillomas. Am. J. Surg. Pathol. 15, 891–898 (1991) 6. Hallden, C., Majmudar, B.: The relationship between juvenile laryngeal papillomatosis and maternal condylomata acuminata. J. Reprod. Med. 31, 804–807 (1986) 7. Healy, G.B.: Neoplasia of the pediatric larynx. Otolaryngol. Clin. North Am. 17, 69–74 (1984) 8. Holinger, P.H., Brown, W.T.: Congenital webs, cysts, laryngoceles and other anomalies of the larynx. Ann. Otol. Rhinol. Laryngol. 76, 744–752 (1967) 9. Kashima, H.K.: Scoring system to assess severity and cause in recurrent respiratory papillomatosis. In: Howley PMB, T. R. (ed.) (1985) Papillomaviruses:molecular and clinical aspects: proceedings of the Burroughs-Wellcome-UCLA Symposium held in Steamboat Springs, Colorado, 08–14 April, 1985: Alan R. Liss, New York, pp 125–135 10. Ohlms, L.A., McGill, T., Healy, G.B.: Malignant laryngeal tumors in children: a 15-year experience with four patients. Ann. Otol. Rhinol. Laryngol. 103, 686–692 (1994) 11. Ravussin, P., Freeman, J.: A new transtracheal catheter for ventilation and resuscitation. Can. Anaesth. Soc. J. 32, 60–64 (1985) 12. Schraff, S., Derkay, C.S., Burke, B., et al.: American Society of Pediatric Otolaryngology members’ experience with recurrent respiratory papillomatosis and the use of adjuvant therapy. Arch. Otolaryngol. Head Neck Surg. 130, 1039–1042 (2004) 13. Shah, K., Kashima, H., Polk, B.F., et al.: Rarity of cesarean delivery in cases of juvenile-onset respiratory papillomatosis. Obstet. Gynecol. 68, 795–799 (1986) 14. Wiatrak, B.J.: Recurrent respiratory papillomatosis. In: Graham, J.M., Scadding, J.K., Bull, P.D. (eds.) Pediatric ENT, pp. 255–265. Springer, Berlin Heidelberg (2008) 15. Wiatrak, B.J., Wiatrak, D.W., Broker, T.R., et al.: Recurrent respiratory papillomatosis: a longitudinal study comparing severity associated with human papilloma viral types 6 and 11 and other risk factors in a large pediatric population. Laryngoscope 114, 1–23 (2004)
IV
Part Surgery for laryngotracheal stenosis
The management of acquired paediatric LTS is challenging for many reasons, not only because some airway reconstructions may be technically difficult, but also because decision making in choosing the most appropriate treatment for a given patient requires a refined judgement. All attempts should thus be made to select the best surgical option based on the patient’s local and general conditions, and not on the surgeon’s limited abilities with only a few reconstructive techniques. In the patient’s best interest, the paediatric airway surgeon should master all endoscopic and surgical techniques available for solving each specific situation, from the least to the most challenging. In essence, this represents the real art of medicine in this field. Cicatricial LTSs mainly result from sequelae of endotracheal intubation. The insult inflicted to the
mucosa and submucosa by the ET-tube is often associated with severe cartilaginous lesions, leading to unsteadiness or distortion of the laryngotracheal framework. The endoscopic aspect may only reflect the tip of the iceberg, when compared with the underlying histological pathology (Fig. IV.1). Needless to say that using severely damaged airway structures as part of an airway reconstruction with cartilage grafts is unlikely to be successful for severe Grade III and IV SGSs. This section is intended to provide insight into the decision-making process for selecting the best surgical option for a given patient, and to describe several closed endoscopic and open surgical techniques for acquired cicatricial stenoses of the larynx and trachea. Treatments of congenital LTS, acute lesions induced by intubation and evolving into incipient LTS, external
Fig. IV.1 Grade IV subglottic stenosis acquired after prolonged intubation: (a) Endoscopic view: complete subglottic cicatricial obstruction. The endoscopic aspect gives no information on the severity of the cricoid cartilage damage. (b) Histological view: distorted cricoid cartilage with complete cicatricial obstruction.
This information is obtained during surgery only. The CT-scan is unlikely to give sufficient details to assess the severity of the cartilaginous distortion and destruction (Reproduced with the permission from Holinger [1])
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laryngeal trauma and caustic injuries have been discussed in previous chapters. Successful management of the whole spectrum of cicatricial LTSs encountered in infants and children is based on the following issues: • Adequate training in laryngotracheal surgery and upper airway endoscopy • Thorough preoperative assessment of the patients’ medical condition and of the stenosis, to select the best surgical option and optimal timing for surgery • Mastery of various surgical options ranging from endoscopic CO2 laser treatments for minor stenoses to LTR and PCTR for more severe stenosis grades
Part IV Surgery for laryngotracheal stenosis
As mentioned earlier, inappropriate initial management of LTS may lead to permanent intractable sequelae, and hence the decisive importance of the first operation.
References 1. Holinger, L.D.: Laryngotracheal stenosis. In: Holinger, L.D., Lusk, R.P., Green, C.G. (eds.) Paediatric Laryngology and Oesophagology, p. 181. Lippincott-Ravent, Philadelphia/ New York (1997)
Preoperative Assessment, Indications for Surgery and Parental Counselling
Contents
Core Messages
17.1
Medical History....................................................... 232
›› Checklist
17.2
Patient’s General Condition.................................. 232
17.3
Preoperative Endoscopic Workup......................... 233
17.4
Modified Myer–Cotton Airway Grading System. 234
17.5 17.5.1 17.5.2 17.5.3 17.5.4
Indications for Surgery.......................................... 234 Grade I SGS (£ 50% Luminal Obstruction)............. 234 Grade II SGS (51%–70% Luminal Obstruction)...... 234 Grade III and IV SGSs.............................................. 235 Isolated Posterior Glottic Stenosis (PGS)................. 236
17.6
Timing for Surgery................................................. 238
17.7
Preoperative Planning............................................ 239
17.8
Preparation for Surgery......................................... 239
References............................................................................ 240
17
content for standardised patient assessment 1. Medical history related to: −− Pregnancy, prematurity and delivery −− Indication for intubation −− Duration of intubation −− ET tube size −− Compromised laryngeal functions (respiration, voice and aspiration) −− Syndromic or non-syndromic anomalies −− Pulmonary, cardiac and neurological status −− Failed previous treatments (endoscopic and open surgery) 2. Endoscopic workup: −− Extralaryngeal sites of obstruction −− Site, degree and extent of LTS −− Glottic involvement and vocal cord mobility −− Site of tracheostomy and localised tra cheomalacia −− Distal tracheal damage 3. Grading of stenosis: −− Modified Myer–Cotton airway grading system encompassing comorbidities, glottic involvement or both 4. Patient’s physical condition −− Pulmonary, cardiac, neurological and gastro-intestinal assessments −− Syndromic or non-syndromic abnormalities
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Careful preoperative evaluation of the patient is essential for the successful management of LTS. This evaluation also provides useful information for prognosticating the outcome when discussing the intervention with the patient’s family. It may also help identify those children who are unlikely to benefit from surgery. The four most important parameters in preoperative assessment are: • • • •
Medical history Patient’s general condition Preoperative endoscopic workup Grade and extent of LTS
For each case, the patient management starts with a thorough discussion within the multi-disciplinary ‘LTS board of specialists’ comprised of physicians from multiple specialities (e.g., ENT surgeons, pulmonologists, gastroenterologists, cardiologists, neurologists, neonatologists, intensivists and geneticists). This discussion is aimed at selecting the optimal surgical approach. Due to practical issues, most hospitals may find it difficult to build up such a team, with the exception of centres where a large number of LTS patients are treated every year. Whenever the ENT surgeon assumes full responsibility for the patient’s care, he/she should not hesitate to seek advice from other medical disciplines in view of a comprehensive assessment of the patient prior to embarking on complex surgical procedures. Every effort should be made to optimise the first surgical attempt, thereby maximising the chances of success.
17.1 Medical History One of the following three clinical scenarios may be encountered in a tracheostomised child with acquired LTS: • A premature or full-term newborn who underwent neonatal intubation for respiratory distress • A child whose neonatal period was uneventful but required intubation for infection or traumatic injury later in life • An older child or adolescent without previous history of ET intubation presenting ‘idiopathic’ LTS In the first scenario, a full medical history should include information on pregnancy, prematurity, ‘small for date’ features, Apgar scores, intubation details (difficult,
Table 17.1 Medical history • Term pregnancy, prematurity, small for date features • Delivery (APGAR scores) • Reason for intubation (difficult? traumatic? repeated? duration?) • Quality of cry, voice • Deglutition (aspiration? choking? regurgitation?) • Pulmonary reserve (need for oxygen supply, bronchodilators) • Neurological and mental status • Cardiac problems • Syndromic and non-syndromic anomalies • Previous treatments
traumatic or multiple), quality of cry, deglutition (e.g., aspiration, choking), pulmonary reserve, cardiac or neurologic problems, syndromic or non-syndromic anomalies and failed previous treatments (Table 17.1). In the second scenario involving an older ‘normal’ child who needed ET intubation for infection or traumatic injury, data on type and severity of injuries, duration of intubation, ET tube size, potential neurological sequelae as well as previous endoscopic/surgical treatments of LTS must be recorded. Compared with acquired neonatal LTS following prolonged intubation, the situation is easier to handle since the child is older and generally in good physical condition. As to the last scenario pertaining to uncommon idiopathic LTS, a complete workup must be performed in collaboration with an immunologist to rule out rare systemic diseases, such as Wegener’s granulomatosis [2, 9].
17.2 Patient’s General Condition Prior to endoscopic assessment, a comprehensive physical examination of the patient’s general condition and a thorough examination of the head and neck are conducted. The physical examination is focused on the overall appearance of the child, with the following details to be noted: bodyweight and height for age, structural and maxillofacial deformities, syndromic or non-syndromic abnormalities, communication skills, neurological and mental abilities including the
17.3 Preoperative Endoscopic Workup
coordination of respiration and swallowing, any history of regurgitation while eating, as well as pulmonary and cardiovascular auscultatory findings (Table 17.2). In a non-tracheostomised child, the degree of respiratory distress and the level of obstruction (based on pathological respiratory sounds and the respiratory cycle phase during which they are produced) are recorded. Neck auscultation is performed when symptoms are mild (see Sect. 3.5, Chap. 3). Except when the infant or child is in acute respiratory distress requiring emergency management in an endoscopy suite, inoffice TNFL is performed in order to assess choanal patency, pharyngolarynx and vocal cord mobility (see Sect. 5.1.1, Chap. 5). In a tracheostomised child, temporary occlusion of the cannula with a finger may allow the surgeon to assess the air egress through the larynx while analysing the quality of the cry or voice. In cooperative children, it may at times be possible to inspect the lower airways through the cannula using a slim bronchofibroscope. Some abnormalities are readily visible, whereas others may need the help of specialists to confirm the diagnosis. Pulmonologists, cardiologists, neurologists, gastroenterologists and geneticists are of great help in providing a detailed assessment of the child. Their input is invaluable for selecting the optimal surgical procedure for each individual patient (see Table 17.2). Table 17.2 Patient’s general condition • Overall appearance • Nutritional aspect – Bodyweight and height for age • Dysmorphic features – Syndromic or non-syndromic • Pulmonary status – Chest deformity – Oxygen requirement, need for bronchodilators • Cardiac anomalies – Pulmonary hypertension – Shunts • Neurologic impairments – Swallowing disorders – Mental retardation • Gastro-oesophageal reflux, eosinophilic oesophagitis
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Correct diagnosis and treatment of associated comorbidities are essential to prevent surgical failures.
17.3 Preoperative Endoscopic Workup A detailed description of the endoscopic assessment of the compromised paediatric airway is provided in Chap. 5. Only a few relevant features are repeated here: • Awake TNFL is the best method for assessing vocal cord mobility, whereas asleep (spontaneous respiration under general anaesthesia) TNFL in the recumbent position provides better information on dynamic airway lesions in the naso-oro-pharyngolaryngeal region, responsible for obstructive sleep apnoea (OSA). This latter procedure may also be used when awake TNFL resulted in an inconclusive assessment of vocal cord mobility, albeit with less accuracy, due to the required sedation that adversely affects vocal cord mobility. • Direct laryngotracheoscopy using a 0-degree endoscope, under general anaesthesia, is the norm for precisely assessing the site, degree and extent of LTS. The stenosis must be graded based on the newly proposed modified Myer–Cotton airway grading system, which encompasses glottic involvement and comorbidities (see Sect 5.3.3.4, Chap 5). In addition, laryngotracheoscopy provides more information on the tracheostomy site and problems associated with tracheostomy cannula (suprastomal collapse and granuloma, localised tracheomalacia and tip of cannula granuloma). • In cases of vocal cord immobility, suspension microlaryngoscopy (SML) is implemented in order to differentiate a neurogenic BVCP from a PGS, with or without cricoarytenoid joint fixation. • Broncho-oesophagoscopy is performed to search for signs of aspiration (lipid-laden macrophages in BAL), gastro-oesophageal reflux and eosinophilic oesophagitis. Tracheal aspirates for bacteriological examination as well as oesophageal biopsies to rule out eosinophilic oesophagitis are routinely taken (Table 17.3). Finally, benefiting from general anaesthesia, the surgeon should conduct a thorough ENT examination in non-cooperative children who could not be examined properly while awake.
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Table 17.3 Preoperative endoscopic workup for LTS • Awake TNFL – VC mobility • Asleep TNFL – Dynamic pharyngeal narrowings
Table 17.4 Modified Myer–Cotton airway grading system SGS Myer–Cotton Isolated Isolated SGS SGS SGS + + glottic + glottic grade involve- involvement comor + bidities ment comorbidities (a) (b) (c) (d)
– VC mobility
I
0–50%
Ia
Ib
Ic
Id
– Localised tracheomalacia
II
51–70%
II a
II b
II c
II d
III
71–99%
III a
III b
III c
III d
IV
no lumen IV a
IV b
IV c
IV d
• Direct laryngotracheoscopy with a bare 0-degree telescope – Site, grade and extent of LTS – Glottic involvement (PGS, VC synechia) – Site of tracheostomy, localised malacia – Associated tracheal damage • Suspension microlaryngoscopy (SML) – Arytenoid palpation – Neurogenic BVCP versus PGS
incorporated into the Myer–Cotton airway grading system. This strategy is instrumental in choosing the best surgical option for each individual patient, especially when deciding on either single-stage or double-stage procedures (Table 17.4).
– Cricoarytenoid joint fixation • Broncho-oesophagoscopy
17.5 Indications for Surgery
– Associated anomalies – Bacteriological aspirate – Chronic aspiration (BAL)
17.5.1 Grade I SGS (£50% Luminal Obstruction)
– Gastro-oesophageal reflux – Eosinophilic oesophagitis (biopsies)
17.4 Modified Myer–Cotton Airway Grading System With the advent of PCTR for the cure of severe SGS, the Myer–Cotton airway grading system has been shown to be less precise in prognosticating the outcome of decannulation [ 6]. Furthermore, this grading system does not provide any predictive information on postoperative voice quality. In fact, the grading system does not encompass vocal cord involvement, which may be associated with SGS [4]. The results of our analysis involving 100 paediatric PCTRs performed for 32 Grade IV, 64 Grade III and 4 Grade II SGSs demonstrated clearly that additional glottic involvement (PGS, VC synechia and CAA) as well as comorbidities (respiratory, cardiac, neurological, gastroenterological or genetic) influenced the final outcomes of postoperative decannulation and voice quality [4, 6]. When discussing the potential outcome of LTS surgery with the child’s parents, the aforementioned parameters must be
Grade I SGS is not usually associated with glottic involvement. In the worst scenario, a slight limitation of vocal cord abduction may be observed without true interarytenoid adhesion. In the majority of cases, Grade I SGS does not require any surgical intervention. Certain SGSs can be managed using CO2 laser radial incisions and gentle dilation according to Shapshay’s technique [7]. Concurrent comorbidities do not preclude this minimally invasive endoscopic procedure (Table 17.5).
17.5.2 Grade II SGS (51%–70% Luminal Obstruction) Grade II SGS may be seen as isolated SGS (SGSa) or in combination with an abnormal glottis. The glottic involvement usually is a moderate PGS without CAA or a partial vocal cord synechia (SGSc). In the absence of glottic involvement, CO2 laser incisions combined with dilations are effective in patients with thin, weblike cicatricial stenoses of the subglottis. For extensive SGS in the cranio-caudal axis, SS-LTR using anterior graft without stenting is preferred.
17.5 Indications for Surgery
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Table 17.5 Treatment algorithm for Grade I SGS
In Grade II SGS with associated glottic involvement (PGS or limited anterior vocal cord synechia = SGSc), CO2 laser surgery is unlikely to provide satisfactory results. In this case, LTR is better. Depending on the location of the glottic pathology, reconstruction of the larynx using anterior or posterior costal cartilage grafts and 1-month stenting with an LT-Mold to prevent recurrence of anterior synechia of the vocal cords and posterior commissure scarring is recommended. Concurrent comorbidities (SGSd) have little influence on the surgical strategy, except for isolated Grade II SGS where a double-stage LTR is preferred to a single-stage procedure (Table 17.6).
17.5.3 Grade III and IV SGSs Minor Grade III SGS (~71–80% luminal obstruction) with thin web-like diaphragms (<5 mm in cranio-caudal axis) is a rare occurrence. Initial CO2 laser treatment with radial incisions combined with dilation may improve the airway. If the stenosis recurs to its original Grade, then open surgery is mandatory. Extensive laser resection is likely to further deteriorate an acquired stenosis.
Thicker (>5 mm in cranio-caudal axis) minor Grade III SGSs (~71–80% luminal obstruction) may benefit from LTR with anterior and posterior cartilage grafts supported by an endoluminal stent, but severe Grade III (>80% luminal obstruction) and Grade IV SGSs are best treated using PCTR. Glottic involvement (PGS, VC synechia or CAA) is common and must be fully integrated into the treatment algorithm. Likewise, the presence of comorbidities calls for a double-stage surgery, even when the glottis is normal. Grade III and IV SGSs with an intact glottis are best treated with SS-PCTR, unless severe comorbidities imply the need for double-stage surgery. Although LTR, another surgical option, may require prolonged stenting in Grade IV SGS, SS-PCTR is able to restore a patent, functional larynx within 3 weeks. Concerns about outcomes following PCTR for severe SGS involving the free border of the vocal cords have recently been clarified by the analysis of our results on 100 patients [4]. Decannulation rates and voice qualities were found to be similar to those observed with isolated SGSs (situated 3– 4 mm below the glottic level). When a severe Grade III or IV subglottic stenosis is associated with significant glottic involvement (PGS
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Table 17.6 Treatment algorithm for Grade II SGS
with or without CAA; total or subtotal synechia of the VC), two surgical options are available: extended PCTR or LTR with anterior and posterior cartilage grafts along with long-term stenting. The author prefers extended PCTR for the following reasons. Extended PCTR involves full resection of the diseased airway segment and cranial mobilisation of the tracheal stump. This helps restore a steady, fully mucosalised airway at the end of the surgery. Treatment for complex glotto-subglottic stenoses with either LTR (with combined posterior and anterior costal cartilage grafts) or extended PCTR includes stenting with an LT-Mold prosthesis. Additional severe comorbidities (e.g., mental retardation or poor cardiopulmonary status) affect the treatment of isolated Grade III or IV SGS with an intact glottis where a double-stage intervention is preferred to an SS-PCTR (Table 17.7). Laryngotracheal reconstruction, however, is the last surgical option after failed PCTR if further tracheal segments cannot be resected. Prolonged stenting with an uncertain final outcome is often necessary following these most complex revision surgeries.
It must be clearly stressed that surgery is not necessarily the best option for every case, as in some patients, the final goal of surgery (i.e. decannulation), cannot be achieved. Such a situation may be found, for example, in a developmentally delayed child with severe Grade IV glotto-SGS along with bilateral cricoarytenoid joint fixation. In this case, extended PCTR may restore a patent airway, albeit with a ‘frozen’ larynx. While most normally functioning children are able to cope with this situation and gain control of aspiration, neurologically impaired or mentally disabled children with swallowing problems may repeatedly aspirate, develop recurrent pneumonia and eventually die. It is therefore important to refrain from operating on these children despite the constant pressure from their parents.
17.5.4 Isolated Posterior Glottic Stenosis (PGS) Isolated PGSs represent a unique group of LTSs limited to the interarytenoid glottis, usually resulting from
17.5 Indications for Surgery
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Table 17.7 Treatment algorithm for Grade III and IV SGS
prolonged intubation. They have been classified into four types according to the Bogdasarian classification (see Fig. 5.11, Chap 5) [1]: Type I and II PGSs may be seen in non-tracheostomised children who are able to tolerate a certain degree of exertional dyspnoea. Endoscopic treatments are appealing to these patients as their parents are often reluctant to accept the need for a temporary tracheostomy during the treatment period. • Type I (interarytenoid adhesion) is likely to benefit from a simple CO2 laser division/resection with dilation. Topical application of mitomycin C is not indicated. • Type II (PGS with preserved active mobility of both arytenoids) should first be treated by CO2 laser resection with dilation and additional topical mitomycin C application. The integrity of both cricoid joints and the abductive force of the posterior cricoarytenoid muscles prevent the recurrence of stenosis during the healing phase. If true abductive movements of the arytenoids cannot be visualised in
TNFL, then CO2 laser endoscopic treatment is likely to fail. In this case, endoscopic posterior cricoid split along with rib grafting, popularised by Inglis (see Fig. 7.8, Chap 7), is a viable option, though this procedure warrants a temporary tracheostomy except in the case of older children and adolescents. Given this event, endoscopic placement of an LT-Mold in order to splint the reconstructed airway for a period of 10–15 days is advisable (see Fig. 14.17, Chap 14). If both endoscopic techniques fail, open surgery (LTR) remains the ultimate option. • Type III and IV (PGS with unilateral or bilateral CAA) are usually associated with thick, severe interarytenoid scarring. The best surgical option for the already tracheostomised child is an open LTR with posterior cricoid split, costal cartilage grafting and stenting with an LT-Mold. However, in minor type III PGS where the unilateral CA fixation is not complete, Inglis’ procedure may be attempted in order to better preserve the anterior laryngeal commissure (Table 17.8).
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Table 17.8 Treatment algorithm for PGS
Table 17.9 Temporary contraindications to surgery for LTS • Local factors – Highly reactive larynx, severe reflux laryngitis – Immature LTS – Other sites of significant airway obstruction – Infected airway – Pharyngolaryngeal discoordination with aspiration • Systemic factors – Persistent pulmonary disease – Uncontrolled GORD – Severe neurological impairment – Severe mental disability – Severe cardiovascular anomalies
17.6 Timing for Surgery Several criteria must be met before an LTS patient qualifies for surgery. In congenital LTS, there must be no other relevant airway obstruction, and the patient must be in good respiratory and neurological condition. In acquired LTS, the original reason for intubation must no longer exist, and the stenosis must be composed of mature scar tissue. Watchful waiting is advisable when the larynx and subglottis appear highly reactive (erythematous and oedematous), if concomitant cardiopulmonary disease requires frequent hospitalisations, or in the presence of severe uncontrolled GOR. Neurological impairment associated with pharyngolaryngeal discoordination and aspiration during feeding may necessitate a longer waiting period before airway reconstruction is envisaged. Associated medical conditions must be treated actively during the waiting period. Should an airway infection occur in a tracheostomised child, a culture must be obtained, and sensitivities of the tracheal aspirates must be determined in order to choose the appropriate antibiotics to be administered in association with chest physiotherapy. Long-term PPI administration, sometimes at high doses, may be necessary to control
gastro-oesophageal reflux disease. Especially in the more severe cases, fundoplication must be considered. If lipid-laden macrophages are found in BAL, then additional investigations are required to identify swallowing disorders and reflux. Temporary contraindications to surgery for LTS are outlined in Table 17.9. Patients with mild stenosis (Grade I or mild Grade II) can be kept under observation, especially if the stenosis is congenital, as the airway is expected to enlarge with growth. Follow-up endoscopies should be carried out every 6 months until complete resolution of the respiratory symptoms. If the respiratory condition deteriorates, then airway reconstruction must be envisaged to avoid emergency tracheostomy. In some cases, however, tracheotomy may be unavoidable as this procedure is the most appropriate way of safely securing a comprised laryngeal airway. As mentioned in Sect 14.3.4, Chap 14, the tracheostomy should be placed either immediately below the cricoid ring to preserve maximally the distal normal trachea, or between the 6th and 7th tracheal rings to spare a sufficient amount of normal tracheal rings between the subglottic stenosis and the tracheostomy site. Further treatment should be planned depending on the patient and disease characteristics, i.e. singlestage PCTR versus SS-LTR, or double-stage LTR versus extended PCTR. Tracheotomy allows the surgeon to ‘buy time’ until the aforementioned local and systemic medical
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17.8 Preparation for Surgery
conditions have improved or been cured. Although the mortality rate of tracheostomised children with significant laryngeal obstruction has declined from 24% in the 1970s to 2–3% by the year 2000, mortality remains a Sword of Damocles for the medical community as well as the parents. When an infant or small child has no significant comorbidities, early intervention during the first months of life is advisable. Our recent review of 53 infants weighing less than 10 kg at the time of PCTR surgery [3, 5] revealed that surgical outcomes were similar to those obtained in older children. Magnifying (3×) glasses provide excellent visualisation of the infant’s airway, enabling the surgeon to perform a technically careful and precise anastomosis. The principle of waiting to intervene until the child reaches 10 kg [ 8] is no longer considered in the management algorithm of LTS. However, it must be kept in mind that the advantage of operating on an older child is offset by the mortality rate associated with the tracheostomy tube as well as the delay in learning effective communication.
17.7 Preoperative Planning The successful outcome following surgery for LTS relies on meticulous preoperative endoscopic assessment and overall evaluation of the child’s general condition. The checklist of all endoscopic steps provided in Table 17.3 should be scrupulously followed, and a thorough medical history be taken, in addition to an assessment of the patient’s general condition with the help of specialised physicians, as necessary (see Table 17.1 and 17.2). Following this, patient management should be discussed within a multidisciplinary airway team to come to a consensus on both the best time and type of surgery. The prognosis should be discussed with and explained in great detail to the parents. The following questions should be addressed: • What type of surgery should be performed? –– Endoscopic, LTR, PCTR or extended PCTR? –– Type of grafting: no graft, anterior, posterior or combined costal cartilage graft(s)? • Single-stage or double-stage surgery? –– With or without stenting?
• Need for PICU and if so, for how long? • Risks involved with the different types of surgery? –– PCTR: anastomotic dehiscence and RLN injury –– LTR: significant recurrence rate in the case of Grade III–IV SGS • Expected results regarding airway, voice and deglutition? • Have all comorbidities been addressed prior to surgery? –– Gastro-eosophageal reflux disease? –– Neurologic, pulmonary and cardiac diseases? –– Nutrition? –– Airway infection/contamination? • Is surgical timing appropriate? –– Maturity of subglottic stenosis? –– Patient’s age in relation to potential comor bidities? • Does the theoretically ideal operation fit with the patient’s comorbidities or other abnormalities? All aforementioned factors must be balanced with the medical resources available, the expertise of the surgical team, and the family’s expectations. It may be necessary to adjust the preoperative plan on a case-by-case basis, as some patients and families travel long distances to seek medical advice and care. The parents must be fully integrated in the decisionmaking process. Videoprints should be used in order to illustrate differences between normal larynges and the pathologic condition of the patient’s larynx so that the scheduled programme can be better understood by the parents. The type of surgery, length of PICU stay, need for long-term follow-up as well as potential life-threatening risks and complications should be clearly addressed before embarking on surgery for difficult airway stenoses.
17.8 Preparation for Surgery All efforts should be made to optimise the patient’s general condition prior to any surgical intervention. With the help of specialists, all local and systemic factors listed in Table 17.9 should be addressed and treated prior to surgery. Some of these factors (infected airway, GOR or eosinophilic oesophagitis) respond to medical therapy, while others require surgery (cardiovascular anomalies, extra-laryngeal site of airway
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obstruction, maxillo-facial abnormalities or severe intractable GOR). A few other factors require a waiting period or rehabilitation period (reactive larynx, immature LTS or pharyngolaryngeal discoordination). However, associated impairments that cannot be corrected should be considered as potential contraindications to surgery (e.g., mental disability, severe syndromic anomaly or severe cardiopulmonary disease with O2-dependency). In a ‘healthy’ child with long-standing tracheostomy, airway colonisation with MRSA or pseudomonas aeruginosa may at times be overlooked, if no tracheal aspirate for bacteriological culture was taken. This simple mistake may cause surgical failure. The same applies to patients with asymptomatic GOR who did not undergo pH-monitoring. The author recommends a 5-day preoperative antibiotic prophylaxis based on bacteriological cultures and sensitivities. If the healing process is uneventful, then antibiotic treatment should be continued during the intra- and postoperative periods for at least 15 days. Depending on the complexity of the reconstruction, or if delayed healing is suspected, this regime may be extended by 1 month or more. In addition, given the significance of a successful primary surgery, the author recommends that all patients be treated with proton pump inhibitors (PPIs) to be started 1 week prior to surgery. This regimen should be continued for 1 month in patients with a doubtful diagnosis of GOR, and up to 6–12 months in children with evident GOR. In the most severe cases, it is recommended that additional H2-blockers be administered at bedtime to suppress nocturnal reflux events. H2-blockers should be continued for 3 months only, as their efficacy diminishes over time. If eosinophilic oesophagitis has been confirmed by biopsy, then surgery must be postponed until the child has completed the entire medical treatment prescribed by the gastroenterologist and allergologist (Table 17.10).
Table 17.10 Optimization of patient’s status prior to airway reconstruction • Address and treat all comorbidities amenable to improvement • Consider potential contraindication to surgery in severely handicapped children who cannot be improved by any means • Start medical treatment of MRSA and pseudomonas aeruginosa airway colonisation 5 days prior to surgery • Treat all patients for GOR, starting in the preoperative period and continuing possibly for 6 months to a year in overt GOR • Postpone surgery and treat for eosinophilic oesophagitis if it has been biopsy-proven
References 1. Bogdasarian, R.S., Olson, N.R.: Posterior glottic laryngeal stenosis. Otolaryngol. Head Neck Surg. 88, 765–772 (1980) 2. Frosch, M., Foell, D.: Wegener granulomatosis in childhood and adolescence. Eur. J. Pediatr. 163, 425–434 (2004) 3. Garabedian, E.N., Nicollas, R., Roger, G., et al.: Cricotracheal resection in children weighing less than 10 kg. Arch. Otolaryngol. Head Neck Surg. 131, 505–508 (2005) 4. George, M., Monnier, P.: Long-term voice outcome following partial cricotracheal resection in children for severe subglottic stenosis. Int. J. Pediatr. Otorhinolaryngol. 74, 154–160 (2010) 5. Ikonomidis, C., George, M., Jaquet, Y., et al.: Partial cricotracheal resection in children weighing less than 10 kilograms. Otolaryngol. Head Neck Surg. 142, 41–47 (2010) 6. Monnier, P., Ikonomidis, C., Jaquet, Y., et al.: Proposal of a new classification for optimising outcome assessment following partial cricotracheal resections in severe pediatric subglottic stenosis. Int. J. Pediatr. Otorhinolaryngol. 73, 1217–1221 (2009) 7. Shapshay, S.M., Beamis Jr., J.F., Hybels, R.L., et al.: Endoscopic treatment of subglottic and tracheal stenosis by radial laser incision and dilation. Ann. Otol. Rhinol. Laryngol. 96, 661–664 (1987) 8. Walner, D.L., Cotton, R.T.: Acquired anomalies of the larynx and trachea. In: Cotton, R.T., Myer III, C.M. (eds.) Practical Pediatric Otolaryngology, p. 522. LippincottRaven, Philadelphia (1999) 9. Wittekindt, C., Luers, J.C., Drebber, U., et al.: ANCAnegative subglottic laryngeal stenosis in childhood. HNO 55, 807–811 (2007)
Endoscopic Techniques for Laryngotracheal Stenosis
Contents
Core Messages
18.1
›› Endoscopic techniques mainly comprise CO2
18.1.1 18.1.2 18.1.3 18.1.4
Anaesthesia for Endoscopic Airway Procedures................................................. 242 Tubeless Microlaryngeal Surgery under Spontaneous Respiration Anaesthesia...................... 242 Apnoeic Anaesthesia with Intermittent Ventilation and Oxygenation.................................... 243 Anaesthetic Techniques for Airway Endoscopies under Controlled Ventilation............... 244 Jet Ventilation........................................................... 245
18.2
Indications for Endoscopic Airway Procedures................................................. 246 18.2.1 Primary Endoscopic Techniques............................... 246 18.2.2 Secondary Endoscopic Techniques........................... 250 18.3 18.3.1 18.3.2 18.3.3
Mitomycin C (MMC).............................................. 251 Mitomycin C Dosage for Topical Application......... 252 Duration of Topical MMC Application.................... 253 Rinsing the Wound after Topical MMC Application..................................................... 253 18.3.4 Risks of Multiple Topical MMC Applications......... 253 18.3.5 Indications and Contraindications of Topical MMC Applications.................................. 253
›› ›› ››
›› ›› ››
References............................................................................ 254
››
››
18
laser, dilations and application of mitomycin C Congenital cartilaginous stenosis is a strict contraindication for dilation or laser resection CO2 laser incisions and dilation may be effective in thin, web-like cicatricial Grade I to III SGSs The success rate (SR) of endoscopic treatment drops drastically with increasing preoperative stenosis grade, from 92% for Grade I SGSs to 13% for thin, web-like Grade III SGSs Further endoscopic treatments are contraindicated if the SGS recurs to its initial grade after the first endoscopic surgery The benefits of intralesional corticosteroid injections have not been proven Mitomycin C: –– Topical application (1–2 mg/ml for 2 min) –– Effective in preventing granulation tissue formation –– Should not be applied on denuded cartilage surfaces Dilation: –– With tapered Savary–Gilliard dilators –– With angioplasty balloons –– Often combined with CO2 laser radial incisions Indications for endoscopic treatments: –– Thin, web-like cicatricial Grade I–III SGS –– Impending subacute SGS –– Acquired subglottic cysts
P. Monnier (ed.), Pediatric Airway Surgery, DOI: 10.1007/978-3-642-13535-4_18, © Springer-Verlag Berlin Heidelberg 2011
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›› Endoscopy as secondary treatment:
››
››
–– Optimisation of postoperative results –– Adjunctive measure in the case of complex LTS –– Partial or total arytenoidectomy –– Supraglottoplasty Endoscopic stenting with LT-Mold: –– Incipient SGS requiring tracheostomy –– Salvage of recurrent SGS during the postoperative period Ancillary endoscopic techniques: –– Inglis’ posterior LTR for bilateral vocal cord palsy (BVCP) or posterior glottic stenosis (PGS) –– Microdebrider for granulation tissue
18.1 Anaesthesia for Endoscopic Airway Procedures Madeleine Chollet-Rivier, MD, Marc-André Bernath, MD, Staff Anaesthesiologists. Different ventilation strategies for endoscopic procedures have been proposed, notably spontaneous respiration anaesthesia, intermittent apnoeic anaes thesia, continuous endotracheal intubation and jet ventilation. Each technique has specific pitfalls and contraindications.
18.1.1 Tubeless Microlaryngeal Surgery under Spontaneous Respiration Anaesthesia Bruce [9] has written an excellent review on the indications of tubeless microlaryngeal surgery. For laryngeal surgery using a microlaryngoscope under spontaneous respiration, two anaesthetic techniques have been proposed: volatile and total intravenous anaesthesia (TIVA).
18.1.1.1 Volatile Anaesthesia In a well-documented article, Best [7] proposed a volatile anaesthesia, with halothane or sevoflurane administered through a small preformed nasotracheal tube positioned in the oropharynx, aimed at delivering highflow (5–6 l/min) oxygen and volatile anaesthetics. Stern et al. [65] have used the same technique while delivering sevoflurane through the modified left channel of the laryngoscope. Analgesia is obtained by using topical laryngeal 4% lidocaine administration. The major pitfall of the technique is hypoxia. If necessary, controlled ventilation is achieved by temporarily obstructing the laryngoscope port with the thumb or by inserting an endotracheal tube. Spontaneous respiration is required for delivering the inhaled anaesthetic gases, but the anaesthesia level is difficult to appreciate [7] as it depends on the alveolar concentration of the volatile anaesthetic. Theatre room pollution by the anaesthetic gases delivered through an open ventilation circuit constitutes another concern [76].
18.1.1.2 Total Intravenous Anaesthesia Total intravenous anaesthesia (TIVA) using short-acting propofol and remifentanil is the most recent and most effective technique for maintaining anaesthesia for paediatric airway procedures [40]. The drugs’ pharmacokinetic properties such as rapid onset of action, ease of titration and rapid clearance by redistribution and metabolism are particularly interesting for TIVA. In comparison to conventional volatile anaesthetics, propofol and remifentanil’s advantages include quicker recovery [23], reduced nausea and vomiting [56], decreased postoperative delirium [25] and no environmental pollution. Other specific effects such as reduced airway reactivity and improved postoperative ciliary function [38] may also be of benefit during airway endoscopic procedures. Propofol acts as an hypnotic, ensures amnesia and has relaxing effects on laryngeal muscles, but does not inhibit the cough reflex at concentrations used to preserve spontaneous respiration. Remifentanil is devoid of hypnotic properties but displays excellent analgesic activity, along with optimal inhibitory effects on the cough reflex. Both drugs act in synergy, with remifentanil having a propofol-sparing effect [66], which reduces the risk of
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lipid overload and propofol infusion syndrome [79]. The narrow therapeutic index of the drugs regarding the preservation of spontaneous respiration constitutes the technique’s main challenge. In adults, a targetcontrolled infusion (TCI) of both drugs allows the anaesthesiologist to precisely control the concentrations to obtain an optimal hypnosis-analgesia match, with preservation of spontaneous respiration. In the absence of paediatric adapted TCI pumps [40], different drug perfusion regimens have been proposed in order to achieve the anaesthetic goals. Barker et al. [5] proposed the first guidelines for remifentanil-propofol administration in order to maintain spontaneous ventilation during invasive procedures. These authors observed that a reduction in respiratory rate £10/min was the best predictor of imminent apnoea [4], and used respiratory rate depression as pharmacodynamic endpoint for remifentanil dose titration. To maintain spontaneous ventilation, a perfusion dose of 0.192 mg/ kg/min remifentanil for children under 3 years of age, 0.095 mg/kg/min for those between 3 and 6 years, and 0.075 mg/kg/min for those between 6 and 9 years was considered adequate. Surprisingly, spontaneous ventilation was shown to be easier to maintain in infants than in older children. Children younger than 3 years of age tolerated higher remifentanil infusion rates while maintaining acceptable ventilation. The effect was most marked in infants less than 1 year of age. In our Lausanne centre, we have adopted a hybrid approach for microlaryngeal surgery under spontaneous respiration in children: inhalation induction is performed with sevoflurane, TIVA with propofol and remifentanil at the dosages proposed by Barker [5] is used for maintenance. Bolus doses of remifentanil (2 mg/kg) and propofol (3 mg/kg) are administered during anaesthesia induction in order to facilitate a rapid rise in plasma concentrations, enabling the installation of the laryngoscope under good airway conditions. The resulting apnoea is of short duration, spontaneously resolving within 5–6 min. To obtain a balanced hypnosis and avoid administering propofol boluses, we use top-up doses of sevoflurane during the intervention to deepen the anaesthesia. Likewise, to obtain a balanced analgesia, at the beginning of the intervention, we combine topical laryngeal administration of 4% lidocaine (£4 mg/kg), remifentanil perfusion and a loading dose of morphine (0.1 mg/kg). Furthermore, 4–6 l/min of oxygen are delivered via a
short naso-pharyngeal tube placed in the oropharynx, whereas 0.5 mg/kg (>1 year of age) of ketorolac and rectal paracetamol (40 mg/kg) are administered to complete postoperative analgesia.
18.1.2 Apnoeic Anaesthesia with Intermittent Ventilation and Oxygenation Provided that cooperation with the surgeon is optimal, this is the least stressful technique for the anaesthesiologist, as he/she utilises a conventional endotracheal tube and anaesthesia circuit [77]. After inducing anaesthesia and assessing the possibility of mask ventilation, the laryngoscope is positioned during an apnoeic period, and an endotracheal tube of appropriate size is slipped into the lumen through the laryngoscope. This technique is adequate for treating laryngomalacia but not indicated in the case of cicatricial subglottic narrowing of the airway. Positive pressure ventilation is initiated until a greater than 98% SaO2 is reached. As soon as the surgeon is ready, the endotracheal tube is removed, and the procedure is conducted through an unobstructed field during 5–6 min. Arterial pCO2 is likely to rise by 11 mmHg during the first minute and by 4.5 mmHg during each subsequent minute [21], without any deleterious effects, provided that there is no pulmonary or intracranial hypertension. The apnoeic period is ended, and the patient reintubated when the SaO2 drops below 90%. Ventilation with recruitment manoeuvres during 1–2 min using the anaesthesia circuit allows for the restoration of oxygenation and normocapnia [78]. The advantages of this technique include improved visualisation of the airway, absence of combustible material and lack of vocal cord motion during surgery. This technique is particularly suitable for microlaryngoscopy in children and infants [77], as well as for certain short-duration laser procedures, provided that using the technique is not prevented by airway stenosis. A few complications have been reported in scientific literature [34], particularly laryngospasm due to inadequate anaesthesia levels. The high safety of this anaesthetic technique is based on periodic airway control with an endotracheal tube and regular measurements of end-tidal carbon dioxide (ET-CO2) levels [78].
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18.1.3 Anaesthetic Techniques for Airway Endoscopies under Controlled Ventilation Controlled ventilation for airway endoscopic procedures is the most common ventilatory technique [77]. Specific but not exhaustive indications are listed in Table 18.1. If carbon dioxide laser use is scheduled, specific methods to secure the airway and deliver ventilation are available. Laser-induced endotracheal fire is the most dreadful complication in endoscopic airway surgery [34]. Ventilation can be delivered during laser work, provided that no flammable material be used, and a low (£30%) oxygen concentration be maintained throughout the procedure. Supraglottic or subglottic jet ventilation and intermittent or continuous use of a variety of endotracheal tubes are recommended.
18.1.3.1 Anaesthetic Drugs Total intravenous anaesthesia (TIVA) using a propofol-opioid combination is mandatory for apnoeic and jet ventilation techniques in order to ensure a constant anaesthesia level, independently of alveolar ventilation [40]. The choice of the opioid to be used depends on the duration of the procedure, the patient characteristics and the anaesthesiologist’s preferences. Fentanyl given as a loading dose followed by repeated boluses has a long duration of action, and a residual analgesic effect during the postoperative period. This agent is particularly suitable in fragile children [1], and when postoperative ventilatory support is scheduled.
Table 18.1 Indications for controlled ventilation in airway endoscopies Patient characteristics
Risk of gastric regurgitation Cardiovascular instability Respiratory insufficiency Emergency
Type of procedure
Rigid bronchoscopy Microlaryngoscopic surgery Laser surgery
Medical indications
Hemorrhagic situations Tracheobronchial obstructive lesions
Association with a muscle relaxant is mandatory, as fentanyl has no relaxant properties on laryngeal muscles [67]. Alfentanil displays an adequate duration of action (20–30 min), is suitable for continuous infusion [8] and offers acceptable intubation conditions when given in association with propofol [47]. Remifentanil, the most recent and appropriate drug for TIVA, displays no cumulative or residual effects at the end of the perfusion (flat context-sensitive half-life) and is best administered via a continuous infusion. Although the use of muscle relaxants has been challenged by the advent of remifentanil, these agents are at times needed to facilitate the surgeon’s work, reduce the risk of airway trauma when using rigid instruments and minimise the amount of anaesthetic agents given to infants and children [42]. A balanced anaesthesia associating a hypnotic, an opioid and a short-acting curare offers optimal conditions for tracheal intubation. The drugs’ synergistic actions allow the anaesthesiologist to lower each agent’s dosage, thereby reducing potential adverse events, in particular cardiovascular toxicity [18]. This technique is particularly indicated for sick, dehydrated and emergency patients. Due to its intermediate duration of action (22–30 min) and its Hofmann elimination pathway, atracurium [42] is the preferred muscle relaxant by most paediatric anaesthesiologists. Unlike other non-depolarising muscle relaxants, regardless of the age group, when used in the normal-dose range, atracurium ensures prompt recovery from neuromuscular blockade, along with a low incidence of side effects. Diminishing the intubation dose by half increases the mean time to intubation from 90 to 150 s, but reduces the time to recovery to 18 min, following pharmacological reverse of the neuromuscular blockade [72].
18.1.3.2 Specific Monitoring As for any paediatric anaesthesia, basic monitoring includes recording of non-invasive blood pressure (NIBP), electrocardiogram (ECG), peripheral oxygen saturation (SpO2) and body temperature. In the absence of an endotracheal tube, the measurement of end-tidal CO2 (ET-CO2) is not feasible. Instead, we routinely use transcutaneous carbon dioxide (TC-CO2) monitoring (Tosca Sensor®; Linde Medical Sensors AG, Basel, Switzerland). Transcutaneous CO2 displays continuous CO2 measurements that better correlate with PaCO2
18.1 Anaesthesia for Endoscopic Airway Procedures
than end-tidal CO2 (ET-CO2), routinely used during anaesthesia [68]. Transcutaneous CO2’s main disadvantage is the time (~5 min) needed for calibration and counterpoising prior to its utilisation, as well as the price of the ear probe and consummates.
18.1.4 Jet Ventilation The concept of jet ventilation is based on using a high working pressure to deliver adequate ventilation through small-diameter (£2 mm) catheters [19]. Jet ventilation can be delivered through supraglottic, transglottic or transtracheal routes: 1. Supraglottic route via the working channel of the suspension microlaryngoscope: Mausser et al. [41] reported no complications when using this technique. However, this technique is not recommended in the presence of laryngotracheal stenosis, as gas exhalation may cause problems [31]. Moreover, this method is also contraindicated for treating papillomatosis, because of the risk of disseminating viral particles into the lungs [19]. 2. Transglottic route via a 2 mm ID polyurethane jet catheter (Acutronic® Medical System AG, Baar, Switzerland): As the most common and the least invasive technique [34], this method presents two drawbacks: the catheter is not laser-safe and cannot be used in neonates with an airway <3 mm in diameter [19]. 3. Transtracheal route via a dedicated polyurethane 14 or 18 gauge jet cannula, developed in Lausanne (Ravussin cannula®, VBM Medizintechnik GmbH, Sulze a.N., Germany): This highly invasive technique is reserved for endoscopic treatment of certain laryngotracheal stenoses, preventing a tracheostomy [17]. High-frequency jet ventilation (HFJV) improves gas exchanges at lower mean airway pressures than conventional ventilation [16], thus improving cardiac function, particularly in the presence of pulmonary arterial hypertension [44]. Inspiratory airflow is always ensured during jet ventilation, owing to the high velocity of the injected gas. Expiratory flow depends on two parameters, notably the patency of the upper airway and the elastic recoil forces of the expanded thorax/lung system [31]. There is a significant risk of
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pneumothorax unless the insufflated air is allowed to egress completely before another inhalation is given to the patient. Failure to provide adequate exhalation time may result in pneumothorax, pneumomediastinum or subcutaneous emphysema. Thus, the main shortcoming of jet ventilation is related to air trapping with a consecutive risk of barotrauma [34], particularly during high-frequency jet ventilation (HFJV) [31]. In small paediatric patients, subglottic transtracheal jet ventilation is dangerous while its usefulness is limited, as small airways do not usually allow air to adequately egress. However, in particular situations, transtracheal jet ventilation may be the only method capable of providing oxygen to the patient. These situations include laser treatment of a narrow airway that cannot accommodate an ET tube or a transglottic catheter. Under these circumstances, supraglottic jet ventilation does not deliver adequate oxygen, whereas an endotracheal tube completely obstructs the airway, rendering the surgical procedure impossible. Given these conditions, tracheostomy is the only alternative to transtracheal jet ventilation. Use of transtracheal jet ventilation to manage stenotic airways requires controlled oxygen insufflations, along with scrupulous monitoring of air egress. As the surgical procedure results in progressive airway enlargement, the risk of barotrauma is highest at the beginning of the procedure. In infants and children, jet ventilation requires close clinical monitoring and high attention levels. As this technique is dangerous and challenging [37], it should be reserved for situations where the only other alternative is to perform a tracheostomy. A well-trained team composed of an anaesthesiologist and an ENT surgeon, familiar with jet ventilation techniques, is a prerequisite for the safe handling of difficult therapeutic procedures on the paediatric airway. In Lausanne, all the above-mentioned techniques of controlled ventilation are used. In our 10-year retrospective analysis of ventilatory modes for paediatric therapeutic microlaryngoscopic procedures (Table 18.2), the apnoeic anaesthesia was the preferred method in infants, followed by controlled ventilation in older children (mainly through a pre-existing tracheostomy) and finally transglottic jet ventilation. Transtracheal jet ventilation was rarely chosen (6% of cases) and if so, mainly for children older than 1 year of age. In our series, we have observed no complications related to jet ventilation and only two cases of minor laryngospasm (1.8%) during the apnoeic ventilation technique. The choice of the
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Table 18.2 Ventilatory modes for paediatric microlaryngoscopy procedures. Lausanne review 1994–2004 [34] Total Mechanical Age Transtracheal jet Transglottal jet Apnoeic controlled ventilation ventilation intermittent ventilation ventilation £1 year
0
4
50
8
62
1–16 year
18
56
61
84
219
Total nb
18
60
111
92
281
Total%
6%
21%
40%
33%
100%
ventilation mode is dependant on the type of laryngeal disease, the scheduled procedure, the patient’s age and comorbidities, the duration of procedure, as well as the relative experience of the anaesthesiologist-ENT surgeon team. Following a thorough discussion with the ENT surgeon, we always aim to apply the least invasive ventilation technique for a given patient and condition.
18.2 Indications for Endoscopic Airway Procedures Closed endoscopic techniques may be used as primary or secondary treatment for the cure of LTS. They mainly comprise CO2 laser, various dilation systems and topical application of mitomycin C, which has been shown to inhibit both neoangiogenesis and proliferation of fibroblasts [26]. Over the last decade, improvements in CO2 lasers with the advent of the microspot and ultrapulse technologies have broadened the indications of the endoscopic CO2 laser for the treatment of LTS. Yet, laser treatment should not be considered as a substitute for open surgery, which remains the cornerstone of treatment of paediatric LTS. Of note is that open and endoscopic techniques often complement each other in the management of LTS. In future years and with the advent of improved stents for paediatric applications, endoscopic treatments are likely to be assigned a major role in the prevention of incipient LTS, prior to the formation of cicatricial stenoses.
18.2.1 Primary Endoscopic Techniques Primary endoscopic dilation or laser resection is strictly contraindicated in children with congenital
cartilaginous stenosis. Any type of endoscopic treatment is liable to worsen the initial condition. When trying to resect a cartilaginous stenosis using the CO2 laser, a raw surface is created, resulting in cartilage exposure in the subglottic lumen. As reepithelialisation does not occur over the denuded cartilage, granulation tissue formation and subsequent scarring are bound to ensue, leading to recurrent stenosis. Likewise, attempted dilation is inevitably ineffective, as the thickened ring of cricoid cartilage cannot be expanded. 18.2.1.1 Cicatricial Subglottic Stenosis (SGS) Only thin, web-like SGSs may benefit from CO2 laser radial incisions and dilation. The cranio-caudal extension of the web should not exceed 5–7 mm in children, and 3–4 mm in infants. As reported by Simpson et al. in 1982 [61], the risk factors for failure of endoscopic treatment of SGS are still valid today. These factors include circumferential cicatricial stenosis with scar tissue greater than 1 cm in the vertical dimension for adults, malacia with loss of cartilage support and posterior laryngeal inlet scarring with arytenoid fixation. Under general anaesthesia in spontaneous respiration, the larynx is suspended with a Benjamin–Lindholm laryngoscope, and the Lindholm self-retaining false cord retractor is placed at the level of the ventricular bands to spread the glottis widely open, thus providing excellent access to the subglottis. The CO2 laser should be set to ultrapulse mode, 100–150 mJ/cm2, 250 m spot size at 400 mm focal distance, and 10 Hz repetition rate, to minimise heat diffusion into the surrounding tissues. Given these parameters, the collateral thermal damage does not exceed 50 m (4–5 cells) and is similar to that of a cold-knife instrument, albeit with no bleeding and more precision. For asymmetrical subglottic webs, a CO2 laser resection comprising less than 50% of the subglottic circumference is very efficient, as it preserves the
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18.2 Indications for Endoscopic Airway Procedures
mucosa of the contralateral side for the reepithelialisation process (Fig. 18.1). For concentric web-like narrowings, radial incisions in the stenosis are made using Shapshay’s technique [58], and gentle dilation is done with tapered bougies such as the Savary–Gilliard dilators or with angioplasty balloons (Fig. 18.2 and 18.3). The author prefers tapered bougies, as they provide tactile feedback for the force needed to dilate the stenosis, as opposed to angioplasty balloons. This procedure is followed by topical application of a mitomycin C soaked cotton swab (1–2 mg/ml) in the subglottis for 2 min. In rare instances, topical application of mitomycin C is associated with excessive fibrin formation, leading to acute dyspnoea 24–48 h after surgery. It is thus advisable to keep the child under close surveillance for at least two postoperative days. The fibrin can easily be removed in SML to relieve the obstruction. In the author’s experience on more than 50 cases (unpublished series), production of excess fibrin never occurred more than once after a single topical application. Repeated mitomycin C applications should, however, be avoided, owing to uncertainties regarding potential late adverse effects (Fig. 18.4).
Fig. 18.1 Web-like, asymmetrical subglottic stenosis: (a) Preoperative view: the thin, web-like diaphragm occupies the left subglottic space. (b) Immediate postoperative view: the web has been fully resected using the CO2 laser. Note the absence of charring. The late outcome was a subnormal airway after a single endoscopic treatment
Fig. 18.2 Diagram of Shapsay’s endoscopic technique for treating a concentric web-like subglottic stenosis: (a) CO2 laser radial incisions at the four cardinal points. (b) Result after dilation: residual mucosal bridges between laser incisions facilitate the reepithelialisation process
Our experience with endoscopic treatments for SGS in 63 paediatric patients [46] revealed a remarkable decrease in success rate as a function of the grade of SGS. An optimal postoperative result, defined as a greater than 80% subglottic airway lumen, was obtained in 92% of preoperative Grade I, 46% of Grade II and only 13% of Grade III SGS.
18.2.1.2 Subglottic Ductal Cysts After prolonged endotracheal intubation, airway compromise may be caused by acquired subglottic ductal cysts. Even though cicatricial subglottic narrowing may be minimal, airway obstruction may be significant due to one or more ductal cysts (Fig. 18.5). The superficial trauma induced by the ET tube eventually causes cicatricial obstruction of the excretory ostium of the submucosal mucous glands, leading to mucus retention in the dilated ducts [6, 70]. The size of ductal cysts may vary widely. While some do not need any treatment and may even shrink spontaneously with time, others are large enough to
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Fig. 18.3 Recurrent subglottic stenosis in a 16-year-old adolescent, treated by CO2 laser incisions and dilation: (a) Peroperative view: three radial incisions are made with the Omniguide CO2 laser fibre at 5, 7 and 12 o’clock (b) Peroperative view: immediate result after dilation. Mucosal bridges are preserved to facilitate reepithelialisation of laser wounds
Fig. 18.4 Recurrent web-like concentric glotto-subglottic stenosis after partial cricotracheal resection: (a) Preoperative view: mild grade III subglottic stenosis treated by CO2 laser incisions, dilation and mitomycin C (2 mg/ml for 2 min). (b) Postoperative view at 6 months showing the result after a
single endoscopic treatment: The airway is adequate, albeit with an anterior synechia of the vocal cords. Parents refused any further treatment over the next 5 years. Initially, the endoscopic treatment was performed solely to “buy time” before considering open revision surgery
Fig. 18.5 Acquired submucosal cysts after prolonged intubation: (a) Endoscopic view: submucosal cysts, resulting from cicatricial obstruction of the excretory ducts, obstructing the subglottis. (b) Histology: large, left submucosal cyst associated
with smaller ductal cysts. Note the presence of a submucosal cleft that possibly avoided development of a severe cicatricial subglottic stenosis (Reproduced from Holinger [39]. With permission)
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18.2 Indications for Endoscopic Airway Procedures
cause airway obstruction, therefore requiring endoscopic removal. Marsupialisation with the CO2 laser set to ultrapulse mode, 150 mJ/cm2, 250 m spot size and 10 Hz repetition rate is efficacious in restoring a patent subglottic airway. Selection of the proper laser parameters is crucial to avoid unwanted collateral thermal damage that will only worsen the initial condition in a small infant’s airway.
18.2.1.3 Posterior Glottic Stenosis (PGS) This entity may present as an isolated condition or be associated with subglottic stenosis (SGS). Glottosubglottic stenosis always requires open surgical repair (see Sect. 17.5, Chap. 17). The endoscopic management of PGS is limited to Bogdasarian Type I and II stenoses (see Fig. 5.11, Chap. 5).
the integrity of both CA joints. A gentle dilation with tapered Savary–Gilliard bougies is used to optimise the final results, and mitomycin C at a concentration of 2 mg/ml is topically applied to the interarytenoid wound with a cotton swab for 2 min. Preserved mobility of the CA joints is a prerequisite for a successful outcome. The repeated abduction of the vocal cords during the healing phase prevents the recurrence of PGS. If CA joint mobility is suboptimal, then the endoscopic treatment is likely to fail. Endoscopic posterior cricoid split and rib-grafting according to Inglis’ technique is an appealing option in non-tracheostomised older children and adolescents. This endoscopic technique has been described in Sect. 7.2.2.2, Chap. 7. Bogdasarian type III and IV PGSs are not indications for simple endoscopic resection of interarytenoid scar tissue, because one or both arytenoids are fixed. A partial or total arytenoidectomy is to be considered if the subglottis is normal. A detailed description of this intervention is provided in Sect. 7.2.2.2, Chap. 7.
Type I Interarytenoid Adhesion Under general anaesthesia in spontaneous respiration, the larynx is suspended with the Benjamin–Lindholm laryngoscope, and the CO2 laser is set to the same parameters as those used for treating cicatricial conditions of the airway (ultrapulse mode, 150 mJ/cm2, 250 m spot size, 10 Hz repetition rate). A Lindholm false cord spreader is installed at the level of the false cords in order to put the interarytenoid scar tissue under tension, and laser platforms are utilised to shield the adjacent laryngeal mucosa. The cicatricial bridge tethering the vocal cords is vaporised without denuding the cartilage on the medial aspect of the arytenoids, and the posterior glottis is then dilated with tapered bougies. A subnormal interarytenoid distance is usually restored. Topical application of mitomycin C is unnecessary, as the residual posterior interarytenoid mucosa prevents recurrence of PGS.
T ype II PGS with Bilateral Preservation of “Active” Arytenoid Mobility The general setting is identical to that used for Type I PGS. The cicatricial tissue constituting the PGS is fully resected, with the CO2 laser set to conventional parameters for this use. Since both cricoarytenoid joints are intact, the vocal cords are progressively splayed open with a Lindholm spreader. This manoeuvre confirms
18.2.1.4 Subacute Lesions of Intubation Evolving into Incipient LTS Although a thorough description of several treatment modalities for this condition is provided in Sect. 14.3, Chap. 14, a few supplementary remarks are worth mentioning as regards the potential of endoscopic therapy in preventing cicatricial LTS after prolonged intubation. The majority of airway reconstructions for cicatricial LTS are splinted with a stent. Hence, to prevent cicatricial stenosis formation from acute or subacute intubation lesions, it seems logical to develop prostheses that resist the contracting forces of scar formation. Until now, the poor design and excessive hardness of laryngotracheal stents have made their use for this indication unsuitable. However, with the introduction of the soft LT-Mold prosthesis, which conforms to the contours of the inner larynx, the situation is likely to change in the near future. Laryngeal rest with 2 weeks of undisturbed intubation, as advised by Graham [24], Hoeve [29] and Albert [3], has proven effective in permitting extubation of infants with early, soft stenosis. In more severe cases with glotto-subglottic ulcerations and granulation tissue necessitating tracheostomy, careful removal of granulation tissue and fibrin along with topical application of mitomycin C is required. After that, endoscopic placement of an LT-Mold prosthesis smeared in Gentamycin-corticosteroid ointment
250
(Diprogenta®) is required, which has proven effective in preventing cicatricial narrowing of the larynx (see Sect. 14.3.3, Chap. 14). The prerequisite for an optimal prosthesis is that the prosthetic device does not induce additional damage to the airway. Since the LT-Mold is snugly fixed to the anterior tracheal wall, without inducing shearing forces at the stent-mucosal interface, the device allows the larynx to rest, thus aiding the healing process.
18.2.2 Secondary Endoscopic Techniques Laser resection and dilation can be used as an additional treatment to open surgery to optimise the final surgical results. These techniques can also be employed as an adjunct in the treatment of complex laryngotracheal stenoses. 18.2.2.1 Postoperative Optimisation of Open Surgical Results After SS-LTR or SS-PCTR, laser resection or dilation should preferably be avoided in the first 6 weeks of the postoperative period. Due to immature scars, earlier intervention is liable to tear the reconstructed area. If the postoperative course after SS-PCTR is uneventful, then the first endoscopic dilation should be performed 3 months after surgery (Fig. 18.6). The CO2 laser is only used when granulation tissue has evolved into an anastomotic web. The laser
Fig 18.6 Optimisation of partial cricotracheal resection results by dilation at 3 months postoperatively: (a) Preoperative view: grade III subglottic stenosis with narrowed interarytenoid distance. (b) Postoperative partial cricotracheal resection results
18 Endoscopic Techniques for Laryngotracheal Stenosis
parameters and type of dilation used during the primary treatment (see Sect. 18.2.1) are employed again. Likewise, topical application of mitomycin C plays a significant role in preventing recurrent scar formation. Arytenoid prolapse or dislocation that impinges on the airway, causing dyspnoea and severe dysphonia, may benefit from partial arytenoidectomy. Under the previously described SML conditions, the CO2 laser is used to partially resect the portion of the arytenoid that obstructs the glottis (Fig. 18.7). This procedure is likely to improve the airway and restore good postoperative voice quality provided that contralateral arytenoid mobility is present. Mitomycin C (2 mg/ml for 2 min) should be applied topically to prevent recurrent scar formation. In some cases, laser supraglottoplasty is required before decannulation can be achieved. Depending on the type of obstruction, the techniques of supraglottoplasty are similar to those used for primary Type III laryngomalacia (Fig. 18.8). For BVCP or bilateral CAA with marginal interarytenoid distance, laser arytenoidectomy is the treatment of choice for larynges that have already been operated on several times. A detailed description of the procedure is provided in Sect. 7.2.2.2 Chap. 7. Arytenoid prolapse may also benefit from submucosal volume reduction with the CO2 laser set to the CW, chopped mode, at 3 W output power with a 0.4 mm spot size (~2,400 W/cm2). These laser parameters are likely to induce submucosal scarring to the patient’s benefit.
at 3 months: annular cicatricial web at the site of the anastomosis. (c) Immediate post-dilatation results: the web has been splayed open
18.2 Indications for Endoscopic Airway Procedures
Fig. 18.7 Dislocated right arytenoid impingement on the laryngeal inlet: (a) Preoperative view: the dislocated right arytenoid blocks the movement of the left arytenoid and partially obstructs the airway. (b) Immediate postoperative view: the partial resection of the right arytenoid restored a triangular shape of the
251
glottis. Note the absence of charring on the laser wound. (c) Late 1-year postoperative results: airway and voice quality significantly improved. The left mobile arytenoid restored a good glottic closure
Fig. 18.8 Epiglottic prolapse preventing decannulation after extended partial cricotracheal resection for grade IV transglottic stenosis: (a) Preoperative view: the epiglottic prolapse almost completely obstructs the laryngeal inlet. (b) Postoperative view: after type III supraglottoplasty and epiglottopexy, the laryngeal inlet is fully patent
18.3 Mitomycin C (MMC) Over the past 10 years [74], mitomycin C (MMC) has been used empirically to improve paediatric airway surgery outcomes following open reconstructions or closed endoscopic techniques. Despite conflicting results as to MMC efficacy in different animal models [12–14, 20, 22, 52–55, 59, 63, 64] and human studies [27, 48–52, 60], the drug is still widely used in clinical practice. Over 80% of patients are reported to have improved outcomes attributable to MMC [75], whereas the use of MMC to improve airway surgery outcomes is supported by only two-thirds of animal studies [75]. Warner et al. [75] examined
drug-related variables, treatment techniques, clinical outcomes, and inter-patient differences that preclude the conduct of properly randomised studies in humans. Even animal experiments have fallen short of this goal and provided contradictory results on significant issues, such as optimal MMC dosage, dose-response trends, as well as duration and frequency of topical application. Clinical observations reveal reduction in granulation tissue and scar formation when MMC is appropriately used for proper indications [48–50, 52, 60, 74]. Mitomycin C, an antibiotic isolated from the streptomyces caespitosus strain of actinomyces [28], acts as a prodrug and is metabolised into an alkylating agent.
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18 Endoscopic Techniques for Laryngotracheal Stenosis
Initially used to treat solid tumours [69], MMC has been found to modulate the wound healing response by inhibiting both neoangiogenesis and fibroblast proliferation [15, 35]. On fibroblasts, topical MMC application was shown to affect cell proliferation by increasing cell apoptosis [30, 36]. Ophthalmology was the first therapeutic area where clinical trials were started. In a randomised study, MMC was shown to reduce recurrence rates after pterygium surgery from 89% to 2.3% [62]. Mitomycin C also proved efficacious in glaucoma surgery, preserving patency rate of the trabeculectomy draining site in more than 90% of cases [11, 45]. Since these early reports, the benefit of topical application of MCC has spread to the otolaryngology community, where it is widely used for choanal atresia, dacryocystorhinostomy and cicatricial stenosis of the airway and oesophagus [51]. In ophthalmology, eye drops at a concentration of 1 mg/ml, applied four times daily, caused conjunctival irritation and mild superficial keratitis [62]. These local side effects were minimised when using a 0.4 mg/ml MMC dosage, which has become the recommended dose regimen for ophthalmological use. Without taking into account the fact that the 0.4 mg/ml dose was applied four times daily for several days in ophthalmology, most clinical studies [48–51, 54], except two [10, 71], utilised the same MMC dose as a single application in the paediatric airway. Currently, many issues pertaining to the topical use of MMC in the paediatric airway remain unresolved. These include: (1) optimal dosage, (2) duration of topical application, (3) appropriateness of rinsing the area with saline after MMC application, (4) potential risks involved with multiple applications, and (5) indications and contraindications in paediatric airway surgery.
similar dosages caused airway obstruction with excess fibrin production and delayed healing in one study [33], or no advantage over control groups treated with saline pledgets in another study [55]. However, when administering higher concentrations of MMC at 0.04 mg/ml, 0.4 mg/ml and 1 mg/ml, Ingram et al. [32] reported that MMC had an increasing beneficial effect in preventing maxillary antrostomy closure in the rabbit model. The only randomised, double-blind, placebo-controlled trial conducted in the paediatric airway [27] revealed no significant differences in the MMC group compared to the placebo group in an interim analysis, and the study was therefore stopped. It should be noted, however, that based on studies from ophthalmology, the selected 0.2 mg/ml dosage might have been too low for the paediatric airway. This “negative” result is in contradiction with the findings of other, albeit non-randomised clinical studies, which revealed clear benefits following topical MMC applications [27, 48–50, 54, 60, 71, 74]. This is in accordance with our own experience involving 50 unpublished cases where MMC was applied topically to the paediatric airway at a concentration of 2 mg/ml for 2 min. As excess fibrin production by small airways without a tracheostomy cover occurred in approximately 5% of the cases, 24–48 h of postoperative hospital observation seems warranted. Based on published reports and clinical experiences, a dosage of 0.2 mg/ml, or even 0.4 mg/ml, may be too low for the paediatric airway. Doses of 1–2 mg/ml are likely to be safe as far as acute adverse events are concerned. Because MMC’s potential late adverse events are unknown, repeated applications must be avoided. One case report on the occurrence of laryngeal cancer in a non-smoking adult patient [2] has been published, although evidence that MMC was the sole responsible factor could not be established.
18.3.1 Mitomycin C Dosage for Topical Application
18.3.2 Duration of Topical MMC Application
Animal studies have failed to provide answers on this issue. In the canine model, solutions of 0.2 mg/ml up to 10 mg/ml MMC were topically applied to the subglottis or the vocal cords without causing significant acute side effects [14, 20, 22, 64]. In the rabbit model,
In the literature, reported exposure times have varied from 1 to 5 min [43, 60, 74], but increasing MMC exposure times from 2 to 5 min did not confer additional benefits [43]. A 2-min application should be used until results of further studies are available.
18.2 Indications for Endoscopic Airway Procedures
18.3.3 Rinsing the Wound after Topical MMC Application In a meta-analysis on the clinical experience with MMC [73], saline rinsing of the wound after topical MMC application was shown to avoid excess fibrin production and potential airway obstruction in children without a tracheostomy cover. However, the exact dilution of the MCC solution after saline rinsing could not be determined, nor was it possible to prove that the dilution was detrimental to the MMC’s anti-fibrotic effects.
18.3.4 Risks of Multiple Topical MMC Applications In cell cultures, inhibition of fibroblast growth lasted as long as 30 days after a single topical MMC application [57]. In dogs, a repeated application after 2 days versus a single application did not prevent laryngotracheal stenosis [20]. When deemed appropriate, a second topical MMC application may be envisaged after 30 days, but further applications should be avoided until worldwide clinical experience confirms that “low-dose” topical MMC applications are innocuous with regard to potential late malignant transformation of the airway mucosa. Other systemic cancers are unlikely to occur, since only traces of MMC have been found in children’s plasma within 1 h following a 2 mg/ml topical application to the larynx (personal communication).
18.3.5 Indications and Contraindications of Topical MMC Applications Although the effects of MMC absorption through intact or injured mucosae have not been studied, clinical experience has shown that the normal mucosa is not macroscopically affected by topical MMC application. On laser wounds or dilation-induced mucosal tears, MMC’s effects are immediately apparent as bleeding decreases. Mitomycin C should be applied to all raw mucosal surfaces after lasering or following granulation tissue removal [14]. It is efficient in preventing regrowth of granulation tissue after extubation or stent removal, CO2 laser incision or excision of
253
cicatricial web-like SGSs. However, MMC should never be applied on denuded cartilage. By preventing granulation tissue formation over the exposed cartilage in the subglottic lumen, MMC is likely to induce cartilage necrosis. Although many uncertainties persist about the use of MMC in the paediatric airway, most clinical studies seem to confirm MMC’s beneficial effects on airway surgery outcomes. As stated by Warner et al. in their meta-analysis [75], “Since none of the studies report significant side effects or complications with MMC usage, it is hard to argue against its use from a risk-benefit analysis standpoint.” Based on the current state of knowledge regarding the adjunctive benefits of topical MMC application in the paediatric airway, the following (clinical but not evidence-based) recommendations can be made: • Dosage: 1–2 mg/ml MMC solution • Application method: topical application on cotton swabs or pledgets soaked in MMC solution • Duration of application: 2 min • Rinsing with saline: this seems to decrease the risk of excess fibrin production but may reduce MMC’s concentration • Frequency of application: only once or perhaps a second application after a 30-day interval. For safety reasons, MMC applications should be limited to less than three until further information on potential late malignancies is made available • Indications and contraindications: –– Prevention of recurrent granulation tissue and scar formation after endoscopic removal of postintubation or poststenting granulation tissue –– Prevention of granulation tissue formation and scarring after CO2 laser excision or incision/dilation of cicatricial airway stenosis –– Topical applications should not be applied to exposed airway cartilage –– Topical applications should not be performed within 6 weeks following PCTR, as MMC may increase the risk of anastomotic dehiscence by reducing scar formation –– When inadvertently applied to the normal mucosa, MMC at a concentration of 1–2 mg/ml is devoid of adverse macroscopic effects These recommendations may change as more MMC data become available over the coming years, though for the time being, these indications and contraindications appear sound.
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18 Endoscopic Techniques for Laryngotracheal Stenosis
References
Box 18 Surgical Highlights of Endoscopic LTS Management • Carefully respect the indications • Use the CO2 laser set to ultrapulse mode, 150 mJ/cm2, 250 m spot size, 400 mm focal distance and 10 Hz repetition rate • Perform radial incisions in the stenosis, and gently dilate with tapered bougies or angioplasty balloons • Do not overdilate an SGS to avoid deep mucosal tears • Apply MMC at 1 or 2 mg/ml concentrations on laser or dilation wounds, but never on denuded cartilage • Avoid repeated MMC applications, due to the uncertainty regarding potential late adverse events • Treat posterior glottic stenosis by closed endoscopic techniques only in the presence of active residual mobility of the arytenoids • If vocal cords are fixed bilaterally, then arytenoidectomy with the CO2 laser is an option • Treat acute intubation-related lesions before performing tracheostomy
1. Abdallah, C., Karsli, C., Bissonnette, B.: Fentanyl is more effective than remifentanil at preventing increases in cerebral blood flow velocity during intubation in children. Can. J. Anaesth. 49, 1070–1075 (2002) 2. Agrawal, N., Morrison, G.A.: Laryngeal cancer after topical mitomycin C application. J. Laryngol. Otol. 120, 1075–1076 (2006) 3. Albert, D.: Post-intubation laryngotracheal stenosis. In: Graham, J.M., Scadding, G.K., Bull, P.D. (eds.) Pediatric ENT, p. 226. Springer, Berlin/Heidelberg (2008) 4. Ansermino, J.M., Brooks, P., Rosen, D., et al.: Spontaneous ventilation with remifentanil in children. Paediatr. Anaesth. 15, 115–121 (2005) 5. Barker, N., Lim, J., Amari, E., et al.: Relationship between age and spontaneous ventilation during intravenous anesthesia in children. Paediatr. Anaesth. 17, 948–955 (2007) 6. Bauman, N.M., Benjamin, B.: Subglottic ductal cysts in the preterm infant: association with laryngeal intubation trauma. Ann. Otol. Rhinol. Laryngol. 104, 963–968 (1995) 7. Best, C.: Anesthesia for laser surgery of the airway in children. Paediatr. Anaesth. 19(Suppl 1), 155–165 (2009) 8. Browne, B.L., Prys-Roberts, C., Wolf, A.R.: Propofol and alfentanil in children: infusion technique and dose requirement for total i.v. anaesthesia. Br. J. Anaesth. 69, 570–576 (1992) 9. Bruce, I.A., Rothera, M.P.: Upper airway obstruction in children. Paediatr. Anaesth. 19(Suppl 1), 88–99 (2009) 10. Cable, B.B., Pazos, G.A., Brietzke, S.E., et al.: Topical mitomycin therapy in the pediatric airway: state of the art. Oper. Tech. Otolaryngol. 13, 57–64 (2002)
18.4 APPENDIX Proposed Adrenalin concentrations for topical endoscopic application (4 µg/kg bodyweight) Adrenaline Concentration Patient 1: 25’000 solution 1mg in 25ml NaCl 0.9 % 40 µg/ml Bodyweight (kg) Maximum Volume Authorised
1: 100’000 solution 1mg in 100ml NaCl 0.9 % 10µg/ml
1: 500’000 solution 1mg in 500ml NaCl 0.9 % 2µg/ml
kg
0.1 ml/kg
0.4 ml/kg
2 ml/kg
5 kg
0.5 ml
2 ml
10 ml
10 kg
1.0 ml
4 ml
20 ml
15 kg
1.5 ml
6 ml
30 ml
20 kg
2 ml
8 ml
40 ml
25 kg
2.5 ml
10 ml
50 ml
30 kg
3 ml
12 ml
60 ml
40 kg
4 ml
16 ml
80 ml
50 kg
5 ml
20 ml
100 ml
References 11. Chen, C.W., Huang, H.T., Bair, J.S., et al.: Trabeculectomy with simultaneous topical application of mitomycin-C in refractory glaucoma. J. Ocul. Pharmacol. 6, 175–182 (1990) 12. Cincik, H., Gungor, A., Cakmak, A., et al.: The effects of mitomycin C and 5-fluorouracil/triamcinolone on fibrosis/ scar tissue formation secondary to subglottic trauma (experimental study). Am J Otolaryngol-Head and Neck Med and Surg. 26, 45–50 (2005) 13. Coppit, G., Perkins, J., Munaretto, J., et al.: The effects of mitomycin-C and stenting on airway wound healing after laryngotracheal reconstruction in a pig model. Int. J. Pediatr. Otorhinolaryngol. 53, 125–135 (2000) 14. Correa, A.J., Reinisch, L., Sanders, D.L., et al.: Inhibition of subglottic stenosis with mitomycin-C in the canine model. Ann. Otol. Rhinol. Laryngol. 108, 1053–1060 (1999) 15. Cummings, J., Spanswick, V.J., Tomasz, M., et al.: Enzymology of mitomycin C metabolic activation in tumour tissue: implications for enzyme-directed bioreductive drug development. Biochem. Pharmacol 56, 405–414 (1998) 16. Davis, D.A., Russo, P.A., Greenspan, J.S., et al.: Highfrequency jet versus conventional ventilation in infants undergoing Blalock-Taussig shunts. Ann. Thorac. Surg. 57, 846–849 (1994) 17. Depierraz, B., Ravussin, P., Brossard, E., et al.: Percutaneous transtracheal jet ventilation for paediatric endoscopic laser treatment of laryngeal and subglottic lesions. Can. J. Anaesth. 41, 1200–1207 (1994) 18. Donati, F.: Tracheal intubation: unconsciousness, analgesia and muscle relaxation. Can. J. Anaesth. 50, 99–103 (2003) 19. El Hammar-Vergnes, F., Cros, A.M.: High frequency jet ventilation in paediatric anaesthesia. Ann. Fr. Anesth. Rèanim. 22, 671–675 (2003) 20. Eliachar, R., Eliachar, I., Esclamado, R., et al.: Can topical mitomycin prevent laryngotracheal stenosis? Laryngoscope 109, 1594–1600 (1999) 21. Emhardt, J., Weisberger, E., Dierdorf, S., et al.: The rise of arterial carbon dioxide during apnea in children. Anesthesiology 69, 779 (1988) 22. Garrett, C.G., Soto, J., Riddick, J., et al.: Effect of mitomycin-C on vocal fold healing in a canine model. Ann. Otol. Rhinol. Laryngol. 110, 25–30 (2001) 23. Glaisyer, H.R., Sury, M.R.: Recovery after anesthesia for short pediatric oncology procedures: propofol and remifentanil compared with propofol, nitrous oxide, and sevoflurane. Anesth. Analg. 100, 959–963 (2005) 24. Graham, J.M.: Formal reintubation for incipient neonatal subglottic stenosis. J. Laryngol. Otol. 108, 474–478 (1994) 25. Grundmann, U., Uth, M., Eichner, A., et al.: Total intravenous anaesthesia with propofol and remifentanil in paediatric patients: a comparison with a desflurane-nitrous oxide inhalation anaesthesia. Acta Anaesthesiol. Scand. 42, 845– 850 (1998) 26. Hardillo, J., Vanclooster, C., Delaere, P.R.: An investigation of airway wound healing using a novel in vivo model. Laryngoscope 111, 1174–1182 (2001) 27. Hartnick, C.J., Hartley, B.E., Lacy, P.D., et al.: Topical mitomycin application after laryngotracheal reconstruction: a randomized, double-blind, placebo-controlled trial. Arch. Otolaryngol. Head Neck Surg. 127, 1260–1264 (2001) 28. Hata, T., Hoshi, T., Kanamori, K., et al.: Mitomycin, a new antibiotic from Streptomyces. I. J. Antibiot (Tokyo) 9, 141– 146 (1956)
255 29. Hoeve, L.J., Eskici, O., Verwoerd, C.D.: Therapeutic reintubation for post-intubation laryngotracheal injury in preterm infants. Int. J. Pediatr. Otorhinolaryngol. 31, 7–13 (1995) 30. Hu, D., Sires, B.S., Tong, D.C., et al.: Effect of brief exposure to mitomycin C on cultured human nasal mucosa fibroblasts. Ophthal. Plast. Reconstr. Surg. 16, 119–125 (2000) 31. Ihra, G.C.: High-frequency jet ventilation in the presence of airway stenosis leads to inadvertent high PEEP levels. Paediatr. Anaesth. 18, 905–906 (2008). author reply 906–907 32. Ingrams, D.R., Volk, M.S., Biesman, B.S., et al.: Sinus surgery: does mitomycin C reduce stenosis? Laryngoscope 108, 883–886 (1998) 33. Iniguez-Cuadra, R., San Martin Prieto, J., Iniguez-Cuadra, M., et al.: Effect of mitomycin in the surgical treatment of tracheal stenosis. Arch. Otolaryngol. Head Neck Surg. 134, 709–714 (2008) 34. Jaquet, Y., Monnier, P., Van Melle, G., et al.: Complications of different ventilation strategies in endoscopic laryngeal surgery: a 10-year review. Anesthesiology 104, 52–59 (2006) 35. Kao, S., Liao, C., Tseng, J., et al.: Dacryocystorhinostomy with intraoperative mitomycin C. Ophthalmology 104, 86 (1997) 36. Khaw, P.T., Doyle, J.W., Sherwood, M.B., et al.: Prolonged localized tissue effects from 5-minute exposures to fluorouracil and mitomycin C. Arch. Ophthalmol. 111, 263–267 (1993) 37. Koomen, E., Poortmans, G., Anderson, B.J., et al.: Jet ventilation for laryngotracheal surgery in an ex-premature infant. Paediatr. Anaesth. 15, 786–789 (2005) 38. Ledowski, T., Paech, M.J., Patel, B., et al.: Bronchial mucus transport velocity in patients receiving propofol and remifentanil versus sevoflurane and remifentanil anesthesia. Anesth. Analg. 102, 1427–1430 (2006) 39. Lusk, R.P., Woolley, A.L., Holinger, L.D.: Laryngotracheal stenosis. In: Holinger, L.D., Lusk, R.P., Green, C.G. (eds.) Pediatric Laryngology and Bronchoesophagology, pp. 165– 186. Lippincott-Raven, Philadelphia/New York (1997) 40. Mani V, Morton NS Overview of total intravenous anesthesia in children. Paediatr Anaesth 20, 211-222 (2009) 41. Mausser, G., Friedrich, G., Schwarz, G.: Airway management and anesthesia in neonates, infants and children during endolaryngotracheal surgery. Paediatr. Anaesth. 17, 942–947 (2007) 42. Meakin, G., Shaw, E.A., Baker, R.D., et al.: Comparison of atracurium-induced neuromuscular blockade in neonates, infants and children. Br. J. Anaesth. 60, 171–175 (1988) 43. Megevand, G.S., Salmon, J.F., Scholtz, R.P., et al.: The effect of reducing the exposure time of mitomycin C in glaucoma filtering surgery. Ophthalmology 102, 84–90 (1995) 44. Meliones, J.N., Bove, E.L., Dekeon, M.K., et al.: Highfrequency jet ventilation improves cardiac function after the Fontan procedure. Circulation 84, III364–III368 (1991) 45. Mirza, G.E., Karakucuk, S., Dogan, H., et al.: Filtering surgery with mitomycin-C in uncomplicated (primary open angle) glaucoma. Acta Ophthalmol (Copenh) 72, 155–161 (1994) 46. Monnier, P., George, M., Monod, M.L., et al.: The role of the CO2 laser in the management of laryngotracheal stenosis: a survey of 100 cases. Eur. Arch. Otorhinolaryngol. 262, 602– 608 (2005) 47. Pavlin, D.J., Coda, B., Shen, D.D., et al.: Effects of combining propofol and alfentanil on ventilation, analgesia, sedation, and emesis in human volunteers. Anesthesiology 84, 23–37 (1996)
256 48. Perepelitsyn, I., Shapshay, S.M.: Endoscopic treatment of laryngeal and tracheal stenosis-has mitomycin C improved the outcome? Otolaryngol. Head Neck Surg. 131, 16–20 (2004) 49. Rahbar, R., Valdez, T., Shapshay, S.: Preliminary results of intraoperative mitomycin-C in the treatment and prevention of glottic and subglottic stenosis. J. Voice 14, 282–286 (2000) 50. Rahbar, R., Shapshay, S.M., Healy, G.B.: Mitomycin: effects on laryngeal and tracheal stenosis, benefits, and complications. Ann. Otol. Rhinol. Laryngol. 110, 1–6 (2001) 51. Rahbar, R., Jones, D.T., Nuss, R.C., et al.: The role of mitomycin in the prevention and treatment of scar formation in the pediatric aerodigestive tract: friend or foe? Arch. Otolaryngol. Head Neck Surg. 128, 401–406 (2002) 52. Roh, J.L., Yoon, Y.H.: Prevention of anterior glottic stenosis after transoral microresection of glottic lesions involving the anterior commissure with mitomycin C. Laryngoscope 115, 1055–1059 (2005) 53. Roh, J.L., Lee, Y.W., Park, H.T.: Subglottic wound healing in a new rabbit model of acquired subglottic stenosis. Ann. Otol. Rhinol. Laryngol. 115, 611–616 (2006) 54. Roh, J.L., Koo, B.S., Yoon, Y.H., et al.: Effect of topical mitomycin C on the healing of surgical and laser wounds: a hint on clinical application. Otolaryngol. Head Neck Surg. 133, 851–856 (2005) 55. Roh, J.L., Kim, D.H., Rha, K.S., et al.: Benefits and risks of mitomycin use in the traumatized tracheal mucosa. Otolaryngol. Head Neck Surg. 136, 459–463 (2007) 56. Rusch, D., Happe, W., Wulf, H.: Postoperative nausea and vomiting following stabismus surgery in children. Inhalation anesthesia with sevoflurane-nitrous oxide in comparison with intravenous anesthesia with propofol-remifentanil. Anaesthesist 48, 80–88 (1999) 57. Senders, C.: Use of mitomycin C in the pediatric airway. Curr. Opin. Otolaryngol. Head Neck Surg. 12, 473–475 (2004) 58. Shapshay, S.M., Beamis Jr., J.F., Hybels, R.L., et al.: Endoscopic treatment of subglottic and tracheal stenosis by radial laser incision and dilation. Ann. Otol. Rhinol. Laryngol. 96, 661–664 (1987) 59. Shvidler, J., Bothwell, N.E., Cable, B.: Refining indications for the use of mitomycin C using a randomized controlled trial with an animal model. Otolaryngol. Head Neck Surg. 136, 653–657 (2007) 60. Simpson, C.B., James, J.C.: The efficacy of mitomycin-C in the treatment of laryngotracheal stenosis. Laryngoscope 116, 1923–1925 (2006) 61. Simpson, G.T., Strong, M.S., Healy, G.B., et al.: Predictive factors of success or failure in the endoscopic management of laryngeal and tracheal stenosis. Ann. Otol. Rhinol. Laryngol. 91, 384–388 (1982) 62. Singh, G., Wilson, M.R., Foster, C.S.: Mitomycin eye drops as treatment for pterygium. Ophthalmology 95, 813–821 (1988) 63. Spector, J.E., Werkhaven, J.A., Spector, N.C., et al.: Prevention of anterior glottic restenosis in a canine model
18 Endoscopic Techniques for Laryngotracheal Stenosis with topical mitomycin-C. Ann. Otol. Rhinol. Laryngol. 110, 1007–1010 (2001) 64. Spector, J.E., Werkhaven, J.A., Spector, N.C., et al.: Preservation of function and histologic appearance in the injured glottis with topical mitomycin-C. Laryngoscope 109, 1125–1129 (1999) 65. Stern, Y., McCall, J.E., Willging, J.P., et al.: Spontaneous respiration anesthesia for respiratory papillomatosis. Ann. Otol. Rhinol. Laryngol. 109, 72–76 (2000) 66. Struys, M.M., Vereecke, H., Moerman, A., et al.: Ability of the bispectral index, autoregressive modelling with exogenous input-derived auditory evoked potentials, and predicted propofol concentrations to measure patient responsiveness during anesthesia with propofol and remifentanil. Anesthesiology 99, 802–812 (2003) 67. Tagaito, Y., Isono, S., Nishino, T.: Upper airway reflexes during a combination of propofol and fentanyl anesthesia. Anesthesiology 88, 1459–1466 (1998) 68. Tobias, J.D.: Transcutaneous carbon dioxide monitoring in infants and children. Paediatr. Anaesth. 19, 434–444 (2009) 69. Tomasz, M., Palom, Y.: The mitomycin bioreductive antitumor agents: cross-linking and alkylation of DNA as the molecular basis of their activity. Pharmacol. Ther. 76, 73–87 (1997) 70. Toriumi, D.M., Miller, D.R., Holinger, L.D.: Acquired subglottic cysts in premature infants. Int. J. Pediatr. Otorhinolaryngol. 14, 151–160 (1987) 71. Unal, M.: The successful management of congenital laryngeal web with endoscopic lysis and topical mitomycin-C. Int. J. Pediatr. Otorhinolaryngol. 68, 231–235 (2004) 72. Ved, S.A., Chen, J., Reed, M., et al.: Intubation with low-dose atracurium in children. Anesth. Analg. 68, 609–613 (1989) 73. Veen, E.J., Dikkers, F.G.: Topical use of MMC in the upper aerodigestive tract: a review on the side effects. Eur. Arch. Otorhinolaryngol. 267, 327–334 (2010) 74. Ward, R.F., April, M.M.: Mitomycin-C in the treatment of tracheal cicatrix after tracheal reconstruction. Int. J. Pediatr. Otorhinolaryngol. 44, 221–226 (1998) 75. Warner, D., Brietzke, S.E.: Mitomycin C and airway surgery: how well does it work? Otolaryngol. Head Neck Surg. 138, 700–709 (2008) 76. Weber, G.: Exposure of operating personnel to inhalational anaesthetics in paediatric surgery. Paediatr. Anaesth. 4, 229– 233 (1994) 77. Weisberger, E.C., Emhardt, J.D.: Apneic anesthesia with intermittent ventilation for microsurgery of the upper airway. Laryngoscope 106, 1099–1102 (1996) 78. Werkhaven, J.A.: Microlaryngoscopy-airway management with anaesthetic techniques for CO(2) laser. Paediatr. Anaesth. 14, 90–94 (2004) 79. Westhout, F.D., Muhonen, M.G., Nwagwu, C.I.: Early propofol infusion syndrome following cerebral angiographic embolization for giant aneurysm repair. Case report. J Neurosurg. 106, 139–142 (2007)
Laryngotracheoplasty and Laryngotracheal Reconstruction
Contents
Core Messages
19.1
Laryngotracheoplasty............................................ 257
›› Use
19.2
Laryngotracheal Reconstruction........................... 258
19.3
Historic Review of Paediatric Laryngotracheal Reconstruction........................................................ 258 19.3.1 Milestones in Paediatric Laryngotracheal Reconstruction............................... 258 19.3.2 Paediatric Cricoid Framework Expansion Without Graft.......................................... 259 19.3.3 Paediatric Cricoid Framework Expansion with Grafts.............................................. 259 19.4
›› ››
Laryngotracheoplasty Without Cartilage Expansion............................................... 260
››
Laryngotracheal Reconstruction (LTR) with Cartilage Expansion........................... 262 19.5.1 Surgical Steps for LTR............................................. 262
››
19.5
19.6
Single-stage Laryngotracheal Reconstruction (SS-LTR)....................................... 268 19.6.1 Surgical Steps of Single-Stage Laryngotracheal Reconstruction (SS-LTR).............. 269 19.7
Postoperative Care and Complications................. 271
19.8
Results of Laryngotracheal Reconstruction (LTR)............................................. 271
19
laryngotracheal reconstruction (LTR) instead of laryngotracheoplasty (LTP), except in rare cases of multiple graft failures due to systemic diseases Use SS-LTR for Grade I to minor Grade III SGSs, in the absence of comorbidities or severe glottic involvement Use DS-LTR with stenting for Grade II to minor Grade III SGSs, associated with comorbidities or severe glottic involvement Use SS-PCTR instead of DS-LTR with longterm stenting for isolated severe Grades III and IV SGSs Use DS-extended PCTR instead of DS-LTR for combined severe glotto-subglottic and transglottic stenoses
19.1 Laryngotracheoplasty
References............................................................................ 275
The term laryngotracheoplasty (LTP) describes a procedure aimed at enlarging the subglottic lumen by vertical incisions of the anterior and posterior cricoid ring and then splinting the two expanded halves by a mould during the healing phase. Originally, the cicatricial subglottic stenosis was partially or totally resected, and the mould subsequently guided reepithelialisation of the subglottic space.
P. Monnier (ed.), Pediatric Airway Surgery, DOI: 10.1007/978-3-642-13535-4_19, © Springer-Verlag Berlin Heidelberg 2011
257
258
19 Laryngotracheoplasty and Laryngotracheal Reconstruction
19.2 Laryngotracheal Reconstruction Though the basic principle of laryngotracheal reconstruction (LTR) is identical to that of LTP, LTR comprises two major modifications. The subglottic airway is kept expanded with the interposition of cartilage grafts, and the cicatricial SGS is not resected so as to preserve residual mucosa in the stenotic tract, thereby facilitating the reepithelialisation process during the stenting and healing periods. Over the last 40 years, constant refinements of these techniques have resulted in high success rates for mild and moderate SGS grades. Due to the scarcity of residual mucosa, LTR results are unconvincing in cases of total or subtotal severe cicatricial SGS grades.
19.3 Historic Review of Paediatric Laryngotracheal Reconstruction 19.3.1 Milestones in Paediatric Laryngotracheal Reconstruction • Modern basic principles –– Rethi (1956): researched adults only • Cricoid framework expansion without graft –– Aboulker (1968) –– Grahne (1971) –– Evans (1974) –– Crysdale (1976) • Cricoid framework expansion with graft –– Fearon and Cotton (1972): animal studies only –– Doig (1973): anterior costal cartilage graft (ACCG) –– Fearon and Cotton (1974): thyroid cartilage –– Cotton (1978): LTR with ACCG –– Cotton and Seid (1980): anterior cricoid split –– Cotton (1984): 100 cases of LTR with anterior and posterior CCG –– Prescott (1988): single-stage-LTR –– Drake and Cotton (1989): four-quadrant cricoid split ± costal cartilage grafts Although open approaches for the treatment of adult laryngotracheal stenosis (LTS) had already been
introduced and popularised in the early 1900s by German and French schools (Killian G [47] and Rabot [68]), the first report on a large paediatric series was published in 1958 by Holinger and Johnston [45]. Acquired LTS was of traumatic or infectious origin, and mainly observed in adults and older children. In 1924, Laurens [50] reported mortality rates of up to 56%, with death cases being mainly due to lung infections, in children undergoing this type of surgery. This explains the reluctance among the medical community, at that time, to use these techniques in the paediatric population. During the first half of the twentieth century, pioneers in airway surgery recommended excision of visible scar tissue using a laryngotracheal fissure [6], with additional long-term stenting [13, 45, 51, 75]. Custom-made rubber tubes or foamrubber sponge moulds were used to splint the reconstructed airway. Thiersch skin grafting was also proposed by several authors to control abundant granulation tissue proliferation that inevitably occurred during healing by secondary intention of large circumferential subglottic areas devoid of mucosal lining [6, 13, 45, 51, 63, 75]. Contrary to this earlier tenet, in 1956, Rethi advocated augmentation of the airway without removing scar tissue so as to preserve the mucosal lining of the inner surface of the mature SGS [71]. A vertical median division of the cricoid ring anteriorly and posteriorly was used to spread open the two cricoid laminae. Additionally, a stent fixed to the tracheostomy tube was left in place for 4 months in order to keep the airway expanded until full reepithelialisation of the denuded subglottic area had occurred. To this date, this forms the basic principle for all paediatric airway reconstructions, with or without grafting. It also accounts for the inconsistent and poor results when using LTR for severe Grade III (> 90% luminal obstruction) and Grade IV (= no residual lumen) SGSs. After vertical division of the subglottis, the absence of any residual mucosa of the reconstructed airway circumference implies healing by secondary intention, with subsequent granulation tissue formation and restenosis in a significant number of cases (see Fig. 20.1, Chap. 20). The modern era of surgical reconstruction for cicatricial stenosis of the paediatric larynx began in the late 1960s when the incidences of acquired LTSs in the paediatric population were on the rise. Long-term intubation providing ventilatory support to neonates and children in the PICU, introduced in the early 1960s and reported by different authors around 1965 [5, 56, 57], accounted for the increased incidences of acquired LTS.
19.3 Historic Review of Paediatric Laryngotracheal Reconstruction
These new techniques shifted the population age, with the majority of LTS patients now being infants and small children. Initially, the incidence of SGS following prolonged endotracheal intubation increased dramatically (12–20% in the early 1970s) [34, 39]. Over the following years, however, the incidence of SGS decreased slowly (1–8% in the early 1980s [66, 70, 84], and around 1–3% in the early 1990s, with a further decline by 2000 [26]). As more premature and smaller babies are now surviving, these figures are likely to remain stable over the coming years [4], although preventive measures have reduced the incidences for a given gestational age.
19.3.2 Paediatric Cricoid Framework Expansion Without Graft In 1966, Aboulker first published minor modifications of Rethi’s procedure in adult cases, introducing his cigar-shaped Teflon prosthesis for stenting the reconstructed airway [3]. In 1969, he reported decannulation in three out of five children having undergone this intervention [2]. This first report was followed by that of Grahne in 1971 on seven children who were operated on following Rethi’s principles and were stented using Aboulker’s stent [40]. In 1985, an update on Grahne’s long-term results was published [72]. Five years later, Crysdale published preliminary results using this same technique in three children [23], followed by another publication on nine children in 1982 [25] and a further publication on 13 in 1983 [24]. In 1974, Evans and Todd approached the technique of cricoid framework expansion without grafts in a different way. They proposed a castellated incision of the anterior cricoid cartilage and upper trachea in order to splay the subglottis open and keep the airway in the expanded position with sutures, using a rolled Silastic sheet as stent. They reported their experience on five children in 1974 [32], with further updates published in 1981 and 1986 [17] [54].
19.3.3 Paediatric Cricoid Framework Expansion with Grafts To the best of my knowledge, Doig, Eckstein and Waterston must be credited with the first report of
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paediatric LTR with anterior costal cartilage grafting in 1973 [28]. In their publication, they provided a thorough explanation of the operative steps, with clear illustrative diagrams. In their series involving seven small children (£3 years of age), good results were achieved in four and failure in one. There were two postoperative deaths: one death was due to severe comorbidities, and the other death was caused by severe airway obstruction due to prolapse of the graft. The most innovative, systematic and comprehensive work in this research area was largely the result of Fearon and Cotton’s animal experiments published in 1972 [35]. Indeed, these experiments shaped the basic principles of what was to become laryngotracheal reconstruction (LTR) with anterior costal cartilage graft (ACCG), where the subglottis is expanded without removing scar tissue. The authors demonstrated that this procedure was innocuous as regards laryngeal growth [36], an observation that was confirmed in 1974 by Calcaterra et al. on the developing canine larynx [12]. At that time, Jackson’s statement that future laryngeal growth would be retarded or arrested if the cricoid ring itself was incised or divided [46] was only questioned by the experimental work of Lapidot et al., published in 1968 [49]. In 1974, Fearon and Cotton (1974) reported their preliminary experience on two children with LTS in whom an anterior vertical incision through the cricoid and the first two tracheal rings was made in order to enlarge the subglottic lumen. A thyroid cartilage graft was fixed into position to maintain expansion of the airway [36]. This report was updated in 1976 with four additional cases [37]. However, soon thereafter, autogenous costal cartilage was found to be superior in terms of texture, thickness and size when compared to the less versatile thyroid cartilage. Over the years, LTR with ACCG slowly superseded other laryngotracheoplasty (LTP) techniques of cricoid framework expansion without grafting [3, 23, 32, 40]. During the late 1970s and early 1980s, more and more expertise was gained with this technique. In 1978, Cotton provided a detailed description of LTR with ACCG, reporting his experience with 11 reconstructions using the autogenous costal cartilage method [14]. Expertise grew rapidly and with the occurrence of more severe stenoses, the use of posterior cartilage grafting (PCCG) between the divided laminae of the cricoid plate began to increase in the early 1980s. In the second half of the 1980s, good overall results were reported for use of this technique [8, 19, 44, 55, 78, 90, 92].
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In 1981, Cotton and Evans [17] published a combined report on LTP and LTR, in which 24 of the 103 reported cases had been treated using costal cartilage grafting. Meanwhile, the anterior cricoid split (ACS) procedure had been described [16]. Although this technique had been designed to avoid tracheostomy in neonates who had failed multiple extubation attempts, it is now often converted into an LTR with thyroid ala cartilage graft [76] in order to prevent donor site morbidity in small premature babies. In 1984, Cotton summarised his experience with LTR, firmly advocating the costal cartilage graft (CCG) operation rather than LTP procedures without CCG [15]. Waiting for SGS to become fully mature prior to surgery made sense, as this gave a mucosal lining to the stenosis before the mucosa was divided and expanded with cartilage graft(s). The advent of single-stage LTR (SS-LTR), first reported by Prescott in 1988, marked another milestone in the management of LTS [67]. In tracheostomised children, the tracheostomy site was incorporated into the subglottic reconstruction, and a longer costal cartilage graft was used in order to bridge the anterior laryngotracheal defect, achieving decannulation and subglottic expansion during the same operative session. Postoperative intubation was maintained for up to 1 week, depending on the severity of the subglottic condition. Subsequently, further reports on SS-LTR were published [18, 52, 79]. During this time, the four-quadrant division of the cricoid ring was introduced to manage more severe SGSs that had not sufficiently responded to a vertical midline division with anterior and posterior costal cartilage grafts. The experimental work underlying this technique was provided in 1989 by Drake under Cotton’s supervision [29], and Cotton’s clinical experience involving 31 patients was published in 1991 [21]. Other grafting materials such as septal cartilage [31] and auricular cartilage [53] were also tested, with the aim of achieving immediate epithelial lining of the graft. Over the years, the versatility of the costal cartilage graft gained recognition, and its preference over other grafting materials grew. In the late 1980s and during the following decade, LTR with CCG became a versatile approach. During this period, in addition to the three largest series [20, 62, 65], various other reports were published. Although refinements in surgical techniques resulted in constant
improvements, operation-specific decannulation rates in patients with isolated (i.e., without supraglottic, glottic or tracheal disease) severe Grades III or IV SGS were still below 60% in the early 2000s [43, 73]. Introduced in the early 1990s [59, 69], partial cricotracheal resection (PCTR) has developed into an alternative approach shown to be superior to LTR in the management of severe Grades III and IV SGSs in the paediatric population.
19.4 Laryngotracheoplasty Without Cartilage Expansion Laryngoplasty (LTP) revolutionised the management of paediatric LTS in the early 1970s [1, 32, 40]. In the mid 1970s and early 1980s, however, it was superseded by laryngotracheal reconstruction (LTR) with costal cartilage graft (CCG), known as the Fearon–Cotton operation [14, 28, 36] (Fig. 19.1). Laryngoplasty without cartilage grafting is seldom used now, except for patients having undergone multiple failed airway reconstructions and for those deemed unsuitable for partial cricotracheal resection (PCTR) or conventional LTR with costal cartilage graft. Repeated local failures due to cartilage necrosis or persistent reactive airways may be accounted for by systemic factors, such as diabetes, immuno-suppression, intractable GORD (after ineffective fundoplication) or other idiopathic conditions. As a procedure of last resort, LTP with anterior and posterior cricoid splits or four-quadrant division of the cricoid ring with very long-term stenting (months to years) may be selected in order to salvage a severely compromised airway. For simpler airway stenoses, as in the case of minor Grade III SGSs, some authors [9] prefer combined LTR and LTP techniques, which may require an anterior graft along with a simple posterior cricoid split supported by an endoluminal stent. The space created between the two cricoid laminae is filled in progressively by granulation tissue, and then by scar tissue. Stenting must be maintained over a sufficient duration (3 to 6 months) until mature scar tissue is obtained so as to prevent secondary scar contraction after stent removal. As costal cartilage graft harvesting is necessary for keeping the anterior cricoid expanded, it is preferable to perform combined posterior and anterior costal
19.4 Laryngotracheoplasty Without Cartilage Expansion
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Fig. 19.1 Laryngotracheoplasty without cartilage expansion: (a) Posterior cricoid split without rib grafting: The anterior midline incision is not extended cranially beyond the anterior commissure in order to preserve optimal steadiness of the laryngeal framework. The posterior cricoid plate is divided vertically in the midline, and curved haemostats are used to spread apart the
two cricoid laminae. Stenting with an LT-Mold is recommended. (b) Four-quadrant division of the subglottis: in addition to the combined anterior and posterior cricoid divisions, lateral transcartilaginous splits are made at 3 and 9 o’clock to further expand the subglottic airway. Long-term stenting is mandatory
cartilage grafting immediately. Reepithelialisation over the costal cartilage perichondrium and maintenance of an adequate posterior interarytenoid space are achieved more safely than with simple division and stenting. Additionally, the cartilage grafts help stabilise the airway reconstruction, thus preventing, to some extent, potential laryngeal distortion after stent removal. The surgical steps for LTP are similar in every respect to those described for LTR (see Sect. 19.5), except that no cartilage graft is employed to keep the airway expanded. If a posterior cricoid split is sufficient to expand the narrowed subglottic airway, then a full laryngofissure should be avoided in order to keep a stable anterior framework of the larynx (Fig. 19.1a). This usually requires longer periods of airway stenting until mature scars are formed. Reactivation of inflammatory processes during upper airway infections is likely to lead to restenosis, necessitating revision surgery later in life.
In many centres, the anterior cricoid split (ACS) operation in neonates is being replaced by LTR with anterior costal cartilage graft (ACCG), as this procedure yields improved results and fewer complications (see Sect. 14.3.2, Chap. 14). With the advent of PCTR and extended PCTR for severe primary or recurrent fibrotic SGSs, the four-quadrant split procedure is now reserved for cases where all other reconstructive and resection procedures have failed. Nevertheless, some centres still use this technique as the primary surgery for severe SGSs [7]. As described by Cotton et al. [21], lateral cuts are made at the 3 and 9 o’clock positions, taking care not to transect the outer perichondrium of the cricoid cartilage that protects the recurrent laryngeal nerves (RLNs) [89] (Fig. 19.1b). Of note is that the author has no experience with the four-quadrant split procedure. For very severe SGS grades requiring a four-quadrant division of the subglottic airway, PCTR or extended PCTR is more likely to achieve
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improved results without the necessity of prolonged endoluminal stenting, as long as segmental airway resection is feasible.
19.5 Laryngotracheal Reconstruction (LTR) with Cartilage Expansion This operation consists of augmenting the laryngotracheal complex by an anterior or posterior midline incision of the cricoid cartilage, along with insertion of cartilage grafts, in order to expand the airway. In the 1970s, during the first decade of the pioneering work on LTR, several grafting materials were tested in both adults and children: costal cartilage [14, 28], thyroid cartilage [35, 37], composite nasal septal cartilage [30], auricular cartilage [53, 61], nasal septal cartilage [86], hyoid bone [80] and mucoperichondrial grafts from the nasal septum [48, 85]. Costal cartilage is considered the best grafting material, due to its rigidity and availability in large quantities. Furthermore, costal cartilage can be easily trimmed and shaped to fit into any desired reconstruction area. Because of its versatility, the majority of paediatric airway surgeons prefer to use this graft instead of other types of grafts. As an exception to this rule, however, thyroid cartilage is preferred as graft material following an anterior cricoid split in premature neonates who have failed multiple extubation attempts (see Sect. 14.3.2, Chap. 14).
19.5.1 Surgical Steps for LTR 19.5.1.1 Cervical Exposure of the Larynx and Trachea A collar incision is made, placed at the superior edge of the tracheostoma, and a subplatysmal flap is elevated cranially up to the level of the hyoid bone. The strap muscles are separated from the midline and reflected laterally. At this stage, a Lone Star disposable retractor ring with elastic stay hooks (Lone Star Medical Products, Stanford, TX 477 USA) may be used rather than manual retractors, thereby reducing the number of assistants required for the surgical procedure.
The thyroid isthmus is divided and retracted laterally. The cricothyroid muscles are carefully preserved. Meticulous dissection is mandatory for controlling the feeding vessels from the thyroid capsule. This provides an optimal view of the airway, from the hyoid bone down to the tracheostoma. In infants, the thyroid cartilage, concealed behind the hyoid bone, must be released by incising the thyrohyoid membrane along its upper rim so as to move it into the surgical field. The thyrohyoid muscles are carefully preserved.
19.5.1.2 Anterior Laryngotracheofissure The length of the vertical midline incision of the airway depends on preoperative endoscopic findings as regards the glottis and subglottis. For isolated SGS, the incision typically extends through the lower third of the thyroid cartilage, the cricothyroid membrane, the anterior cricoid arch and the upper two or three tracheal rings. For an SGS involving the glottis (PGS, VC synechia and CAA), the incision must be extended into a full laryngofissure to provide optimal exposure of the cricoid plate for the posterior cricoid split and adequate room for fixing the posterior costal cartilage graft into position (Fig. 19.2). Great care must be taken to divide the thyroid alae directly in the midline at the anterior commissure. When the VCs and anterior laryngeal commissure are intact, this procedure is carried out from below by palpating the slit of the anterior commissure with a blunt elevator. If the VCs are fused together by acquired synechiae or congenital webs, the airway is opened through the epiglottis slightly cranially to the thyroid notch. Skin hooks are used to improve supraglottic exposure, and section of the thyroid cartilage is made under visual control from cranial to caudal, thereby dividing the fused vocal cords exactly in the midline. Peroperative endoscopy has been recommended, allowing for adequate visualisation of the anterior commissure on the monitor when performing the laryngofissure [89]. Yet, this technique is substantially more cumbersome, and the tip of the endoscope often becomes blurred with blood.
19.5.1.3 Posterior Cricoid Split The posterior cricoid split must be carried out precisely in the midline and strictly perpendicular to the
19.5 Laryngotracheal Reconstruction (LTR) with Cartilage Expansion
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Fig. 19.2 Full laryngotracheofissure for subglottic stenosis combined with glottic involvement: (a) The incision is first made just above the thyroid notch in order to provide complete visualisation of the glottis during the midline laryngofissure. The posterior cricoid split must be placed precisely in the midline. The cuts should be perpendicular to the plane of the cricoid plate. (b) Results after posterior costal cartilage grafting: The interarytenoid and subglottic spaces have been enlarged
plane of the cartilage. Great care must be taken to ensure that the retrocricoid mucosa is not harmed, and that the incision is placed through the raphe of the posterior cricoarytenoid muscles. A blunt, curved haemostat is used in order to spread apart the divided cricoid laminae until the desired width is obtained (see Fig. 19.2). Cranially, the incision must extend into the interarytenoid region by incising fibrous tissue and fully transecting the interarytenoid muscle without entering the pharynx. Caudally, the vertical incision should be prolonged for 5–10 mm into the membranous tracheal wall, while incising the fibrous attachment of the party wall to the cricoid plate. This is essential for adequate distraction for placing the cartilage graft.
19.5.1.4 Costal Cartilage Graft Harvesting Prior to surgery, the thoracic region is draped separately and isolated with adhesive plastic sheeting (Steridrape). A horizontal 2–3 cm long incision is
made in the skin crease below the mammary gland, starting medially at the bony-cartilaginous junction to its sternal attachment. The subcutaneous fatty tissue is then dissected and retracted to expose the thoracic wall. The costal cartilage is usually flat or slightly concave medially in the lower sternal insertion. This favourable configuration can easily be palpated, which allows the surgeon to select the best site for harvesting the graft, usually at the level of the seventh to eighth or ninth ribs (Fig. 19.3). Furthermore, the costal cartilages are often fused together at this level, thus allowing the selection of the appropriate width of the cartilage graft. Once the proper area for harvesting has been selected, the muscles attached to the rib cage are cauterised and sectioned, with careful preservation of the perichondrium on the rib cartilage. Using a #15 blade, the perichondrium is incised at mid-distance of the rib thickness on both superior and inferior edges, and a small elevator is used to dissect the rib cartilage in a subperichondrial plane on the inner surface (Fig. 19.4). The entire length of the costal cartilage is prepared and later sectioned at both extremities,
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19.5.1.5 Carving the Posterior Costal Cartilage Graft
Fig. 19.3 Costal cartilage graft harvesting: the seventh, eighth and ninth rib cartilages frequently present a flat and slightly concave surface at the bony-cartilaginous junction to the sternum. As they are often fused together, they provide adequate width for the graft
depending on the required length. Usually, a 3–4 cm long segment of rib cartilage may be obtained. If necessary, a second rib cartilage is harvested above or below the initial site. Meticulous dissection in the proper plane helps maintain a bloodless operative field. Lastly, the surgical wound is filled with sterile saline solution to verify that no pneumothorax has occurred. A manovac drain is inserted into the bed of the wound, and a three-layer closure is performed using absorbable sutures.
Fig. 19.4 Technique for obtaining a costal cartilage graft: (a) Incision at mid-distance of the rib thickness on the superior and inferior borders of the costal perichondrium. (b) Dissection in a subperichondrial plane on the deep chest surface and transsec-
The cranio-caudal distance as well as the thickness of the cricoid plate must be measured with precision prior to carving the costal cartilage graft. For PGS, the graft must be rectangular in shape. When the interarytenoid distance is normal, and posterior grafting is aimed at enlarging an isolated SGS, the upper extremity of the CCG must be slightly trimmed in a conical fashion to avoid overexpansion of the interarytenoid distance, which results in poor postoperative voice quality. For rectangular CCGs, the graft is cut to the appropriate length, corresponding to the height of the cricoid lamina, while at the same time keeping small, 1-mm long flanges of perichondrium on its inner side. According to Cotton [89], the width of the graft should correspond to approximately 1 mm for each year of age (up to 10 mm), however, the smallest graft should not be narrower than 4 mm, which corresponds to the interarytenoid distance of the glottis in neonates. The graft is first trimmed to a thickness that corresponds to that of the cricoid plate, with an additional 1 or 2 mm for the posterior lateral flanges. The lateral cuts for trimming the graft to the appropriate final size are made at the end by removing a rectangular piece of cartilage laterally on the perichondrial side in order to design the flanges of the cartilage graft (Fig. 19.5). Ideally, the graft should fit flush between the two cricoid laminae, with the perichondrium facing the lumen. If the width of the rib cartilage is not sufficient to create the lateral flanges of the CCG, then the cartilage is shaped into a simple rectangular piece, with strong perpendicular cuts providing the best contact with the
tion of the cartilage at both extremities. A 2–4 cm long costal graft can usually be obtained. (c) Axial view of subperichondrial dissection on the deep chest surface
19.5 Laryngotracheal Reconstruction (LTR) with Cartilage Expansion
Fig. 19.5 Design of the posterior cartilage graft: (a) The cartilage must be trimmed to the appropriate thickness (~cricoid plate plus 1 or 2 mm) by removing cartilage on the side opposite
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to the perichondrium. (b) Additional removal of lateral wedges of cartilage in order to design a rectangular graft with flanges of cartilage postero-inferiorly and laterally
For more complex glotto-subglottic stenoses (VC synechiae or webs) or severe posterior glottic stenoses (PGSs), with or without cricoarytenoid ankylosis (CAA), the anterior cricoid split must be extended into a full laryngofissure.
19.5.1.6 Fixing the Posterior Costal Cartilage Graft (Fig. 19.7)
Fig. 19.6 Distorted laryngeal framework after failed primary laryngotracheal reconstruction: recurrent glotto-subglottic stenosis with overlapping arytenoids
incised surface of the divided cricoid laminae. Meticulous suturing is essential to prevent any tilting of the graft into the subglottic lumen. However, despite stenting, the combined anterior and posterior division of the airway may destabilise the laryngeal framework and lead to cartilage migration, resulting in a distorted larynx (Fig. 19.6). To avoid this complication, incomplete laryngofissure has been proposed if glottic involvement is limited to posterior commissure scarring. Although exposure is limited, a posterior cricoid split with cartilage grafting is still possible, albeit without cranial fixation of the cartilage. The rectangular costal cartilage graft is simply slid into position from caudal to cranial, with lateral flanges resting behind the denuded cricoid laminae. The advantage of this technique is the preservation of an intact anterior laryngeal commissure and a steady laryngeal framework.
After confirming the size and shape of the costal cartilage, 4.0 or 5.0 vicryl sutures are placed through the graft. Every stitch must enter the cartilage graft on the perichondrial side and emerge exactly at the angle created by the posterior flanges of the graft (Fig. 19.7a). Multiple punctures must be avoided to prevent breakage of the cartilage and subsequent necrosis. If lateral flanges could not be shaped in the posterior costal cartilage graft, then the stitch must emerge at a 1-mm distance from the posterior angle of the graft on its dorsal side. Exact positioning of the stitch through the cricoid lamina is best achieved by lifting up the cricoid lamina using a skin hook. This permits rotation of the hemicricoid, facilitating the placement of subsequent stitches (Fig. 19.7b). The four stitches are placed in the same manner, with the knots tied inside the lumen (Fig. 19.7c). At the upper and lower extremities of the cartilage graft, the mucosae of the interarytenoid region and membranous trachea are sutured with 5.0 or 6.0 vicryl stitches to the perichondrium of the graft facing the lumen. This step is instrumental in improving tightness of the mucosal-perichondrium interface, thus preventing superinfection of the graft. Additionally, fibrin-thrombin glue (Tisseel® or Tissucol®) is applied to the perichondrium in order to promote reepithelialisation from the edges of the reconstructed area.
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Fig. 19.7 Diagrammatic representation of suturing the posterior graft into position: (a) The needle must be inserted through the perichondrium and emerge exactly at the angle created by the lateral flanges of the cartilage. Four stitches are sufficient to stabilise the graft. (b) Correct placement of the stitches through the cricoid plate: The edge of the cricoid lamina is lifted using a skin
hook. The needle is inserted obliquely from the postero-inferior crest of the cricoid plate so as to fit exactly the height of the costal cartilage graft. (c) Final result in cross section with additional anterior graft. Note the exact placement of the stitches, which is different for anterior and posterior costal cartilage grafts
19.5.1.7 Selecting Appropriate Stent Materials
lengths are available, providing the ability to accommodate different tracheal lengths in relation to the stoma site.
If a single-stage procedure is planned for a limited reconstruction with posterior grafting alone (i.e., PGS without significant SGS), then nasotracheal intubation using a soft Portex Blue Line® Tube matching the child’s age is selected. The tracheostomy cannula is then removed, the ET tube is pushed into the distal trachea, and the tracheostoma is closed by placing stitches in the cranio-caudal axis. An additional anterior costal cartilage graft (ACCG) is often necessary in order to maximise anterior airway expansion at the stoma site. If, due to the complexity of the underlying condition (SGS associated with severe PGS, CAA or VC synechiae), long-term stenting is required, then an appropriate LT-Mold must be selected. Gauges are used to determine the proper diameter and length of the LT-Mold stent, and the distal extremity should fit flush with the upper edge of the tracheostoma (Fig. 19.8). For a given prosthesis size, four different
Fig. 19.8 Metallic LT-Mold gauges for intra-operative use: during the surgery, these LT-Mold gauges allow for proper selection of the prosthesis size to fit the reconstructed airway in calibre and length
19.5.1.8 Stent Fixation and Closure of Laryngofissure Before closing the laryngofissure, the LT-Mold stent must be carefully fixed using non-resorbable 4.0 or 3.0 prolene sutures. Precise reconstruction of the anterior laryngeal commissure is essential. This is achieved using 4.0 or 5.0 vicryl sutures, placed submucosally through the thyroid cartilage, at the vocal cord level. The 3.0 prolene stitch is placed horizontally through the tracheal wall and the prosthesis at mid-distance from the cricoid ring to the upper pole of the tracheostoma. An additional 5.0 resorbable vicryl suture is applied in order to affix the anterior commissure of the LT-Mold to that of the reconstructed larynx. Although
19.5 Laryngotracheal Reconstruction (LTR) with Cartilage Expansion
this stitch is reabsorbed before the LT-Mold is removed, proper placement of the prosthesis at the anterior commissure is facilitated by this stitch during the first few weeks after stenting. The LT-Mold is not fixed until the laryngofissure is fully reconstructed and closed, usually with 4.0 vicryl sutures. In the supraglottis, the epiglottic petiole must be fixed anteriorly to the thyroid cartilage by mattress pexy sutures in order to avoid epiglottic prolapse and supraglottic narrowing. If the subglottic space is large enough, and closure may be achieved in the midline without undue tension, then closure of the laryngotracheofissure is performed, after verifying that proper restoration of the anterior laryngeal commissure is achieved. Care should be taken not to overtighten the 3.0 prolene stitches used to fix the LT-Mold in place, in order to avoid any ischemia of the reconstructed airway. Following placement of the LT-Mold stent and restoration of a sharp anterior laryngeal commissure, some cases may require additional anterior grafting. The oval-shaped residual anterior opening reflects the exact shape and size of the anterior graft needed.
19.5.1.9 Carving and Positioning the Anterior Costal Cartilage Graft Precise measurement of the oval defect in the anterior subglottis and trachea is essential. This measurement should be taken while a properly sized stent expands the airway to its normal size, leaving an anterior defect in the exact size of the graft needed. The costal cartilage is carved to a boat-shaped graft, keeping large flanges all around the designed graft, as shown in Fig. 19.9.
Fig. 19.9 Carving of the anterior cartilage graft: (a) On the perichondrial side, a boat-shaped template is drawn to match exactly the anterior laryngotracheal defect, preserving superior, inferior and lateral flanges of the cartilage. (b) Results after proper carving of the anterior costal cartilage graft
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The perichondrial side of the graft should face the lumen, and the thickness of the boat-shaped portion of the graft should match as closely as possible that of the subglottic and tracheal walls. The large flanges of cartilage are likely to prevent prolapse of the graft into the airway, once the stent is removed. 19.5.1.10 Positioning and Fixing the Anterior Costal Cartilage Graft The 4.0 vicryl stitches used to suture the graft into position are placed from the outside to the luminal side of the ACCG. The stitches must emerge exactly at the angle created by the perichondrial interface, with the cut edge of the boat-shaped portion of the ACCG, as shown in Fig. 19.10. The same principle holds here as for the posterior graft. The corresponding stitch through the tracheal or cricoid wall is placed to exactly match the thickness of both the ACCG and the wall of the reconstructed airway (see Fig. 19.7c). This precise approximation facilitates the reepithelialisation process over the perichondrium of the cartilage inset (Fig. 19.11). 19.5.1.11 Neck Closure A Penrose drain is placed in the tracheal bed without contacting the cartilage graft. The thyroid lobes are slightly mobilised, and the thyroid isthmus is resutured over the cartilage graft in order to maintain an optimal vascular supply to the reconstruction. The strap muscles are sutured on the midline, and the skin is closed in two layers (Figs. 19.12 and 19.13).
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Fig. 19.10 Correct placement of stitches through the boatshaped anterior costal cartilage graft for laryngotracheal reconstruction: the stitch, inserted through the dorsal portion of the cartilage, must emerge exactly at the edge of the perichondrium on the boat-shaped portion of the costal cartilage graft
Fig. 19.12 Laryngotracheal reconstruction with anterior costal cartilage graft for Grade II congenital subglottic stenosis: (a) Preoperative view: elliptical cricoid. (b) Postoperative view at 3 months: large, round-shaped subglottis with perfect integration of the anterior costal cartilage graft (dotted white line)
19.6 Single-stage Laryngotracheal Reconstruction (SS-LTR)
Fig. 19.11 Double-stage laryngotracheal reconstruction with anterior costal cartilage graft: the costal cartilage graft is sewn into position, with the perichondrium facing the lumen. Large cartilage flanges prevent prolapse of the costal cartilage graft into the airway. For details on suturing in cross section, refer to Fig. 19.7c)
Various conditions must be met before considering SS-LTR: 1. The patient must not present significant congenital anomalies, pulmonary, cardiac and neurological abnormalities, or mental disabilities.
19.6 Single-stage Laryngotracheal Reconstruction (SS-LTR)
269
Fig. 19.13 Laryngotracheal reconstruction for Grade III subglottic stenosis combined with posterior glottic stenosis: (a) Preoperative view: the posterior glottic stenosis is thin, and the cricoarytenoid joints are passively mobile during palpation.
(b) Postoperative view at 3 months: restoration of an adequate airway following laryngotracheal reconstruction with anterior and posterior costal cartilage grafts, and 1-month stenting using an LT-Mold
2. The stenosis must involve only one airway level (i.e., isolated PGS or isolated SGS), and the SGS must be mild-Grade III (~75% luminal obstruction), or less. 3. The tracheostoma, if present, must be close to the SGS, and thus easily included in the reconstructed area (see Sect. 14.3.4, Chap. 14). 4. Adequate airway reconstruction must be possible with a single (anterior or posterior) CCG to preserve optimal steadiness of the laryngeal framework. If posterior grafting is necessary, then the anterior midline division of the cricoid and upper tracheal rings should not be extended into a full laryngofissure. Although an SS-LTR with combined anterior and posterior CCG can be performed, the risk of postoperative distortion of the reconstructive airway is greater should a full laryngofissure be necessary. A 7-day stenting period with an ET tube is generally sufficient for an anterior graft alone, but the stenting time must be extended to at least 14 days for a posterior graft alone or a combined anterior-posterior graft. Postoperative sedation without administering paralysing agents is sufficient in most cases.
during the same surgical session. To this end, two modifications to the surgical procedure are necessary:
19.6.1 Surgical Steps of Single-Stage Laryngotracheal Reconstruction (SS-LTR) The surgical steps of single-stage and double-stage LTR are similar, except that in SS-LTR, the tracheostoma is included into the reconstruction and closed
1. The ACCG must be longer and shaped in a more triangular fashion to accommodate the round opening of the tracheostoma caudally. A significant distal flange of cartilage must be preserved to avoid graft prolapse into the lumen at the stoma site. If the long rib cartilage is slightly bowed and does not adapt to the anterior subglottic defect, then small transverse wedge excisions of cartilage are performed opposite to the perichondrial side, in order to flatten the cartilage for approximation with the anterior tracheal wall (Fig. 19.14). The graft is sutured in place using the previously described technique. 2. An ET tube must be inserted during surgery, while the tracheostomy ventilating tube is removed. For an anterior graft alone, this can be done immediately after splitting the airway open. A normal sized ET tube corresponding to the patient’s age must be easily passed into the lower airway. The expanded subglottis provides an adequate estimate of the length and width of the ACCG to be harvested for the reconstruction. For a posterior graft alone or a combined posterior– anterior graft, the ET intubation is performed after the posterior graft has been sutured into position. After performing a posterior cricoid split and expansion of the cricoid lamina, the ET tube is first inserted into the larynx. Through the anterior subglottic opening, the tip of the ET tube is recaptured in the operative field and secured with a mercilene thread placed at its most distal extremity (not through the Murphy’s eye). The ET tube is then withdrawn by the anaesthetist into the pharynx,
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Nevertheless, the surgeon should not hesitate to resort to a double-stage LTR in the case of severe, multilevel or hyper-reactive stenosis, or in the presence of significant comorbidities. Another factor pertinent to the decision-making process is the expertise of the surgical, anaesthesiological and PICU teams. A DS-LTR may be preferred to a SS-LTR by a less experienced group.
Box 19.3 and 19.4 Surgical Highlights for LTR
Fig. 19.14 Single-stage laryngotracheal reconstruction with anterior costal cartilage graft: the shape of the cartilage inlet is more triangular in order to accommodate the round opening of the tracheostoma. The anterior costal cartilage graft is sutured into position, including the tracheostomy site. The suturing technique is identical to that used for double-stage surgery
with the leading thread lifted towards the anterior commissure to provide a free operative field for the posterior costal cartilage grafting. Upon completion of this procedure, the ET tube is gently advanced into the subglottis by pulling on the mercilene thread, ensuring that the bevelled tip of the tube does not get stuck in a ventricle. After removing the ventilating tube of the tracheostoma, the ET tube is gently pushed into the distal airway. Anterior costal cartilage grafting may then be performed, as previously described. Due to the absence of a tracheostoma, which perpetuates the risk of suprastomal collapse and bacterial contamination, the use of an SS-LTR facilitates the healing process, resulting in improved postoperative outcomes. Moreover, to the patient’s benefit, single-stage surgery helps shorten tracheostomy dependency.
• Do not perform a full laryngofissure for anterior or posterior CCG alone • Extend the midline thyrotracheal incision from the lower third of the thyroid cartilage down to the first two tracheal rings for a simple LTR with ACCG alone • Avoid incising the thyroid cartilage cranially to the anterior commissure of the vocal cords (middistance from the thyroid notch to the inferior border of the thyroid cartilage) in order to preserve good voice quality • Extend the vertical midline thyrotomy into a full laryngofissure for a combined ACCG and PCCG • Carefully divide the thyroid cartilage in the midline in order to preserve an intact anterior laryngeal commissure • Extend the posterior cricoid split through the transverse interarytenoid muscle in the case of posterior glottic scarring • Harvest the rib cartilage with the perichondrium on its flat or slightly concave surface • Systematically check for pneumothorax after harvesting a CCG • Carve the PCCG in a rectangular fashion with the perichondrium facing the lumen and preserve lateral flanges of cartilage in order to wedge the graft between the two divided cricoid laminae • Carve the ACCG in an oval shape on the perichondrial side and preserve flanges of cartilage on the opposite side in order to avoid prolapse of the ACCG into the airway • Always place the perichondrial side of the CCG intraluminally
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19.8 Results of Laryngotracheal Reconstruction (LTR)
• Select an appropriate stent shape, diameter and length in order to splint the reconstructed airway • For single-stage LTR, avoid full laryngofissure in order to maintain optimal laryngeal stability • Carve and suture the ACCG into position after reintubation with a normal size ET tube, corresponding to the patient’s age, in the case of SS-LTR
19.7 Postoperative Care and Complications The duration of postoperative surveillance in the PICU or semi-ICU depends on the child’s age and the type of surgery (SS-LTR vs. DS-LTR) performed. A postoperative chest film is routinely taken to rule out pneumothorax (after rib cartilage harvesting) or atelectasis from plugged bronchial secretions or blood clots. To prevent this latter complication, rinsing with a saline solution at the end of surgery is recommended, as is the suctioning of mucus plugs or blood clots that may have migrated from the operative field into the distal airway. Antibiotics and PPIs, initiated prior to surgery, are continued and adjusted during postoperative follow-up as necessary (in the case of superinfection, change in bacteriological sensitivities, need for increased PPI dosage or adjunction of H2-blockers). Inspection of the neck for subcutaneous emphysema, haematoma, seroma or superinfection is carried out over 10 days. After the child has stabilised, even following an SS-LTR, he or she is transferred to the ward. With proper postoperative care, a conscious patient may tolerate the nasotracheal tube used for splinting in SS-LTR. However, proper humidification and saline instillation into the ET tube are critical in order to avoid clogging of the ET tube by dried secretions. Proper monitoring by parents and nursing personnel is a prerequisite for a successful surgical outcome. The Penrose drain is removed when the dressing is dry, typically after 48 h. Special attention is given in the case of double-stage reconstructions with stenting, when the caudal extremity of the anterior costal cartilage graft abuts the upper edge of the tracheostoma. Indeed, the cartilage graft is at high risk of superinfection, due to the
proximity of the tracheostomy cannula. Because of improved awareness among the medical community, proper tracheostomy placement (see Sect. 14.3.4, Chap. 14) is likely to improve surgical outcomes following LTR and PCTR. A tracheostoma located at a distance from the reconstructed subglottis favours wound healing, in contrast to the conventionally placed tracheostoma at the second to third tracheal rings, with suprastomal collapse reaching the reconstructed site. Typically, early complications are linked to pulmonary or operative site problems. During the first week, the neck must be inspected twice daily. Parents are instructed to look for signs of local complications after hospital discharge. Such signs include neck swelling and tenderness with erythema due to late superinfection of the graft, or stent migration in the case of double-stage surgery. The rate of graft failures after LTR is estimated to be approximately 2% [27]. Moreover, pneumothorax, atelectasis and bronchopneumonia must be regularly searched for. Numerous causes of failure following LTR have been described in the literature [27]. Overall failures account for 10–20% of the reported series [22, 43, 62, 87], with most occurring after primary surgery for isolated Grade III/IV SGS or SGS with associated glottic involvement [41]. Refinements of the therapeutic steps (preoperative evaluation, surgical technique and postoperative care) have led to improved outcomes [73]. Nonetheless, in spite of attention to detail, a significant number of reconstructions still fail, particularly in cases of severe Grades III or IV SGS (even without associated glottic involvement) [43]. Revision surgery is necessary in up to 70% of Grade IV SGSs, primarily treated using LTR [41].
19.8 Results of Laryngotracheal Reconstruction (LTR) The comparison of worldwide experience in airway reconstruction surgery (ARS) for paediatric airway stenosis is a difficult task. Indeed, because various conditions may lead to the same Myer-Cotton stenosis grade, very large sample sizes are required to allow for patient stratification into comparable subgroups (Table 19.1). Except for Cincinnati, where on average 100 airway reconstruction procedures are performed every year [43], other major institutions perform
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Table 19.1 Variables influencing outcomes of airway recon structions for the same initial grade of airway stenosis [60] • Primary versus salvage surgery • Isolated SGS versus SGS combined with glottic involvement ± cricoarytenoid joint fixation • Single-stage versus double-stage surgery • No comorbidities versus additional comorbidities • LTR versus PCTR
fewer interventions, ranging from 10 to 20 ARSs per year in the reported series [62, 65, 87]. The publications involved a heterogeneous patient population with respect to the pathology and surgical strategy (i.e., SGS of different grades, with or without glottic involvement, single- or double-stage surgeries, patients with or without comorbidities), with overall decannulation rates being used as the primary outcome measure [7, 11, 33, 38, 55, 73, 74, 77, 78, 81, 88]. Consequently, experience is limited and widely dispersed. When outcome assessment is based on patient or disease characteristics, this inevitably leads to smaller patient groups, which are irrelevant from a statistical perspective. A worldwide uniform reporting system is mandatory in order to gather accurate information on disease-specific outcomes of ARS in the paediatric age group. This would enable the surgeon to predict the ARS outcome when discussing the intervention with the child’s parents (Table 19.2). To date, only one published report has involved a sufficiently large number of patients with homogenous inclusion criteria (i.e., isolated SGS), permitting the analysis of operation-specific and overall decannulation or extubation rates after ARS [43]. In this series, data on 1,296 ARSs was collected over a 12-year period (1988 to 2000) and stratified into grade-specific decannulation or extubation rates after double-stage (DS) or single-stage (SS) LTRs. This series contained 199 LTRs for a sole diagnosis of SGS (i.e., without supraglottic, glottic or upper tracheal disease). The results are shown in Table 19.3. Single-stage LTRs were selected for less severe grades of SGS when compared to DS-LTRs (49% vs. 22% for Grade II SGSs and 51% vs. 78% for Grades III–IV SGSs, respectively). Data analysis showed that approximately half of the patients required revision surgery after doublestage surgery, compared to only 18% after single-stage surgery. The operation-specific and overall decannulation rates for combined DS- and SS-LTRs were 65% (121/187 cases) and 87% (162/187 cases), respectively.
Single-stage LTR is preferred in the case of less severe SGS grades (Grades I and II and some minor Grade III). The likelihood of reintubation or secondary tracheostomy during the postoperative period is higher with anterior and posterior costal cartilage grafting when performed for severe Grades III or IV SGS. The overall decannulation rate reported in the literature for SS-LTR ranged from 84% to 96%, with 70% of the cases pertaining to Myer–Cotton Grades I or II SGS [10, 22, 42, 52, 58, 79, 82, 91]. One-third of the patients needed reintubation and approximately 15% required tracheostomies. In children younger than 4 years of age, those with a gestational age of less than 30 weeks, and those presenting moderate to severe tracheomalacia, the likelihood of successful extubation was decreased. Upon analysis of the three largest series involving LTR for Grades II–IV SGSs (Table 19.4), the operation-specific and overall decannulation rates were 68% (range: 65–70%) and 89% (range: 87–95%), respectively. In the published series, the failure rate after first surgery was 33% (range: 30–35%) (Table 19.5). To achieve the overall decannulation rates listed in Table 19.4, one to four additional open procedures (with an average of 1.4 per child) were necessary. When compared to Grade II SGS, operation-specific and overall decannulation rates following LTR tended to be less optimal in patients with Myer–Cotton Grades III and IV SGS, except for cohorts too small for stringent data analysis (see Table 19.3). This again illustrates the difficulty in gathering data from a single institution, albeit with the largest series worldwide. In 2001, the same group [41] published a report on 56 cases with Grade IV SGS recruited over a 20-year period. Among this patient population, 39 (70%) required more than one procedure (range: 2–9 open surgeries) for achieving decannulation, the mean time to decannulation being 28 months (range: 0.1– 120 months). With increasing expertise, the decannulation rate following LTR for Grade IV SGS improved from 67% in the 1980s to 86% in the 1990s. In the same article, the authors reported a decannulation rate of 92% after PCTR for Grade IV SGSs versus 81% after LTR, with 18% versus 46% revision surgery rates, respectively. These findings supported the use of PCTR for severe Grades III and IV SGSs, as previously advocated by several authors [59, 69, 83, 88]. In conclusion, PCTR is now widely accepted as the treatment of choice for severe Grades III and IV SGS in the paediatric age group.
273
19.8 Results of Laryngotracheal Reconstruction (LTR) Table 19.2 Reporting system for airway reconstructions • Subglottic stenosis Grade
I
II
III
IV
• Glottic involvement > Absent
> Posterior glottic stenosis
> VC synechia or web
> Transglottic stenosis (supraglottic, glottic, subglottic)
• Impairment of VC mobility > Neurogenic
> Cicatricial
> Combined
> Unilateral
> Bilateral
• Comorbidities
> Airway: – OSA-related obstruction – Tracheal stenosis/malacia
> Patient: – respiratory insufficiency (O2 dependence)
– Severe cardiovascular anomaly
– Neurologic, mental impairment
– Severe GORD, eosinophilic oesophagitis
– Severe syndromic/non-syndromic anomalies
• New Myer-Cotton airway grading system: Ia
Ib
Ic
Id
IIa
IIb
IIc
IId
IIIa
IIIb
IIIc
IIId
IVa
IVb
IVc
IVd
Isolated SGS
SGS + comorbidities
SGS + glottic involvement
SGS + comorbidities + glottic involvement
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Table 19.3 Results of the Cincinnati experience in 199 LTRs for a sole diagnosis of SGS[43] Myer–cotton Grade Double-stage LTR (n = 101) Single-stage LTR (n = 98) OP specific DR Overall DR OP specific DR II
III
IV
II, III, IV
Revision surgery
Overall DR
85%
95%
82%
100%
(18/21)
(20/21)
(37/45)
(45/45)
37%
74%
79%
86%
(23/61)
(45/61)
(34/43)
(37/43)
50%
86%
67%
100%
(7/14)*
(12/14)*
(2/3)*
(3/3)*
~ 50%
~ 80%
~ 80%
~ 93%
(48/96)
(77/96)
(73/91)
(85/91)
48% of all cases~ 1.6 per child
18% of all cases~ 1.3 per child
OP = Operation DR = Decannulation rate * = Please note the small numbers
Table 19.4 Operation-specific and overall decannulation rates of LTRs from the largest world series Myer–cotton GOS* 1992 London [65] Robert-Debré 1999 Paris [62] CCHMC 2001 Cincinnati [43] Grade* OP specific DR Overall DR Op specific DR Overall DR OP specific DR Overall DR II
NR
89%(41/46)
83%(30/36)
NR
83%(55/66)
95%(65/66)
III
NR
78%(21/27)
75%(33/44)
NR
55%(57/104)
79%(82/104)
IV
NR
50%(4/8)
24% (5/21)
NR
53%(9/17)
88%(15/17)
II, III, IV
70%
81%
68%
NR
65%
87%
+
*GOS (Great Ormond Street) series used the old Cotton airway grading system (ref 7, chapter 5) + The overall DR is reported to be 89%, some Grade I falling into Grade II SGS in the Myer–Cotton airway grading system ([22], Chap. 5) OP = Operation DR = Decannulation rate NR = not reported
Table 19.5 Surgical failures after primary* LTRs Institution Failure rate
GOS 1992 London [64] 30% (32/108)
Robert-Debré 1999 Paris [62] 33% (33/101)
CCHMC 2001 Cincinnati [43] 35% (66/187)
Distribution according to Myer–Cotton Grade+
II: 57%
II: 36%
II: 35%
III: 33%
III: 44%
III: 56%
IV: 10%
IV: 20%
IV: 9%
NR
1.18
1.49
Average nb. of revisional surgeries per child
GOS = Great Ormond Street *Primary = first surgery of the published series, not primary operation on a child’s airway + The old Cotton airway grading system was used in the GOS series + The new Myer–Cotton airway grading system was used in the Paris and Cincinnati series
References
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39. Gaudet, P.T., Peerless, A., Sasaki, C.T., et al.: Pediatric tracheostomy and associated complications. Laryngoscope 88, 1633–1641 (1978) 40. Grahne, B.: Operative treatment of severe chronic traumatic laryngeal stenosis in infants up to three years old. Acta Otolaryngol. 72, 134–137 (1971) 41. Gustafson, L.M., Hartley, B.E., Cotton, R.T.: Acquired total (grade 4) subglottic stenosis in children. Ann. Otol. Rhinol. Laryngol. 110, 16–19 (2001) 42. Gustafson, L.M., Hartley, B.E., Liu, J.H., et al.: Singlestage laryngotracheal reconstruction in children: a review of 200 cases. Otolaryngol. Head Neck Surg. 123, 430–434 (2000) 43. Hartnick, C.J., Hartley, B.E., Lacy, P.D., et al.: Surgery for pediatric subglottic stenosis: disease-specific outcomes. Ann. Otol. Rhinol. Laryngol. 110, 1109–1113 (2001) 44. Hof, E.: Surgical correction of laryngotracheal stenoses in children. Prog. Pediatr. Surg. 21, 29–35 (1987) 45. Holinger, P.H., Johnston, K.C.: The management of chronic laryngeal stenosis. Ann. Otol. Rhinol. Laryngol. 67, 496– 515 (1958) 46. Jackson, C.: Stenosis of the larynx with special reference to curative treatment with core moulds. Trans. Am. Laryng. Rhin. Otol. Soc. 42, 12–24 (1936) 47. Killian, G.: On the treatment of laryngeal tuberculosis. Dtsch Med. Wochenschr. 38, 585–589 (1912) 48. Krizek, T.J., Kirchner, J.A.: Tracheal reconstruction with an autogenous mucochondrial graft. Plast. Reconstr. Surg. 50, 123–130 (1972) 49. Lapidot, A., Sodagar, R., Ratanaprashtporn, S., et al.: Experimental repair of subglottic stenosis in piglets. “Trapdoor” thyrochondroplasty flap. Arch. Otolaryngol. 88, 529–535 (1968) 50. Laurens, G.: Chirurgie de l’oreille, du nez, du pharynx et du larynx. Masson et cie, Paris (1924) 51. LeJeune, F., Owens, N.: Chronic laryngeal stenosis. Ann. Otol. Rhinol. Laryngol. 44, 354–363 (1935) 52. Lusk, R.P., Gray, S., Muntz, H.R.: Single-stage laryngotracheal reconstruction. Arch. Otolaryngol. Head Neck Surg. 117, 171–173 (1991) 53. Lusk, R.P., Kang, D.R., Muntz, H.R.: Auricular cartilage grafts in laryngotracheal reconstruction. Ann. Otol. Rhinol. Laryngol. 102, 247–254 (1993) 54. MacRae, D., Barrie, P.: “Swiss roll” laryngotracheoplasty in young children. J. Otolaryngol. 15, 116–118 (1986) 55. Maddalozzo, J., Holinger, L.D.: Laryngotracheal reconstruction for subglottic stenosis in children. Ann. Otol. Rhinol. Laryngol. 96, 665–669 (1987) 56. Markham, W.G., Blackwood, M.J., Conn, A.W.: Prolonged nasotracheal intubation in infants and children. Can. Anaesth. Soc. J. 14, 11–21 (1967) 57. McDonald, I.H., Stocks, J.G.: Prolonged Nasotracheal Intubation. A review of its development in a Paediatric Hospital. Br. J. Anaesth. 37, 161–173 (1965) 58. McQueen, C.T., Shapiro, N.L., Leighton, S., et al.: Singlestage laryngotracheal reconstruction: the Great Ormond Street experience and guidelines for patient selection. Arch. Otolaryngol. Head Neck Surg. 125, 320–322 (1999)
59. Monnier, P., Savary, M., Chapuis, G.: Partial cricoid resection with primary tracheal anastomosis for subglottic stenosis in infants and children. Laryngoscope 103, 1273–1283 (1993) 60. Monnier, P., Ikonomidis, C., Jaquet, Y., et al.: Proposal of a new classification for optimising outcome assessment following partial cricotracheal resections in severe pediatric subglottic stenosis. Int. J. Pediatr. Otorhinolaryngol. 73, 1217–1221 (2009) 61. Morgenstein, K.M.: Composite auricular graft in laryngeal reconstruction. Laryngoscope 82, 844–847 (1972) 62. Ndiaye, I., Van de Abbeele, T., Francois, M., et al.: Traitement chirurgical des sténoses laryngées de l’enfant. Ann. Otolaryngol. Chir. Cervicofac. 116, 143–148 (1999) 63. Negus, V.: Treatment of chronic stenosis of the larynx with special reference to skin grafting. Ann. Otol. Rhinol. Laryngol. 47, 891–901 (1938) 64. Ochi, J.W., Evans, J.N., Bailey, C.M.: Pediatric airway reconstruction at Great Ormond Street: a ten-year review. II. Revisional airway reconstruction. Ann. Otol. Rhinol. Laryngol. 101, 595–597 (1992) 65. Ochi, J.W., Evans, J.N., Bailey, C.M.: Pediatric airway reconstruction at Great Ormond Street: a ten-year review. I. Laryngotracheoplasty and laryngotracheal reconstruction. Ann. Otol. Rhinol. Laryngol. 101, 465–468 (1992) 66. Papsidero, M.J., Pashley, N.R.: Acquired stenosis of the upper airway in neonates. An increasing problem. Ann. Otol. Rhinol. Laryngol. 89, 512–514 (1980) 67. Prescott, C.A.: Protocol for management of the interposition cartilage graft laryngotracheoplasty. Ann. Otol. Rhinol. Laryngol. 97, 239–242 (1988) 68. Rabot, de Barlatier, L., Garel, J., et al.: Rétrécissements du larynx et de la trachée consécutifs au tubage et à la trachéotomie. Maloine, Paris (1908) 69. Ranne, R.D., Lindley, S., Holder, T.M., et al.: Relief of subglottic stenosis by anterior cricoid resection: an operation for the difficult case. J. Pediatr. Surg. 26, 255–258 (1991) 70. Ratner, I., Whitfield, J.: Acquired subglottic stenosis in the very-low-birth-weight infant. Am. J. Dis. Child. 137, 40–43 (1983) 71. Rethi, A.: An operation for cicatricial stenosis of the larynx. J. Laryngol. Otol. 70, 283–293 (1956) 72. Rinne, J., Grahne, B., Sovijarvi, A.R.: Long-term results after surgical treatment of laryngeal stenosis in small children. Int. J. Pediatr. Otorhinolaryngol. 10, 213–220 (1985) 73. Rizzi, M.D., Thorne, M.C., Zur, K.B., et al.: Laryngotracheal reconstruction with posterior costal cartilage grafts: outcomes at a single institution. Otolaryngol. Head Neck Surg. 140, 348–353 (2009) 74. Saunders, M.W., Thirlwall, A., Jacob, A., et al.: Single-ortwo-stage laryngotracheal reconstruction; comparison of outcomes. Int. J. Pediatr. Otorhinolaryngol. 50, 51–54 (1999) 75. Schmiegelow, E.: Stenosis of the larynx: a new method of surgical treatment. Arch. Otolaryngol. 9, 473–493 (1929) 76. Schroeder Jr., J.W., Holinger, L.D.: Congenital laryngeal stenosis. Otolaryngol. Clin. North Am. 41, 865–875 (2008) 77. Schultz-Coulon, H.J.: The management of postintubation stenoses in children. HNO 52, 363–377 (2004)
References 78. Schultz-Coulon, H.J., Laubert, A.: Laryngotracheoplasty in early childhood. HNO 36, 1–12 (1988) 79. Seid, A.B., Pransky, S.M., Kearns, D.B.: One-stage laryngotracheoplasty. Arch. Otolaryngol. Head Neck Surg. 117, 408–410 (1991) 80. Shapiro, R.S.: Surgical repair of complete subglottic stenosis. J. Otolaryngol. 7, 223–229 (1978) 81. Silva, A.B., Lusk, R.P., Muntz, H.R.: Update on the use of auricular cartilage in laryngotracheal reconstruction. Ann. Otol. Rhinol. Laryngol. 109, 343–347 (2000) 82. Stenson, K., Berkowitz, R., McDonald, T., et al.: Experience with one-stage laryngotracheal reconstruction. Int. J. Pediatr. Otorhinolaryngol. 27, 55–64 (1993) 83. Stern, Y., Gerber, M.E., Walner, D.L., et al.: Partial crico tracheal resection with primary anastomosis in the pediatric age group. Ann. Otol. Rhinol. Laryngol. 106, 891–896 (1997) 84. Strong, R.M., Passy, V.: Endotracheal intubation. Complications in neonates. Arch. Otolaryngol. 103, 329– 335 (1977) 85. Toohill, R.J.: Autogenous graft reconstruction of the larynx and upper trachea. Otolaryngol. Clin. North Am. 12, 909– 917 (1979)
277 86. Toohill, R.J., Martinelli, D.L., Janowak, M.C.: Repair of laryngeal stenosis with nasal septal grafts. Ann. Otol. Rhinol. Laryngol. 85, 600–608 (1976) 87. Triglia, J.M., Belus, J.F., Portaspana, T., et al.: Laryngeal stenosis in children. Evaluation of 10 years of treatment. Ann. Otolaryngol. Chir. Cervicofac. 112, 279–284 (1995) 88. Vollrath, M., Freihorst, J., von der Hardt, H.: Surgery of acquired laryngotracheal stenoses in childhood. Experiences and results from 1988 to 1998. I: laryngotracheal reconstruction. HNO 47, 457–465 (1999) 89. Walner, D.L.: Acquired anomalies of the larynx and trachea. In: Cotton, R.T., Myer III, C.M. (eds.) Practical Pediatric Otolaryngology. Lippincott-Raven, Philadelphia/New York (1999) 90. Weerda, H., Lange, G.: Die Chirurgie der zervikalen trachea. Praxis der Pneumologie vereinigt mit Der Tuberkulosearzt 28, 1007–1016 (1974) 91. Younis, R.T., Lazar, R.H., Bustillo, A.: Revision single-stage laryngotracheal reconstruction in children. Ann. Otol. Rhinol. Laryngol. 113, 367–372 (2004) 92. Zalzal, G.H.: Rib cartilage grafts for the treatment of posterior glottic and subglottic stenosis in children. Ann. Otol. Rhinol. Laryngol. 97, 506–511 (1988)
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20
Contents
20.9.2 Continuing PostOperative Care for SS-PCTR........ 310 20.9.3 Follow-Up Care for SS-PCTR................................ 310
20.1 Historical Review of Paediatric Partial Cricotracheal Resection (PCTR)........................... 282 20.1.1 Milestones in Paediatric PCTR............................... 282
20.10 Postoperative Management After Double-Stage PCTR............................................... 311 20.10.1 Initial Intensive Care Management Following DS-PCTR............................................... 311 20.10.2 Continuing Postoperative Care for DS-PCTR........ 311 20.10.3 Follow-Up Care for DS-PCTR............................... 312
20.2 Anaesthesia for PCTR............................................ 283 20.2.1 Anaesthesia for Single-Stage PCTR in Non-tracheostomised Children........................... 284 20.2.2 Anaesthesia for Single-Stage PCTR in Tracheostomised Children...................................... 285 20.3 Surgical Technique for Simple PCTR................... 285 20.3.1 Position of the Patient and Incisions....................... 286 20.3.2 Tracheal Dissection................................................. 286 20.3.3 Laryngeal Dissection.............................................. 287 20.3.4 Resection of Subglottic Stenosis............................ 287 20.3.5 Reshaping of the Subglottic Space......................... 288 20.3.6 Anastomosis............................................................ 289 20.4
Surgical Technique for Extended PCTR.............. 293
20.5
Surgical Technique for Extended PCTR with Intussusception of Thyrotracheal Anastomosis............................... 297
20.6
Management of Supraglottic Stenosis................... 300
Decision-Making Process in the Operating Theatre.................................................. 300 20.7.1 Extent of Airway Resection.................................... 300 20.7.2 Laryngeal and Tracheal Release Manoeuvres........ 302 20.7.3 Management of Malacic Tracheal Segments.......... 302
20.11 Complications of PCTR......................................... 313 20.11.1 Anastomotic Dehiscence......................................... 313 20.11.2 Recurrent Laryngeal Nerve Injury After PCTR..... 315 20.11.3 Delayed Recurrent Stenosis After PCTR................ 315 20.11.4 Tracheostomy-Related Stenosis After DS-PCTR... 315 20.12 Results of Paediatric PCTR................................... 315 20.12.1 Surgical Data on PCTR for Severe Grades III and IV LTS............................................ 316 References............................................................................ 319
Core Messages
›› Use
20.7
Perioperative Intensive Care After Major Laryngotracheal Surgery in Infants and Children: The Intensivist’s Perspective......... 303 20.8.1 Developmental Anatomy and Physiology of the Pharyngolarynx and Trachea During Childhood................................................... 304 20.8.2 General Aspects of Peri-operative Intensive Care Management After Laryngotracheal Surgery......... 304 20.8.3 Post-Extubation Respiratory Care Management..... 306
››
20.8
20.9
Postoperative Management After Single-Stage PCTR................................................. 309 20.9.1 Initial Intensive Care Management Following SS-PCTR............................................... 309
›› ››
simple single-stage partial cricotracheal resection (SS-PCTR) for isolated severe Grade III or IV SGS in patients without comorbidities Use simple double-stage partial cricotracheal resection (DS-PCTR) for isolated severe Grade III or IV SGS in patients with comorbidities, or when the tracheostomy is distally placed, requiring resection of more than five tracheal rings Use extended PCTR with stenting for Grade III or IV SGS combined with severe glottic involvement (PGS or VC fusion) Use extended PCTR with thyrotracheal intussusception for transglottic laryngotracheal stenosis (LTS) or LTS requiring a long (³5 rings) tracheal resection
P. Monnier (ed.), Pediatric Airway Surgery, DOI: 10.1007/978-3-642-13535-4_20, © Springer-Verlag Berlin Heidelberg 2011
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280
Simple PCTR In an attempt to improve the mediocre surgical results following primary laryngotracheal reconstruction (LTR) for severe (Grades III and IV) LTS, the concept of removing the diseased airway segment has developed into an attractive alternative to cartilage expansion of the subglottic airway. PCTR with primary thyrotracheal anastomosis spares the glottis with reconstruction of a ‘normal,’ rounded, mucosalised subglottic airway. Additionally, this approach minimises the problems of wound-healing encountered with costal cartilage grafts and stenting in LTR. When appropriate, the operation is performed as a single-stage procedure, that is, the tracheostoma is excised as part of the resected specimen, and an endotracheal tube is left in place for 3–7 days, depending on the child’s age. When the tracheostoma is at a sufficient distance (³5 tracheal rings) from the SGS, and if there is no suprastomal collapse, PCTR is performed as a double-stage procedure. The tracheostoma is closed secondarily after the healing of the subglottic anastomosis is complete. The term ‘simple PCTR’ refers to the resection of an isolated SGS (i.e. with normal vocal cords). This procedure is more challenging than LTR and has the double risk of injuring the RNLs or that of anastomotic dehiscence. When more than five tracheal rings are to be resected, the trachea must be mobilised extensively in order to achieve a tension-free anastomosis. A laryngeal release procedure is advisable.
Extended PCTR When PCTR is combined with an additional open airway procedure, it is referred to as an extended PCTR. This procedure is suggested for patients presenting LTS with glottic involvement. Glottic involvement may present itself as posterior glottic stenosis with possible cricoarytenoid joint fixation, cicatricial fusion of the vocal cords, and transglottic
20 Partial Cricotracheal Resection
cicatricial stenosis, or as a completely distorted larynx due to previous failed LTRs [46, 57]. Extended PCTR consists of a posterior cricoid split with costal cartilage graft, resection of subglottic stenosis, and stenting for 4–6 weeks. Extended PCTR cannot be performed as a single-stage procedure, and a tracheostomy must be left in situ until the airway is fully healed and stable.
Extended PCTR with Intussusception of Thyrotracheal Anastomosis In an attempt to diminish the risk of anastomotic dehiscence and better preserve the function of the lateral cricoarytenoid muscles, the author has recently modified the extended PCTR operation as follows: Instead of resecting the anterior and lateral portions of the cricoid ring, the airway is opened transversally at the lower limit of the glotto-subglottic stenosis, typically the inferior border of the cricoid ring. A full laryngofissure with posterior cricoid split is created in order to expand the interarytenoid distance in a similar manner as for an LTR with anterior and posterior costal cartilage grafts. The cicatricial tissue forming the subglottic obstruction is fully resected, while any residual mucosa at the glottic level is carefully preserved. Next, the divided lateral arches of the cricoid ring are trimmed with a diamond burr until the cartilage becomes more pliable. The outer surface of the cricoid ring is kept fully intact. With additional interposition of the posterior costal cartilage graft between the divided cricoid laminae, a large subglottic space is created, which accommodates the narrower tracheal stump as an intussuscepted airway inside the enlarged cricoid ring. The thyrotracheal anastomosis is performed inside the expanded cricoid in order to obtain a fully mucosalised glottosubglottic airway. Additional external stitches are placed between the lateral portions of the cricoid and the tracheal wall to reinforce the anastomosis and diminish tension on the suture line. A 6-week stenting period is necessary.
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LTR Versus PCTR While the debate is still ongoing as to the advantages of one technique over the other, LTR is easier from a technical standpoint, but the procedure may distort the laryngeal framework. In addition, expanded cartilage may increase the risk of granulation tissue formation, with delayed wound healing and subsequent restenosis. Primary LTR has been reported to yield good results in patients with Grades I and II or minor Grade III SGS, and less optimal results in those with severe Grades III and IV SGS. After airway reconstruction with anterior and posterior costal cartilage grafts for severe Grade III or IV SGS, lack of residual mucosa in the reconstructed portion of the subglottis implies healing by secondary intention, with granulation tissue formation and subsequent restenosis (Fig. 20.1). The concept of simple PCTR and extended PCTR offsets these shortcomings by resecting the diseased airway segment with end-to-end anastomosis, creating a fully mucosalised airway upon completion of surgery. Although a stenosis at a 3–4 mm distance from the vocal cords represents the most favourable situation, this is not an absolute prerequisite for performing PCTR. A recent analysis of our results on airway patency and voice quality after PCTR revealed no difference when the stenosis did not involve the vocal cords or when it just reached the free border of the vocal cords. However, when SGS was associated with vocal cord fusion or posterior glottic stenosis, postoperative voice quality was found to be less optimal [21]. Although there are no published data comparing LTR and PCTR in matched patient groups, it is now generally accepted that PCTR is appropriate as the primary surgery for severe Grades III and IV LTS [34] and as salvage surgery after failed LTR for Grades II (with airway collapse), III, and IV SGS.
a
b
Fig. 20.1 Diagram of laryngotracheal reconstruction with anterior and posterior costal cartilage grafts for grade IV laryngotracheal stenosis: (a) Prior to surgery, the subglottic airway is fully obstructed by cicatricial tissue. (b) Diagram of airway expansion with anterior and posterior costal cartilage grafts: The reconstructed airway is fully devoid of any mucosal lining. A circumferential (up to 1.5 cm in length) airway segment must heal by secondary intention around the stent (displayed in white), which leads to difficult wound healing, granulation tissue formation, and restenosis
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20.1 Historical Review of Paediatric Partial Cricotracheal Resection (PCTR) 20.1.1 Milestones in Paediatric PCTR Adult experience: Conley (1953)
Subperichondrial resection of the cricoid ring with stenting
Shaw et al. (1961)
PCTR for traumatic stenosis
O gura and Powers (1964)
PCTR for traumatic stenosis
G erwat and Bryce (1974)
PCTR with preservation of RNLs
Pearson (1975)
First description of the original PCTR technique
Grillo (1982)
Slight modification of the PCTR technique
Couraud (1996)
PCTR extended cranially to the glottis and supraglottis
with damaged recurrent laryngeal nerves(RNLs)
Paediatric experience: Savary (1978)
First PCTR on a 9-year-old child
Ranne (1991)
First reported series of PCTR on 7 children
Monnier (1993)
Lausanne experience in the first 15 PCTRs
Stern, Cotton (1997)
Cincinnati experience in the first 16 PCTRs
Monnier (1999)
PCTR combined with posterior cricoid split and costal cartilage graft
Rutter, Cotton (2001)
Introduction of the term, ‘extended PCTR’ (i.e. PCTR combined with an additional open airway procedure)
G arabedian et al. (2005)
PCTR in children weighing less than 10 kg
Monnier (2009)
Extended PCTR with intussusception of thyrotracheal anastomosis
In 1953, Conley [7] reported a case of subperichondrial dissection and resection of the cricoid for removing a subglottic chondroma. He repaired the wound ‘by carefully suturing the mucoperichondrium over the cricoid bed and maintaining it in position with a foam rubber sponge dressing wrapped with vaseline gauze.’ Although the description does not match that of a cricotracheal resection, this was the first report of a successful partial resection of the cricoid ring. Almost 10 years later, Shaw et al. [58] followed by Ogura and Powers (1964) [52] described a true resection of the cricoid cartilage with primary thyrotracheal anastomosis for subglottic stenosis secondary to blunt trauma. All of the patients presented bilateral RNL injury resulting from the original trauma. The first description of partial cricotracheal resection with preservation of the posterior cricoid plate and RNLs was made in 1974 by Gerwat and Bryce, reporting on a small series of four patients, of which one was a 14-year-old adolescent [24]. The resection line of the anterior cricoid arch was carried out in a very oblique manner limiting the resection of the posterior subglottic airway. In 1975, Pearson et al. [54] introduced the technique of transverse resection of the subglottic airway. This technique resulted in improved access for removing the scar tissue forming the posterior aspect of the subglottic stenosis, while preserving the RNLs, and a shell of the cricoid plate. The anterolateral arch of the cricoid ring was entirely removed, and the thyrotracheal anastomosis was performed within 1 cm or less from the vocal cords. Excellent functional results were reported in 5 out of 6 patients, with further updates on 38 patients published in 1986 [53] and 1992 [41]. This significant contribution is still considered to be the basis of what is now referred to as partial cricotracheal resection with primary thyrotracheal anastomosis. Couraud et al. applied the procedure successfully in 1979 [13], with additional reports published in 1987 and 1995 [10, 11], extending the limits of resection cranially to the glottis and supraglottis [12]. Meanwhile, in 1982, Grillo described a slight modification of the original PCTR technique, with preservation of a pedicled flap of membranous trachea so as to resurface the posterior cricoid plate [27]. In 1992, he updated his experience involving 80 adult patients [31]. By that time, PCTR was already considered to be the best surgical option for the cure of subglottic stenosis in the adult population. In 2001, Macchiarini et al. [40] reported their own experience including 45 patients,
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20.2 Anaesthesia for PCTR
while reviewing worldwide experience. Of the 249 PCTRs performed, 95% were considered to be a success and 4% a failure, with a death rate amounting to 1%. The experience gained with this technique in the adult population formed the basis for its implementation in the paediatric population. Ranne et al. (1991) [55] are credited with the first report of a series of seven PCTRs performed in small children (mean age, 3.6 years; range 1.3–5.7 years) with recurrent subglottic stenosis. Successful decannulation was achieved 3–12 weeks after surgery in all cases. For unknown reasons, this short-lived experience went unheeded and failed to stimulate otolaryngologists, wary about the risk of RNL injury and interference with normal laryngeal growth. Savary’s pioneering work with paediatric PCTR dated back to 1978. However, this surgical procedure did not emerge as a preferred alternative to LTR for the cure of severe paediatric SGS until publication of the Lausanne experience involving 15 cases [43] in 1993, with further updates on 60 cases published in 2003 [47], and 100 cases in 2009 [22]. In 1997, the Department of Paediatric Otolaryngology in Cincinnati [59], Ohio, USA supported the use of this technique for selective indications, reporting results on 16 paediatric cases, with updates on 44 cases published in 2001 [57], and 100 cases in 2005 [69]. In 1985, Fearon and McMillin [19] published an experimental study demonstrating that cricotracheal resection with primary thyro-tracheal anastomosis was perfectly feasible on growing primates. However, as the follow-up period was too short, it was difficult to confirm that laryngotracheal growth was fully normal after this type of operation. This concern has now been resolved by the Lausanne group. Thirty of the patients who underwent PCTR have now reached adulthood, showing stable results, without requiring further endoscopic or open surgeries (unpublished series on 108 patients). In 1991, the Lausanne group started using a pedicled flap of membranous trachea to resurface the denuded cricoid plate and the interarytenoid region after resection of posterior commissure scarring combined with subglottic stenosis. This technique was published in 1995 [44]. Partial cricotracheal resection combined with posterior cricoid split and costal cartilage grafting for severe glotto-subglottic stenosis was implemented in 1998, with reports published in 1999 [45]. This technique combining resection of the subglottic space with either additional widening of the posterior glottis or
separation of fused vocal cords was later termed ‘extended PCTR’ by the Cincinnati group [57]. At the beginning of 2009, Monnier developed the concept of extended PCTR with intussusception of thyrotracheal anastomosis to better preserve the function of the lateral cricoarytenoid muscles and diminish the risk of anastomotic dehiscence (unpublished data). This technique is described in detail in this chapter. Over the last two decades, PCTR has been advocated as a superior alternative to LTR for the cure of severe Grades III and IV SGS by several authors [1, 22, 64, 67, 69], even in very small children [20, 35, 38].
20.2 Anaesthesia for PCTR Madeleine Chollet-Rivier, MD, Marc André Bernath, MD, Staff Anaesthesiologists Anaesthesia in a tracheostomised child is straightforward if a double-stage surgery is scheduled. The entire intervention is carried out through a RAE tube or an armoured Rüsch tube inserted through the tracheostoma into the distal trachea. The surgery is usually performed above the tracheostoma, which is kept in place at the end of the procedure (see Sect. 20.4 on extended PCTR). When PCTR is scheduled in a non-tracheostomised child with moderately severe Grade III SGS, it may be necessary to buy time until definitive surgery can be planned. To alleviate symptoms of obstructive dyspnoea, the following temporising measures are helpful (Table 20.1). Anaesthesia for PCTR is more challenging in singlestage surgeries, where either a moderately severe Grade III SGS is resected in a non-tracheostomised child or the tracheostoma is resected as part of a severe Grade III or IV SGS. At some time during surgery, the infant or child must be ventilated through the opened tracheal stump. Three main anaesthesiological techniques are possible: • Positive pressure ventilation via a sterile endotracheal tube inserted by the surgeon into the distal tracheal stump • High frequency jet ventilation (HFJV) via a long catheter inserted through the endotracheal tube into the distal trachea • Temporary spontaneous respiration anaesthesia with an opened trachea
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Table 20.1 Temporising measures to alleviate obstructive dyspnoea prior to definitive surgical management Prevention and support Measures Airway obstruction
Sitting position Avoidance of unnecessary upper airway manipulations
Cough suppression
Hydrocodone i.v. 0.1 mg/kg
Alleviation of dyspnoea
Light sedation: Midazolan 0.1–0.2 mg/kg or Propofol 1–3 mg/kg/h and/or Remifentanil 0.05 mg/kg/h Heliox® (70:30): Helium 70% in O2 30%
Prevention of oedema
Epinephrine aerosol: 50 mg/kg every 10 min, if necessary Humidification of inspired air Dexamethasone 0.1 mg/kg
Respiratory support
Oxygen supply Positive end-expiratory pressure (PEEP) and/or continuous positive airway pressure (CPAP)
20.2.1 Anaesthesia for Single-Stage PCTR in Non-tracheostomised Children
As the cervical trachea is usually normal in nontracheostomised children with subglottic stenosis, the circumferential tracheal incision is first made at the inferior edge of the cricoid ring around the ET tube or the Cook exchange catheter. At this stage, one of the three above mentioned anaesthesiological techniques may be used:
20.2.1.1 Ventilation Through the Tracheal Stump with a Sterile ET Tube The trachea is freed from its laryngeal attachment, and a second set of sterile anaesthesia tubing is temporarily used to ventilate the patient with a flexible armoured Rüsch tube through the tracheal stump. The tip of the original nasotracheal Portex Blue line tube is securely fixed with a mercilene thread, and it is withdrawn into the pharynx to provide a free operative field to the surgeon. The next steps are identical to those used in tracheostomised children, which is the more common setting with severe SGS (see Sect. 20.2.2).
20.2.1.2 High Frequency Jet Ventilation When PCTR is performed in a non-tracheostomised child with a moderately severe Grade III SGS, inhalation induction with sevoflurane using mask ventilation is the preferred method [71]. Anaesthesia maintenance is achieved with propofol, fentanyl, and vecuronium as necessary under mask positive pressure ventilation. The stenosis is gently dilated with tapered-bougies during an apnoeic period, and the child is intubated with the smallest nasotracheal tube that provides adequate ventilation. The trauma to the subglottis induced by dilation has no adverse effects on the final outcome, as the cicatricial stenosis is fully resected. Fayoux et al. [18] have described another useful ventilation method for infants undergoing surgery for a stenotic airway. For this procedure, the trachea is intubated using a paediatric Cook exchange catheter (internal diameter of 1.6 mm), and the patient is manually ventilated with gentle positive pressure through the anaesthesia circuit via the supplied connexion. However, this setting requires a sufficiently large airway to allow air to freely egress around the catheter. The authors reported one case of total obstruction which needed an emergency tracheotomy.
Once the proximal trachea is opened, the ET tube is withdrawn until the tip appears in the operative field. The tip of the tube is secured using a mercilene thread. A small paediatric Cook exchange jet catheter is then passed through the tube and placed by the surgeon distally in the trachea. After the jet catheter has been correctly placed, the ET tube is withdrawn out of the operation field into the pharynx. HFJV [42] is then instituted using a Monsoon HF-J ventilator (Acutronic® Medical System AG, Baar, Switzerland). The parameters should be set as follows for children: rate, 100– 200/min; driving pressure 0.02 bar/kg; Ti/Tot, 0.3. During the entire procedure, the distal part of the trachea must be moistened continuously in order to prevent mucosal dessication. Resection of the stenosis and creation of the anastomosis are performed in a free operative field under optimal conditions. The tiny catheter can be temporarily removed from the surgical field in order to optimally place the stitches. Once the posterior anastomosis has been completed, and a few additional stitches have been placed laterally, the ET tube is pulled back from
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the pharynx and pushed down into the trachea over the jet catheter. Conventional ventilation is restored until the end of the operation. Although optimal from a theoretical point of view, this is not always the best technique for the surgeon. The pressure induced by the jet ventilation constantly splashes blood and secretion from the distal tracheal stump, and great care must be taken to avoid temporary closure of the tracheal stump during surgical manipulations. The author’s preferred technique is a temporary intubation of the distal tracheal stump using a normal cuffed-endotracheal tube.
20.2.1.3 Spontanous Respiration Anaesthesia with an Opened Trachea Only a few reports on this technique have been published in scientific literature [25, 39]. After opening the trachea, the operative field is bathed with a constant oxygen flow supplied by the endotracheal tube, which is maintained at the glottic level using the leading mercilene thread. The technique is delicate, and the surgeon must constantly moisten and suck the distal trachea so as to avoid aspiration of blood and debris. A sterile endotracheal tube is intermittently inserted by the surgeon into the distal tracheal stump to provide positive pressure ventilation aimed at managing actelectasis and reoxygenating the child as necessary. Coughing fits are frequently reported, which may interfere with the surgical procedure. However, since the advent of short-acting intravenous drugs such as propofol and remifentanil, which allow for an entirely intravenous anaesthesia (TIVA) in children, spontaneous ventilation anaesthesia has regained some interest. Its advantage is to temporarily provide a free operative field enabling the surgeon to perform the thyrotracheal anastomosis under optimal conditions, even if at times an endotracheal tube must be inserted into the distal trachea to improve recruitment in order to optimally treat atelectasis and reoxygenate the child. When the posterior anastomosis has been completed and a few lateral stitches have been placed, the distal trachea is rinsed with saline and carefully suctioned before the nasotracheal tube is pulled by the leading mercilene thread beyond the anastomosis. The last anterior stitches are placed when the ET tube is securely fixed at the level of the nose.
This technique combines the advantages of safe distal ventilation through a cuffed endotracheal tube and those of a free operative field in a child under spontaneous respiration.
20.2.2 Anaesthesia for Single-Stage PCTR in Tracheostomised Children Before draping the patient, two sets of ventilating tubes are prepared, one on the thorax for ventilation through the tracheostoma, and another one at the head end of the patient for ventilation through the nasotracheal tube. The entire dissection and resection of the stenosis is carried out under optimal conditions in a free operative field, while the patient is ventilated through the tracheostoma. Before starting the thyrotracheal anastomosis, the anaesthesiologist exposes the larynx with an intubation laryngoscope in order to pass the nasotracheal tube through the vocal cords under visual control. The retrograde Seldinger technique with a Cook airway exchange catheter passed from the operative field to the pharynx is inappropriate for paediatric surgery, as nasotracheal intubation is required during the postoperative period. The surgeon recaptures the nasotracheal tube in the operative field, securing the tip of the tube with a mercilene thread. The tube is withdrawn into the pharynx in order to provide a free operative field to the surgeon for resection of the stenosis and accomplishment of a safe anastomosis. The suture of the posterior anastomosis and two lateral cricotracheal stitches are placed and tied, while the child is still ventilated through the tracheal stump. Using the leading mercilene thread, the nasotracheal tube is retrieved through the larynx and gently pushed beyond the posterior anastomosis into the distal trachea. The remainder of the lateral and anterior sutures are placed around the ET tube, with the knots tied on the outside (Fig. 20.2).
20.3 Surgical Technique for Simple PCTR In infants and small children, the use of magnifying (3x) glasses is recommended.
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Fig. 20.2 Use of two sets of anaesthesia tubes for partial cricotracheal resection: The child is initially ventilated through the tracheostoma, then through the tracheal stump using a RAE or flexible armoured Rüsch tube (a) after resection of the subglottic stenosis. Once the posterior anastomosis has been completed, the nasotracheal tube (b) is gently pulled through the vocal cords with the leading mersilene thread (c) and pushed into the distal airway to ventilate the patient. The lateral and anterior thyrotracheal stitches are then placed and tied on the outside
20.3.1 Position of the Patient and Incisions The patient is placed in the supine position, with a bolster under the shoulders. An RAE tube is inserted into the tracheostoma and fixed to the chest, slightly to the left of the sternum. The cervical and thoracic regions are cleaned and draped separately to provide access for harvesting a costal cartilage graft, should it become necessary during surgery. In non-tracheostomised children, a second sterile anaesthetic tube is prepared and
Fig. 20.3 Peritracheostomal ellipse of skin used to hold the trachea during dissection: (a)Skin-resection design around the tracheostoma. (b) Hold of the skin around the tracheostoma in order to pull on the trachea during dissection
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fixed to the left of the neck to provide temporary ventilation through the tracheal stump, while the surgeon performs the thyrotracheal anastomosis. With the neck fully extended, a horizontal crescentshaped excision of the skin is made around the tracheostoma. It is helpful to place haemostats for traction on either side of the skin ellipse left around the stoma. This provides a hold during the tracheal dissection phase, enabling the surgeon to pull cranially and laterally on the thoracic trachea so as to improve exposure of the tracheo-oesophageal grooves on both sides (Fig. 20.3). This manoeuvre enormously facilitates tracheal dissection, particularly when the trachea is fixed by dense scar tissue to the structures surrounding the tracheostoma. In children without tracheostomy, the collar incision is placed at a mid-distance from the cricoid to the sternum, usually at the level of the fourth tracheal ring.
20.3.2 Tracheal Dissection The subplatysmal flaps are elevated, and the strap muscles are separated from the midline above and below the tracheostoma in order to provide exposure from the hyoid bone to the sternal notch. The isthmus of the thyroid gland is transected in the midline, and the lobes are reflected laterally. At this stage, the use of a Lone Star retractor ring (Lone Star Medical Products, Stafford TX, USA) facilitates optimal airway exposure. As the dissection progresses, elastic stay hooks are positioned into deeper tissues in order to improve exposure. As a result, fewer personnel are required and overcrowding is avoided when operating on a small child (Fig. 20.4).
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Fig. 20.4 Retractor ring with elastic stay hooks: This device provides perfect exposure of the trachea during the entire surgical procedure
Dissection of the trachea is done only anteriorly and slightly laterally, without identifying the RNLs. This is best achieved by staying in close contact with the outer-perichondrium of the tracheal rings. The vascular supply originating laterally from the tracheooesophageal grooves must be carefully preserved, particularly in the case of an extensive mobilisation of the intrathoracic trachea. Over the tracheal segment that is to be resected around and above the tracheostoma for an SS-PCTR, the feeding vessels of the trachea are first coagulated and then divided. Bleeding must be avoided, as the small vessels retract into the peritracheal fatty tissue of the tracheo-oesophageal grooves, where the RLNs are at risk of injury during bipolar coagulation. To minimize the risk of RNL injury, dissection must be carried out meticulously against the trachea without visualizing the nerves, often embedded in the scar tissue. Dissection is performed safely up to the lower edge of the cricoid cartilage. A high lateral or posterior dissection of the cricoid ring must be avoided, as this is likely to injure the RNLs that run posteriorly to the cricothyroid joints (Fig. 20.5).
20.3.3 Laryngeal Dissection The sternohyoid muscles are retracted laterally by the elastic stay hooks, resulting in optimal exposure of the sternothyroid and thyrohyoid muscles, which are
Fig. 20.5 Tracheal dissection: The recurrent laryngeal nerves are not identified. The left recurrent laryngeal nerve is shown for anatomical purposes only. The feeding vessels of the trachea are only coagulated over the segment that is to be resected (black spots of coagulation on the trachea)
divided transversally at the level of their insertion on the thyroid cartilage. This provides exposure of the lower edge of the thyroid cartilage over its entire width. At the level of the cricoid arch, the cricothyroid muscles are sharply dissected off the cricoid cartilage from the midline towards the cricothyroid joints. The cricothyroid muscles are thus reflected over the cricothyroid joints, protecting the RNLs from injury (Fig. 20.6). Along the upper rim of the thyroid cartilage, the thyrohyoid membrane is incised until the upper thyroid cornua are reached. This results in a mini-laryngeal drop. The upper thyroid cornua are sectioned only if a full laryngeal release procedure is carried out. Before incising the trachea, a tentative approximation of the airway reveals the degree of tension placed on the anastomosis.
20.3.4 Resection of Subglottic Stenosis The superior incision is started at the inferior margin of the thyroid cartilage on the midline and is passed laterally just anterior to the cricothyroid joint, thus avoiding injury to the RLNs that run posteriorly to the joint (see Fig. 20.6). This lateral cut is best performed with a 15-blade knife. Once the skeleton of the anterior cricoid arch has been freed, a view of the posterior cricoid plate is obtained through the former cricothyroid
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Fig. 20.6 Laryngeal dissection for partial cricotracheal resection: The sternothyroid and thyrohyoid muscles are sectioned from their thyroid insertion (not shown on the diagram). The cricothyroid muscles are reflected laterally in order to protect the recurrent laryngeal nerves (yellow arrow). The thyrohyoid membrane is incised to provide a mini-laryngeal drop (dotted red line). The resection lines (dotted blue lines) are shown for single-stage partial cricotracheal resection
membrane. Under visual control, the posterior subglottic mucosa is incised transversally just above the upper limit of the stenosis with a beaver knife. The cicatricial stenosis obliterating the cricoid cartilage is then dissected from the cricoid plate in a subperichondrial plane with a sharp elevator or a beaver knife. The membranous trachea is dissected and separated from the anterior wall of the oesophagus over a distance that corresponds to the height of the cricoid plate in nontracheostomised children. This dissection is extended caudally to the tracheostoma level for single-stage PCTR in tracheostomised children, but the vascular supply to the trachea is carefully preserved beyond this lower limit. Unnecessary extensive separation of the trachea from the oesophagus must be avoided in order to preserve an optimal vascular supply to the tracheal stump (Fig. 20.7). After having placed stay sutures on the distal normal tracheal wall, the inferior resection line is made at the lower margin of the stenosis in non-tracheostomised children or one ring below the lower margin of the tracheostoma (which is fully resected with its stoma tract) in the case of single-stage surgery. Anteriorly, a rectangular wedge of tracheal wall pedicled to the tracheal stump must be preserved to increase the subglottic diameter at the level of the anastomosis (see Fig. 20.8). If a long tracheal resection is required, then
20 Partial Cricotracheal Resection
Fig. 20.7 Tracheoesophageal separation: The dissection is extended caudally to the tracheostoma level, while avoiding a compromise of the vascular supply to the distal tracheal stump
the anteriorly pedicled wedge of tissue is taken from the stoma tract to preserve the normal tracheal rings. During this stage, the RAE tube is moved from the tracheostoma to the tracheal stump in order to ensure proper ventilation of the patient. The cranial mobilisation of the distal tracheal stump is now possible without creating an anterior bulge of the oesophagus, which shortens spontaneously, due to its elasticity.
20.3.5 Reshaping of the Subglottic Space As the luminal diameter of the tracheal stump is larger than that of the proximal subglottic resection line, additional measures must be envisaged to reshape the neo-subglottis. Any attempt to reduce the calibre of the trachea must be avoided. Instead, the subglottic lumen must be enlarged as much as possible without compromising voice quality. This is best achieved by the following means: • The immediate subglottic space is typically seen as a slit instead of an oval-shaped opening. By suturing the lateral subglottic mucosa with 5.0 or 6.0 vicryl sutures to the inferior edge of the thyroid cartilage, the subglottic airway is widened significantly (Figs. 20.8 and 20.9). Moreover, this manoeuvre approximates the subglottic mucosa to the suture line of the future thyrotracheal anastomosis, thus diminishing the risk of granulation tissue formation.
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Fig. 20.8 Reshaping of the subglottic space after partial cricotracheal resection: The slit-like subglottis is enlarged by suturing the lateral subglottic mucosa to the inferior edge of the thyroid cartilage. The red dotted line shows the cranial extent of the inferior midline thyrotomy that must not extend cranially beyond the mid-distance from the thyroid notch to the inferior border of the thyroid cartilage
Fig. 20.10 Reshaping of the subglottic space after partial cricotracheal resection: The inferior borders of the thyroid alae are spread apart using skin hooks to enlarge the subglottic lumen without affecting voice quality. The V-shaped cricoid is flattened and widened with a diamond burr to easily accommodate the distal tracheal stump (red dotted line)
(see Fig. 20.9). Due to the soft and pliable nature of the thyroid cartilage in infants and children, the inferior edge of the thyroid alae can be easily spread apart. This provides significant enlargement of the subglottic lumen, while the anterior laryngeal commissure is kept intact. • The V-shaped cricoid plate is widened posteriorly and laterally with a diamond burr until a flat surface is obtained to accommodate the distal tracheal stump (Fig. 20.10).
20.3.6 Anastomosis Fig. 20.9 Reshaping of the subglottic space after partial cricotracheal resection: The subglottis has been widened by lateral mucosal stitches. A midline inferior thyrotomy (not extending cranially beyond the mid-distance from the thyroid notch to the inferior edge of the thyroid cartilage) is made with a 15 blade knife
• An inferior midline thyrotomy kept below the anterior laryngeal commissure is created using a 15-blade knife. The thyroid transection should not extend cranially beyond the mid-distance from the thyroid notch to the inferior border of the thyroid cartilage in order to preserve optimal voice quality
Depending on the child’s age, 3.0, 4.0 or 5.0 vicryl sutures are used for the lateral and anterior anastomoses. Before performing the posterior anastomosis, which is sensitive to mucosal tears, two posterolateral stitches must be placed in order to release tension on the posterior suture line. The first stitch is passed through the posterolateral aspect of the second normal tracheal ring and must emerge in a submucosal plane on the inner surface of the trachea. On the laryngeal side, the same stitch is passed through the posterolateral subglottic mucosa and then through the cricoid plate, laterally. It should emerge in a subperichondrial plane from the outer surface of the cricoid plate so as
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to avoid any lesion to the RLNs. This stitch is essential and must be placed as meticulously as possible to achieve a perfect approximation of the subglottic and tracheal mucosae. For this reason, the length of the stitch on the trachea should be slightly greater than that on the cricoid plate (Fig. 20.11). The posterior anastomosis is performed with interrupted 5.0 or 6.0 vicryl sutures. On the tracheal side, the stitch must be placed full-thickness through the mucosa to match that of the thinner subglottic mucosa exactly. At the subglottic level, the stitch must be placed half-thickness through the posterior cricoid cartilage and mucosa in order to obtain perfect mucosal approximation (Fig. 20.12) [4]. Generally, three posterior stitches placed between the two transcartilaginous posterolateral stitches suffice (Fig. 20.13). The knots of the posterior anastomosis are tied inside the lumen, after having pulled the trachea cranially with traction sutures to avoid undue tension on the more fragile posterior anastomosis. Placing the stitches in a reversed fashion to tie the knots on the outside is virtually impossible and should not be attempted. Fibrin glue (Tisseel® or Tissucol®) is used to secure the membranous trachea to the cricoid plate (Fig. 20.14). At this stage, the distal trachea is rinsed with saline solution to clear it of potential mucous plugs and blood
20 Partial Cricotracheal Resection
Fig. 20.12 Details of posterior cricotracheal anastomosis in sagittal view: The three posterior stitches are placed at fullthickness through the mucosa of the tracheal side and at halfthickness through the posterior cricoid plate and mucosa on the laryngeal side to achieve perfect mucosal approximation
Fig. 20.13 Posterior cricotracheal anastomosis after partial cricotracheal resection: Due to the adherence of the posterior subglottic mucosa to the cricoid plate, passing the stitches in a reverse fashion to tie the knots on the outside is virtually impossible and not recommended. All stitches are placed before they are tied inside the lumen. A vicryl thread does not cause granulation tissue formation, which is usually due to a defective anastomosis technique with inappropriate mucosal approximation
Fig. 20.11 Thyrotracheal anastomosis after partial cricotracheal resection: The posterolateral stitches are actually cricotracheal stitches. They are first passed through the posterolateral subglottic mucosa, and then through the cricoid plate where they must emerge in a subperichondrial plane on the outer surface in order to avoid injury to the recurrent laryngeal nerves. As these two stitches dictate the quality of mucosal approximation for the posterior anastomosis, they are essential to avoid recurrent stenosis
clots by gentle suction. The nasotracheal soft Portex Blue Line® Tube is retrieved from the pharynx through the vocal cords by pulling gently on the leading mercilene thread (see Fig. 20.2) and is pushed into the distal trachea, while the RAE tube is removed. The thyrotracheal anastomosis is completed by placing 3.0 or 4.0 vicryl sutures alternately through the first and second tracheal rings on the tracheal side
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Fig. 20.14 Completion of posterior cricotracheal anastomosis: Great care should be taken to achieve perfect mucosal approximation, the only guarantee for primary healing without scar tissue formation
and through the thyroid cartilage on the laryngeal side. They must be placed proportionately, using the midlateral sutures as guiding points. These latter stitches must be placed precisely at the angle formed by the tracheal ring and the pedicled wedge of anterior trachea on the tracheal side, and by the inferior midline laryngofissure and the inferior edge of the thyroid cartilage on the laryngeal side. All sutures are placed before they are tied on the outside, after removing the shoulder bolster. At this stage, the triangular wedge of pedicled cartilage used to fill in the anterior subcommissural defect is trimmed to its appropriate size. It is then stitched to the thyroid cartilage by two or three 5.0 vicryl sutures. Next, a tension-releasing suture is placed through the third or fourth tracheal ring laterally and through the inferior border of the cricoid plate. Great care should be taken in order to avoid RNL injury by staying in a subperichondrial plane at the cricoid level (Fig. 20.15). The integrity of the anastomosis is checked by pouring normal saline into the surgical field, while the patient is ventilated using positive pressure to detect any leakage of air. Fibrin glue (Tisseel® or Tissucol®) is applied on the suture line to obtain a perfect seal, preventing early local superinfection. The lobes of the thyroid gland are slightly mobilised and resutured on the midline over the anastomosis to provide an optimal vascular supply. A Penrose drain is placed on the anterior surface of the trachea distally to the anastomotic site. The strap muscles are resutured in the midline, and a two-layer skin closure is performed with interrupted 5.0 or 6.0
Fig. 20.15 Completion of thyrotracheal anastomosis: Note the alternate position of the stitches through the first and second tracheal rings so as to distribute the anastomotic tension onto different levels. An additional tension-releasing suture is placed between the posterolateral aspect of the cricoid plate and the trachea (displayed in turquoise). Staying in a subperichondrial plane at the cricoid level is essential to avoid injury to the recurrent laryngeal nerves. The triangular wedge of pedicled trachea is trimmed to the size of the corresponding subcommissural defect and sutured in place with two or three 5.0 vicryl sutures
prolene sutures on the skin. At the end of the procedure, the neck is maintained in a flexed position. In our institution, we do not use chin-to-chest sutures to limit the extension of the neck during the postoperative period, although this measure has been recommended by several authors [28, 68] (Fig. 20.16).
20.3.6.1 Single-Stage Versus Double-Stage PCTR For a single-stage PCTR, the patient must be in good general condition, the SGS must not extend cranially to the glottic level, and the location of the tracheostoma must not require resection of more than five tracheal rings (Table 20.2). In a single-stage PCTR, the tracheostoma is excised as part of the resected stenotic segment. During the postoperative period, proper healing of the anastomosis is thereby facilitated, but longer tracheal resections carry greater risks of anastomotic dehiscence. If the location of the tracheostoma is low (requiring resection of six or more tracheal rings along with the SGS), then the anastomosis is best performed by using a steady, normal tracheal ring situated between the SGS and the
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Fig. 20.16 Single-stage partial cricotracheal resection for isolated grade III subglottic stenosis: (a) Preoperative view: The grade III subglottic stenosis is away from the normal vocal cords. (b) Postoperative view: patent subglottic airway 2 years after single-stage partial cricotracheal resection. The anastomotic line is barely visible posterolaterally under the left vocal cord
Table 20.2 Indications for single-stage PCTR • Grade IIIa and IVa SGS > Intact vocal cords/glottis > Absence of severe comorbidities • Resection of £5 tracheal rings with the SGS
Table 20.3 Indications for double-stage PCTR • Grade III b,c,d and IV b,c,d SGSs > Glottic involvement > Severe comorbidities > Combined features • Resection of >5 tracheal rings with the SGS
tracheostoma. In this setting, the tracheostoma is closed separately, either during the same procedure (uncommon situation) or a later time point (doublestage surgery). Due to proximal tracheal damage, in some cases, no steady tracheal ring may be available for the anastomosis. Should this situation arise, a longer tracheal resection combined with laryngeal release must be envisaged (see Sect. 20.7). In our series, this occurred in 13/100 PCTRs. Of note is that two of the 13 (15%) children sustained an anastomotic dehiscence, as compared with three of the 49 (6%) children in whom tracheal resection did not involve more than five tracheal rings. A double-stage PCTR is preferred when LTS is more complex with involvement of the glottis, extralaryngeal sites of airway obstruction, associated severe comorbidities, or a combination of the aforementioned conditions (Table 20.3).
20.1 Box 20.1 Surgical Highlights for Simple PCTR • Place a haemostat for traction on either side of the ellipse of skin left around the stoma in order to facilitate tracheal dissection and mobilisation. • Use a retractor ring with elastic stay hooks to optimise the exposure throughout the surgical procedure. • Do not attempt to visualise or dissect the RLNs. • Tracheal dissection is performed by staying over the outer perichondrium of the tracheal rings. • Carefully preserve the vascular supply to the trachea from the tracheo-oesophageal grooves, except for the segment that is to be resected. • Coagulate before dividing the feeding vessels of the trachea using a bipolar forceps to avoid retraction of the vessels into the peri-tracheal fat pad and prevent injury to the RLNs during coagulation. • Do not dissect the larynx and trachea using a monopolar coagulation probe. • Avoid dissection above the posterolateral border of the cricoid plate in order to avoid injury to the RLNs. • Dissection is safe up to the cricoid ring, short of the trachea. • Reflect the cricothyroid muscles over the cricothyroid joints by sharp dissection off the cricoid ring from the midline so as to protect the RLNs. • Carry out infrahyoid laryngeal release and extensive intrathoracic tracheal mobilisation if five or more tracheal rings must be resected for a single-stage PCTR.
20.3 Surgical Technique for Simple PCTR
• Open the airway first at the lower edge of the cricoid ring in order to determine the distal extent of the SGS. • Perform the upper resection line along the inferior edge of the thyroid cartilage and stay anterior to the cricothyroid joint laterally in order to avoid injury to the RLNs. • Remove any cicatricial tissue from the cricoid plate and flatten it down with a diamond burr to optimise adaptation of the tracheal ring used for the anastomosis. • Keep an anterior cartilaginous wedge pedicled to the tracheal stump used for the anastomosis, perform an inferior midline thyrotomy to enlarge the subglottic lumen, and suture the anterior pedicled wedge of the trachea into the subcommissural defect upon completion of the anastomosis. • Meticulous surgical technique is required throughout the entire surgical procedure, particularly for the thyrotracheal anastomosis. • Perfect mucosal approximation is the only way of preventing granulation tissue formation and subsequent restenosis at the anastomotic level. • Use magnifying (3x) glasses when operating on infants and small children.
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Fig. 20.17. The original tracheostoma is kept intact and repositioned in the neck at the end of surgery. Contrarily, when the original tracheostoma is close to the subglottis, it must be excised as part of the resected specimen, and a new tracheostomy must be placed three to four tracheal rings below the former tracheostoma. This step is performed at a later time point, upon completion of the posterior anastomosis (Fig. 20.18).
Fig. 20.17 Severe glotto-subglottic stenosis with distally placed tracheostoma: Subglottic resection is limited to the anterior cricoid ring and first or second tracheal ring laterally to keep a wedge of cartilage pedicled to the anterior tracheal wall
20.4 Surgical Technique for Extended PCTR As extended PCTR is performed in patients presenting more complex LTS with glottic involvement, postoperative stenting and a double-stage procedure are required. The patient is ventilated through the tracheostomy with an RAE or flexible armoured Rüsch ET tube during the entire procedure. The initial surgical steps are identical to those of a classical PCTR. Although a tracheostomy is left in situ upon completion of the procedure, the original tracheostoma must be fully dissected from its cutaneous attachments so as to facilitate cranial mobilisation of the tracheal stump. Tracheal dissection and subglottic resection are conducted, as described in Sect. 20.3. When four or five good-quality tracheal rings remain between the cricoid ring and the tracheostoma, a short subglottic resection (comprising the anterior arch of the cricoid and part of the first tracheal ring) is performed, as shown in
Fig. 20.18 Severe glotto-subglottic stenosis with tracheostoma placed at the third tracheal ring: The segment of residual trachea between the subglottic stenosis and the tracheostoma is too short to be used for the anastomosis. The original tracheostoma must be excised as part of the resected specimen, and a new tracheostoma must be repositioned more distally (yellow arrow)
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As for classical PCTR, the SGS is fully resected. On the tracheal side, however, one or two additional rings are partially resected in order to provide a pedicled flap of membranous trachea posteriorly to resurface the subglottis, and a pedicled wedge of cartilage anteriorly to optimise the subglottic lumen size. The pedicled flap of membranous trachea is easily taken from the tracheostoma site if the original tracheostoma must be resected, while the anteriorly based triangular wedge of cartilage is obtained from the stoma tract itself. Next, a full laryngofissure is created. The airway is opened first through the epiglottis in the supraglottic region. This enables separation of the fused vocal cords under visual control, exactly through the midline, with preservation of the anterior laryngeal commissure (Fig. 20.19). The posterior cricoid plate is divided vertically in the midline, and the transverse interarytenoid muscle is fully transected, if embedded in the scar tissue. Great care should be taken to avoid any tear of the retrocricoid pharyngeal mucosa. The divided cricoid laminae are spread apart using a blunt curved haemostat to allow for correct positioning of the costal cartilage graft harvested from the seventh or the eighth rib (Fig. 20.20).
Fig. 20.19 Status after resection of the subglottic stenosis: The cricoid arch and cicatricial stenosis have been removed, leaving the cricoid plate denuded. On the tracheal side, a pedicled flap of membranous trachea is created by resecting the tracheostoma site, and an anterior wedge of cartilage is preserved attached to the anterior tracheal wall. The full laryngofissure is started just above the thyroid notch (red dotted line) in order to separate the vocal cords and anterior laryngeal commissure precisely on the midline under visual control
20 Partial Cricotracheal Resection
Fig. 20.20 Posterior cricoid split: Through the anterior laryngofissure, the cricoid plate is divided exactly in the midline. This transsection is fully extended through the posterior commissure scarring and interarytenoid muscle. A blunt haemostat is used to spread apart the divided portions of the cricoid plate, and a costal cartilage is harvested
The width of the costal cartilage graft must be selected with precision in order to avoid overexpansion of the interarytenoid distance, which may cause a breathy voice. The rectangular posterior costal cartilage graft (with or without bilateral flanges) is carefully sutured with four 4.0 vicryl stitches to the divided portions of the cricoid laminae, as described for LTR with posterior costal cartilage grafting (see Fig. 19.7, Chap. 19). The graft must fit flush with the divided halves of the cricoid plate, and the perichondrium must be placed intraluminally (Fig. 20.21). The tracheal stump is pulled cranially, and its pedicled posterior membranous flap is sutured with 5.0 or 6.0 (interrupted or running) vicryl sutures to the mucosa of the posterior laryngeal commissure. The posterolateral cricotracheal stitches serve as traction sutures to approximate the trachea to the thyroid cartilage (Fig. 20.22). Using metallic LT-Mold gauges (see Fig. 19.8, Chap. 19), a proper size prosthesis whose length and calibre fit the reconstructed airway is selected. The distal extremity of the LT-Mold must abut the upper extremity of the tracheostoma in order to prevent the occurrence of suprastomal collapse of the reconstructed airway (Fig. 20.23). Before closing the supraglottic portion of the laryngofissure, a 3.0-prolene suture is passed through the thyroid alae, the ventricular bands, and the head of the
20.3 Surgical Technique for Simple PCTR
Fig. 20.21 Enlargement of the interarytenoid space and cricoid lamina: A rectangular costal cartilage graft, trimmed to the exact thickness of the cricoid plate, is sutured into position with four 4.0 vicryl sutures, thus restoring an adequate interarytenoid space
Fig. 20.22 Resurfacing of the cartilage graft and interarytenoid space: The pedicled flap of membranous trachea is sutured in a horseshoe fashion to the interarytenoid mucosa, thus providing full cover of the posterior costal cartilage graft. Two posterolateral cricotracheal stitches are used as traction sutures to reduce tension on the posterior suture line
prosthesis in order to secure the LT-Mold in position in the supraglottic area. A second 5.0 resorbable suture is used to restore the anterior laryngeal commissure and fix the LT-Mold exactly at this level. This thread is likely to be resorbed within a few weeks, thus preventing granulation tissue formation and subsequent
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Fig. 20.23 Selection of a properly sized LT-Mold prosthesis: After selecting an LT-Mold of optimal diameter and length with a metallic gauge (see Fig. 19.8), the thyroid cartilage is temporarily closed over the prosthesis to check for any excess mucosal pressure. If necessary, a one-size smaller prosthesis is chosen
Fig. 20.24 Fixation of the LT-Mold to the thyroid cartilage: The supraglottic portion of the laryngofissure is closed after securely fixing the LT-Mold at the supraglottic level (red thread) with 3.0 non-resorbable prolene sutures. At the glottic level, a 5.0 vicryl thread is used to temporarily fix the LT-Mold exactly at the level of the vocal cords (turquoise thread). Precise reapproximation of the anterior laryngeal commissure is essential to avoid postoperative vocal cord synechia
webbing of the anterior laryngeal commissure. The rest of the supraglottic laryngofissure is closed using mattress sutures on the epiglottic petiole to avoid secondary prolapse of the epiglottis after stent removal (Fig. 20.24).
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Before completing the thyrotracheal anastomosis, a second 3.0 prolene stitch is passed through the lateral walls of the trachea and the LT-Mold so as to secure the prosthesis in place. This thread is tied loosely to preserve the vascular supply to the tracheal stump. At last, the lateral and anterior parts of the anastomosis are completed, as described for a simple PCTR, using 3.0 or 4.0 vicryl sutures alternately placed through the first and second rings on the tracheal side. The wedge of cartilage pedicled to the anterior tracheal wall is trimmed to its definite triangular shape and sutured into position with 5.0 vicryl sutures between the inferiorly distracted thyroid alae in order to enlarge the subglottic lumen without compromising voice quality (Fig. 20.25). Fibrin glue (Tisseel® or Tissucol®) is applied on suture lines so as to provide a perfect seal during the first postoperative days. The isthmus of the thyroid gland, resutured in the midline over the anastomosis, helps optimise vascular supply to the reconstructed airway. Not only does extended PCTR provide a fully mucosalised reconstruction with excellent steadiness
Fig. 20.26 Extended partial cricotracheal resection for glotto-subglottic stenosis with cicatricial fusion of the vocal cords: (a) Preoperative view: acquired on congenital glotto-subglottic stenosis with fusion of the vocal cords and pinhole residual posterior opening. (b) Postoperative view: patent glottosubglottic airway, albeit with an overexpanded interarytenoid space. The posterior mucosal flap was sutured above the glottic level (white arrows) Fig. 20.25 Completion of thyrotracheal anastomosis with LT-Mold in situ: The lateral and anterior thyrotracheal stitches are placed alternately through the first and second rings on the tracheal side. An additional transverse 3.0 prolene stitch is used to fix the prosthesis at the upper tracheal level, and the anterior wedge of cartilage is trimmed to its final triangular shape and sutured into position using 5.0 vicryl threads
of the laryngotracheal framework, but it is also avoids the risk of contracting scars, as the reconstruction is non-circumferential at the level of the anastomosis (Figs. 20.26 and 20.27).
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20.3 Surgical Technique for Simple PCTR
Fig. 20.27 Extended partial cricotracheal resection for severe posterior glottic stenosis combined with a grade III subglottic stenosis: (a) Preoperative view: The arytenoids are fused together by a dense posterior glottic stenosis. The grade III subglottic stenosis cannot be seen through the adducted vocal cords.
Box 20.2 Surgical Highlights for Extended PCTR • Keep an ellipse of skin around the initial tracheostoma so as to facilitate tracheal dissection and mobilisation. • Create a new tracheostoma at the end of the surgery. • Perform a full laryngofissure under visual control in order to preserve the integrity of the vocal cords and anterior laryngeal commissure, in case of a tight posterior glottic stenosis or vocal cord fusion combined with a subglottic stenosis. • Expand the posterior cricoid plate using the same technique as for LTR with PCCG. • On the tracheal stump, create a pedicled flap of membranous trachea in order to resurface the posterior subglottis, and use a cartilage wedge anteriorly so as to increase the size of the reconstructed subglottic lumen. • Select an appropriately sized LT-Mold and recreate a perfect anterior laryngeal commissure by proper realignment of the vocal cords during closure of the supraglottic portion of the laryngofissure. • Reposition the tracheostoma more distally, if deemed appropriate.
(b) Postoperative view: After extended partial cricotracheal resection, the glotto-subglottic airway is restored to normal size. Distally, a suprastomal granuloma is seen at the level of the tracheostomy
20.5 Surgical Technique for Extended PCTR with Intussusception of Thyrotracheal Anastomosis After extended PCTR and stenting with an LT-Mold, a slow progressive dehiscence of the anastomosis may occur around the stent, without causing significant symptoms. After removal of the stent several weeks or months later, the resultant localised subglottic malacia may compromise the outcome. This complication, which was observed in one of our cases, gave rise to the idea of intussuscepting the distal tracheal stump inside the preserved lateral arches of the cricoid ring. By reinforcing the thyrotracheal anastomosis, such a procedure would prevent anastomotic dehiscence. This technical variant was also likely to better preserve both the function of the lateral cricoarytenoid muscles and the stability of the arytenoids. Extended PCTR with intussusception of the thyrotracheal anastomosis is carried out as follows: The exposure of the thyroid cartilage, cricoid cartilage, and trachea is performed as described for extended PCTR. The subglottic airway is opened through the normal-sized trachea just below the cricoid ring, or at the level of the tracheostoma if the distance from the cricoid to the stoma does not provide healthy tracheal rings for the anastomosis. A full laryngofissure transecting the
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Fig. 20.28 Subglottic resection with intussusception of thyrotracheal anastomosis: The airway is opened transversally at the inferior edge of the cricoid ring. The distal tracheal stump is prepared with anterior and posterior pedicled flaps of cartilage and membranous trachea. A full laryngofissure and posterior cricoid split are performed, displaying the total or subtotal cicatricial subglottic stenosis
anterior cricoid ring is performed as described in Sect. 20.4. As this technique is essentially used for the most severe cases of transglottic or glotto-subglottic stenoses, the midline laryngofissure is extended through the cricoid plate (as for an LTR) until a satisfactory expansion of the posterior glottis is obtained (Fig. 20.28). The dense cicatricial tissue forming the glottic or supraglottic stenosis is simply transected in the midline. In the subglottic space, beginning at the level of the inferior edge of the thyroid cartilage, the cicatricial tissue filling the inner portion of the cricoid ring is cored out and fully removed in a subperichondrial plane using a sharp elevator or beaver-knife. The lateral arches of the cricoid ring are thinned down from the inside using a diamond burr until they become slightly pliable. A costal cartilage graft is harvested in order to expand the posterior glottis and subglottis in a similar manner as described for conventional LTR or extended PCTR (Fig. 20.29). As the widening of the posterior subglottis permits easy approximation of the tracheal stump to the thyroid cartilage inside the expanded cricoid cartilage, the procedure is termed ‘thyrotracheal intussusception.’ The pedicle flap of membranous trachea is used to resurface the costal cartilage graft and is sutured to the posterior interarytenoid mucosa, approximately at
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Fig. 20.29 Subglottic resection with intussusception of thyrotracheal anastomosis/status after midline transection of the glottis, full resection of the cicatricial subglottic stenosis, and posterior expansion of the cricoid plate : From the undersurface of the vocal cords to the inferior edge of the cricoid ring, the dense cicatricial tissue forming the subglottic stenosis is fully resected in a subperichondrial plane. A diamond burr is used to thin out the lateral cricoid arches, and a posterior costal cartilage graft is used to keep the posterior glottis and subglottis expanded
the pharyngeal level, as for extended PCTR. The posterolateral stitches that secure the trachea to the cricoid plate are tied, just at the lower edge of the cricoid ring (Fig. 20.30). At this stage, the LT-Mold is secured at the supraglottis prior to closing the anterior midline laryngofissure down to the level of the anterior commissure. The lateral and anterior thyrotracheal stitches are placed in the same manner as for conventional PCTR, albeit inside the thinned lateral arches of the cricoid ring. Upon completion of the surgery, the thyrotracheal anastomosis is fully intussuscepted inside the cricoid ring. Additional sutures are placed between the cricoid arch and the trachea, thus reinforcing the thyrotracheal anastomosis. A second non-resorbable 3.0-prolene stitch is placed through the trachea in order to secure the LT-Mold above the tracheostoma. A new tracheostoma can be created three to four rings below the thyrotracheal anastomosis, if deemed necessary. Great care should be taken so that the distal end of the LT-Mold matches with the upper edge of the new tracheostoma in order to avoid suprastomal collapse of the reconstructed airway (Fig. 20.31).
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Fig. 20.30 Subglottic resection with intussusception of thyrotracheal anastomosis: The tracheal stump is advanced cranially (yellow arrow), and the pedicled flap of membranous trachea is sutured to the interarytenoid pharyngeal mucosa. The posterolateral stitches are placed exactly as in conventional partial cricotracheal resection but inside the lateral cricoid arches. The position of the thyrotracheal stitches does not differ from that used for normal thyrotracheal anastomosis. The LT-Mold is inserted when the first two thyrotracheal lateral stitches have been placed on both sides
Fig. 20.31 Completion of the intussuscepted thyrotracheal anastomosis: The final outcome is similar to that of a conventional thyrotracheal anastomosis, except that the lateral cricoid arches surround the trachea. Additional stitches (displayed in turquoise) act as a reinforcement of the thyrotracheal anastomosis
Fig. 20.32 Subglottic resection with thyrotracheal intussusception for grade IV transglottic stenosis: (a) Preoperative view: larynx severely damaged from previous failed treatments. Complete synechia of the false vocal cords, no identifiable vocal cords, and grade IV subglottic stenosis reaching the lower edge of the cricoid ring. (b) Postoperative view: restoration of a patent laryngotracheal airway with a triangular neo-glottis after extended partial cricotracheal resection with thyrotracheal intussusception and 6-month stenting using an LT-Mold prosthesis
The final result is a fully mucosalised reconstructed airway except at the glottic and supraglottic levels where the LT-Mold facilitates the healing process. Additionally, the lateral cricoarytenoid muscles are
preserved, and the thyrotracheal anastomosis is strongly reinforced, which diminishes the risk of anastomotic dehiscence (Fig. 20.32).
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Box 20.3 Surgical Highlights for Extended PCTR with Intussusception of Thyro-tracheal Anastomosis • Do not resect the anterior arch of the cricoid ring as done for classical PCTR. • Open the trachea transversally just below the cricoid ring. • Perform a full midline thyrocricoidotomy and a posterior cricoid split. • Core out the cicatricial SGS in a subperichondrial plane inside the cricoid ring and preserve any supraglottic residual mucosa. • Trim down the divided lateral cricoid arches using a diamond burr in order to increase their pliability. • Expand the posterior cricoid plate with a PCCG as done for LTR. • Perform the intussuscepted thyrotracheal anastomosis inside the expanded cricoid ring. • Place additional tension-releasing sutures between the lateral cricoid arches and the trachea.
20.6 Management of Supraglottic Stenosis Due to blunt trauma or following failed previous surgical airway reconstructions, the laryngeal framework may be severely distorted, and the epiglottic petiole may be displaced posteriorly, up to the arytenoid level. This is often associated with recurrent glotto-subglottic stenosis (Fig. 20.33). This supplementary problem at the supraglottic level is addressed during LTR or PCTR as follows: 1. The thyrohyoid membrane is largely exposed through a full laryngofissure reaching the hyoid bone. 2. The scar tissue filling the thyro-hyo-epiglottic space is removed in its midportion in order to preserve the superior laryngeal nerves laterally. 3. An epiglottopexy is performed using transfixion sutures. The epiglottic petiole may be wedged into the thyroid notch, where it is firmly stitched to the thyroid cartilage. The lateral edges of the epiglottis are sutured
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over a certain distance to the upper rim of the thyroid cartilage. With a few additional stitches, the epiglottis is fixed to the hyoid bone. Stenting with an LT-Mold prosthesis helps maintain the reconstructed supraglottis, glottis, and subglottis in place above the tracheostoma, thereby facilitating re-epithelialisation (Figs. 20.34 and 20.35).
20.7 Decision-Making Process in the Operating Theatre Even after careful planning of the surgical strategy based on a thorough preoperative assessment, several questions may arise during PCTR surgery: 1. What is the permissible length of airway resection that allows for the anastomosis to be accomplished safely? 2. Is there a need for a laryngeal or tracheal release manoeuvre? 3. How should the problem of a malacic tracheal segment be addressed?
20.7.1 Extent of Airway Resection The indications for single-stage versus double-stage PCTR encompass a variety of factors that must be identified and discussed with the child’s parents prior to surgery (see Tables 20.2 and 20.3). Yet, the exact location of the tracheostomy site and the quality of the tracheal rings situated just above the tracheostoma can only be appreciated during surgery. In most cases, the tracheostoma is placed at the level of tracheal rings 3 and 4. This necessitates the excision of the tracheostoma along with the resected specimen, due to the poor-quality tracheal rings surrounding the stoma tract (see Fig. 20.6). Improved awareness among the medical community for placing the tracheostoma either immediately below the cricoid ring through the first tracheal ring or, very low in the neck, at the level of the seventh or eighth tracheal rings in children with impending SGS would facilitate further management, especially when a resection-anastomosis is contemplated. Although intraoperative assessment of tension at the anastomotic site is possible, this requires a certain
20.7 Decision-Making Process in the Operating Theatre
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Fig. 20.33 Complex laryngotracheal stenosis after multiple failed laryngotracheal reconstructions in the same patient: (a) Epiglottic petiole prolapse reaching the posterior laryngeal com-
missure. (b) Overlapping arytenoids obscuring the glottic level. (c) Recurrent glotto-subglottic stenosis
Fig. 20.34 Diagram of supraglottic reconstruction for epiglottic petiole prolapse: (a) Due to blunt trauma or failed airway reconstruction, the epiglottic petiole was severely displaced posteriorly to the arytenoid level. (b) The scar tissue of the thyrohyo-epiglottic space is fully resected through the thyro-hyoid
membrane by skeletonising the epiglottic cartilage. (c) The epiglottis is resutured anteriorly to the thyroid cartilage and hyoid bone using mattress pexy stitches. An LT-Mold prosthesis supports the airway reconstruction
surgical expertise. Prior to incising the airway, the distal trachea is carefully dissected, while sparing the blood supply to the lateral pedicles; it is then mobilised cranially by pulling with a haemostat on the ellipse of the skin left around the stoma. With sufficient experience, the degree of tracheal ascent that helps avoid tension at the anastomosis can be appreciated. This manoeuvre
must always be performed prior to any airway incision or resection. Depending on the child’s age and individual anatomy, five tracheal rings can easily be resected with a partial laryngeal release manoeuvre. In our series involving 108 paediatric PCTRs, up to eight tracheal rings were removed, albeit with a full laryngeal release procedure.
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Fig. 20.35 Postoperative results after extended partial cricotracheal resection and epiglottopexy (same patient as in Fig. 20.33): (a) Reconstructed airway with an LT-Mold in situ. (b) Restoration of a patent laryngosubglottic airway. The cannula is still present in the distal trachea
20.7.2 Laryngeal and Tracheal Release Manoeuvres In almost all cases, a partial thyrohyoid release is carried out by dividing the sternohyoid and thyrohyoid muscles at the level of their attachment to the thyroid cartilage. This procedure is performed during the systematic dissection of the thyroid cartilage in order to expose the inferior border in a transverse plane towards the cricothyroid joints on both sides. Next, the thyrohyoid membrane is incised along the upper rim of the thyroid cartilage, with the superior cornua as the lateral extent. Pulling caudally on the thyroid notch using a skin hook helps achieve a complete division of the thyrohyoid ligament in the midline. If deemed necessary, the upper cornua of the thyroid cartilage may be sectioned with straight Mayo scissors in order to obtain a full infra-hyoid laryngeal release. In contrast to adults [30], this infra-hyoid release manoeuvre does not induce swallowing difficulties in infants and children. This may be explained by the relatively high position of the paediatric larynx in the neck. When performed as described above, the infra-hyoid laryngeal release spares the superior laryngeal neurovascular bundle. Thus, the procedure is less bloody and results in a 1- to 1.5-cm laryngeal drop. It is therefore considered to be the preferred method of laryngeal release in the paediatric age group (Fig. 20.36). In our series involving 100 paediatric PCTRs, a hilar release was never required for benign SGSs, even when stoma-related tracheal damage necessitated
resection of five to eight tracheal rings. The incidence of revision surgery for partial anastomotic dehiscence was 6%. Though Grillo does not advocate the routine use of hilar release in adults (except for extensive resections in the case of neoplastic lesions), he admits that a bilateral hilar release may be the preferred method in the case of a lengthy benign stenosis in a young and fit patient [29]. Recently, a joint report was published by otolaryngologists and thoracic surgeons on a series of 16 children who underwent PCTR (requiring resection of at least four tracheal rings), with a systematic hilar release performed in all of the cases [60]. One patient had a near-total resection of the trachea because of a longsegment severe tracheomalacia. None of the patients in this series developed anastomotic dehiscence. Although the routine use of this procedure is not indicated, the published report highlights the benefits of a hilar release in the case of long-segment laryngotracheal resections, albeit with additional morbidity.
20.7.3 Management of Malacic Tracheal Segments The congenital forms of diffuse and localised tracheomalacia have been described in Chap. 13, Sects. 13.1.1 and 13.1.2. In most paediatric cases, acquired localised malacia is due to the tracheostoma. The incidence of cuff-induced tracheomalacia is exceedingly rare, as low-pressure cuffed and non-cuffed tubes are used in
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Fig. 20.36 Infra-hyoid laryngeal release manoeuvre: (a) Laryngeal release: The larynx is exposed between the retracted sternohyoid muscles. The sternothyroid and thyrohyoid muscles are divided at their insertion level on the thyroid cartilage. The thyrohyoid membrane is sectioned along the upper rim of the thyroid cartilage, reaching the superior cornua of the thyroid cartilage which is sectioned using Mayo scissors (blue dotted lines). (b) Results of the laryngeal release: A 1.0–1.5 cm drop of the larynx is obtained (blue arrows)
both smaller and older children. The best treatment for tracheostomal malacia is simple resection and anastomosis, which facilitates the restoration of a steady tracheal vault with near normal anatomy. If resection proves impossible because of previous surgeries, then tracheoplasty with a costal cartilage graft is the sole remaining option. Partial cricotracheal resection associated with congenital diffuse or localised tracheomalacia is performed as a double-stage procedure. Although the malacic airway segment is typically addressed in the second stage, the tracheostomy tube is kept in place in most cases until the child outgrows the problem. In the meantime, the cannula acts as a stent preventing distal airway collapse. In this regard, it must be stressed that external splinting of the airway with cartilaginous autografts leads to disappointing results. Though the grafts may survive, they are often not sufficiently incorporated into the tracheal wall to provide stability. Any synthetic foreign material used for external splinting or self-expandable internal metallic stents must be proscribed (see Sect. 2.8, Chap. 2). At present, smooth silicone T-tubes are a viable option for older children whose trachea can accommodate size 8 tubes so that the tube does not become clogged with dried secretions. Until bioresorbable, self-expandable stents become available, stenting of the lower trachea with a tracheostomy tube is the safest treatment option for severe tracheomalacia.
20.8 Perioperative Intensive Care After Major Laryngotracheal Surgery in Infants and Children: The Intensivist’s Perspective Jacques Cotting, MD, Marie Hélène Perez, MD, Staff Paediatric Intensivists The paediatric intensive care unit (PICU) is a major cornerstone as regards the multidisciplinary team approach for providing care to neonates and older children suffering from major airway problems in both the pre and postoperative settings. In many unspecialised centres, these conditions are uncommon, and the related medical literature is scarce. For the paediatric intensivist, it is thus difficult to gain sufficient knowledge and acquire the necessary management skills enabling her/him to provide adequate medical care to a child undergoing major airway surgery and offer appropriate support to the family until they can return home safely. A meticulous evaluation and a thorough understanding of the pathophysiological aspects of each child with severe laryngotracheal problems may help achieving these objectives, while taking into account that many of these children also suffer from other comorbidities. To provide optimal pre and postoperative care to neonates and children with laryngotracheal stenoses, both the medical and the nursing teams of the PICU
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must have a clear understanding of the major anatomical and physiological differences between paediatric and adult airways [2].
20.8.1 Developmental Anatomy and Physiology of the Pharyngolarynx and Trachea During Childhood The infant’s nose is short, soft, and flat with small, nearly circular nares. By 6 months of age, the nares have nearly doubled in size [62]. Physiologically, the nasal passage accounts for 25% of the total resistance to airflow compared to 60% in adults [63]. As the basicranium is flat, the nasopharyngeal volume is small. Other significant differences include the large infant’s occiput, the relatively large tongue, the high position of the larynx at the C3–4 level rather than the C6–7 level as seen in the adult, as well as the configuration of the larynx [3] (see Chap. 2). Until the age of 8 years, the cricoïd cartilage is the narrowest part of the child’s upper airway, and the subglottic area is predisposed to oedema caused by infection (croup) or mechanical trauma (endotracheal intubation or bronchoscopy). The trachea’s internal dimension in the newborn is approximately one-third of that of the adult, and absolute resistance to airflow is higher than in older children and adults (see Sect. 2.7.2, Chap. 2). Physiologically, the infant is an obligate nose breather during the first months of life. Forty percent of term newborns are unable to breathe by mouth. By 5 months of age, nearly all infants are capable of regular oral breathing [63]. During infancy, several factors such as inflammation, secretions, external pressure at the nasal nares, and decreased lingual or pharyngeal muscle tone may induce potentially severe airway obstruction, given that laminar flow resistances increase proportionally with the fourth power of the luminal radius. The larynx, trachea, and bronchi are considerably more compliant in infants than adults, rendering these structures highly susceptible to distensible and compressive forces [63]. Supra-normal inspiratory efforts due to laryngotracheal obstruction may result in significant and dynamic extrathoracic airway collapse below the obstruction. The same phenomenon occurs at the supraglottic level, causing further airway obstruction,
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adding to that already present. Furthermore, agitation and crying lead to marked transmural pressure changes that may further increase airway collapse. In infants, basal metabolism is threefold higher than in adults. The infant’s respiratory rate and minute ventilation are increased in the same proportions. Their adaptation to chronic upper airway obstruction may lead to a particular physiopathological pattern. Inspiratory time is fixed and often prolonged depending on the severity of the airway stenosis. Therefore, infants and children adapt themselves by decreasing the expiratory time via forced expiration. This results in increased intrathoracic pressure and dynamic expiratory collapse. With time, severe and diffuse peripheral broncho(tracheo)malacia develops with a wheezy auscultation that possibly leads to the erroneous diagnosis of asthma. Typically, b2-agonist inhalations are totally ineffective in these patients. As for severe tracheomalacia, long-term positive end-expiratory pressure (up to 15 cm H2O) delivered via a face mask or a tracheostomy can counteract the positive intrathoracic pressure. This particular respiratory pattern may also be seen in severely neurologically impaired children with chronic supraglottic dynamic obstruction due to impaired laryngopharyngeal neuromuscular coordination [9]. In this context, chronic forced expiratory efforts create large intrathoracic pressure swings, leading to severe and at times intractable gastro-oesophageal reflux, which is less often observed in other patients with laryngotracheal problems but without active expiration.
20.8.2 General Aspects of Peri-operative Intensive Care Management After Laryngotracheal Surgery It is beyond the scope of this section to describe in detail all the postoperative conditions the paediatric intensivist may be confronted with. There are short PICU stays after minor endoscopic procedures or major laryngotracheal procedures when the child remains tracheostomy-dependent after surgery. The aim of this section is to focus on major single-stage surgery without postoperative tracheostomy. Children remain electively intubated for several days in order to bypass vocal cord oedema and
20.8 Perioperative Intensive Care After Major Laryngotracheal Surgery in Infants and Children
facilitate wound healing. When considering partial cricotracheal resections, single-stage surgery represented 62% of the procedures performed on 100 patients in a recent review conducted by our institution [22]. Of these, 91 patients were from other countries, and 82% were tracheostomy-dependent. In total, 38 children had undergone previous surgery. When children are admitted to the PICU, a meticulous clinical history must be obtained, and any aspect of the surgical and anaesthetic procedures be retrieved. Given that 40% of patients present comorbidities such as heart defects or congenital syndromic or non-syndromic anomalies, special attention must be paid to these conditions in order avoid additional complications. A past history of reactive airways or chronic dyspnoea must be searched for. The length of intubation and the need for sedation should be discussed with the surgeon, along with the planning of the pre-extubation laryngoscopic examination. Generally, patients are intubated using the nasotracheal route with a very soft Portex® Blue line endotracheal tube. The nasotracheal route is preferred as it is more comfortable for conscious patients, causes less stimulation of the gag reflex, and is more easily secured. Moreover, using the nasotracheal route prevents children from biting the tube, as they often do with the paediatric endotracheal tube, which is smaller and less rigid than that used on adults [62]. In these patients, mechanical ventilation is usually simple, as their lung function is not severely impaired. Modern artificial ventilators easily monitor any decrease in respiratory compliance or increase in resistance. Flow and pressure curves are continuously registered. In our institution, online end-tidal CO2 (ET-CO2) monitoring is the rule. With respect to intubated children, a one-to-one ratio for nurses and patients is ensured. Finally, it should be noted that positive ventilation pressure, even at a low mean airway pressure, increases fluid retention, often requiring small diuretic doses so as to stabilise the fluid balance. In more complex cases, a smaller endotracheal tube than the one recommended for age should be inserted. Pressure-controlled ventilation must be used, with an acceptable 50% air-leak. This ensures accurate monitoring of the first portion of the expiratory CO2 curve. Furthermore, closer nursing survey, fine positioning of the patient’s head, and more frequent blood gas analyses are necessary.
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More complex is the management of analgesia and sedation, with or without neuromuscular blockade following PCTR. Preventing head and neck movements as well as those of the endotracheal tube in order to minimise the risk of anastomotic dehiscence constitutes the rationale for deep sedation and analgesia with continuous muscular paralysis [33]. In 2001, the Cincinnati group reported that older developmentally appropriate children who were not sedated and allowed unrestricted activities, presented shorter PICU and hospital stays, with a decreased incidence of postoperative adverse events [36]. It should be noted that this technique can only be applied after single-stage LTR but not single-stage PCTR due to the risk of anastomotic dehiscence. In a recent publication, Roeleveld reported that short-term use of muscle relaxants was associated with shorter mechanical ventilation, as well as shorter PICU and hospital stay [56]. From a practical point of view, morphine at a rate of 20–30 mg/kg/h and midazolam at a rate of 30 mg/ kg/h are used as a continuous infusion for analgesia and sedation. Midazolam dosage has decreased dramatically during the last years, due to frequent paradoxical excitement seen in small children following administration of this drug [33]. As for other PICU patients, this regimen may be adequately applied to 70–80% of the children. Chloral hydrate is given as necessary, and at times small doses of propofol are added to older patients. If analgesia and sedation are needed during more than 1 week, tolerance develops and dosage increases are required, with the subsequent risk of a withdrawal syndrome. This necessitates a slow tapering of the drug. More recently, in severe cases, we administer a2-adrenergic agonists prior to opioid weaning in order to prevent the occurrence of a withdrawal syndrome. Over time, the use of muscular paralysing drugs has dramatically decreased in our institution. Currently, in most patients, intermittent doses of vecuronium are tapered over 3 to 4 days. In some patients, muscular paralysis is totally avoided, even following SS-PCTR with limited airway resection. When the use of paralysing drug is prolonged, special attention must be paid to prevent pressure sores. In addition, frequent changes of the patient’s position decrease lung atelectases. Moreover, protective dressings and air mattresses appear very useful. Peri-operative prophylactic use of antibiotics has not been extensively debated in scientific literature. In
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tracheotomised children who represent the majority of LTS patients, colonisation of the lower airways was reported to occur in 95% of the cases. When infection developed, Haemophilus influenzae, Staphylococcus aureus, Acinetobacter baumanii, and Pseudomonas aeruginosa were the main causative pathogens [49]. The last named two bacteria are not sensitive to usual peri-operative antibioprophylaxis, such as cefuroxim or aminopenicillin. Therefore, preoperative assessment of tracheal colonisation is beneficial for the choice of the best perioperative antibiotic. Providing optimal nutrition to infants and children requiring intensive care is another significant challenge. Preoperative malnutrition may be observed in tracheotomised children with increased breathing work. Contrarily to adult ICU patients, sedated, analgesied and afebrile PICU patients are not hypermetabolic during artificial ventilation. In over 70 artificially ventilated patients, our daily indirect calorimetric measurement revealed stable energy expenditure during the first postoperative week. Measured energy expenditure amounted to 55% of the recommended dietary allowances (RDA) for healthy children. In fact, children admitted to the PICU following laryngotracheal reconstruction may be fed enterally on the day of admission, with progressive increases over the following days in order to reach 60% of RDA after 4–5 days, and 80% at day 10. In addition, supplements of calcium, magnesium, oligo-elements, and vitamins must be provided. If the patient has no past history of gastro-oesophageal reflux, gastric feeding may be administered, provided it is well tolerated. Otherwise, transpyloric feeding is prescribed. Lastly, proton pump inhibitors and prokinetics are routinely administered to these patients.
20.8.3 Post-Extubation Respiratory Care Management Prior to scheduled extubation, endoscopic examination is performed in order to ascertain that the child can be safely extubated. In small children and complicated cases, extubation may be facilitated by the administration of low doses of analgesics and sedatives that decrease anxiety and crying, which inevitably aggravate respiratory distress. The following drug dosages
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are used in our PICU: 1–3 mg/kg/h Propofol and 10–30 mg/kg/h Morphin. Additional 20–30 mg/kg per dose Chloral hydrate or 0.5–1.0 mg/kg per dose Chlorpromazin thrice daily may also be given on an individual basis if necessary. Following major laryngotracheal procedures, most children present signs of partial upper airway obstruction at extubation, mainly due to oedematous swelling of the vocal cords after PCTR. Prednison (2 mg/kg) given intravenously the day prior to extubation, along with adrenaline aerosols (50–100 mg/kg in 5 mL saline solution) administered at extubation, has been shown to decrease glotto-subglottic oedema. In a significant proportion of infants and small children, airway obstruction persists for a prolonged time period after PCTR, and persistent increased inspiratory efforts contribute to a further increase in airway resistance and breathing work. To alleviate this vicious circle that inevitably leads to reintubation, two techniques have been recommended, notably use of non-invasive face mask ventilation with continuous positive airway pressure (CPAP) or inhalation of heliox, a helium–oxygen mixture delivered through a face mask.
20.8.3.1 Non-Invasive Ventilation in Infants and Children Non-invasive ventilation (NIV) delivers respiratory support without the need of endotracheal intubation or tracheostomy. This minimises the risk of nosocomial infections, upper airway injuries, as well as sedation and analgesia requirements. Since the introduction of CPAP in neonatal units [26] in the 1970s, NIV has increasingly been used in various paediatric patient groups. Bilevel positive airway pressure (BiPAP) provides both inspiratory and expiratory airway pressure, resulting in lung recruitment. This maintains an adequate functional residual capacity while decreasing the inspiratory muscle load. However, data related to bilevel NIV in children refers mainly to highly heterogeneous groups and small case series [5]. Furthermore, in the paediatric patient population, comparative data on the non-invasive interface is virtually absent, despite the crucial role of this equipment piece in causing both successful ventilation and adverse effects. In addition, there is an appalling paucity of face masks available for paediatric use, particularly for infants [51].
20.8 Perioperative Intensive Care After Major Laryngotracheal Surgery in Infants and Children
In the paediatric population, the use of bilevel NIV has been reported in various acute settings, such as respiratory failure after extubation, communityacquired pneumonia in PICU [14], acute lower airway obstruction [61], upper airway obstruction as laryngotracheomalacia [15], and for the optimum timing of subglottic stenosis surgery [70]. Non-invasive positive pressure ventilation is also commonly used in chronic home-care settings for children with neuromuscular disease or obstructive sleep apnoea [16]. Both the ventilator and the interface (tubing and mask) have been poorly described in the literature. In the 1990s, conventional artificial ventilators were used with inspiratory and expiratory tubings. Such a set-up dramatically increased the weight of the interface, requiring a tighter mask fixation resulting in an increased risk of pressure sores. During the last 10 years, turbine-driven flow generators have been developed, with modern ventilators for invasive ventilation including practically all features and modes. They comprise a tube with an expiratory valve at the patient’s end or a mask with holes, providing a continuous airflow leak in the system. Pressure variations are delivered by increasing the turbine speed. As in adults, pressure support constitutes the most comfortable mode to assist inspiratory efforts. The trigger function senses either pressure or flow changes within the system. Its sensitivity is of fundamental importance in small children with low tidal volumes and high respiratory rates. The end of inspiration (expiratory trigger) is mostly defined by the decline in inspiratory flow. Most devices use room air without humidification. Only for the last-generation devices was a humidification chamber added. If higher FiO2 is required, adding oxygen flow into the inspiratory tube may dramatically decrease the device’s trigger sensitivity. In our PICU, oxygen is added at the room air entry in the machine, and the fraction of oxygen is measured at its output port. Our experience with non-invasive ventilation in children began approximately 10 years ago [65], with continuous learning curves towards younger and smaller children. Medical, nursing, and physiotherapy staffs are collaborating in these patients’ care management. Small children under non-invasive ventilation require the same close survey and monitoring as those under artificial ventilation. Indeed, acute
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dysfunctions, such as mask displacement which may obstruct the nostrils, are likely to present the same dramatic consequences as accidental extubation in a ventilated child. To prevent rapid deterioration following extubation in small children having undergone major laryngotracheal surgery, we adopt the following rules: • Extubation is scheduled to occur during the day. Both the anaesthesiologist and ENT surgeon must be available. Beforehand, the physiotherapist has carefully prepared the necessary equipment, including different face masks to initiate non-invasive ventilation. • In infants and toddlers, extubation is mostly performed under light sedation so as to avoid excessive agitation. Close observation of spontaneous breathing by the medical and nursing staff provides precious hints towards the forthcoming scenario. • For most patients, non-invasive ventilation is initiated within the first 10 min. The pressure support mode is used, with positive and expiratory pressure (PEEP: 5–6 cm H2O), Pmax (12–14 cm H2O), and maximal sensitivity of the inspiratory trigger. When using modern devices, it is possible to set up a maximal inspiratory time in order to bypass the expiratory trigger system, when the end of inspiration is not sensed due to numerous air leaks. For this age group, custom silastic smooth nasal masks are used and fixed to a cap (see Fig. 20.38). • Close nursing attention with respect to ideal positioning (30° tilt head) and skin protection with colloidal dressing must be provided. Adequate continuous monitoring (ECG, pulse oxymetry, and impedance respiratory rate) is also essential. • Occurrence of respiratory distress or stridor (typically, 15–30 min after extubation) requires intervention. Chest physiotherapy, adrenaline aerosols, or b2-agonist aerosolisation may be beneficial. • Aerosolisation under NIV requires special attention. Conventional jet nebulizers placed in the inspiratory limb dramatically interfere with the trigger system and are not suitable in this setting. Only ultrasonic and new-generation micropump nebulizers with vibrating plate do not interfere with the NIV settings. Micropump mesh nebulizers (Aerogen Pro, Aerogen, Ireland) are more potent, and drug dosages must be adjusted.
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• In most cases, 6–8 h after extubation, enteral feeding is progressively reinitiated, mostly by using a small naso- or oro-duodenal feeding tube. A second small gastric tube is inserted for gastric air emptying, using an intermittent suctioning pump. • In the majority of cases, NIV may be gradually weaned within a few days. First, NIV parameters are decreased, following which NIV pauses are permitted, while in some patients, NIV is maintained during sleep for a few days until complete weaning occurs. In more severe cases, prolonged periods of NIV are necessary due to tracheomalacia, prolonged mucosal oedema, intercurrent viral or bacterial infection, or other residual problems [6]. Some patients require reintubation owing to ongoing deterioration. Endoscopic evaluation during the reintubation process is crucial in order to better understand the reasons contributing to extubation failure. A major risk of NIV is to wait too long, while deterioration is already in progress. Emergency reintubation in an exhausted and desaturated child should be avoided at all costs. In rare cases, particularly in patients with neurologic impairment and abnormal laryngopharyngeal coordination, erratic respiration may be observed under NIV. Asynchrony between patient and ventilator may be accepted provided blood gas values remain in a clinically acceptable range. In our series, only patients with severe neurologic deficits eventually required a new tracheotomy. Recently, secondary tracheotomy weaning with non-invasive positive pressure ventilation has been used [17]. Lastly, panic attacks may be observed in patients with prolonged cannulation who have never breathed through their upper airways. The continuous presence of parents, along with administration of light neuroleptic medication, is of great help in preventing reintubation or tracheotomy.
20.8.3.2 Use of Helium–Oxygen Gas Mixture During the Peri-operative Period The rationale for using a helium–oxygen gas mixture in patients with upper airway stenosis is based on the ninefold lower helium’s density as compared to the air. This lower density is maintained for a helium:oxygen (He:O2 )mixture containing up to 40% oxygen. The
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heliox gas mixture used for medical purposes is composed of 78% He and 22% O2. By decreasing the Reynolds number, flow remains laminar with heliox at much higher flow rates than an oxygen-air mixture. Heliox decreases the resistance to gas flow in the respiratory system, where the air-flow is turbulent, especially at the level of a stenosis. Although Barach’s first description on the use of He in upper airway obstruction and asthma exacerbation dates back to 1934, reports on the optimal use and efficacy of the He:O2 mixture in the paediatric population have only been sporadic, without being supported by evidence-based medicine. A recent review by Myers has further stressed these conclusions [50]. From a theoretical point of view, upper airway obstructions with locally high turbulent flow patterns represent the best indication for He administration in children. Post-extubation stridor, subglottic congenital or acquired stenosis, trauma, tumours, airway infections, as well as post-operative oedema following major laryngotracheal surgery are the principal indications. While using heliox in 42 children admitted for severe upper airway obstruction of various aetiologies, Grosz reported a 73% decrease in breathing work. All prematurely born children were responders, whereas two-thirds of the children with congenital anomalies or syndromes were non-responders [32]. In another report, 10 of 14 patients with severe upper airway obstruction did not require intubation, while the four children who did require intubation had a prior history of mechanical ventilation, with three of them presenting subglottic stenosis [8]. In clinical practice, heliox is rarely used in infants. In our PICU, over a 13-year period, heliox was administered in 55 of 4,170 admissions, and in 36 of 370 children undergoing laryngotracheal endoscopic or open surgery, or following tracheostomy closure. Of 34 patients treated for post-extubation dyspnoea, 5 required reintubation, while 2 patients were re-tracheostomised. It was immediately obvious that these 2 patients were non-responders. Although heliox decreases the breathing work in patients with high airway resistance, its high costs and rarity in the nature must be taken into account. Currently, NIV is our first-line method to support the vast majority of patients. The care of children after major laryngotracheal procedures, particularly SS-PCTR, implies a strong interdisciplinary team approach. Infants and toddlers
20.9 Postoperative Management After Single-Stage PCTR
are particularly vulnerable because of their limited respiratory reserve. A meticulous pre-operative evaluation of comorbidities is of primary importance. Although major surgical and endoscopic progresses have been made, postoperative care is still highly challenging for both medical and nursing teams after single-stage surgery, owing to the permanent risk of rapid deterioration. In the absence of rapid intervention, dramatic events often lead to major neurological sequellae. Over the last 10 years, the medical device industry has made significant technological progress in equipments that provide accurate non-invasive respiratory support, also in infants. It should be noted, however, that NIV needs the same close monitoring and survey as invasive ventilation. In this context, the exact place of He-O2 mixture in the therapeutic arsenal needs to be further defined.
20.9 Postoperative Management After Single-Stage PCTR 20.9.1 Initial Intensive Care Management Following SS-PCTR Children older than 10 years are extubated in the operating theatre upon completion of surgery. Younger children are transferred while still intubated to the PICU. Great care must be taken to maintain the neck in the flexed position by supporting pillows to avoid tension on the anastomosis. We do not use any chin-to-chest position by stay sutures but rather rely on adequate sedation.
Fig. 20.37 Results of single-stage partial cricotracheal resection at postoperative day 7: (a) Preoperative view: minor grade III subglottic stenosis. (b) Postoperative view: patent subglottic airway at postoperative day 7. The absence of fibrin deposits reflects an excellent anastomotic mucosal approximation
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Antibiotics started prior to surgery, based on culture and sensitivity results, are continued for at least 7 days following the intervention. Proton pump inhibitors (PPI), with or without H2-blockers at bedtime, are routinely prescribed for at least 6 weeks or up to 6 months to 1 year in children with established reflux. Great care should be taken to titrate the sedative agent towards the optimal degree of sedation until extubation of the child can be safely performed. Chest X-rays are taken every second day to check for any atelectasis or early bronchopneumonia. Routine chest physiotherapy (gentle percussions or vibrations, with or without devices) is aimed at mobilising distal airway secretions and mucous plugs for alleviating atelectasis. If these measures prove inefficient, a smallsized rigid open-tube bronchoscope is used to clean the lower airways in an atraumatic way, although this is a rare event. Corticosteroid therapy is initiated 1 day prior to the first control endoscopy performed under general anaesthesia in the morning of day 5. The larynx is exposed using the Macintosh anaesthesia laryngoscope, after which a 4-mm adult rigid sinuscope (0°) is passed in order to inspect the larynx for supraglottic or glottic oedema. Under visual control, the Portex nasotracheal tube is withdrawn into the pharynx, and a quick look at the subglottis provides critical information on the quality of mucosal approximation at the site of the anastomosis (Fig. 20.37). The absence of any fibrinous deposit is indicative of a good-quality thyrotracheal anastomosis. The infant or child is reintubated with a one-size smaller soft Portex nasotracheal tube, smeared with a Gentamycin-corticosteroid (Diprogenta®) ointment if vocal cord oedema is prominent and precludes
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tentative extubation. Using a syringe and a large needle, the same ointment is injected around the tube in the supraglottic region. Following this, the child is taken back to the PICU and kept sedated for another 2 days until a further extubation attempt is undertaken. The initial ET tube is gently reinserted through the vocal cords using a Magill forceps if laryngeal oedema is minor or moderate. On the same morning, the child is slowly weaned off sedative drugs until spontaneous breathing is restored. The ET tube must only be removed when the child is still sufficiently sedated to avoid coughing and agitation. A face mask supplying oxygen along with an aerosol of adrenalin is maintained, with careful monitoring of SpO2 levels. Low dose systemic corticosteroids (2 mg/kg of prednisone stat, then 1 mg/kg twice daily) are continued for a few days, and then discontinued gradually. Due to the small airway size in infants and small children, some inspiratory stridor is inevitable during the postoperative period. To counteract the Bernouilli effect created by the swollen vocal cords during inspiration, ventilation of the patient using slight CPAP may be initiated, as this is the only way to break the vicious cycle of fostering vocal cord oedema by mechanical stimulation during inspiration. A triangular face mask surrounding the nasal region is snugly fixed to the head with elastic bands (Fig. 20.38). Heliox, a mixture of He and O2, can also be used to diminish the viscosity of the inspired gas mixture, as it has been shown to reduce stridor, significantly.
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Although the postextubation period may be hectic in small children, spontaneous breathing provides constant information on airway patency. Progressive improvement in breathing is indicative of a normal healing process at the anastomotic site. However, if an initial period of normal breathing is followed by progressive deterioration with stridor, then prompt endoscopic control of the subglottic anastomosis is warranted. The management of anastomotic complications is described in Sect. 20.11.
20.9.2 Continuing PostOperative Care for SS-PCTR As soon as the extubated child breathes comfortably, and tracheal secretions are minimal, feeding is resumed. Thick fluids or soft solid diets are given under close supervision in order to detect any aspiration. In the case of an uneventful recovery, mobilisation or ambulation is begun at the tenth postoperative day. Chest physiotherapy is continued as necessary throughout hospitalisation. The central venous line must be kept in place until the last control endoscopy has been performed at the third week postoperatively, following which patients from foreign countries are allowed to return home. Transnasal fibreoptic laryngoscopy (TNFL) through face mask ventilation is necessary to assess the postoperative mobility of the vocal cords, and a direct laryngotracheoscopy with a 0° rigid 4-mm adult sinuscope is used to carefully inspect the glottis and subglottis for any abnormality. Granulation tissue, if any, is gently removed using a biopsy forceps. At this stage, dilation is avoided to prevent the breakdown of the anastomosis. In most cases, the first endoscopic dilation is carried out during the sixth postoperative week, if deemed necessary.
20.9.3 Follow-Up Care for SS-PCTR
Fig. 20.38 Face mask for continuous positive airway pressure ventilation in the paediatric intensive care unit: The small triangular face mask is adapted to the midface around the nose and is held with elastic bands placed around the head. Continuous positive airway pressure is delivered to alleviate inspiratory stridor
Ideally, patient follow-up after PCTR begins at 6 weeks, with further visits planned at 3 months and 1 year following hospital discharge. On each occasion, a control endoscopy is performed under general anaesthesia, consisting of TNFL and direct laryngotracheoscopy, in order to assess both the laryngeal dynamics and the size of the subglottis.
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20.10 Postoperative Management After Double-Stage PCTR Fig. 20.39 CO2 laser resection of a left subglottic stenosis 3 months after single-stage partial cricotracheal resection: (a) Significant cicatricial tissue at the anastomotic level below the left vocal cord. (b) Status after endoscopic resection using the CO2 laser
At the sixth postoperative week, gentle dilation with tapered bougies may be tried, although true endoscopic dilation for optimising the final outcome is envisaged at 3 months only, when a mature cicatricial anastomosis has been constituted. Suboptimal results necessitate carbon dioxide (CO2) laser resection/incision as well as gentle dilation with additional topical application of mitomycin C. These measures are usually effective in restoring a fairly normal subglottic airway (Fig. 20.39). Tapered bougies provide a precise measurement of the subglottic calibre obtained for the child’s age. For patients from foreign countries, a control endoscopy is scheduled to take place between the third and sixth postoperative months. Our long-term follow-up data on paediatric PCTRs performed for severe LTS have clearly shown that the results obtained at 3 months are maintained in the long run, as evidenced by normal laryngeal growth [37]. None of the patients in whom a satisfactory subglottic airway had been achieved at the third postoperative month needed revision surgery at a later date.
20.10 Postoperative Management After Double-Stage PCTR 20.10.1 Initial Intensive Care Management Following DS-PCTR A double-stage surgery may have been selected for an isolated SGS in a child with a distally placed tracheostomy or additional comorbidities. In this situation, the
subglottic airway is not stented upon completion of the anastomosis. Yet, the majority of double-stage surgeries are the consequence of an extended PCTR in which the SGS is combined with glottic involvement, requiring postoperative stenting with an LT-Mold. The immediate postoperative management is more straightforward, as the child is ventilated through the tracheostomy cannula. After overnight monitoring in the PICU, a chest X-ray is taken to rule out postoperative atelectasis that would require prompt bronchoscopic cleansing of the distal airway. The medical management is similar to that described for SS-PCTR, except for the sedation level. The child is monitored for a short period in a semi-ICU before being transferred to the ward. As the children’s parents are often familiar with care of the tracheostomy, they may efficiently participate in the postoperative routine. Anastomotic separation may occur without giving rise to any symptoms, particularly in a stented airway reconstruction. For that reason, a control endoscopy must be performed on the tenth postoperative day without exception.
20.10.2 Continuing Postoperative Care for DS-PCTR Feeding is resumed early during the immediate postoperative days. The LT-Mold prosthesis ensures efficacious protection of the glotto-subglottic airway, even if the child tends to aspirate. Medication and chest physiotherapy are continued as described for SS-PCTR. At the tenth postoperative day, control endoscopy is
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performed under general anaesthesia. In the setting of a non-stented airway, inspection of the anastomotic site is the only guarantee that no partial separation has occurred, unless the neck dressing is stained with mucous secretions. In extended PCTRs with postoperative stenting using an LT-Mold, a slow and progressive anastomotic separation may occur without giving rise to any clinical signs. The neck may look completely normal, and the old dressing may remain dry, because granulation tissue formation has progressively sealed the air leak around the stent. Only endoscopy under general anaesthesia is able to rule out an anastomotic separation clearly. In the supraglottic region, the prosthesis is usually still in place, as its larger head cannot migrate distally through the vocal cords. If retrograde inspection through the tracheostoma with a 70° or 90° sinuscope reveals cranial migration of the distal extremity of the LT-Mold, then the possibility of an anastomotic separation must be considered (Fig. 20.40). In this case, immediate revision surgery is mandatory (see Chap. 23).
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When endoscopic control at day 10 is satisfactory with no suspicion of incipient anastomotic dehiscence, the
patient is discharged from the hospital and followed up at the outpatient clinic. Patients from foreign countries are advised to stay nearby for another 15 days prior to returning home. The child should refrain from normal activities for another 2 weeks, until the anastomotic site has fully healed. Depending on the complexity of the glotto-subglottic reconstruction, the LT-Mold prosthesis is kept in situ for 6 weeks, or up to 3 or 6 months. The next endoscopy under general anaesthesia is scheduled to remove the prosthesis. Outpatient consultations are recommended to rule out early migration of the LT-Mold stent in between the procedures. During the control endoscopy, the larynx is suspended with a Lindholm laryngoscope placed in the valleculae. This fully exposes the laryngeal inlet. With curved microscissors, the head of the LT-Mold is uncapped, and the fixing prolene threads are cut inside the prosthesis (Fig. 20.41). The LT-Mold is grasped with alligator forceps and easily removed. The prolene threads are firmly seized with cup forceps and pulled out. Usually, the threads come out completely with the knot. If this proves impossible, then the threads are simply cut close to the endolaryngeal mucosa in order to prevent foreign body reactions. Excess granulation tissue is removed using a biopsy forceps, and mitomycin C is applied topically for 2 min at a concentration of 2 mg/ml. Should an initial Grade IV complex
Fig. 20.40 Diagram of clinically unnoticed thyrotracheal separation after extended partial cricotracheal resection with LT-Mold stenting: (a) Initial postoperative status: The LT-Mold is correctly placed with its distal extremity matching the upper edge of the tracheostoma (yellow arrow). (b) Postoperative status after anastomotic dehiscence: The head of the prosthesis lies
correctly in the supraglottic larynx, but the distal extremity has migrated cranially following anastomotic dehiscence (yellow arrows). As the neck is fully normal, this can only be visualised by retrograde subglottic endoscopy using a 70° sinuscope through the tracheostoma. The distal end of the LT-Mold has effectively migrated cranially
20.10.3 Follow-Up Care for DS-PCTR
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20.11 Complications of PCTR
20.11.1 Anastomotic Dehiscence
Fig. 20.41 Endoscopic removal of the LT-Mold: The larynx is exposed with a Lindholm laryngoscope, and the head of the prosthesis is uncapped with curved microscissors. The prolene fixation threads are cut inside the prosthesis, which is removed with an alligator forceps. The prolene threads are pulled out with a cup forceps
transglottic stenosis have induced excessive granulation tissue formation, it is best to reinsert an LT-Mold endoscopically for another 4-week period after topical mitomycin C application (see Sect. 18.3, Chap. 18). During the next control endoscopy, the stent is removed if the glotto-subglottic airway is fully healed.
20.11 Complications of PCTR Neck haematomas and wound infections are exceedingly rare in the postoperative period. These complications never occurred at our institution in our series of 108 PCTRs. Pulmonary complications such as lobar atelectasis or bronchopneumonia may be observed. Normally, they respond well to medical treatment and pulmonary physiotherapy. Bronchoscopic intervention to dislodge a mucous plug is seldom necessary. Broncospasm with episodes of wheezing may require bronchodilator administration for several weeks or months. Among the complications, anastomotic dehiscence, RLNs injury, and delayed recurrent stenosis are the most frightening. In DS-PCTR, tracheostomy-related problems (i.e. stenosis with A-frame deformity, suprastomal collapse, and localised malacia) may require additional surgery for tracheostoma closure (see Sect. 21.4.1, Chap. 21).
Though an infrequent complication (6/108 PCTRs = 5.6%) in our series, dehiscence may be lifethreatening if it occurs after hospital discharge. It is also a common cause of surgical failure. It is noteworthy that this complication usually occurs after the tenth postoperative day (five out of six in our series), so the need for a careful follow-up after the first postoperative week must not be underestimated. A perfect mucosal approximation with no fibrinous deposit at the anastomotic level is unlikely to evolve into an anastomotic separation within the next days. Alternatively, fibrinous deposits may represent an incipient anastomotic separation. Some may heal fully, while others may lead to late recurrent stenosis, as granulation tissue progressively fills the gap. When the airway is chronically contaminated with MRSA or Pseudomonas aeruginosa, the risk of restenosis is markedly increased. It is noteworthy that an anastomotic dehiscence never occurs abruptly. The signs of dehiscence are always present, though discrete in some patients. After an initial uneventful postoperative period, a slight biphasic stridor with a ‘washing machine’ type of respiration should alert the physician. This noisy breathing results from the back and forth movements of tracheal secretions at the partially dehiscent anastomotic level. The neck may remain normal, but the suspicion of anastomotic dehiscence is strengthened by mucous stains on the neck dressing around the Penrose drain. Immediate endoscopic assessment of the subglottic airway followed by revision surgery should then be performed as necessary. Endoscopy findings may not reflect the severity of anastomotic dehiscence in all cases (Fig. 20.42). Revision surgery consists of refreshing the tracheal stump by resecting one or two further tracheal rings. An additional full laryngeal release procedure and more mobilisation of the intrathoracic portion of the trachea may be needed. On the laryngeal side, the thyroid cartilage cannot be partially resected. If its inferior portion is altered by the anastomotic dehiscence, then new anastomotic stitches must be sewn around the superior thyroid edge, as shown in Fig. 20.43. A strong reinforcement of the anastomosis on the laryngeal side results from this procedure. When the situation is dire and a new thyrotracheal anastomosis cannot be accomplished without excessive tension, a tracheostomy must
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Fig. 20.42 Anastomotic dehiscence 3 weeks after single-stage partial cricotracheal resection for grade III subglottic stenosis: (a) Preoperative view: grade III subglottic stenosis. (b) Anastomotic dehiscence 3 weeks after single-stage partial
Fig. 20.43 Revision surgery for anastomotic dehiscence after partial cricotracheal resection: The tracheal side is refreshed by further resecting one or two tracheal rings. Tracheal mobilisation and a full laryngeal release procedure are performed. On the laryngeal side, which cannot be re-resected, anastomotic stitches must be shrouded around the superior edge of the thyroid cartilage (white arrows)
be placed distally to the thyrotracheal anastomosis. An LT-Mold prosthesis is introduced through the dehiscent anastomosis and fixed to the larynx to calibrate the airway. The anastomosis is then reinforced anteriorly with a large strip of tibial periosteum sutured at different levels of the thyroid cartilage and suprastomal
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cricotracheal resection due to respiratory syncytial virus infection with severe coughing. (c) Final outcome 3 weeks after revision surgery: patent glotto-subglottic airway, albeit with thinned vocal cords
Fig. 20.44 Reinforcement of thyrotracheal anastomosis during revision surgery for anastomotic dehiscence after partial cricotracheal resection: A patch of tibial periosteum is additionally placed over the thyrotracheal anastomosis, glued to the trachea using Tisseel®, and fixed at different levels of the thyroid cartilage and trachea (red threads). The airway is calibrated by an LT-Mold, and a distal tracheostomy is placed in the lower neck
trachea, with additional fibrin glue applied to seal the anastomosis underneath the periosteum (Fig. 20.44). In DS-PCTR, the subglottic airway has usually been splinted by the LT-Mold prosthesis. After having performed a laryngeal release procedure and extensive intrathoracic tracheal mobilisation, the anterior anastomosis is simply reaccomplished and reinforced as described above.
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20.12 Results of Paediatric PCTR
20.11.2 Recurrent Laryngeal Nerve Injury After PCTR In SS-PCTR, a unilateral RLN injury may complicate the postoperative recovery, particularly in small children. If extubation is not tolerated despite a patent subglottic airway, then a distally placed tracheostomy is required. A bilateral RLN injury should not occur if the surgery is carried out as described. Should this uncommon event occur, a temporary tracheostomy must be created before definite treatment is envisaged (see Sect. 7.2.2, Chap. 7).
20.11.3 Delayed Recurrent Stenosis After PCTR Recurrent stenosis generally results from a slow and progressive partial anastomotic dehiscence occurring over a 3- to 6-week period. As in the case of postintubation stenosis, the child experiences progressive dyspnea with biphasic stridor, requiring an endoscopic assessment along with therapeutic measures (CO2 laser and/ or dilation) or revision open surgery if the recurrent stenosis is severe or extensive in the craniocaudal axis.
20.11.4 Tracheostomy-Related Stenosis After DS-PCTR Suprastomal collapse and granuloma or an A-frame deformity of the trachea with localised malacia at the former site of the tracheal stoma are the two main causes of stenosis. Treatment of these two conditions consists of either resection and anastomosis of the diseased tracheal segment or tracheoplasty with anterior costal cartilage graft. These procedures are described in Sects. 22.1.1 and 22.6, Chap. 22.
20.12 Results of Paediatric PCTR Mercy George, MD Evaluation of outcomes following LTR or PCTR suggests the possibility of establishing an international standard of treatment for children with LTS. This
endeavour is difficult and often biased by a number of parameters (e.g. grade of stenosis, glottic involvement, or severe comorbidities) that may influence the operation-specific and overall decannulation rates, without considering the outcomes in voice quality. A small case series, more often than not, comprises a mixture of several conditions in which only one parameter is analysed (e.g. decannulation rates) based on the grade of stenosis. In contrast, analyses of results in larger series (100–200 patients), when classified into different subgroups, fail to achieve statistical significance due to the small number of patients in each subgroup. It should be noted that the initial experience with any technique (e.g. PCTR or LTR) shows better results due to the bias in patient selection (more favourable cases), as can be seen in Table 20.4. A strict comparison of results in a matched series of patients is extremely difficult and warrants the introduction of an internationally recognised reporting system for surgical outcomes following LTR and PCTR (see Table 19.2, Chap. 19). The two major published case series [22, 69] of paediatric PCTRs for severe LTS are compared in Table 20.5. These series are well matched for most variables analysed. In the Lausanne cohort, there were slightly more patients with associated glottic involvement (a known factor for a less favourable outcome) and less salvage surgeries than in the Cincinnati cohort. The operation-specific and overall success rates were roughly comparable; however, the Lausanne cohort had fewer revision surgeries and a slightly lower overall success rate. This small difference may not be relevant since some children are awaiting decannulation. Among the variables analysed as potential risk factors for delayed decannulation or unsuccessful Table 20.4 Published results of overall decannulation rates after paediatric PCTR for severe Grade III and IV SGS Ranne et al. [55]
(1991)
7/7
~
100%
Monnier et al. [43]
(1993)
14/15
~
93%
Vollrath et al. [67]
(1999)
8/8
~
100%
Triglia et al. [64]
(2000)
10/10
~
100%
Garabedian et al. [20]
(2005)
16/17
~
94%
Alvarez-Neri et al. [1]
(2005)
20/22
~
91%
White et al. [69]
(2005)
87/93
~
94%
George et al. [22]
(2009)
90/100
~
90%
Total
(2009)
238/257
~
92.6%
316
20 Partial Cricotracheal Resection
Table 20.5 Results of PCTR for severe Grade III and IV LTS Lausanne Patients’characteristics Cincinnati [22] [69] n = 100 n = 93 Stenosis Grade II
5%
4%
III
60%
64%
IV
35%
32%
Glottic involvement
23%
33%
Comorbidities
NR
45%
Tracheostomy at surgery
85%
82%
Primary PCTR
46%
62%
Salvage PCTR
59%
38%
Extended PCTR
27%
23%
Revision surgery
29%
14%
Operation-specific success rate
71%
76%
Overall success rate
94%
90%
Anastomotic dehiscence
2%
4%
RNL injury
2%
0%
Results
underwent PCTR between 1978 and 2008 in Lausanne. Data on 100 patients with at least a 1-year follow-up were collected and analysed. At the time of surgery, the mean age was 5 years (ranging from 1 month to 14 years with a median of 3 years). Ninety-one patients were referred from other centres. Postintubation injury was the most frequent aetiology. Overall, 38 patients had prior endoscopic dilations, laser surgery or open airway surgery before being treated in Lausanne. Among previously failed open surgical procedures, the most common was LTR. Most of the patients presented severe Grade III stenosis (n = 64, pinhole residual opening). In our series, 32 patients had Grade IV and 4 patients had Grade II stenosis. Subglottic stenosis combined with vocal cord involvement was seen in 33 patients. A further 82 patients were tracheostomised upon arrival. Postoperative assessment with a minimum 1-year follow-up included endoscopic evaluation of the airway as well as vocal cord mobility; duration of stenting (after extended PCTR); the need for open or endoscopic revision procedures; decannulation status; and long-term assessment of breathing, voice, and swallowing based on patients’ or parents’ views as described in a 2008 questionnaire.
NR = not reported
decannulation, glottic involvement (neurogenic or cicatricial impairment of vocal cord mobility, posterior glottic stenosis or vocal cords fusion) was the most significant risk factor, often requiring extended PCTR [22, 23, 48, 69]. The presence of severe congenital anomalies, associated comorbidities (e.g. gastro-oesophageal reflux), eosinophilic oesophagitis, preoperative airway contamination with MRSA or Pseudomonas aeruginosa, secondary airway obstructions (e.g. pharyngeal collapse, mandibular hypoplasia, obesity), or tracheal damage warrants evaluation of larger patient cohorts to establish statistically significant predictors of failure. On the contrary, salvage surgery or surgery on patients with Down syndrome did not influence final outcomes (decannulation rates) following PCTR.
20.12.1 Surgical Data on PCTR for Severe Grades III and IV LTS Using an ongoing database, a retrospective chart review was conducted on 108 paediatric patients who
20.12.1.1 Overall and Operation-Specific Decannulation Rates Ninety patients underwent successful decannulation after partial cricotracheal resection for severe SGS. Seven patients are still on a tracheostomy tube. One patient who developed restenosis after PCTR refused further treatment and hence could not be decannulated (n = 1). The reasons for unsuccessful decannulation in the six remaining patients included neurologic dysfunction and respiratory insufficiency due to campomelic dystrophy (n = 1), upper airway collapse and aspiration in a patient with CHARGE syndrome (n = 1), and gastro-oesophageal reflux and aspiration (n = 2). After establishing an initial satisfactory airway, one patient with idiopathic progressive subglottic stenosis is still undergoing treatment due to the progressive nature of the disease (n = 1). The last patient is on an LT-Mold after extended PCTR and awaits decannulation (n = 1). Three patients died before decannulation could be achieved, the cause of death being tracheostomy tube obstruction at home in two patients, and in the remaining patient, respiratory insufficiency despite
317
20.12 Results of Paediatric PCTR
a tracheostomy cover due to thoracic cage malformation secondary to spondylo-epiphyseal dysplasia (SED). Overall mortality was 7%. No death was directly related to the surgical procedure. Both overall and operation-specific decannulation rates were 100% in the Grade II stenosis group (n = 4). In the Grade III stenosis group (n = 64), the overall decannulation rate was 95% (61/64), and the operation-specific decannulation rate was 80% (51/64). In the Grade IV stenosis group (n = 32), overall decannulation rate was 78% (25/32), and operation-specific decannulation rate was 66% (21/32). It is noteworthy that in the entire series, the reason for unsuccessful decannulation was restenosis in only one patient.
20.12.1.2 Single-Stage PCTR (N = 62) In 62 patients, single-stage PCTR was used to treat either isolated severe subglottic stenosis (n = 47) or severe SGS with minor glottic or supraglottic involvement (n = 15). In the entire group of 62 patients, 6 required secondary tracheotomy among which 4 could be decannulated at a later date. The reason for secondary tracheostomy was mucosal prolapse due to posterior submucosal cleft (n = 1), tracheomalacia (n = 2), upper airway obstruction due to hypoplastic mandible (n = 1), respiratory insufficiency due to campomelic dystrophy (n = 1), and posterior glottic stenosis (n = 1). Overall decannulation rate was 97% (60/62). For isolated severe Grades III and IV SGSs, overall decannulation was 98% (46/47), and the operation-specific decannulation (signifying no need for a second procedure) was 91% (44/47).
20.12.1.3 Double-Stage PCTR (N = 38) In the remaining 38 patients, there were 17 with isolated subglottic stenosis and 21 with combined glottosubglottic stenosis. The overall decannulation rate is currently 79% in this group (30/38). Among the 17 patients with isolated subglottic stenosis, decannulation could be achieved in 14/17 patients (82%), whereas only 16/21 (76%) achieved decannulation in the glottosubglottic stenosis group. These results reinforce the importance of glottic involvement as a significant prognosticator of failure to decannulate.
20.12.1.4 Children Weighing Less Than 10 kg at the Time of Surgery At the time of surgery, 36 children (21 males, 15 females) weighed less than 10 kg of bodyweight. Their mean age was 16 months, and their mean bodyweight was 8.8 kg (range 4.4–9.9 kg). A single-stage procedure was performed in 27 (75%) patients, with a mean period of 10 days (range 5–21 days) until final extubation. The decannulation rate following single-stage PCTR was 100% (27/27). Nine children underwent a double-stage procedure, and six out of nine (67%) children are at present decannulated. Of these nine children, five were decannulated within 6 months, one within 20 months, and one is awaiting decannulation, while two children died before decannulation could be achieved. The first of these two children suffered from congenital spondylo-epiphyseal dysplasia and died of respiratory insufficiency at home after PCTR while he was still tracheostomy-dependent. The second child died at home of cannula obstruction 1 year after surgery. The present overall decannulation rate for the entire children’s group is 92% (33/36 patients).
20.12.1.5 Glotto-subglottic Stenosis Thirty-three children with combined glotto-subglottic stenosis underwent PCTR with repair of glottic pathology. Their ages ranged from 6 months to 16 years (median, 5.3 years). Thirty-two (97%) of 33 patients had Myer Cotton Grade III (n = 16) or IV (n = 16) stenosis, whereas one patient had Grade II stenosis with glottic involvement. Thirty-one (94%) patients were tracheostomised, and two patients (6%) had severe stridor on their arrival. The glottic pathology included posterior commissure stenosis with bilateral fixed cords in 19 patients, bilateral restricted abduction of vocal cords in 7 patients, and unilateral fixed vocal cord in 7 patients. Ten out of 33 patients underwent a single-stage PCTR with interarytenoid scar excision (with free or pedicled mucosal graft) and the endotracheal tube used as a stent in the postoperative period. Extended PCTR was done in 23 patients. The additional procedure included posterior cricoid split with (n = 18) or without (n = 1) costal cartilage graft, and separation of fused vocal cords (n = 4). A pedicled flap of the membranous trachea was used to realign the cartilage graft of the
318
denuded cricoid plate in all cases. The reconstruction was splinted with a Montgomery T-tube in 8 patients at the beginning, and with an LT-Mold in the next 15 patients. Postoperative endoscopies were performed in all patients, and a majority required several endoscopies (mean, 4.2; range, 1–11), with or without dilation or granulation tissue removal. In the series of 33 patients, extubation or decannulation was achieved in 26 patients (overall decannulation rate = 79%) within a period ranging from 1 week to 3 years (mean, 8 months; median 3 months). The reason for unsuccessful decannulation (n = 4) was association of comorbidities or syndromic anomalies, which included neurological dysfunction, gastro-oesophageal reflux disease, or extra-laryngeal obstruction regardless of a satisfactory postoperative airway. One patient with idiopathic stenosis and associated fructosemia developed restenosis after an initially satisfactory result. Another child who still awaits decannulation had to undergo endoscopic laser epiglottopexy for epiglottic prolapse. A patient with spondylo-epiphyseal dysplasia with thoracic cage malformation succumbed to the primary pathology prior to decannulation.
20.12.1.6 Revision Open Surgery In total, 14 patients (14%) needed revision open surgery. Their ages ranged from 2 months to 12 years (mean, 4.5 years; median, 2.9 years). Ten patients had severe Grade III stenosis, and four had Grade IV stenosis. Association of glottic involvement was observed in six patients. Recurrent or residual posterior glottic stenosis was the most common cause of revision open surgery (five patients). Four patients (4%) had revision surgery for partial anastomotic dehiscence. One patient underwent supraglottoplasty. One patient had anterior LTR for suprastomal collapse. Three patients required revision PCTR for flap necrosis (n = 2) and restenosis (n = 1).
20.12.1.7 Delayed Decannulation Group (>1 year) Nine patients who had delayed decannulation (>1 year) belonged either to Grade III (n = 4) or Grade IV (n = 5) stenosis categories. The mean age of these patients was 4.9 years (median, 2.9 years). Eight patients had
20 Partial Cricotracheal Resection
associated glottic involvement or comorbidities contributing to the delay in decannulation. Five had prior endoscopic laser or surgical interventions (LTR before management in Lausanne). The delayed decannulation was due to recurrence of posterior glottic stenosis (n = 3), flap necrosis (n = 1), laryngomalacia (n = 1), upper airway obstruction secondary to mandible hypoplasia (n = 1), or prolonged stenting (n = 3).
20.12.1.8 Long-Term Follow-Up In 2008, a questionnaire intended to assess the current functional state of the patient was sent. Seventyseven children were available for long-term follow-up, meeting the criterion of a minimum 1-year followup. Eighteen patients had reached adulthood and were able to respond to the questionnaire by themselves. Laryngotracheal development was found to be normal in all.
Breathing During long-term follow-up, 50 of 77 patients (65%) had normal breathing, and 33 demonstrated dypnoea during major physical exercises (30%). Four patients reported having dyspnoea even with mild exertion. None had dyspnoea at rest.
Voice Among the 77 patients available for a long-term outcome, 31 patients had isolated SGS free of the vocal cords, and 30 had SGS reaching the under surface of the vocal cords, with or without partial impairment of abduction. Twelve patients presented associated posterior glottic stenosis (PGS) or vocal cord fusion (without cricoarytenoid ankylosis), and four patients had transglottic stenosis or bilateral cricoarytenoid ankylosis. The long-term voice outcome following PCTR, as perceived by the parents or patients, was normal in 18% of patients (14 of 77), and the remaining 62 demonstrated mild to severe dysphonia. Patients with isolated SGS or SGS reaching the undersurface of the vocal cords had normal voice quality or mild dysphonia following PCTR. Patients with associated posterior glottic stenosis but no cricoarytenoid joint fixation had
20.12 Results of Paediatric PCTR
dysphonia, which was mild to moderate in severity. All patients with transglottic stenosis or cricoarytenoid joint fixation exhibited severe dysphonia.
Swallowing No patient developed new symptoms of dysphagia or worsening of dysphagia following PCTR, even after a laryngeal release procedure. During long-term followup, swallowing was normal in 72 patients (94%). Four patients with postoperative mild dysphagia experienced occasional coughing episodes during meals. One patient with oesophageal atresia and laryngeal malformation continued to need a naso-gastric tube after PCTR.
Global Satisfaction The postoperative result was assessed as ‘excellent or very good’ in 64 patients (83%). Thirteen (17%) patients rated the results ‘good or fair’ due to the residual dysphonia.
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321 Otolaryngology, p. 533. Lippincott-Raven, Philadelphia/ New York (1999) 69. White, D.R., Cotton, R.T., Bean, J.A., et al.: Pediatric cricotracheal resection: surgical outcomes and risk factor analysis. Arch. Otolaryngol. Head Neck Surg. 131, 896–899 (2005) 70. Wormald, R., Naude, A., Rowley, H.: Non-invasive ventilation in children with upper airway obstruction. Int. J. Pediatr. Otorhinolaryngol. 73, 551–554 (2009) 71. Wrightson, F., Soma, M., Smith, J.H.: Anesthetic experience of 100 pediatric tracheostomies. Paediatr. Anaesth. 19, 659– 666 (2009)
Part Tracheal Surgery and Revision Surgery
Acquired isolated tracheal stenoses are less common in children than in adults. Since the introduction of soft non-cuffed ET tubes for use in infants and small children, and low-pressure, high-volume cuffs for use in older children [1], post-intubation tracheal stenoses have become insignificant. In a series published by Weber et al., among 62 non-tracheostomised children treated for acquired tracheal stenosis [2], there were 44 (71%) with post-intubation stenosis and only 15 (24%) with stenoses involving the mid- or lower trachea. All the other post-intubation stenoses affected the subglottis or upper trachea. The remaining aetiologies, accounting for less than 30% of all cases, comprised caustic injuries, recurrent infections, endoscopic trauma and gastric aspiration. In the paediatric age group, acquired tracheal stenoses are mainly related to tracheostoma-related problems. It is important to stress that prevention of complications at the stoma site begins with using an adequate surgical technique and selecting a tracheostomy tube ideally adapted to the anatomy of the individual patient. Furthermore, careful nursing of the cannula, that is, endoscopic tracheal inspection at regular time intervals, enables prompt treatment of superinfection, thereby preventing granulation tissue formation at the stoma tract or cannula tip.
With the exception of congenital tracheal anomalies (see Chap. 13), paediatric tracheal surgery mainly consists of performing tracheotomy and treating its associated complications. This chapter focuses on tracheotomy and its related complications, such as tracheal stenosis, tracheoinnominate artery fistula and tracheo-oesophageal fistula. Furthermore, decannulation strategies, as well as methods for surgical closure of the tracheostomy, are described. Tracheal resection and anastomosis, cervical slide-tracheoplasty and tracheoplasty with costal cartilage graft for the management of cicatricial tracheal stenoses are also addressed. Lastly, an entire chapter is devoted to revision procedures following laryngotracheal surgery.
References 1. Morris, L.G., Zoumalan, R.A., Roccaforte, J.D., et al.: Monitoring tracheal tube cuff pressures in the intensive care unit: a comparison of digital palpation and manometry. Ann Otol Rhinol Laryngol 116, 639–642 (2007) 2. Weber, T.R., Connors, R.H., Tracy Jr., T.F.: Acquired tracheal stenosis in infants and children. J Thorac Cardiovasc Surg 102, 29–34 (1991)
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Tracheotomy
Contents
Core Messages
21.1
›› Current indications for tracheotomy include:
Indications............................................................... 326
21.2 Technique of Tracheotomy..................................... 326 21.2.1 Location of Tracheotomy.......................................... 326 21.2.2 Operative Technique for Tracheotomy..................... 327 21.3 Complications.......................................................... 329 21.3.1 Early Complications................................................. 329 21.3.2 Late Complication.................................................... 330
›› ››
21.4 Decannulation and Tracheostoma Closure........... 334 21.4.1 Surgical Closure of the Tracheostoma...................... 335 References............................................................................ 336
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–– Laryngotracheal stenosis (LTS) –– Prolonged ventilatory support –– Pulmonary toilet for permanent aspiration Mortality due to paediatric tracheostomies is estimated at 1–3%. Common causes of tracheostomy-related fatalities encompass accidental decannulation and tracheostomy tube plugging. Proper tracheostomy placement: –– For prolonged ventilatory support or pulmonary toilet: –– Third and fourth tracheal ring –– For impending LTS: –– First tracheal ring or –– Sixth and seventh tracheal ring –– For tracheal stenosis or recurrent stenosis at the tracheostomy site: –– Through tracheal stenosis –– Through former tracheostoma –– For distal intrathoracic stenosis: –– Close to thoracic inlet (sixth or seventh tracheal ring), with long cannula to stent the distal stenosis Tracheostomy management at home requires full training for the child’s parents as well as constant support from caregivers.
In medical practice, the terms ‘tracheotomy’ and ‘tracheostomy’ are often used interchangeably. While tracheotomy (=cutting) refers to the surgical act of P. Monnier (ed.), Pediatric Airway Surgery, DOI: 10.1007/978-3-642-13535-4_21, © Springer-Verlag Berlin Heidelberg 2011
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incising the trachea, the term ‘tracheostomy’ should be reserved for describing the presence of an opening (=stoma) in the trachea.
21 Tracheotomy Table 21.1 Indications for paediatric tracheotomy • Airway obstruction – Laryngotracheal stenosis (congenital, acquired) – Bilateral vocal cord paralysis
21.1 Indications Prior to the early 1960s, short-term tracheostomies were mainly used to treat airway obstructions due to acute infections (epiglottitis, pharyngeal abscesses or laryngotracheo-bronchitis) or trauma (foreign bodies) [4]. The concomitant development of airway endoscopy and PICUs made it possible to secure an obstructed airway under visual control, while keeping the child intubated until the medical problem was resolved. This obviated the need for a tracheostomy. With the development of neonatology units, long-term intubation for ventilatory support of premature babies suffering from hyaline membrane disease represented another significant change in the indications for tracheostomies [1, 9, 10]. At present, almost two-thirds of tracheostomies are performed in infants less than 1 year of age [2, 7]; they usually stay in place for longer periods of time (several weeks, months or even years) [11, 12]. The main indications include congenital or acquired LTSs, prolonged ventilatory support beyond a reasonable timeframe and regular pulmonary toileting for persistent aspiration in cases of pharyngolaryngeal discoordination and neurological problems (Table 21.1). The duration of ET intubation before a tracheostomy is recommended and varies widely and must be decided on a case-by-case basis, depending on the nature and prognosis of the primary disease, as well as the presence of comorbidities. Severe anterior neck burns, vascular anomalies of the lower neck and the need for high peak inspiratory pressures that may cause pneumomediastinum/pneumothorax are all contraindications to performing a tracheotomy.
– OSA-related naso-oropharyngeal obstruction – Tracheomalacia – Laryngo-tracheo-oesophageal cleft • Ventilatory support – Respiratory distress syndrome – Central nervous system disorder – Neuromuscular disease • Pulmonary toilet – Pharyngolaryngeal discoordination with aspiration – Laryngo-tracheo-oesophageal cleft – Laryngotracheal fistula
Table 21.2 Location of tracheotomy • Tracheotomy for ventilatory support or aspiration (normal airway) – Third or fourth tracheal ring • Tracheotomy for incipient laryngotracheal stenosis – First tracheal ring or – Sixth or seventh tracheal ring • Tracheotomy for incipient tracheal stenosis – Through tracheal stenosis • Tracheotomy for intrathoracic tracheal stenosis – Sixth or seventh tracheal ring with long cannula to stent the distal stenosis • Tracheotomy for recurrent stenosis at former tracheostomy site – Through former tracheostomy
21.2 Technique of Tracheotomy 21.2.1 Location of Tracheotomy (Table 21.2) • Jackson’s warning against ‘high tracheotomy’ or cricothyroidotomy as a cause of subglottic stenosis
is still valid today [5]. When tracheostomy is required for ventilatory support or lung protection from aspiration in the absence of any LTS, the tracheal incision must be made at the level of the third or fourth tracheal rings. • When tracheotomy is indicated for incipient LTS due to prolonged intubation, it must be placed either at the first tracheal ring, to preserve as many normal
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tracheal rings distally as possible, or low in the neck, at the sixth or seventh tracheal ring, so as to spare a sufficient number of normal rings between the stenosis and tracheostoma (see Sect. 14.3.4 and Fig. 14.18, Chap. 14). In the former case, an SS-PCTR or SS-LTR can be used to rectify the problem. A short airway resection is performed (cricoid plus one or two tracheal rings) in SS-PCTR with a minimal risk of anastomotic dehiscence, whereas an anterior costal cartilage is incorporated into the tracheostoma in SS-LTR. In the case of a distally placed tracheostomy, PCTR is limited to the cricoid, and an anastomosis is performed with good-quality tracheal rings. Laryngotracheal reconstruction with CCG is limited to the laryngeal complex, while the longer distance from the tracheostoma favours the healing process. Anterior costal cartilage graft, when close to the tracheostoma, is more prone to superinfection and graft failure (see Fig. 14.18, Chap. 14). • The options available to stabilise the airway of a patient with impending post-intubation tracheal stenosis are either an emergency resection and anastomosis or a tracheostomy across the tracheal stenosis. The patient is ventilated using a rigid bronchoscope placed proximally to the stenosis. The site of the neck incision is determined by transillumination. After careful dissection of the anterior tracheal wall, a needle is inserted into the trachea under visual bronchoscopic guidance in order to investigate the exact level of the stenosis. Next, a resection and anastomosis or a tracheotomy may be carried out safely without damaging the normal tracheal rings (see Fig. 22.2, Chap. 22). • In the case of an isolated intrathoracic tracheal stenosis, a rare occurrence in children, the tracheostomy must always be placed in the lower neck, usually at the sixth or seventh tracheal ring. The length of the cannula must be carefully chosen so that it can pass through the low stenotic lesion without abutting the carina (see Fig. 14.19b, Chap. 14). Fibre-optic control of proper cannula positioning is essential to avoid complications. In the event of poor positioning of a long cannula, a modified Portex endotracheal tube acting as a cannula may be used to splint the lower trachea. • Should recurrent stenosis occur at the level of the former stoma site, a new tracheotomy must be performed at the previous tracheostomy site (see Fig. 14.19a, Chap. 14).
21.2.2 Operative Technique for Tracheotomy Surgery is performed under general anaesthesia; the airway is secured by an ET tube or a rigid ventilating bronchoscope, as necessary. In congenital SGS, dilation of the stenosis should not be attempted to avoid any mucosal trauma to the subglottis. An elliptical cricoid may be able to accommodate a tiny catheter for jet ventilation, in contrast to a Cohen’s Grade IV glotto-subglottic web with a pinhole residual posterior opening. Laryngeal mask ventilation or a face mask with pharyngeal airway tubes are the two preferred options that ensure adequate working conditions for the surgeon during tracheotomy, while preserving an intact larynx for further airway reconstruction. The surgical procedure starts with the infant or child being placed in the supine position and the neck extended using a shoulder bolster. For cosmetic reasons, a small horizontal midline neck incision is used. The incision is deepened through the subcutaneous fat plane to the strap muscles. As most of the dissection is performed bluntly with S-shaped retractors, great care is taken to stay in the midline. Before proceeding to deeper tissue layers, the fascia over the strap muscles is clearly visualised, cauterised and then divided vertically in the midline. At this stage, the curved retractors are advanced deeper underneath the strap muscles and retracted laterally in order to expose the pretracheal space. Bipolar diathermy is used to cauterise the small vessels within the surgical field. A bloodless surgical field facilitates performance of the paediatric tracheotomy. Depending on the selected location for the tracheotomy, the thyroid isthmus is clamped, divided and tied with 4.0 vicryl ligatures. The anterior surface of the trachea is exposed over three to four rings. The debate is still ongoing as to whether a vertical or horizontal tracheal incision, with or without flap, should be made. In a study including 93 tracheostomised children with various tracheal incisions, Mac Rae et al. [8] reported no difference in results or complications when comparing the different types of tracheal incisions. The basic principle consists of incising as few tracheal rings as possible. Irrespective of the type of tracheal incision used, the tracheostomy tube is likely to inflict some damage on the tracheal vault and cartilage. The most effective preventive measure is to
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exercise great care while suturing the skin around the edges of the tracheal opening. This ensures a particularly secure stoma in the event of accidental extubation following surgery. The author uses an inferiorly based Björk flap, transecting only a single tracheal ring. The flap is sutured to the inferior edge of the skin to facilitate reinsertion of the tracheostomy tube while it is being changed or during accidental extubation. The rest of the skin is sutured around the small tracheal opening (Fig. 21.1). The endotracheal tube is withdrawn to the level of the tracheostomy, and an appropriately sized cannula, coated with a gentamycin-corticosteroid (Diprogenta®) ointment, is inserted with a tapered introducer that slightly dilates the new tracheal stoma. The smallest tracheostomy tube that ensures specifically adapted gas exchange in relation to the child’s age is selected. The cannula is slid into position and connected to the anaesthesia tube in order to ensure adequate bilateral lung ventilation. The flanges of the cannula are fixed around the patient’s neck with Velcro ties, and a dedicated dressing is placed underneath to protect the peristomal skin. The position of the distal tip of the tracheostomy tube, which should rest at least two to three rings above the carina, is checked using a flexible fibre-optic bronchoscope. A chest X-ray is taken during the immediate postoperative period in order to rule out a pneumomediastinum or pneumothorax. Antibiotics are administered for 48 h following surgery, and a gentamycin-corticosteroid ointment (Diprogenta®) is applied around the stoma twice daily to protect the skin from soaking in mucus secretions. The Velcro neck-ties are checked regularly to ensure a fit that allows one single finger to pass under the ties. Suctioning of the cannula is
Fig. 21.1 Björk flap for paediatric tracheotomy: (a) Only one single ring is incised. The width of the flap should not be larger than its length to obtain a square opening. (b) The neck-skin is sutured to the Björk flap inferiorly and all around the tracheal window. The cannula calibrates the opening to its own size
21 Tracheotomy
performed as often as deemed necessary, but should be limited to the tracheostomy tube length in order to avoid severe coughing spells and trauma to the distal airway. Saline may be administered into the cannula to facilitate suction of viscid secretions. The suction catheter must be gently introduced deeper into the airway only when ‘washer machine’ type respiration is not alleviated by aspirating the tracheostomy tube. Distal trauma to the carina and bronchi can lead to granulation tissue formation and bleeding, which should be avoided by careful and gentle suctioning. The first tracheostomy tube change is made one week after the operation in a fully equipped endoscopy suite. The frequency of tracheostomy tube changes varies on an individual basis. Initially, once per week is sufficient, provided that the airway, stoma and peritracheostomal skin are not infected or inflamed.
Box 21.1 Surgical Highlights for Tracheotomy • Select a proper site for tracheotomy tube placement depending on the indication. • Regardless of the technique selected, perform a limited incision of the trachea and suture the skin around the edges of the tracheal opening. • A ‘one ring’ Björk flap prevents anterior accidental subcutaneous dislodgment of the cannula. • The final tracheostoma must be calibrated to the size of the cannula rather than that of the tracheal incision.
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• Always check adequate positioning of the tracheostomy tube with respect to the distal trachea and carina. • The first tube change is made 1 week after the operation in a fully equipped endoscopy suite. • Tracheo-innominate artery fistula and tracheooesophageal fistula are extremely rare in children, but must be recognised and treated quickly. • Tracheostoma closure should be performed surgically after a difficult laryngotracheal reconstruction in order to optimise the tracheal calibre. • When closing a tracheostoma surgically, always place stitches in the cranio-caudal axis to restore the Roman vault of the trachea. • Diagnose any localised malacia at the stoma site prior to tracheostomy closure. • A malacic tracheostoma requires either a resection and anastomosis or a tracheoplasty with ACCG.
Table 21.3 Complications of paediatric tracheotomy • Early complications of tracheotomy – Haemorrhage – Subcutaneous emphysema, pneumomediastinum and pneumothorax – Local infection – Accidental decannulation, tubal obstruction • Late local complications of tracheostomy – Suprastomal collapse and granuloma – Tip of cannula granuloma or stenosis – Granulation tissue along stoma tract – Tracheal innominate artery fistula (rare) – Tracheo-oesophageal fistula (rare) – Lower airway infection, pneumonia – Accidental decannulation, tubal obstruction • Post-decannulation complications – Tracheomalacia at tracheostomy site – A-frame tracheal deformity
21.3 Complications (Table 21.3) 21.3.1 Early Complications Complications are defined as ‘early’ when they occur within the first postoperative week, before the stoma tract is well formed around the tracheostomy tube. They include haemorrhage, pneumomediastinum or pneumothorax, local infection, airway obstruction due to accidental decannulation, or mucous plugging of the tracheostomy tube. These complications are most often caused by technical errors during the surgery, or poor tracheostomy tube care during the early postoperative period. Acute haemorrhage may be prevented by meticulous attention to haemostasis throughout the procedure. As a basic principle, all vessels must be coagulated prior to being divided. In ‘virgin’ cases, it is easy to keep the operative field bloodless until the trachea is incised. The thyroid isthmus must be ligated by running sutures bilaterally to obtain perfect haemostasis, and the lower thyroid veins must be tied, if they cannot be displaced laterally. When an innominate artery is located aberrantly high in the neck, it can be protected by an inferiorly pedicled sternohyoid muscular flap, and by placing the stoma higher in the neck.
– Tracheal stenosis
Creating a ‘mature’ stoma tract, by suturing the skin to the edges of a Björk flap and the remaining tracheal window, offers many advantages. The Björk flap prevents anterior dislodgement of the cannula into the subcutaneous tissue. If positive pressure ventilation is attempted, then it also prevents subcutaneous emphysema and pneumomediastinum. Furthermore, the cutaneous-mucosal approximation prevents air and mucus leaks around the stoma, possibly leading to subsequent subcutaneous emphysema or pneumomediastinum. Peristomal cellulitis is thus prevented. Systemic antibiotics are rarely needed, but regular application of a gentamycin-corticosteroid ointment (Diprogenta®) around the stoma helps avert skin maceration. Finally, fibre-optic control of proper size, length and placement of the tracheostomy tube significantly diminishes the risk of accidental decannulation, as well as the formation of cannula tip lesions in the distal trachea. To avoid further complications, skilled nursing care in an appropriate setting with 24-h surveillance is necessary. Correct tracheostomy tube care is key to preventing postoperative complications. In order to reduce the risk of the tracheostomy tube becoming plugged with dried secretions, frequent suctioning with
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instillation of saline solution and constant humidification of the inspired air are essential. Should accidental decannulation occur despite these preventive measures, parents and nurses must be instructed to stretch the skin around the stoma to prevent inward collapse during inspiration, thus alleviating respiratory distress. This prevents the necessity of quickly reinserting the cannula.
21.3.2 Late Complications With the exception of accidental decannulation and cannula obstruction, which may occur at any time during the tracheostomy, late complications are usually provoked by local trauma induced by the cannula itself. Late complications include (Figs. 21.2–21.4): • Granulation tissue along the stoma tract. • Suprastomal collapse and granuloma (Fig. 21.2a). Fig. 21.2 Complications of tracheostomy: (a) Suprastomal collapse and granuloma. (b) Tip of cannula granuloma creating an asymmetrical distal tracheal stenosis
Fig. 21.3 Sequelae of tracheostomy: (a) A-frame deformity and malacia at the former tracheostoma site. (b) Distal annular cicatricial stenosis resulting from circumferential tip of cannula lesions
21 Tracheotomy
• Granuloma and stenosis at the cannula tip (Figs. 21.2b and 21.3b). • A-frame deformity at the stoma tract after decannulation (Fig. 21.3a). • Tracheo-innominate artery fistula and tracheooesophageal fistula, both life-threatening complications, are extremely rare in the paediatric age group (see Fig. 21.4). Severe granulation tissue formation along the stoma tract is generally due to insufficient tracheostomy care and poor hygiene at home. The exuberant granulation tissue is often infected, which necessitates a short hospital stay to remove it under general anaesthesia using bipolar coagulation and biopsy forceps. Aggressive local treatment with a gentamycin-corticosteroid ointment (Diprogenta®) along with frequent tracheostomy tube changes is required until the stoma tract is fully epithelialised. Any lower airway infection must be treated with systemic antibiotics based on bacteriological culture and sensitivity test results.
21.3 Complications
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Fig. 21.4 Extremely rare complications of tracheostomy: (a) Ill-placed cannula impinging on the anterior tracheal wall, with possible tracheo-innominate artery fistula. (b) Ill-placed cannula
impinging on the posterior tracheal wall, due to a cervical mass, with possible tracheo-oesophageal fistula
Suprastomal collapse and granuloma are most frequently seen in very young children with long-term tracheostomy tubes. Both complications may remain asymptomatic until decannulation; their management is discussed in Sect. 21.4 on tracheostoma closure. Cannula tip granulomas may also lead to symptoms such as haemoptysis and airway obstruction (see Fig. 21.2b). These potentially life-threatening complications require immediate rigid bronchoscopy in order to reopen the distal airway. To this end, a KTP or CO2 laser beam is delivered through a flexible fibre fixed with steristrips to the 0° telescope (see Fig. 4.16, Chap. 4). After reopening the airway, a longer cannula or a non-cuffed endotracheal tube must be used to bypass the stenotic segment during the healing phase. However, proper positioning of the tube may be extremely difficult to achieve due to the proximity of the carina. With any body movement, the tip of the tube abuts against the carina and induces granulation tissue formation and bleeding. It may also move cranially into the trachea, failing to stent the stenotic lesion. A-frame deformity or localised malacia of the trachea at the former stoma site causes symptoms only after decannulation (see Fig. 14.20, Chap. 14). This complication must be anticipated by proper endoscopic assessment prior to decannulation, and a segmental tracheal resection or tracheoplasty with ACCG should be considered, as described in Sect. 21.4 on tracheostoma closure. Although tracheo-innominate artery fistula and tracheo-oesophageal fistula (TOF) are extremely uncommon in the paediatric age group, it is important to include information on their treatment (Fig. 21.4). The presence of a ‘pulsating’ cannula should prompt the
physician to consider the possibility of an impending innominate artery fistula (Fig. 21.4a). This is a dreadful complication that must be anticipated in order to avoid the occurrence of uncontrollable and fatal bleeding. The airway must be inspected through the tracheostomy tube using a small fibrescope while slowly withdrawing the cannula to display the anterior tracheal wall. Bleeding granulation tissue at this level is indicative of an imminent tracheo-innominate artery fistula. Should this be the case, the child is reintubated through the tracheostoma with a cuffed ET tube inflated at the level of the impending tracheo-innominate artery fistula. The thoracic surgeon is notified, and the child is immediately brought to the operating theatre. If the diagnosis is confirmed by the endoscopic findings, then there is no need for an angio-CT scan to be performed. However, if the diagnosis is uncertain, and provided that the patient’s condition is not critical, an angio-CT scan facilitates the localisation of the brachiocephalic trunk in relation to the tip of the cannula in axial and sagittal slices. Upon confirmation of the diagnosis of imminent tracheo-innominate artery fistula during surgical exploration, there is only one option: performing a sternotomy with division and resection of the innominate artery. The anterior tracheal defect is closed and covered with an inferiorly pedicled sternohyoid or intercostal muscle. In children and adolescents, if the carotid-subclavian junction remains intact after division of the brachiocephalic artery, then neither neurologic sequelae nor a subclavian ‘steal’ syndrome are encountered [3, 6]. Tracheo-oesophageal fistula rarely occurs in children. Pressure necrosis on the posterior tracheal wall is habitually induced by misplacement of the
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tracheostomy tube’s distal tip in patients with anatomic abnormalities such as kyphoscoliosis or a lower neck mass (Fig. 21.4b). At times, a cuffed cannula in a patient requiring ventilatory support may squeeze the posterior membranous trachea against an inappropriately hard or large nasogastric tube, thereby inducing pressure necrosis, leading to a TOF. The use of lowpressure, high-volume cuffed tracheostomy tubes and soft nasogastric tubes has reduced the frequency of such complications in children. In children without ventilatory support, an inexplicable increase in tracheal secretions or the occurrence of lung infection should suggest the development of TOF. In children requiring assisted positive airway pressure ventilation, eructation with ventilated breaths are the first suggestive signs. In such cases, the only successful treatment is surgical repair. Prior to surgery, major efforts must be made to control local and pulmonary infections and wean the child off the ventilator. Satisfactory nutritional status is another prerequisite for successful surgery.
a
As the TOF is generally close to the tracheostoma, the cuff of the cannula or ET tube must be positioned and inflated below the fistula. Depending on the underlying pathology, two options are available: closure of TOF with or without tracheal resection.
21.3.2.1 Closure of TOF with Tracheal Resection (Fig. 21.5) In this scenario, the tracheotomy is performed due to the need for prolonged ventilatory support using a cuffed tube. Closure of the TOF with tracheal resection is only considered when the child meets the pulmonary requirements for decannulation and does not present LTS or upper airway obstruction. Additional tracheal damage/stenosis around the TOF is another indication to perform this procedure. A new soft nasogastric tube or a percutaneous endoscopic gastrostomy must be installed prior to surgery.
b
c
Fig. 21.5 Management of tracheo-oesophageal fistula (TOF) with tracheal resection and anastomosis: (a) Identification of the TOF: The exact site of the fistula is identified endoscopically, and the corresponding tracheal segment, including the tracheostoma, is resected, leaving the posterior membranous wall in situ. (b) Resection of the membranous trachea under visual control:
The membranous trachea is incised at the upper and lower borders of the tracheal resection, and progressively elevated to circumscribe the neck of the fistula. (c) Closure of the TOF: The oesophageal fistula is closed in two layers longitudinally and covered with the pedicled sternohyoid muscle, used as a sealing intermediate tissue layer
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The child is ventilated with a flexible anaesthesiology tube placed through the tracheostoma. The initial steps of the intervention are identical to those of a single-stage tracheal resection in a tracheostomised child. A horizontal ellipse of skin is excised around the tracheostoma. After elevating the subplatysmal flap, the strap muscles are reflected laterally, and the trachea is dissected by staying close to the cartilaginous rings at or below the stoma. The recurrent laryngeal nerves (RLNs) are not dissected, but displaced laterally during tracheal dissection. After clearly identifying the level of the TOF in relation to the stoma at endoscopy, and recognising that the length of the tracheal resection is likely to avoid hazardous anastomotic tension, the trachea should be opened vertically on its anterior wall to visualise the TOF. Next, without separating the membranous wall from the oesophagus, the inferior transverse section is performed between two tracheal rings, and the cartilaginous wall of the trachea is bilaterally resected towards the tracheostoma. This procedure leaves the posterior membranous trachea with the TOF in place (Fig. 21.5a). The upper transverse incision of the trachea is made just above the stoma, and the cartilaginous tracheal segment is then resected, providing unsurpassed access to the oesophageal fistula. The proximal and distal transverse sections of the membranous trachea are performed subsequently, preserving the entire vascular supply to both tracheal stumps. By removing the membranous tracheal wall on the immediate oesophageal dissection plane, the TOF is progressively circumscribed to its neck (Fig. 21.5b). It is closed on its vertical axis in two layers using 4.0 or 5.0 vicryl sutures. In the end, an inferiorly pedicled flap of the left sternohyoid muscle is mobilised, sutured and glued to the anterior oesophageal repair (Fig. 21.5c). At this stage, the child is intubated transnasally by the anaesthetist, and the tube is recaptured in the operative field, secured with a 4.0 mersilene thread, and withdrawn to the subglottic level. The surgeon then creates the minimal tracheo-oesophageal separation required to perform the posterior anastomosis safely over the muscular flap. Inverted 5.0 vicryl stitches are placed over the entire length of the posterior anastomosis. The knots are tied on the outside after placement of lateral transcartilaginous stitches, used as traction sutures. Finally, the distal ventilating tube is removed, and the nasotracheal ET tube is inserted into the distal trachea by pulling on the mersilene thread. The lateral and anterior anastomosis
is then completed with 4.0 vicryl sutures tied on the outside. A soft Blue Line Portex tube not exerting any significant pressure on the posterior anastomosis should be used, but extubation must be considered as soon as possible, typically on the next postoperative day, depending on the child’s age and the ventilation parameters. The advantage of this single-stage repair is to avoid the presence of a cannula, which may lead to fistula recurrence.
21.3.2.2 Closure of TOF Without Tracheal Resection (Fig. 21.6) Since the introduction of non-cuffed, low-pressure, high-volume ET tubes in paediatric PICUs, TOF without a tracheotomy has become exceedingly rare. However, a TOF induced by a tracheostomy tube in a child with SGS is extremely challenging to treat. Both conditions cannot be addressed during the same surgery. Priority must be given to TOF repair, albeit under suboptimal conditions, as the tracheostomy must be maintained during the postoperative period. A collar incision with an ellipse of skin around the stoma is created, and bilateral dissection of the tracheal wall is then performed around the stoma and the distal trachea. However, proximal and distal devascularisation of the trachea is more extensive than in single-stage repair with tracheal resection. A plane of dissection between the trachea and oesophagus must be established above and below the TOF in order to circumscribe its neck, from normal to cicatricial tissues (Fig. 21.6a). Unless the neck of the fistula is transected, the oesophagus cannot be separated from the membranous trachea. This operation is more difficult than TOF repair with tracheal resection. After the oesophagus is completely freed from the trachea over 1–2 cm around the fistula, a two-layer closure of the anterior oesophageal defect is made with 5.0 vicryl sutures. The trachea is rotated in order to expose its posterior wall laterally, and a single-layer closure is made. The left sternohyoid muscle is sectioned from its hyoid attachment, mobilised, interposed and then sutured between the trachea and oesophagus (Fig. 21.6b). In addition, fibrin glue is applied to seal the reconstruction. The neck is closed with Penrose drains placed in the tracheo-oesophageal grooves, and a new tracheostoma is created by suturing the skin around the edges of the former stoma.
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Fig. 21.6 Management of tracheo-oesophageal fistula without tracheal resection: (a) Dissection of the tracheo-oesophageal plane must be extensive to isolate the neck of the tracheooesophageal fistula. (b) Simple suture of the posterior tracheal defect, two-layer longitudinal suture of the oesophageal defect,
and cover with a sternohyoid muscular flap. A soft Blue Line Portex Tube® is customised as a new tracheostomy tube to avoid pressure on the posterior membranous wall of the trachea at the site of fistula repair
This operation has one major disadvantage: the tracheostomy tube must be kept in during the postoperative period because of the SGS. It is easy to understand that the cannula, initially responsible for the TOF, will favour its recurrence. Often, pressure on the posterior tracheal wall just below the stoma can only be minimised using a soft Blue Line Portex tube as a tracheostomy tube. Should this be the case, ventilation under deep sedation for more than 1 week may be required until the TOF has completely healed.
granuloma component of the stenosis must be resected before a capping trial of the tracheostomy tube is considered. The collapsed portion of the anterior tracheal wall cannot be corrected as long as the cannula is in place. This requires surgical closure of the tracheostomy. Failure to remove the tracheostomy tube during the dynamic evaluation of the airway may cause decannulation failure, despite a successful plugging trial during the day and night. With the fibre-optic scope placed just above the tracheostoma, the stoma site is inspected to rule out localised malacia, while the child is breathing spontaneously with the stoma temporarily occluded by the anaesthetist’s finger. As long as the cannula is in place, it functions as a stent, preventing lateral collapse of the tracheal wall at the stoma site. Several of our patients were referred to our centre due to this unidentified problem, which required either closure of the stoma with an ACCG or a simple resection and anastomosis. With the exception of this scenario, a successful plugging trial is highly indicative of uneventful decannulation. In clinical practice, progressively smaller tracheostomy tubes are inserted, and plugging trials are started during the day, while the patient is under close supervision. If the results are satisfactory, then the plugging trial is extended during the night using SpO2 monitoring or nocturnal polygraphy. Decannulation is only considered when the child tolerates day and night occlusion of the tracheostomy tube, without showing
21.4 Decannulation and Tracheostoma Closure In infants and children, decannulation is only considered after thorough airway evaluation, when progressive down-sizing and plugging of the tracheostomy tube have been successfully achieved. Transnasal fibre-optic laryngoscopy and direct laryngotracheoscopy are performed under general anaesthesia in order to identify any residual dynamic or structural narrowing of the upper airway, assess vocal cord function and evaluate the status of the underlying primary airway pathology that necessitated tracheostomy. Following successful primary surgery, residual airway obstruction is most often caused by suprastomal collapse and granuloma formation due to the back of the curved cannula (see Fig. 14.21, Chap. 14). In case of subtotal or total suprastomal obstruction, the
21.4 Decannulation and Tracheostoma Closure
signs of respiratory distress. This evaluation is more complicated in infants where the tracheostomy tube occludes the small airways, despite satisfactory dynamic and static endoscopy control. In small children, the best way to achieve decannulation consists of surgical closure of the tracheostomy with short-term endotracheal intubation and follow-up in the PICU after extubation.
21.4.1 Surgical Closure of the Tracheostoma In our institution, the tracheostoma is closed surgically after successful airway reconstruction for LTS. Particularly in infants and small children, the airway size at the tracheostoma site is never fully optimal, either due to suprastomal collapse or stomal malacia. Furthermore, surgical closure allows the surgeon to eliminate the unsightly scar resulting from spontaneous closure at the tracheostomy site. After inducing general anaesthesia through the tracheostomy tube, the child is intubated transorally, after which the cannula is removed. The ET tube is passed beyond the tracheostoma. This manoeuvre pushes the suprastomal granuloma anteriorly into the opening of the tracheostoma, where it can easily be removed with a biopsy forceps after bipolar coagulation. This is a simpler and faster way of removing the suprastomal granuloma than using a sphenoid punch or broncholaser. Through a small collar incision, a small ellipse of skin around the tracheostoma is removed; the tract is
Fig. 21.7 Surgical closure of the tracheostoma: (a) The anterior orifice of the trachea is isolated by resecting the cutaneous stoma tract completely. (b) Closure of the tracheal orifice is always performed by placing stitches in the cranio-caudal axis to restore a steady tracheal vault. This prevents the sequela of an A-frame deformity of the trachea at the former stoma site
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then dissected to the trachea and excised. This leaves a round opening in the anterior tracheal wall that must be snugly closed with 4.0 vicryl stitches placed in the cranio-caudal axis (Fig. 21.7), which restores the vault of the tracheal wall and the steadiness of the trachea at the stoma site. This manoeuvre is particularly satisfactory in infants and small children with a partial suprastomal collapse that can be stabilised and fixed to the anterior infrastomal wall of the trachea. Placing stitches transversally must be avoided at all costs, as such a procedure would lead to A-frame deformity of the trachea (see Fig. 14.20b, Chap. 14). The strap muscles are sutured in the midline after placing a small Penrose drain below the tracheostoma closure on the anterior tracheal wall, and the skin is then closed in two layers. This simple surgical closure of the tracheostomy is only possible when the stoma has not migrated cranially over time, leaving an anterior subcutaneous tracheal cleft below the tracheostoma. This abnormal condition, encountered in long-term tracheostomies and due to a cheesewire mechanism, must be treated using ACCG tracheoplasty. Another potential indication requiring ACCG grafting for tracheostoma closure is a long, oval-shaped stoma where simple horizontal closure using stitches placed in the cranio-caudal axis is not an option (Fig. 21.8). Lastly, severe localised malacia at the stoma site is best treated with a resection and anastomosis, as the steadiness of the lateral tracheal wall is insufficient to restore a good tracheal framework after ACCG tracheoplasty. A previous extensive airway resection, however, may preclude a secondary resection.
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21 Tracheotomy
Fig. 21.8 Large, oblong tracheostoma preventing simple primary closure: (a) Large oblong tracheostoma (white arrows) in a patient who underwent PCTR for LTS. (b) Tracheostoma closure with an ACCG
References 1. Allen, T.H., Steven, I.M.: Prolonged endotracheal intubation in infants and children. Br. J. Anaesth. 37, 566–573 (1965) 2. Ang, A.H., Chua, D.Y., Pang, K.P., et al.: Pediatric tracheotomies in an Asian population: the Singapore experience. Otolaryngol. Head Neck Surg. 133, 246–250 (2005) 3. Brewster, D.C., Moncure, A.C., Darling, R.C., et al.: Innominate artery lesions: problems encountered and lessons learned. J. Vasc. Surg. 2, 99–112 (1985) 4. Hoeve, H.: Tracheostomy: an ancient life saver due for retirement of vital aid in modern airway surgery ? In: Graham, J.M., Scadding, J.K., Bull, P.D. (eds.) Pediatric ENT, p. 247. Springer, Berlin/Heidelberg (2008) 5. Jackson, C.: High tracheostomy and other errors: the chief causes of chronic laryngeal stenosis. Surg. Gynecol. Obstet. 32, 392–398 (1921) 6. Jones, J.W., Reynolds, M., Hewitt, R.L., et al.: Tracheoinnominate artery erosion: successful surgical management
of a devastating complication. Ann. Surg. 184, 194–204 (1976) 7. Kremer, B., Botos-Kremer, A.I., Eckel, H.E., et al.: Indications, complications, and surgical techniques for pediatric tracheostomies-an update. J. Pediatr. Surg. 37, 1556– 1562 (2002) 8. MacRae, D.L., Rae, R.E., Heeneman, H.: Pediatric tracheotomy. J. Otolaryngol. 13, 309–311 (1984) 9. Markham, W.G., Blackwood, M.J., Conn, A.W.: Prolonged nasotracheal intubation in infants and children. Can. Anaesth. Soc. J. 14, 11–21 (1967) 10. McDonald, I.H., Stocks, J.G.: Prolonged nasotracheal intubation a review of its development in a paediatric hospital. Br. J. Anaesth. 37, 161–173 (1965) 11. Palmer, P.M., Dutton, J.M., McCulloch, T.M., et al.: Trends in the use of tracheotomy in the pediatric patient: the Iowa experience. Head Neck 17, 328–333 (1995) 12. Wetmore, R., Thompson, M., Marsh, R., et al.: Pediatric tracheostomy: a changing procedure? Ann. Otol. Rhinol. Laryngol. 108, 695–699 (1999)
Tracheal Resection and Anastomosis
Contents
Core Messages
22.1
›› Simple tracheal resection is less common than
Isolated Post-Intubation Stenosis.................................................................... 338 22.1.1 Tracheal Resection with End-to-End Anastomosis.......................................... 338 22.1.2 Cervical Slide-Tracheoplasty.................................... 340
››
22.2
Isolated Post-Tracheostomy Stenosis and Tracheostoma-Related Stenosis..................... 341
››
22.3
Tracheal Stenosis in a Tracheostomised Child........................................... 342
››
22.4
Postoperative Management of Single-Stage Tracheal Resection and Anastomosis.................... 344
››
22.5
Complications of Tracheal Resection and Anastomosis..................................................... 344 22.5.1 Anastomotic Separation............................................ 344 22.5.2 Granulation Tissue at Anastomosis.......................... 345 22.5.3 Recurrent Laryngeal Nerve (RLN) Injury................ 345 22.6
Tracheoplasty.......................................................... 345
22.7
Results of Tracheal Resection................................ 345
References............................................................................ 346
22
PCTR or LTR in children. Acquired conditions such as tracheostomarelated stenosis, post-intubation stenosis or a combination of both, are the main indications. Congenital tracheal stenosis is an additional indication. Both preoperative assessment and surgical principles are similar to those of PCTR. For the management of severe malacia at the stoma site, resection and anastomosis is favoured over performing tracheoplasty with ACCG.
Although isolated tracheal stenoses are uncommon in the paediatric age group, the vast majority are caused by ET intubation or sequelae of tracheostomy performed for post-intubation LTS. Congenital, traumatic or neoplastic aetiologies are very rare. In infants and small children, tracheostoma-related stenoses are predominant, whereas in older children, post-intubation stenoses due to oversized ET tubes or overinflated cuffed tubes are more common. The preoperative assessment is, in every respect, similar to that used in children with LTS (see Chap. 17). Careful endoscopic evaluation is still the cornerstone of successful management of tracheal stenoses, with every effort made to rule out potential localised malacia at the tracheostoma level (see Sect. 17.3, Chap. 17).
P. Monnier (ed.), Pediatric Airway Surgery, DOI: 10.1007/978-3-642-13535-4_22, © Springer-Verlag Berlin Heidelberg 2011
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In clinical practice, three main situations are encountered: • Isolated post-intubation stenosis • Isolated post-tracheostomy stenosis or tracheostoma-related stenosis • Tracheal stenosis in a tracheostomised child
22.1 Isolated Post-Intubation Stenosis Short, web-like cicatricial stenoses are successfully managed using CO2 laser incisions and dilatations [31], but cicatricial scars of the posterior membranous trachea are likely to recur, because of the lack of cartilaginous support (Fig. 22.1). Anteriorly situated, shortsegment stenoses may benefit from CO2 laser excision. Unsteadiness of the tracheal framework, however, warrants immediate open surgery. Any endoscopic treatment that does not significantly improve the airway on the first attempt should not be repeated, and an open surgical approach must be considered instead. Short-segment tracheal stenoses represent the best indication for a safe, straightforward resection and anastomosis. Though minimally invasive, endoscopic treatment still requires multiple ambulatory sessions that may inconvenience the patient. A simple resection and anastomosis resulting in a permanent optimal airway is unquestionably worth
Fig. 22.1 Tracheal stenosis with cicatricial involvement of the posterior membranous trachea: This situation represents a relative contra-indication to CO2 laser radial incisions and dilation. The likelihood of recurrent stenosis is high when the posterior membranous trachea is involved in the cicatricial stenosis. A simple resection and anastomosis is preferable in such cases
22 Tracheal Resection and Anastomosis
undertaking, as it requires only a short (<10–15 days) hospital stay. Successful endoscopic treatment may not restore the trachea to its normal anatomy. Additionally, airway infections in later life are likely to reactivate a dormant scar, leading to recurrent stenosis. In the case of an isolated post-intubation stenosis, tracheal resection with end-to-end anastomosis is the sole reasonable option. Tracheoplasty with ACCG is reserved for patients with post-tracheostomy stenosis or those previously operated on and for whom further resection cannot be performed.
22.1.1 Tracheal Resection with End-to-End Anastomosis The patient is placed in a supine position with the neck extended using a shoulder roll. At anaesthesia induction, the tracheal stenosis is gently dilated with tapered Savary–Gillard bougies, and an oro- or nasotracheal intubation is performed, depending on the child’s age as well as the need for maintaining the ET tube during the postoperative period. The dilatation-induced trauma to the stenosis has no adverse consequences, as the tracheal segment is fully resected during the procedure. A horizontal collar incision is made 2 cm above the sternal notch, the subplatysmal flaps are elevated, and the strap muscles are divided in the midline from the thyroid cartilage down to the thoracic inlet. The Lone Star® ring retractor is installed, and the elastic stay hooks are positioned in order to facilitate exposure of the anterior tracheal wall (see Fig. 20.4, Chap. 20). At times, the exact location of the stenosis is easily recognisable by the bottleneck deformity of the trachea. Should this not be the case, the exact location of the stenosis is identified using a fibroscope inserted through the ET tube, which is temporarily withdrawn to the subglottic level. Visual control on a monitor enables the surgeon to insert a needle into the stenotic segment with precision, and to mark the site with a thread on the anterior tracheal wall (Fig. 22.2). If the stenosis is located in the lower neck, then the thyroid isthmus must not be transected in order to preserve optimal vascular supply to the trachea. In all other cases, the thyroid gland is divided, ligated and reflected laterally. Distal mobilisation of the trachea is achieved by antero-lateral dissection only, staying short of the
22.1 Isolated Post-Intubation Stenosis
Fig. 22.2 Location of a tracheal stenosis not clearly identifiable externally: A fine needle is inserted through the middle of the stenosis under visual bronchoscopic guidance, and a stitch is temporarily placed as a landmark
tracheal rings, and passing underneath the innominate artery. The vascular supply from the tracheoesophageal groves is carefully preserved. The RLNs are not identified but simply displaced laterally with the peritracheal fat pad or cicatricial tissue. Bipolar coagulation of the feeding vessels to the trachea should be strictly limited to the stenotic tracheal segment to be resected. Circumferential tracheal dissection must be avoided, as this procedure is likely to unnecessarily sacrifice further tracheal feeding vessels. Before incising the airway, cranial traction on the distal trachea provides an estimation of the length of trachea that can be resected and anastomosed without performing a laryngeal release procedure. In most children, onethird of the tracheal length (approximately six rings) may easily be resected. The trachea is opened transversally at the midpoint of the stenosis, which is marked by a thread in the absence of a bottleneck deformity. The trachea is then progressively sliced cranially and caudally until normal steady tracheal rings are reached (Fig. 22.3a). As Grillo stated [15]: ‘The tracheal tailor quickly runs out of cloth’. The surgeon can always remove more tracheal segments, but he or she cannot replace them. The orotracheal ET tube is withdrawn up to the subglottic level after securing its tip with a mersilene thread, and a second anaesthetic tube is inserted into the distal trachea in order to ventilate the patient. Horizontal cuts are then progressively made on the membranous trachea at the extremities of the stenosis,
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until reaching the anterior oesophageal wall. The posterior component of the stenosis is resected with the incised tracheal rings under visual control. When endoscopy reveals a long tracheal stenosis, the best option is to divide the trachea anteriorly on its vertical midline from its midpoint to either of its extremities until reaching normal tracheal rings. If tracheal mobilisation shows excessive tension when attempting to approximate the two tracheal stumps, then the procedure can still be converted into a tracheoplasty with ACCG. However, stepwise tracheal mobilisation with laryngeal release or, less commonly, hilar release should enable a safe resection and anastomosis. This procedure yields results that are superior to an extensive tracheoplasty with temporary stenting. In children, however, hilar release should be the exception [32]. The posterior anastomosis is carried out first. The membranous trachea is freed from the oesophagus over several millimetres in order to place inverted, interrupted 5.0 vicryl stitches with the knots tied on the outside. Some surgeons favour a running suture, thus obtaining an improved mucosal approximation. The oesophagus shortens spontaneously and does not create any anterior bulging that would prevent optimal mucosal approximation of the membranous trachea. The trachea should be rinsed with saline solution, and mucous and blood clots should be gently suctioned off prior to converting to orotracheal ventilation (see Sect. 20.3, Fig. 20.2, Chap. 20). The lateral and anterior anastomosis is then performed with interrupted 4.0 vicryl stitches. As the two tracheal stumps are well matched in size, the anastomosis is technically easier to perform than a thyrotracheal anastomosis in the case of PCTR. All tracheal stitches are placed prior to being tied. They are alternately inserted through the first and second normal rings on either side of the tracheal stumps in order to prevent persistent tension at the same level (Fig. 22.3b). Great care should be taken to keep the needle in a submucosal plane throughout the length of the transcartilaginous stitch, thus avoiding devascularisation of the mucosa at the site of anastomosis (Fig. 22.4). The tracheal cartilages are nourished from the inside by the submucosal capillary network (see Fig. 2.12, Chap. 2). Devascularisation of the mucosa, combined with extensive circumferential mobilisation of the trachea, may result in anastomotic failure. In paediatric airway surgery, meticulous care is essential, as every detail counts. At the end of the procedure, the shoulder roll is removed, the head is elevated and the chin is drawn
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22 Tracheal Resection and Anastomosis
a
towards the chest wall. The attending surgeon exerts traction on the stitches, which are tied with the knots on the outside. Upon completion of the anastomosis, fibrin glue (Tisseel®) is applied to the suture line, and a Penrose drain is placed distally towards the thoracic inlet, but never on the suture line. If possible, the thyroid lobes are sutured at the midline over the anastomosis in order to provide adequate sealing and vascular supply. The strap muscles are resutured at the midline, and the skin is closed in two layers. Depending on the child’s age, extubation is performed in the operating room. In infants and small children, nasotracheal intubation is preferable and maintained for 24–48 h. Contrary to PCTR, tracheal resection and anastomosis is not associated with significant postoperative laryngeal oedema (Fig. 22.5).
b
22.1.2 Cervical Slide-Tracheoplasty (Fig. 22.6)
Fig. 22.3 Simple tracheal resection with end-to-end anastomosis: (a) Slight bottle neck deformity of the trachea: Feeding vessels to the trachea are only coagulated over the segment that will be resected. The airway is sliced cranially and caudally from the midpoint of the stenosis until normal rings are found (dotted blue lines). (b) Completion of tracheo-tracheal anastomosis: All stitches are placed submucosally and alternatively through the first and second tracheal rings on either side of the anastomosis
Fig. 22.4 Close-up view of correct stitch placement for tracheotracheal anastomosis: The needle should pass in a submucosal plane to preserve all vascular supply to the anastomosis. Through and through stitches must be avoided as they compromise the capillary network of the submucosa, which provides the sole vascular supply to the anastomosis
In 2008, de Alarcon and Rutter [8] advocated the use of cervical slide-tracheoplasty for treating acquired tracheal stenoses located in the upper two-thirds of the trachea. The authors reported two main advantages in comparison with standard tracheal resection, notably less tension on the suture line spread over a large area, and a further increase in the airway’s luminal diameter. If mild restenosis does occur at the anastomotic site, it tends to be clinically insignificant. Contrary to long-segment congenital tracheal stenoses with ‘O’ circular cartilaginous rings with a normal tracheal framework and mucosa, acquired tracheal stenoses are made of cicatricial, abnormal tissue. This abnormal tissue is a real disadvantage when compared to performing an anastomosis with normal tracheal rings, as is the case in segmental resection and anastomosis. Although the author has no experience with the slide-tracheoplasty technique for acquired tracheal stenosis, he supports the idea of transversally resecting the narrowest portion of a long bottleneck stenosis (Fig. 22.6a) and performing a slide-tracheoplasty with the remains of the two tracheal stumps. This allows the surgeon to diminish the length of total resection and increase the luminal diameter at the anastomotic site
22.2 Isolated Post-Tracheostomy Stenosis and Tracheostoma-Related Stenosis
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Fig. 22.5 Post-tracheostomy stenosis: (a) Preoperative view: The broken vault of the tracheal cartilaginous ring is easily recognisable, but there is an important intrinsic component to the tracheal stenosis. (b) Postoperative view: normal size and steadiness of the trachea. Only resection and anastomosis can achieve an optimal result
(Fig. 22.6b and c). However, a simple resection-anastomosis without undue tension is favoured over slide-tracheoplasty, whenever possible. This procedure restores a normal and steady trachea, with excellent long-term results and no risk of recurrent stenosis (see Fig. 22.5).
22.2 Isolated Post-Tracheostomy Stenosis and TracheostomaRelated Stenosis This scenario is similar to that of an isolated post-intubation stenosis, except that the exact level of the stenosis is immediately identifiable, as it is either at the former stoma site or at the stoma itself. Caution must be taken in the case of very long-term tracheostomas that have slowly migrated cranially over time. The anterior tracheal wall may have been destroyed over 1–2 cm, leaving an acquired anterior subcutaneous cleft below the site of the current stoma, due to a cheesewire mechanism. This problem must be identified before discussing alternative measures of reconstruction with the child’s parents. A simple palpation of skin immediately below the tracheostoma reveals the defect on the anterior tracheal wall. This cleft is likely to increase the amount of tracheal resection needed to restore the normal airway. In cases of previous tracheal resection, tracheoplasty with ACCG may be the only remaining alternative. In this situation, a cervical slide-tracheoplasty might also be considered as a valuable surgical option. In all other cases, tracheal resection and anastomosis is the best surgical option to treat localised malacia
at the stoma site in order to restore a steady, normally sized airway. This technique is superior to tracheoplasty with ACCG, which is unlikely to correct the malacic component of the lateral tracheal walls. The collar incision typically includes a crescentshaped excision of the skin around the pit of the former stoma or the tracheostoma itself. To facilitate tracheal dissection, a haemostat is used for traction on either side of the ellipse of skin left around the stoma. As the peritracheostomal region is embedded in scar tissue, midline division of the strap muscles must begin at some distance from the stoma, in normal tissues above the sternal notch whenever possible. The anterior wall of the trachea is identified first, and dissection is progressively carried out towards the former stoma or the tracheostoma, by keeping in close contact with the tracheal rings. The strap muscles adhering to the trachea are reflected laterally. In post-tracheostomy stenosis, the stenotic segment is generally well-identified by its bottleneck shape despite endoluminal stenting with the ET tube. Blood supply in the lateral pedicles is carefully preserved above and below the stenotic segment of the tracheostoma. When dealing with a tracheostoma-related stenosis, the tracheal segment to be resected is clearly identified. Following the transverse section immediately below the stoma, the surgeon must check that the tracheal rings are normal in size and steadiness. Above the stoma, any residual granuloma must be resected with great care. The stenotic or malacic segment of trachea is resected by applying the same principles as those described for isolated tracheal stenoses, and the remainder of the procedure is carried out in a similar fashion (see Sect. 22.1.1 and Fig. 22.3).
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a
b
c
22 Tracheal Resection and Anastomosis
22.3 Tracheal Stenosis in a Tracheostomised Child This condition is due to an ill-placed tracheostomy, outside the stenotic tracheal segment (Fig. 22.7): • When the stoma is located very close to the stenosis, the best option is to include it in the tracheal resection. Extensive tracheal mobilisation and laryngeal release procedures are frequently necessary to achieve a tension-free anastomosis (Fig. 22.7a). • When the stenosis is located at a distance from the stoma, a thoracic surgeon may be needed to perform a partial sternotomy, as well as an intrathoracic tracheal resection and anastomosis. Provided the child is in overall good health, the stoma opening can be closed simultaneously. If the tracheostoma must be retained at the end of surgery, a tracheostomy cannula must never be used as it is likely to impinge on the lower anastomosis, thereby preventing proper healing. A customised Portex Blue Line tube® is used as a tracheostomy cannula to avoid pressure at the anastomotic site (Fig. 22.7b). • When an isolated tracheal stenosis is located proximally to the tracheostomy, its position is generally very close to the stoma. This situation is highly uncommon in children. Treatment consists of resecting the stenosis and the tracheostoma in a single-stage procedure. In rare cases where the stenosis is located away from the tracheostomy, a simple resection and anastomosis of the stenosis is carried out. The proximity of the stoma, however, is not conducive to healing at the anastomotic site. The curved back of the cannula may cause constant damage to the suprastomal tracheal rings, thereby weakening the stability of the tracheal wall at the anastomotic site (Fig. 22.7c).
Box 22.1 Surgical Highlights for Tracheal Resection and Anastomosis Fig. 22.6 Cervical slide-tracheoplasty: (a) Peritracheostomial stenosis extending cranially and caudally to the stoma site: The stoma is resected segmentally with the corresponding tracheal cartilages. (b) Vertical tracheal slits are created over the stenotic segment anteriorly and posteriorly on the distal and proximal tracheal stumps, respectively. (c) Completion of the oval-shaped anastomosis. The drawback of this technique is that it uses abnormal cicatricial tissue to expand the airway, in contrast to the same technique used for congenital long-segment tracheal stenosis with circular ‘O’ tracheal rings (see Sect. 13.2.1.3.4, Chap. 13)
• Apply all basic surgical principles as outlined for simple PCTR in Sect. 20.3, Chap. 20. • Specific measures for tracheal resection with end-to-end anastomosis: –– Gently dilate an isolated upper tracheal stenosis before intubation and resection-anastomosis in a non-tracheostomised child.
22.3 Tracheal Stenosis in a Tracheostomised Child
Fig. 22.7 Tracheal stenosis located cranially or caudally to the tracheostoma: (a) Tracheal stenosis located below, but close to the tracheostoma: Tracheal resection includes the stenosis and the stoma, provided that the patient can tolerate a single-stage surgery. (b) Tracheal stenosis located below but at some distance from the tracheostoma: Most likely, the stenosis is located in the upper mediastinum. If possible, resection-anastomosis must include the tracheostomy site. If this proves impossible
–– Identify the exact position of the stenosis under peroperative bronchofibroscopy guidance, whenever indicated. –– Always check tracheal mobilisation and approximation of the tracheal stumps prior to performing any tracheal resection. –– Incise the posterior membranous wall progressively until the tissue ‘party wall’ between the trachea and oesophagus is identified, and resect the posterior component of the stenosis on the anterior oesophageal wall. –– Never perform unnecessary circumferential dissection of the trachea, as this procedure devascularises the proximal and distal tracheal stumps.
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during surgery, a soft Blue Line Portex® is customised as a cannula to avoid pressure on the suture line of the anastomosis. (c) Tracheal stenosis situated above the stoma: Tracheal resection usually includes the stenosis and stoma. If the stenosis is located at some distance from the stoma, it can be resected separately, but the proximity of the cannula is not conducive to anastomotic site healing
–– Open the airway at the narrowest point of the stenosis, and progress cranially and caudally until normal tracheal rings are found. –– Use steady and normal tracheal rings for anastomosis. –– Place tracheal stitches alternately through the first and second tracheal rings on either side of the anastomosis in order to avoid tension on the suture line. –– Place tracheal stitches strictly in a submucosal plane to prevent potential devascularisation at the anastomotic site. –– Work meticulously with 3x magnifying glasses in infants and small children.
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22.4 Postoperative Management of Single-Stage Tracheal Resection and Anastomosis Tracheal resection and anastomosis is usually performed as a single-stage procedure except for certain rare cases among children (see Sect. 22.3). Although the general postoperative management is similar to that of single-stage PCTR (see Sect. 20.9, Chap. 20), airway control is simpler. As tracheo-tracheal anastomosis does not induce postoperative oedema of the vocal cords, children older than 2 years are often extubated in the operating theatre. The use of corticosteroids is not indicated in the postoperative period. The advantage of using a nasotracheal tube as a temporary stent is offset by the foreign body effect in the trachea. Pressure on the suture line at the anastomosis in addition to the retention of secretions around the ET tube may compromise the healing process. In smaller children, extubation occurs after 24–48 h, when spontaneous breathing and respiratory parameters allow for the procedure to be conducted safely. A meticulously accomplished tracheal anastomosis is not associated with significant local oedema, even in small airways. A non-invasive technique such as face mask ventilation with continuous positive airway pressure (CPAP) (see Fig. 20.38, Chap. 20) is far preferable to keeping the child intubated. A patent upper airway and larynx, and normal lung function are the only requirements. Should the patient need to be intubated, all vital parameters must be monitored, and expertise in managing difficult airways is mandatory. Furthermore, the absence of an ET tube provides constant information on the patency of the airway and the quality of the healing process at the level of the anastomosis. If everything runs smoothly, then the first postoperative endoscopy control is performed at Day 10. If mucosal approximation at the anastomotic site is excellent, then it is likely to remain so until the anastomosis has fully healed. The presence of significant fibrin deposits on the suture line is indicative of a suboptimal result that warrants close monitoring of the child during the next 2 weeks. A new control endoscopy where granulation tissue is gently removed under bronchoscopic guidance with a biopsy forceps is scheduled at 3 weeks postoperatively. When the postoperative course
22 Tracheal Resection and Anastomosis
is uneventful, one follow-up tracheoscopy at 3 months is sufficient. Final assessment should always include a dynamic evaluation of laryngeal function. If necessary, a small dilation with tapered bougies or angioplasty balloons may be performed. In our experience, a good result obtained at 3 months is a life-long guarantee of successful repair following PCTR or tracheal resection and anastomosis. This does not hold true for tracheoplasties and laryngotracheal reconstructions with costal cartilage grafts, as airway infections may reactivate scars that lead to recurrent stenosis later on in life.
22.5 Complications of Tracheal Resection and Anastomosis Early and late complications of tracheal resection and anastomosis are very similar to those of a single-stage PCTR. Haemorrhage, early air leak, wound infection and pulmonary complications are managed in the same fashion. Section 20.11, Chap. 20 has important detailed information on this subject. A few points are worth additional mention here.
22.5.1 Anastomotic Separation Anastomotic separation is typically due to excessive tension at the anastomotic site. Performing a full laryngeal release procedure and extensive antero-lateral mobilisation of the intrathoracic trachea, while carefully preserving its vascular supply can prevent this. Newly trained surgeons are often hesitant to mobilise the trachea sufficiently, although it is actually a safe and easy procedure. Anastomotic separation may also occur as a result of tracheal necrosis due to unnecessary circumferential tracheal dissection and excessive coagulation of the tracheal feeding vessels. Dissection with a monopolar probe should never be used for this procedure. Rather, the surgeon must favour careful and precise bipolar coagulation of individual vessels. As an additional measure to avoid anastomotic separation, all stitches must be placed submucosally instead of through the tracheal wall (see Fig. 22.4) in order to prevent ischaemia from occurring around the anastomosis.
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22.7 Results of Tracheal Resection
22.5.2 Granulation Tissue at Anastomosis Granulation tissue can no longer be attributed to the type of thread used, since vicryl has been universally adopted. Grillo reported a decrease in granulation tissue formation from 23% to 1.6% when using vicryl instead of non-resorbable threads [16]. Other monofilament threads such as the polydioxanone suture (PDS) have no biological advantage over vicryl. Presently, granulation tissue is invariably linked to slow and progressive partial anastomotic dehiscence. Granulation tissue, often asymmetrical, proliferates at the location where fibrin deposits have been noticed during endoscopy control performed at Day 10 postoperatively. When granulation tissue is considerable and circumferential, it may evolve into contracting scars and restenosis.
22.5.3 Recurrent Laryngeal Nerve (RLN) Injury The RNLs should not be identified during dissection of the trachea. Staying short of the tracheal rings displaces the RNLs laterally with the peritracheal soft tissue. The RNLs are endangered during coagulation rather than during dissection. Tracheal feeding vessels must be coagulated using the bipolar forceps prior to their division, in order to avoid their retraction into the peritracheal soft tissues, where cauterisation can cause thermal damage to the RLNs.
LTR are also applicable to tracheoplasty (see Sect. 19.4.1, Chap. 19). In older children, stenting with a straight, plain silicone tube at least 8 mm in diameter is useful for supporting a long costal cartilage graft in a highly damaged, unsteady tracheal segment caused by multiple and unsuccessful surgeries. The tube is simply fixed with two 3.0 prolene stitches placed transversally at both extremities of the reconstruction, before suturing the ACCG into position. It is very unlikely that the tube will be clogged with dried secretions, as the child moisturises the air through the normal upper airway during respiration. Furthermore, tightly fixing the tube to the trachea avoids shearing forces at the stent– mucosal interface, thus preventing granulation tissue formation. In such situations, a simple smooth silicone tube is tolerated better than a Montgomery T-tube with the side-arm kept open. The healing process is improved, and the tracheostoma is addressed during the single-stage surgical procedure (see Fig. 21.8, Chap. 21). However, when sizes smaller than 8 mm in outer diameter are needed in smaller children, there is a life-threatening risk of the tube becoming plugged with dried secretions. Such small tubes, whether straight silicone or Montgomery T-tubes, are proscribed when sizes below 8 mm in outer diameter are required. A proximal LT-Mold must be used under tracheostomy cover with a cannula. Postoperative management and complications are, in all respects, similar to those of LTR with ACCG (see Sect. 19.5, Chap. 19).
22.7 Results of Tracheal Resection 22.6 Tracheoplasty Whenever possible, a tracheal resection with end-toend anastomosis is superior to enlargement tracheoplasty of the stenotic airway, particularly at the site of the current or former tracheostoma. Tracheoplasty with ACCG must be reserved for cases where a simple tracheal resection and anastomosis is no longer feasible because of previous airway resections. From a technical point of view, tracheoplasty is identical to LTR with ACCG. The same principles for harvesting, carving and suturing the ACCG used in
In the medical literature, reports of paediatric tracheal surgery for acquired post-intubation or post-tracheostomy stenoses are limited and widely dispersed [5, 17, 19, 28, 30, 35]. To the best of my knowledge, Carcassonne et al. [5] are credited with having published one of the first series of paediatric tracheal resection and anastomosis. They performed three to five ring-segmental resections of the trachea for acquired stenoses in four children aged 5 years or more, reporting successful surgical results in all cases. Since these early days, most published series have included a mix of congenital and acquired tracheal stenoses that presented different therapeutic challenges [1, 4, 9, 11, 24].
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Congenital tracheal stenoses are typically longer, and present an intact, albeit abnormal cartilaginous framework. Except for short-segment congenital stenoses treated by simple resection and anastomosis, all other cases are treated by slide, or less optimally, by patch tracheoplasty [3, 10, 14, 20, 21]. Most acquired cervical tracheal stenoses result from post-intubation or post-tracheostomy injuries, and are often associated with laryngotracheal stenosis. Their management by otolaryngologists has essentially consisted of tracheoplasty with costal cartilage grafts [6, 25–27]. Thoracic surgeons, however, have always favoured resection and anastomosis to restore a more normal and steady tracheal framework (see Fig. 22.5), based on their experience in adults [7, 22, 35]. It is noteworthy that two airway centres in the United States [28, 35] have developed different surgical strategies for managing acquired post-intubation stenosis. In 2004, the Cincinnati paediatric ENT group [28] published four cases of tracheal resection and anastomosis for acquired tracheal stenosis among several hundred paediatric laryngotracheal stenoses. In 2002, the Boston thoracic school, which specialises in adults, had already published 46 cases of paediatric tracheal resection-anastomoses for acquired stenoses [35]. Although bias in referral patterns to these centres might have played a significant role, the different philosophies of addressing similar issues are apparent. Although little information can be gathered from very small series of tracheal resections for acquired stenoses [5, 19, 28, 30], the conclusions based on the combined experiences of tracheal [35] and laryngotracheal resections [13, 32, 34, 35] in children have an impact on future research: • The principles of adult tracheal operations are directly applicable to children. • Complication rates and anastomotic failures of tracheal resection are higher in children than in adults. • In the largest single institutional series [35], success rates of tracheal resection were nearly 80% in children compared to 94% in adults [18]. • More recent series of laryngotracheal resections for isolated SGSs obtained similar (>90%) success rates to that of adults [2, 12, 13, 23, 29, 33, 34]. • Children do not tolerate anastomotic tension as well as adults.
22 Tracheal Resection and Anastomosis
• Up to 30% of the tracheal length (approximately six tracheal rings) can be resected, and the anastomosis can be carried out safely [35]. • When more than 30% of the tracheal length has to be resected, a full laryngeal release and sometimes a hilar release procedure are required [13]. • The limits of tracheal resection can be increased to 50% (eight to ten rings) when using an additional hilar release procedure [32]. • Anastomosis of the distal tracheal stump to the thicker cricoid ring is favourable to maintain the stability and patency of the anastomosis [28]. • Application of cervical slide-tracheoplasty for treating acquired tracheal stenoses is attractive as it diminishes tension on the suture line. However, an anastomosis performed with abnormal cicatricial tissue complicates the healing process [8]. Further experience is needed in this area before definite conclusions can be drawn. It can also be argued that while paediatric tracheal cartilages are thinner than the thyroid cartilage used for the thyrotracheal anastomosis during PCTR, tension on the suture line is identical given that the tracheal resections are of the same length. In the author’s opinion, resection of six rings can be safely performed in previously non-resected paediatric tracheae, either for PCTR or for simple tracheal resection with end-to-end anastomosis. A laryngeal release procedure is recommended. Assuming all basic principles outlined for the surgical technique (see Sect. 22.1.1) are followed to avoid localised devascularisation of the trachea, resection and anastomosis in children should be as safe as in adults. Working with 3x magnifying glasses aids in the meticulous suturing technique using 5.0 and 4.0 vicryl sutures for small and older children, respectively.
References 1. Acosta, A.C., Albanese, C.T., Farmer, D.L., et al.: Tracheal stenosis: the long and the short of it. J. Pediatr. Surg. 35, 1612–1616 (2000) 2. Alvarez-Neri, H., Penchyna-Grub, J., Porras-Hernandez, J.D., et al.: Primary cricotracheal resection with thyrotracheal anastomosis for the treatment of severe subglottic
References stenosis in children and adolescents. Ann. Otol. Rhinol. Laryngol. 114, 2–6 (2005) 3. Backer, C.L., Mavroudis, C., Dunham, M.E., et al.: Reoperation after pericardial patch tracheoplasty. J. Pediatr. Surg. 32, 1108–1111 (1997) 4. Backer, C.L., Mavroudis, C., Gerber, M.E., et al.: Tracheal surgery in children: an 18-year review of four techniques. Eur. J. Cardiothorac. Surg. 19, 777–784 (2001) 5. Carcassonne, M., Dor, V., Aubert, J., et al.: Tracheal resection with primary anastomosis in children. J. Pediatr. Surg. 8, 1–8 (1973) 6. Cotton, R.T., Gray, S.D., Miller, R.P.: Update of the Cincinnati experience in pediatric laryngotracheal reconstruction. Laryngoscope 99, 1111–1116 (1989) 7. Couraud, L., Jougon, J.B., Velly, J.F.: Surgical treatment of nontumoral stenoses of the upper airway. Ann. Thorac. Surg. 60, 250–259 (1995) 8. de Alarcon, A., Rutter, M.J.: Revision pediatric laryngotracheal reconstruction. Otolaryngol. Clin. North Am. 41, 959– 980 (2008) 9. deLorimier, A.A., Harrison, M.R., Hardy, K., et al.: Tracheobronchial obstructions in infants and children. Experience with 45 cases. Ann. Surg. 212, 277–289 (1990) 10. Elliott, M., Hartley, B.E., Wallis, C., et al.: Slide tracheoplasty. Curr. Opin. Otolaryngol. Head Neck Surg. 16, 75–82 (2008) 11. Elliott, M.J., Speggiorin, S., Vida, V.L., et al.: Slide tracheoplasty as a rescue technique after unsuccessful patch tracheoplasty. Ann. Thorac. Surg. 88, 1029–1031 (2009) 12. Garabedian, E.N., Nicollas, R., Roger, G., et al.: Cricotracheal resection in children weighing less than 10 kg. Arch. Otolaryngol. Head Neck Surg. 131, 505–508 (2005) 13. George, M., Ikonomidis, C., Jaquet, Y., et al.: Partial cricotracheal resection in children: potential pitfalls and avoidance of complications. Otolaryngol. Head Neck Surg. 141, 225–231 (2009) 14. Grillo, H.C.: Slide tracheoplasty for long-segment congenital tracheal stenosis. Ann. Thorac. Surg. 58, 613–619 (1994) 15. Grillo, H.C.: Preoperative consideration. In: Grillo, H.C. (ed.) Surgery of the Trachea and Bronchi, p. 445. BC Decker, Hamilton/London (2004) 16. Grillo, H.C.: Complications of tracheal reconstruction. In: Grillo, H.C. (ed.) Surgery of the Trachea and Bronchi, p. 487. BC Decker, Hamilton/London (2004) 17. Grillo, H.C., Zannini, P.: Management of obstructive tracheal disease in children. J. Pediatr. Surg. 19, 414–416 (1984) 18. Grillo, H.C., Donahue, D.M., Mathisen, D.J., et al.: Postintubation tracheal stenosis. Treatment and results. J. Thorac. Cardiovasc. Surg. 109, 486–492 (1995) 19. Healy, G.B., Schuster, S.R., Jonas, R.A., et al.: Correction of segmental tracheal stenosis in children. Ann. Otol. Rhinol. Laryngol. 97, 444–447 (1988)
347 20. Kimura, K., Mukohara, N., Tsugawa, C., et al.: Tracheoplasty for congenital stenosis of the entire trachea. J. Pediatr. Surg. 17, 869–871 (1982) 21. Lang, F.J., Hurni, M., Monnier, P.: Long-segment congenital tracheal stenosis: treatment by slide-tracheoplasty. J. Pediatr. Surg. 34, 1216–1222 (1999) 22. Mathisen, D.J.: Surgery of the trachea. Curr. Probl. Surg. 35, 453–542 (1998) 23. Monnier, P., Savary, M., Chapuis, G.: Partial cricoid resection with primary tracheal anastomosis for subglottic stenosis in infants and children. Laryngoscope 103, 1273–1283 (1993) 24. Nakayama, D.K., Harrison, M.R., de Lorimier, A.A., et al.: Reconstructive surgery for obstructing lesions of the intrathoracic trachea in infants and small children. J. Pediatr. Surg. 17, 854–868 (1982) 25. Ndiaye, I., Van de Abbeele, T., Francois, M., et al.: Traitement chirurgical des sténoses laryngées de l’enfant. Ann. Otolaryngol. Chir. Cervicofac. 116, 143–148 (1999) 26. Ochi, J.W., Evans, J.N., Bailey, C.M.: Pediatric airway reconstruction at Great Ormond Street: a ten-year review. I. Laryngotracheoplasty and laryngotracheal reconstruction. Ann. Otol. Rhinol. Laryngol. 101, 465–468 (1992) 27. Ochi, J.W., Bailey, C.M., Evans, J.N.: Pediatric airway reconstruction at Great Ormond Street: a ten-year review. III. Decannulation and suprastomal collapse. Ann. Otol. Rhinol. Laryngol. 101, 656–658 (1992) 28. Preciado, D., Cotton, R.T., Rutter, M.J.: Single-stage tracheal resection for severe tracheal stenosis in older children. Int. J. Pediatr. Otorhinolaryngol. 68, 1–6 (2004) 29. Ranne, R.D., Lindley, S., Holder, T.M., et al.: Relief of subglottic stenosis by anterior cricoid resection: an operation for the difficult case. J. Pediatr. Surg. 26, 255–258 (1991) 30. Sasano, S., Onuki, T., Nakajima, H., et al.: A two-year-old child with tracheal stenosis due to tracheostomy treated by end-to-end anastomosis of the trachea. Nippon Kyobu Geka Gakkai Zasshi 38, 1227–1230 (1990) 31. Shapshay, S.M., Beamis Jr., J.F., Hybels, R.L., et al.: Endoscopic treatment of subglottic and tracheal stenosis by radial laser incision and dilation. Ann. Otol. Rhinol. Laryngol. 96, 661–664 (1987) 32. Taylor, J.C.: Cricotracheal resection with hilar release for paediatric airway stenosis. Arch. Otolaryngol. Head Neck Surg. 136, 256–259 (2010) 33. Triglia, J., Nicollas, R., Roman, S., et al.: Cricotracheal resection in children: indications, technique and results. Ann. Otolaryngol. Chir. Cervicofac. 117, 155–160 (2000) 34. White, D.R., Cotton, R.T., Bean, J.A., et al.: Pediatric cricotracheal resection: surgical outcomes and risk factor analysis. Arch. Otolaryngol. Head Neck Surg. 131, 896–899 (2005) 35. Wright, C.D., Graham, B.B., Grillo, H.C., et al.: Pediatric tracheal surgery. Ann. Thorac. Surg. 74, 308–313 (2002)
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Revision Surgery
Contents 23.1 Insufficient Preoperative Assessment.................... 350 23.1.1 Incorrect or Incomplete Airway Assessment............ 351 23.1.2 Poor Evaluation of the Patient’s Comorbidities............................................. 351 23.1.3 Inadequate Parental Counselling.............................. 351 23.1.4 Inappropriate Selection of the Operative Procedure....................................... 352 23.2 Failure of Surgical Technique................................ 352 23.2.1 Laryngotracheal Reconstruction with CCG............. 352 23.2.2 Tracheal Resection and PCTR.................................. 353 23.3
Factors Unrelated to the Child’s Primary Medical Condition................................... 354
23.4 23.4.1 23.4.2 23.4.3 23.4.4 23.4.5
Late Failures............................................................ 354 Suprastomal Collapse and Granuloma..................... 354 A-Frame Tracheal Deformity................................... 355 Arytenoid Prolapse................................................... 355 Recurrent Posterior Glottic Stenosis......................... 355 Epiglottic Petiole Prolapse........................................ 355
23.5 Unresolved Issues.................................................... 355 23.5.1 Bilateral Cricoarytenoid Joint Fixation.................... 356 23.5.2 Extensive Tracheal Damage..................................... 356
Core Messages
›› Surgical failures of LTS may result from:
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References............................................................................ 356
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–– Insufficient preoperative assessment –– Inappropriate selection of the operative procedure –– Failure of the surgical technique –– Factors inherent to the child’s general condition Prior to any surgery, a comprehensive assessment of the child’s general condition and airway is essential. A refined selection of the best surgical option is based on: –– Grade, location and extent of LTS –– Dynamic assessment of the larynx and upper airways –– Adequate evaluation of the patient’s comorbidities Surgeons managing paediatric airway problems must be fully trained in upper airway endoscopy and all technical aspects of surgical airway reconstruction. Technical failures of LTR with CCG are mainly due to: –– Off-midline laryngofissure and posterior cricoid split –– Inappropriate width of the PCCG –– Poor carving and suturing of the CCG –– Selection of an inappropriate stent for splinting the airway reconstruction –– Inadequate coverage of the reconstruction Technical failures of PCTR or tracheal resection and anastomosis are mainly due to: –– Anastomotic dehiscence: –– Insufficient mobilisation of the intrathoracic trachea
P. Monnier (ed.), Pediatric Airway Surgery, DOI: 10.1007/978-3-642-13535-4_23, © Springer-Verlag Berlin Heidelberg 2011
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Absence of laryngeal release procedure Excessive devascularisation of the trachea Inappropriate suturing technique Inadequate sedation of the patient during the postoperative period –– Recurrent laryngeal nerve injury –– Technical failure during tracheal and cricoid dissection –– Blind coagulation in peritracheal soft tissues –– Inappropriate placement of stitches on the thyrotracheal anastomosis –– Late restenosis –– Slowly progressive anastomotic dehiscence –– Suboptimal approximation of the tracheal stumps at the anastomotic site An airway stent should always be removed 4–6 weeks prior to revision surgery in order to delineate the exact extent of airway reconstruction needed. Other airway problems may compromise decannulation after successful PCTR or LTR for LTS: –– Suprastomal collapse and granuloma at the tracheostomy site –– A-frame deformity of the tracheostomy site –– Arytenoid prolapse –– Epiglottic petiole prolapse Recurrent posterior glottic stenosis accounts for most surgical failures following airway reconstruction for glotto-subglottic stenosis. Unresolved issues requiring further research in paediatric airway surgery include: –– Bilateral cricoarytenoid joint fixation –– Extensive tracheal damage
Fig. 23.1 Recurrent glotto-subglottic stenosis after failed LTR for severe grade III subglottic stenosis with glottic involvement: The endoscopic view shows a thick anterior synechia of the vocal cords and a severe shortening of the anteroposterior distance of the glottis. Cigar-shaped prostheses of the Aboulker or Montgomery T-tube types are inadequate for splinting glottosubglottic reconstructions
is illustrated by the most challenging cases resulting from previous failed surgeries (Fig. 23.1). Attention to details is of paramount importance during the entire management, as minute errors may have devastating consequences. According to Grillo [8] and Rutter [3], complications of laryngotracheal reconstruction result from: • Insufficient preoperative assessment with inappropriate selection of the operative procedure • Failure of surgical technique • Factors inherent to the child’s general condition
23.1 Insufficient Preoperative Assessment Despite a thorough preoperative assessment, surgical planning and meticulous attention to technical details, surgery may fail due to unforeseen complications. In the absence of a comprehensive preoperative appraisal, the surgical outcome is unlikely to be successful. In fact, it may worsen the initial condition, as
Incomplete appraisal may occur at different stages of the preoperative workup: 1. Incorrect or incomplete airway assessment 2. Poor evaluation of the patient’s comorbidities 3. Inadequate interview of the parents 4. Inappropriate selection of the operative procedure
23.1 Insufficient Preoperative Assessment
23.1.1 Incorrect or Incomplete Airway Assessment A detailed description of endoscopic airway assessment is provided in Chap. 5 and Sect. 17.3 of Chap. 17. The most common mistakes include: • • • •
Inadequate evaluation of the nature of the stenosis Imprecise assessment of vocal cord function Missed concomitant airway lesions Failure to obtain a bacteriological aspirate of the trachea
Any of the aforementioned errors may result in extubation or decannulation failure.
23.1.2 Poor Evaluation of the Patient’s Comorbidities Comorbidities may be numerous and gravely compromise the surgical outcome. They include: • • • • • • • • •
Syndromic and non-syndromic anomalies Lung disease caused by prematurity Airway infection and hyper-reactivity Gastro-oesophageal reflux (GOR) Eosinophilic oesophagitis (EO) Feeding difficulties and aspiration Neurological impairment and/or mental disability Cardiovascular anomalies Long-lasting corticosteroid treatment
All efforts must be made to optimise the patient’s general condition before any airway surgery is undertaken. Airway infection and hyper-reactivity, gastro-oesophageal reflux and eosinophilic oesophagitis are amenable to medical treatment [1, 2, 5, 10, 15, 18, 20]. More complex situations such as maxillo-facial or cardiovascular anomalies and intractable GOR require surgical correction. Feeding difficulties with aspiration and neurological impairment may call for a long rehabilitation period. Lastly, surgery should not be considered for severe syndromic or non-syndromic anomalies or lung diseases with O2 requirements unless voice restoration rather than decannulation is the final goal.
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The ‘lost’ preoperative time used for optimising the patient’s status is regained during the postoperative period as complications and potential surgical failures are less likely to occur if careful preoperative assessments are conducted.
23.1.3 Inadequate Parental Counselling Before engaging in any airway reconstruction, the surgeon must clearly explain to the child’s parents what outcome is expected. For parents, understanding the differences in the prognosis of two clinical conditions that both show aphonia and tracheostomy is impossible if not properly explained (see Fig. 5.13, Chap. 5). For a child suffering from a ‘simple’ Grade IV SGS with normal vocal cord function, the prognosis is good and he/ she can expect to lead an almost normal life after a successful PCTR (see Fig. 5.13a, Chap. 5). In contrast, for a child with a severely damaged larynx with transglottic stenosis and bilateral cricoarytenoid joint fixation, the best postoperative result that can be anticipated is a trade-off between voice quality and airway patency with possible aspiration (see Fig. 5.13b, Chap. 5). However, parents are not able to comprehend the difference in outcomes if they are not fully informed. Likewise, similar airway problems such as isolated Grade III SGS with normal vocal cord function must be treated differently in otherwise healthy children in comparison to those with respiratory insufficiency. Single-stage PCTR may be a reasonable option for the healthy child, whereas either DS-PCTR or DS-LTR must be considered for the child with respiratory insufficiency. In order to choose the optimal surgical strategy for the right patient, the surgeon must demonstrate refined judgement, and ensure that the parents share in the realistic expectations about the outcome. Only if the surgeon has made a thorough and complete preoperative assessment of the child’s general condition and airway can the parental interview be meaningfully conducted. Decannulation is not the sole outcome measure in compromised airway surgeries. For example, restoring a laryngeal opening for voice production is likely to improve communication skills in a child with an initial
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Grade IV SGS even when decannulation is impossible due to chronic respiratory insufficiency. In such a case, surgery may be considered a success even though the ultimate goal of decannulation could not be achieved. Again, the preoperative interview with the parents is critical in order for them to be properly informed in advance about the limited expectations.
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play a significant role in selecting the surgical strategy for a given case.
23.2 Failure of Surgical Technique Enlargement LTR with CCG must be clearly distinguished from airway resection and anastomosis.
23.1.4 Inappropriate Selection of the Operative Procedure
23.2.1 Laryngotracheal Reconstruction with CCG As a rule, surgeons managing paediatric airway problems must be fully trained in endoscopy and all other technical aspects of laryngotracheal reconstructions, laryngeal framework augmentation with cartilage grafts, tracheal or cricotracheal resections, slide-tracheoplasty and endoscopic therapeutic procedures. Only if the team in charge of the patient correctly masters the entire range of endoscopic and surgical interventions can the optimal option for each particular patient be chosen. Selecting a technique that is not the optimal surgical option (e.g., LTR for a Grade IV SGS) should not be due to a surgeon’s lack of training, but based on a decision that airway resection would have been too risky in a particular child. Likewise, choosing a single-stage rather than a double-stage LTR or PCTR requires sound judgement. Although the healing process is generally easier in single-stage surgeries, the postoperative period may be more difficult, requiring skilled management in the PICU. In addition, the risk of graft or anastomotic superinfections is higher when there is a tracheostomy. Singlestage surgery may not be possible in certain impaired or disabled children. In fact, if the indication criteria were clearly established and respected, the same operations would be performed for similar cases in all institutions; however, experience proves the contrary. In that respect, it is worth noting that in 2008, LTR (85% of cases) was used more frequently than PCTR (15% of cases) for treating LTS in children [12] by the Cincinnati group, whereas in our institution, the ratio was reversed, with PCTR (75% of cases) being used more frequently than LTR (25% of cases). Selection biases may explain this significant difference; nevertheless, the surgeon’s preference and familiarity with a surgical procedure also
This intervention is technically simple, and the approach to the larynx is at the midline with no lateral neck dissection. Technical failures may result from: • Off-midline laryngofissure and posterior cricoid split: The vocal cords may be damaged anteriorly and the cricoarytenoid joint posteriorly. • Inappropriate width of the CCG: Under- or overexpansion of the posterior laryngeal commissure may lead to an insufficient airway or to a breathy voice with possible arytenoid prolapse and aspiration, respectively. • Poor carving and suturing technique of the CCG: Suboptimal mucosal-perichondrial approximation leads to increased superinfection risks, granulation tissue formation or graft migration with subsequent laryngeal distortion. • Inappropriately designed stent: Additional damage to the reconstructed airway, such as blunting of the anterior laryngeal commissure after vocal cord separation for synechia, and supra- or infraglottic trauma with subsequent granulation tissue formation and restenosis may ensue when using inappropriate stents for the larynx, such as Montgomery T-tubes or Aboulker stents. • Inadequate coverage of the reconstruction: Failure to resuture the thyroid isthmus or the strap muscles over the ACCG may delay the vascular supply to the reconstructed airway, thereby contributing to graft necrosis. • Additional perioperative conditions such as prolonged steroid usage or inappropriate antibiotic selection may be responsible for graft failure. Meticulous attention to detail cannot be overemphasised.
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23.2 Failure of Surgical Technique
23.2.2 Tracheal Resection and PCTR Technically, these interventions (and particularly PCTR) are more challenging than LTR, as they require careful dissection of the trachea and larynx with preservation of RLNs and vascular supply to the trachea. They are, however, largely superior to LTR for the management of severe (Grade III and IV) SGS, complete transglottic stenosis and tracheal stenosis with loss of cartilage support. Serious complications include:
23.2.2.1 Anastomotic Separation Anastomotic separation is due to a technical failure, likely because of excessive anastomotic tension resulting from insufficient tracheal mobilisation or laryngeal release at initial surgery. If suspicion of dehiscence is confirmed by laryngotracheoscopy, then immediate reexploration is warranted. It is often possible to salvage the situation by several means, including refreshing the distal tracheal stump by resecting one or two additional rings, performing a full infrahyoid laryngeal release manoeuvre, mobilising the intrathoracic trachea extensively and recreating the anastomosis. For a thyrotracheal anastomosis, the best option is to shroud the laryngeal stitches around the upper edge of the thyroid cartilage (see Fig. 20.43, Chap. 20). An additional reinforcement using tibial periosteum may be envisaged (see Fig. 20.44, Chap. 20). If these manoeuvres prove impossible because of prior extensive resection, then efforts should be made to recreate the anastomosis around the LT-Mold prosthesis and perform a distal tracheostomy in order to release the tension on the suture line and fix the distal trachea to the skin (see Fig. 20.44, Chap. 20).
23.2.2.2 Tracheal Stenosis This early complication, occurring during the first postoperative week, results from technical errors, such as extensive circumferential mobilisation and devascularisation of the trachea, or improper placement of the anastomotic stitches. The trachea must never be dissected circumferentially before being resected, as this
procedure unnecessarily devascularises the proximal and distal tracheal stumps. Inadequate technique of anastomosis may further compromise the vascular supply to the edges of the tracheal stump. If all stitches are placed through the tracheal wall instead of passing submucosally at the anastomotic level, then they may devascularise the mucosa over a distance of one or two tracheal rings, due to a cheesewire mechanism (see Fig. 22.4, Chap. 22). It is essential to keep in mind that the cartilages are nourished by the inner mucosa and not by the outer perichondrium of the trachea (see Sect. 2.5, Chap. 2).
23.2.2.3 Anastomotic Granulation Tissue and Restenosis This late complication, occurring between the 10th and 15th postoperative day, is due to suboptimal mucosal approximation at the anastomotic site. Since the introduction of vicryl for performing airway anastomoses, suturing material is no longer the cause for anastomotic granulation tissue formation. Magnifying (3x) glasses help achieve optimal results. Single-stage PCTR in small children requires the surgeon’s full expertise, but allows for early extubation without anastomotic problems (see Fig. 20.37, Chap. 20). Late, slowly progressive anastomotic dehiscence may also cause granulation tissue formation and restenosis. At the first endoscopy control at 1 week postoperatively, even when the initial anastomotic site looks perfect, the child must stay quiet for another 2 weeks until the anastomosis has been stabilised by scar tissue. During the postoperative course of a single-stage resection and anastomosis, chronic coughing may be responsible for anastomotic disruptions, which occurred in one patient of our series (see Fig. 20.42, Chap. 20). Airway stenting with an LT-Mold for PCTR and a plain silicone or Montgomery T-tube for tracheal resection and anastomosis frequently solves the problem of anastomotic granulation with impending restenosis. Scars exert their retraction effects in the cranio-caudal axis, while the airway prosthesis prevents the airway’s recurrent circumferential narrowing. However, this positive effect is observed only in the case of a short and partial dehiscence. Longer airway separations evolve into localised malacia, with a bottleneck recurrent stenosis of the airway.
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23.2.2.4 Recurrent Laryngeal Nerve Injury This complication results from failure to follow the basic principles of laryngotracheal surgery, namely dissection of the trachea short of the tracheal rings, preventative coagulation of all tracheal feeding vessels, avoidance of posterior and lateral cricoid dissection above the lower edge of the cricoid plate, section of the lateral cricoid arches anteriorly to the cricothyroid joints, as well as accurate placement of the posterolateral cricoid stitches in a subperichondrial plane during PCTR. All of these technical details must be studied during training in paediatric airway surgery.
23.3 Factors Unrelated to the Child’s Primary Medical Condition Besides the comorbidities to be addressed and treated prior to surgery, some children are prone to developing laryngeal oedema, granulation tissue, keloids or infections in wounds or the lower airway. In small children, vocal cord oedema after PCTR is not considered a complication, as it results from the interruption of the lymphatic flow at the level of the subglottic anastomosis. Adrenaline aerosols and a short course of systemic corticosteroids are sufficient to alleviate symptoms of obstruction with the help of a slight CPAP delivered through the face mask. Airway and wound infections are fairly rare and respond well to antibiotics based on bacteriological cultures and sensitivity. Despite careful optimisation of both concomitant airway stenoses and the patient’s general condition, some children present higher tissue reactivity with a strong propensity to develop excessive granulation tissue and keloids. Although parameters such as gastrooesophageal reflux, eosinophilic oesophagitis and bacteriological airway colonisation may have been adequately treated, the postoperative result may be less favourable than expected for unknown reasons. If revision surgery is deemed necessary, then a full reassessment of the patient with the help of specialists (e.g., gastroenterologists, pulmonologists, infectiologists, immunologists) must be carried out prior to any new surgical intervention. In the most difficult cases, revision surgery may have to be postponed until after puberty when growth hormone activity has decreased. Although rare, this scenario did occur on one occasion in our series of 100 PCTRs performed for severe LTS. The
23 Revision Surgery
last chance treatment should always be meticulously prepared in order to avoid another surgical failure that may leave the child crippled with a permanent tracheostomy.
23.4 Late Failures Acute revision surgery aims at salvaging a critical situation, particularly after a resection and anastomosis procedure. The goal should be to recreate a safe airway, while optimising conditions for revision surgery. At times, endoscopic stent placement is sufficient, hopefully alleviating the need for a second open surgery. In all other cases, the reasons for surgical failure should be sought before considering open revision surgery. These include a more detailed examination for unidentified OSA problems, severe gastro-oesophageal reflux requiring pH-impedance monitoring or undiagnosed eosinophilic oesophagitis possibly warranting new oesophageal biopsies [5]. Revision surgery for failed primary treatment should not be considered until restenosis has matured into a full cicatricial stricture. A 6-month waiting period is usually enough before attempting a revision procedure. If a stent is left in situ, it should be removed 4–6 weeks prior to the revision surgery. This allows a diseased malacic airway segment to shrink to its final position and helps determine what portion of the airway should be reconstructed. Various factors, such as the degree, length, location and steadiness of the airway should be evaluated prior to selecting the technique used for resection or augmentation. As for the primary surgery, scrupulous judgement should be exercised in choosing the most appropriate revision surgery, taking into account previous surgeries that may preclude certain interventions, such as further airway resection after extensive primary resection. Even after correcting the primary stenosis, decannulation may fail in some patients due to other laryngeal or stomal problems.
23.4.1 Suprastomal Collapse and Granuloma The author believes that the best strategy is to close all tracheostomae surgically following challenging airway reconstructions. By reapproximating the tracheal rings of
355
23.5 Unresolved Issues
the stoma in the cranio-caudal axis, a steady tracheal framework is reconstructed, thus avoiding recurrent anteroposterior stenosis (see Fig. 21.7, Chap. 21). Furthermore, an A-frame tracheal deformity is prevented. Optimising the airway size from the nostrils to the carina can only benefit the child, as multiple minor extrathoracic narrowings have negative additive effects on respiration.
23.4.2 A-Frame Tracheal Deformity This condition develops after spontaneous closure of the tracheostoma. The interrupted vault of the Roman tracheal arch is progressively retracted by scar tissue and leads to laterally collapsed airway (see Figs. 14.20 and 21.3a, Chaps. 14 and 21). This complication may be prevented by primary surgical closure of the stoma, placing all tracheal stitches in the cranio-caudal axis (see Fig. 21.7, Chap. 21).
23.4.3 Arytenoid Prolapse The exact mechanisms responsible for the airway’s dynamic obstruction are not completely understood. Following previous surgery, one arytenoid may fall antero-medially into the glottic inlet during each inspiration, thereby obstructing the airway. De Alarcon and Rutter [3] believe that arytenoid prolapse results from injury to the cricoarytenoid joints or the posterior cricoarytenoid ligament during LTR or PCTR, with further destabilisation of the arytenoid when the lateral cricoarytenoid muscle is partially cut during PCTR. Our own observations provide a different scenario. Arytenoid prolapse is essentially seen when glottic closure is incomplete, particularly when the glottic chink is large. In order to make sounds, the child uses the arytenoid to create mucosal vibrations against the laryngeal aspect of the epiglottis as a compensatory mechanism. The same mechanism is observed in adult patients following supracricoid partial laryngectomy with crico-hyoido-epiglottopexy. Although their residual arytenoid has not experienced any cricoarytenoid joint or posterior cricoarytenoid ligament trauma, it prolapses into the glottic inlet during phonation. In most cases, a partial or complete endoscopic CO2 laser arytenoidectomy, with preservation of a medially
based mucosal flap, is effective in alleviating symptoms of arytenoid prolapse.
23.4.4 Recurrent Posterior Glottic Stenosis As the most common cause of secondary stenosis [6, 7, 17, 21], recurrent posterior glottic stenosis is due to insufficient width of the costal cartilage graft, posterior graft loss or migration, and may be associated with severe laryngeal distortion. It is more frequently seen after SS-LTR than DS-LTR with long-term stenting, but can also occur after extended PCTR [7]. Surgical correction necessitates revision LTR with posterior cricoid split and PCCG. To avoid another failure, patients require stenting until full healing has occurred after revision surgery.
23.4.5 Epiglottic Petiole Prolapse Epiglottic petiole prolapse (EPP), unless caused by blunt laryngeal trauma, is secondary to a laryngofissure with section-disruption of the thyro-epiglottic ligament during the course of an LTR or extended PCTR (see Fig. 15.12, Chap. 15 and Fig. 20.34, Chap. 20). Awareness of this potential complication has improved the technique of laryngofissure closure, in which the base of the epiglottis is fixed to the hull of the thyroid cartilage with pexy sutures. Late correction of EPP requires full resection of the scar tissue of the pre-epiglottic space as well as anterior pexy of the epiglottis with mattress sutures through the thyroid cartilage and possibly around the hyoid bone (see Fig. 20.34, Chap. 20). Postoperative care of revision surgery is similar to that of primary surgery. Formal capping and decannulation trials, for instance, are performed in a similar fashion. Surgical closure of the tracheostoma is strongly recommended.
23.5 Unresolved Issues Despite major progress made in the management of paediatric LTS over the last few decades, bilateral cricoarytenoid joint fixation and extensive tracheal damage remain unresolved issues.
356
23.5.1 Bilateral Cricoarytenoid Joint Fixation Bilateral fixed vocal cords are frequently associated with severe, dense posterior commissure scarring. Although LTR or extended PCTR with PCCG recreates an adequate interarytenoid distance, a ‘frozen larynx’ (with no vocal cord mobility) is the final outcome. In clinical practice, a trade-off between airway patency and voice quality, with potential aspiration, must be made. Children without neurological problems can cope with this situation after a rehabilitation period for deglutition. However, their voice often remains breathy, thereby diminishing their ability to communicate. After prolonged intubation, the arytenoids are not fused with the cricoid plate. Severe medial peri-articular fibrosis is responsible for arytenoid fixation. If peroperative palpation reveals complete arytenoid fixation after removing interarytenoid scar tissue, then remobilising the arytenoid cartilages by deliberately opening and freeing the cricoarytenoid joints should be attempted. This cannot worsen the initial condition of bilaterally fixed arytenoids. The medial aspect of the cricoarytenoid joints is then covered by a large pedicled flap of the membranous trachea that is sutured to the vocal process of the arytenoid laterally and the pharyngeal interarytenoid mucosa posteriorly. Next, the reconstructed airway is stented using an LT-Mold prosthesis. Although our attempts at remobilising the arytenoids have been partially successful, this problem deserves further attention and research. Restoring arytenoid mobility in severely damaged larynges would greatly benefit the children who have sustained this injury.
23.5.2 Extensive Tracheal Damage In children, the limits of safe tracheal resection have been fixed at 30%, based on experimental studies in puppies [13, 14]. However, longer and more dependable resections are feasible, notably with the adjunct of infrahyoid and hilar release manoeuvres [16, 19]. Subtotal resections of the trachea have been reported by some authors in isolated paediatric cases [11, 19]. Nevertheless, tracheal replacements will probably not be available in the near future for the few paediatric cases where they might be used.
23 Revision Surgery
Over the last 40 years, countless animal experiments have been performed to create a dependable and predictable tracheal substitute for adult patients, albeit with little success. For a thorough and thoughtful discussion on this matter, the reader is referred to the work of HC Grillo on tracheal replacement [9]. Recently an interesting article on adult tracheal allotransplantation with temporary immunosuppressive therapy was published in the New England Journal of Medicine [4]. This concept is certainly opening new horizons for tracheal replacement in severely damaged adult tracheas. In children, the endeavour is even more challenging, taking into account the small size of the airway and the necessity for potential growth and development. This remains a biosurgical challenge for future generations. It should stimulate thoughtful research in the field of bioengineered tissues, but the challenges are overwhelming, as any suitable conduit needs to be comprised of a laterally rigid and longitudinally flexible scaffold, an inner lining of ciliated respiratory epithelium and an adequate vascular supply over its whole length.
References 1. Brown-Whitehorn, T., Liacouras, C.A.: Eosinophilic esophagitis. Curr. Opin. Pediatr. 19, 575–580 (2007) 2. Dauer, E.H., Freese, D.K., El-Youssef, M., et al.: Clinical characteristics of eosinophilic esophagitis in children. Ann. Otol. Rhinol. Laryngol. 114, 827–833 (2005) 3. de Alarcon, A., Rutter, M.J.: Revision pediatric laryngotracheal reconstruction. Otolaryngol. Clin. North Am. 41, 959– 980 (2008) 4. Delaere, P., Vranckx, J., Verleden, G., et al.: Tracheal allotransplantation after withdrawal of immunosuppressive therapy. N Engl J. Med. 362, 138–145 (2010) 5. Furuta, G.T., Liacouras, C.A., Collins, M.H., et al.: Eosinophilic esophagitis in children and adults: a systematic review and consensus recommendations for diagnosis and treatment. Gastroenterology 133, 1342–1363 (2007) 6. Gardner, G.M.: Posterior glottic stenosis and bilateral vocal fold immobility: diagnosis and treatment. Otolaryngol. Clin. North Am. 33, 855–878 (2000) 7. George, M., Jaquet, Y., Ikonomidis, C., et al.: Management of severe pediatric subglottic stenosis with glottic involvement. J. Thorac. Cardiovasc. Surg. 139, 411–417 (2010) 8. Grillo, H.C.: Complications of tracheal reconstruction. In: Grillo, H.C. (ed.) Surgery of the Trachea and Bronchi, pp. 483–487. BC Decker, Hamilton/London (2004) 9. Grillo, H.C.: Tracheal replacement. In: Grillo, H.C. (ed.) Surgery of the Trachea and bronchi, pp. 839–854. BC Decker, Hamilton/London (2004)
23.5 Unresolved Issues 10. Halstead, L.A.: Extraesophageal manifestations of GERD: diagnosis and therapy. Drugs Today (Barc) 41(Suppl B), 19–26 (2005) 11. Jacobs, J.P., Haw, M.P., Motbey, J.A., et al.: Successful complete tracheal resection in a three-month-old infant. Ann. Thorac. Surg. 61, 1824–1826 (1996) 12. Koempel, J.A., Cotton, R.T.: History of pediatric laryngotracheal reconstruction. Otolaryngol. Clin. North Am. 41, 825– 835 (2008) 13. Kotake, Y., Grillo, H.C.: Reduction of tension at the anastomosis following tracheal resection in puppies. J. Thorac. Cardiovasc. Surg. 71, 600–604 (1976) 14. Maeda, M., Grillo, H.C.: Effect of tension on tracheal growth after resection and anastomosis in puppies. J. Thorac. Cardiovasc. Surg. 65, 658–668 (1973) 15. McGuirt Jr., W.F.: Gastroesophageal reflux and the upper airway. Pediatr. Clin. North Am. 50, 487–502 (2003) 16. Monnier, P., Lang, F., Savary, M.: Partial cricotracheal resection for severe pediatric subglottic stenosis: update of the
357 Lausanne experience. Ann. Otol. Rhinol. Laryngol. 107, 961–968 (1998) 17. Rutter, M.J., Cotton, R.T.: The use of posterior cricoid grafting in managing isolated posterior glottic stenosis in children. Arch. Otolaryngol. Head Neck Surg. 130, 737–740 (2004) 18. Suskind, D.L., Zeringue 3rd, G.P., Kluka, E.A., et al.: Gastroesophageal reflux and pediatric otolaryngologic disease: the role of antireflux surgery. Arch. Otolaryngol. Head Neck Surg. 127, 511–514 (2001) 19. Taylor, J.C.: Cricotracheal resection with hilar release for paediatric airway stenosis. Arch. Otolaryngol. Head Neck Surg. 136, 256–259 (2010) 20. Yellon, R.F., Goldberg, H.: Update on gastroesophageal reflux disease in pediatric airway disorders. Am. J. Med. 111(Suppl 8A), 78S–84S (2001) 21. Zalzal, G.H.: Posterior glottic stenosis. Int. J. Pediatr. Otorhinolaryngol. 49(Suppl 1), S279–S282 (1999)
Appendix
Manufacturer Information Armoured cuffed tracheal tube (SilkoClear Flex Silicone): Willy Rüsch GmbH, Willy-Rüsch Strasse 4-10, 71394 Kernen/Germany www.ruesch.de Balloon dilators: Boston Scientific, Customer service, Corporate Headquarters, One Boston Scientific Place, Natick, MA 01760-1537, USA www.bostonscienfific-international.com CO2 laser, Digital AcuBlade robotic laser microsurgery: Lumenis Inc. Main Office, 5302 Betsy Ross Drive, Santa Clara, CA 95054, USA www.lumenis.com Diprogenta®: Gentamycin-corticosteroid ointment: Essex Chemie AG, Weystrasse 20, 6006 Luzern, Switzerland www.essex.ch Disposable retractor ring: Lone Star, Medical products, 11211 Cash Road, Stafford TX 77477, USA www.lsmp.com Eliachar stents: Hood Laboratories, E. Benton Hood Laboratories Inc., 575 Washington Str., Pembroke, MA 02359, USA www.hoodlabs.com
Endoscopic needle holders: Karl Storz GmbH, Mittelstrasse 8, D-78532 Tuttlingen, Germany www.karlstorz.de Medtronic International Trading Sarl, Rte du Molliau 31, CP 84, CH – 1131 Tolochenaz, Switzerland www.medtronic.com ET tubes, laser-safe ET tubes, and tracheostomy cannulas: Mallinckrodt Inc., 675 Mcdonnell Blvd, St. Louis, MO 63134, USA www.mallingckrodt-rx.com Portex Smiths Medical International Ltd, 1500 Eureka Park, Lower Pemberton, Ashford, Kent, TN25 4 BF, UK www.smiths-medical.com Ruesch, Teleflex Medical, PO Box 12600, Research Triangle Park, NC 27709, UK www.teleflexmedical.com Lasershield, Xomed-Treace, 6743 Southpoint Drve, North, Jacksonwille, FL 32216-6218, USA www.bizdays.com Face mask for transnasal fibre-optic laryngoscopy: VBM® Medizintechnik GmbH, Einsteinstrasse 1, 72172 Sulz am Neckar, Germany
[email protected] www.vbm-medical.de Fibrin glue: Baxter, One Baxter Parkway, Deerfield, IL 600154625, USA www.baxter.com
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Flexible bronchoscopes, oesophagoscopes: Olympus Medical Systems Corp., Shinjuku Monolith, 3-1 Nishi-Shinjuku-chome, Shinjuku-Kum Tokyo 163-0914, Japan www.olympus-global.com Pentax Corp., 2936-9 Maeno-cho, Itabashi-ku, Tokyo 1748639, Japan www.pentax.co.jp Fujinon: Fujifilm Corp., 1-324 Uetaki, Kita-ku, Saitama City, Saitama 331-9624, Japan www.fujifilam.com Food thickener (ThickenUp®): Nestlé, avenue Nestlé 55, 1800 Vevey, Switzerland www.nutrition.nestle.ca, www.dysphagia-diet.com High frequency jet ventilator: Acutronic® Medical System AG, Haldenstrasse 3, 6342 Baar(ZH), Switzerland www.acutronic-medical.ch KTP, diode, Nd-YAG lasers: Laserscope, 3070 Orchard Drive, San Jose, California, USA www.laserscope.com Laryngoscopes, rigid bronchoscopes, oesophagoscopes, and forcepses: Karl Storz GmbH, Mittelstrasse 8, D-78532 Tuttlingen, FRG www.karlstorz.de Lichtenberger needle-carrier: Richard Wolf GmbH, Pforzheimerstr. 32, D-75438 Knittlingen, Germany www.richard-wolf.com LT-molds: Bredam SA, Rue des Jordils 40, 1025 St-Sulpice, Switzerland www.bredam.ch Actimed SA, Rue des Jordils 40, 1025 St-Sulpice, Switzerland www.actimed.ch
Appendix
Micropump mesh nebulizer: Aerogen Ltd., Galway Business Park, Dangan, Galway, Ireland
[email protected] Montgomery T-tubes: Hood Laboratories, E. Benton Hood Laboratories Inc., 575 Washington Str., Pembroke, MA 02359, USA www.hoodlabs.com MRI non-magnetic monitoring (Maglife C Plus®): Schiller AG, Altgasse 68, 6341 Baar, Switzerland www.schiller.ch Savary-Gilliard tracheal dilators: Cook Medical Inc. PO Box 4195, Bloomington, IN 47402-4195, USA www.cookmedical.com Silicone glue: NuSil Technology Headquarter, 1050 Cidy Lane. Carpinteria, CA 93013, USA www.nusil.com Transcutaneous carbon dioxide monitoring (TC-CO2) (Tosca Sensor®): Linde Medical Sensors AG, Ausstrasse 25, 4051 Basel, Switzerland www.highbeam.com Transglottic Polyurethane Jet Catheter (Tosca Sensor®): Acutronic® Medical System AG, 8816 Hirzel (ZH), Switzerland www.acutronic-medical.ch Transtracheal Jet Cannula (Ravussin Cannula®): VBM® Medizintechnik GmbH, Einsteinstrasse 1, 72172 Sulz am Neckar, Germany www.vbm-medical.de
Index
Abductor muscles, 11 Aberrant innominate artery, 36, 161–162, 164–165, 197 Aberrant subclavian artery, 161–162 Aboulker stent, 19–20, 259, 352 Acquired fistula tracheo-innominate artery, 329–331 tracheo-oesophageal, 197, 331–334 Acquired on congenital (mixed) subglottic stenosis, 123, 184 Acquired stenosis larynx, 184–189, 194–195 predisposing factors, 189 prevalence, 181 subglottis, 184–186, 190 trachea, 195–197 AcuBlade micromanipulator, 63–64 Acute postintubation injuries endoscopic treatment, 189–194 obstructive granulation tissue, 191–194 pathogenesis, 184–185, 189 prevention, 186–189 soft tissue stenosis, 189–190 Acute respiratory distress syndrome (ARDS), 78–79 Acute trauma, larynx and trachea, 199–212 Adductor muscles, 11 Adhesion, interarytenoid, 86–87, 89, 188, 234, 237–238, 249 A-frame deformity, tracheostomy, 197, 315, 330, 335, 350 Airway anatomy, 15–16, 19 assessment, incorrect or incomplete, 350, 351 fire, lasers, 68–70 management, for severe respiratory distress, 78–80 Airway compression extrinsic, 158, 164 mediastinal masses, 164 vascular causes, 161, 164–165 Airway compromise anaesthetic techniques for MRI, 40–42 emergency airway support, 78–80 emergency surgical airway access, 80 Airway dimensions larynx, 16–18 trachea, 18–19 Airway endoscopy, 78–91 direct laryngoscopy, 84–85 rigid bronchoscopy, 80
suspension microlaryngoscopy, 48–50, 67, 85–90, 194, 233 transnasal fiberoptic laryngoscopy, 79, 82–84 Airway grading system modified according to Monnier, 89–90, 231, 231, 234 Myer–Cotton, 85, 87–89, 234, 273, 274 Airway obstruction causes, 33–35 clinical evaluation, 31–42 dynamic obstruction, 34, 40–41, 82–84 fixed, 34–35 medical history, 36–37 physical examination, 37–38 site, 33–34 variable extrathoracic, 34 variable intrathoracic, 34 worsening factors, 36 Airway reconstruction complications, 271 laryngotracheal reconstruction (LTR), 257–271 laryngotracheoplasty (LTP), 259–262 postoperative care, 271 reporting system, 272, 273 results of LTR, 271–274 single-stage LTR, 268–271 surgical highlights for LTR, 270–271 Algorithm for isolated PGS, 238 for treatment of LTS, 234–237 Alpha-2A interferon, for recurrent respiratory papillomatosis, 226 Anaesthesia for endoscopic airway procedure under controlled ventilation, 244–245 intermittent apnoeic technique, 243 jet ventilation, 245–246 under spontaneous respiration, 242–243 Anaesthesia for PCTR under controlled ventilation, 284–285 high frequency jet ventilation, 284–285 under spontaneous respiration, 285 SS-PCTR in non-tracheostomised patient, 284 SS-PCTR in tracheostomised patient, 285 Anaesthetic techniques high frequency jet ventilation, 245–246 with intermittent apnoeas, 243 for MRI, 40–42 in obstructive dyspnoea, 40–42
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362 in spontaneous respiration, 81–82, 242–243 Anastomosis dehiscence, 195, 239, 280, 283, 291, 299, 302, 305, 312–316, 318, 327, 345, 349, 350 restenosis, 353 Anatomy endoscopic anatomy, 15–16 innervations, 12–14 intrinsic musculature, 11–12 laryngotracheal framework, 9–11 larynx and trachea, 7–27 larynx morphometry, 16–18 position in the neck, 8–9 trachea morphometry, 18–19 vascular supply, 14–15 Anomalous left pulmonary artery sling, 161–162 Ansa Galeni, 12–13 Anterior costal cartilage graft (ACCG), 12, 123, 236, 259, 262, 267–268, 270, 272 Anterior cricoid split (ACS), 190–191, 260–262 Anterior laryngeal commissure, 20, 49, 128–131, 184, 190, 194, 266–267, 294–295, 297, 352 Anterior laryngotracheofissure, 262 Antibiotics for airway surgery, 105, 151, 153, 189, 193, 238, 271, 305, 309 Antireflux therapy for airway surgery, 271, 309 Aortic arch, double, 163 Argon (Ar) laser, 55, 59–60, 65, 67 Arnold–Chiari malformation, 110 Articulated speech, 9, 10 Aryepiglottic (AE) folds anatomy, 15, 16 in laryngomalacia, 100–103 Aryepiglottoplasty, in laryngomalacia, 102 Arytenoid cartilage anatomy, 9, 10 luxation, dislocation, 205–206 palpation, 86 prolapse, 355 Arytenoidectomy endoscopic CO2 laser, 111–113, 254, 355 open surgery, 111 Asleep transnasal flexible laryngoscopy, 82–84 Aspiration, as contraindication to airway surgery, 238, 240 Assessment, preoperative, 231–240 Atresia larynx and trachea, 175–176, 126 oesophagus, 165–167 Augmentation laryngotracheal reconstruction (LTR), 258, 262–274 laryngotracheoplasty (LTP), 258, 260–262 Avulsion, arytenoid, 201, 206–207 Awake transnasal flexible laryngoscopy, 80, 83, 108, 160, 233, 234 B Bacteriological aspirate, 91, 105, 351 Balloon dilation, for laryngotracheal stenosis, 72 Barium contrast studies, 40 Benign tumours, larynx and trachea, 134, 181, 217–227 Benjamin–Haves light-clip, 50
Index Benjamin–Lindholm laryngoscope, 47, 48, 50, 85, 101–102,104, 144, 213, 246, 312–313 Bilateral vocal cord immobility neurogenic paralysis, 77, 84 neurogenic vs. cicatricial, 86–87 posterior glottic stenosis, 87–89 Bilateral vocal cord paralysis (BVCP) aetiology, 110 endoscopic surgical techniques, 111–115 open surgical techniques, 111 prevalence, 107–108 symptoms, 107–108 treatment, 110–115 Bilevel positive airway pressure (BiPAP), 25, 42, 149, 153, 160, 306 Björk flap, tracheotomy, 328–329 Bleach ingestion, 210 Blood supply, larynx and trachea, 14–15 Blunt neck trauma clinical presentation, 203–205 larynx and trachea, 200–209 management, 205–209 mechanisms of injury, 200–203 radiological evaluation, 205 Bouchayer dissectors, 50 grasping forceps, 49, 51, 103, 112 Brachiocephalic (innominate) artery, 161–162 Brachiocephalic subclavian system, 14–15 Bridge bronchus, 168, 169, 175 Bronchoalveolar lavage (BAL), 91, 234 Bronchogenic cyst, 158, 164 Bronchomalacia. See Tracheomalacia Broncho-oesophagoscopy, for airway assessment, 77, 80, 90–91 Bronchoscopes flexible, 53 rigid, 52–53 sizes, 52–54 Bronchoscopy, rigid, 17–18, 80, 101, 159, 204, 207, 331 Bronchus suis, 168–169 Burns, larynx and trachea, 199, 209–214 C Cannula, tracheostomy, 19, 91, 160, 195–197, 224, 233, 266, 271, 311, 342 related stenosis, 196–197 sizes, 19 Carbon dioxide (CO2) laser, 53, 59–61,102, 246–251 Cardiac anomalies, congenital, 42–43, 164 with extrinsic airway compression, 164 Cartilage graft carving, 264–265, 267 harvesting, 263–264 stenting, 266–267 suturing technique, 265–268, 270 CATCH 22 (Shprintzen, DiGeorge) syndrome, 127 Caustic ingestion, 209–214 cicatricial sequelae, 212–214 endoscopic assessment, 210–211 injuries, 209–210
Index management, 211–212 patient assessment, 210 CHARGE syndrome, 148, 316 Choanal atresia, 83, 148 Chopped (gated) mode, laser, 61 Cicatricial intubation sequelae non-stenotic, 185, 187 stenotic, 185–186, 188 Cidofovir, for recurrent respiratory papillomatosis, 226–227 Cleft, laryngotracheal associated syndromes, 148 classification, 148–149 diagnosis, 149–150 endoscopic repair, 151–153 extrathoracic LTOC, 153–154 intrathoracic LTOC, 154–155 management, 150–155 open surgical repair, 153–155 pathogenesis, 148 symptoms, 149 Comorbidities, in patients with LTS, 5, 233, 316 Complete tracheal rings, 158, 168–175 Complications of PCTR anastomotic dehiscence, 313–314 arytenoid prolapse, 355 delayed recurrent stenosis, 315 epiglottic petiole prolapse, 355 recurrent laryngeal nerve injury, 315 tracheostomy-related stenosis, 315 Complications of tracheal resection anastomotic separation, 344 recurrent laryngeal nerve injury, 345 recurrent stenosis, 345 Compromised airway, 4, 36, 77–90, 83, 101, 168, 206, 351 Computerized tomography (CT), 16, 18, 38–40, 127, 135, 150, 158–159, 168, 202, 203, 205, 207, 331 Congenital anomalies larynx, 97–156 mediastinum, 161–167 trachea, 97, 157–179 Congenital clefts. See Laryngotracheo-oesophageal cleft (LTOC) Congenital laryngeal anomalies, prevalence, 97 Congenital subglottic stenosis (C-SGS) classification, 120–121 endoscopic assessment, 121–122 indication for surgery, 122–123 pathogenesis, 120–121 prevalence, 119–120 surgery for, 122–124 symptoms, 121 Congenital tracheal anomalies assessment, 158–159 cardiac anomalies, 164 complete vascular rings, 163 diffuse tracheomalacia, 158–160 incomplete vascular rings, 161–163 localised tracheomalacia, 160–165 pathogenesis, 158 prevalence, 97, 157 symptoms, 158 treatment, 159, 160, 164–165, 168–175
363 Congenital tracheal stenosis (CTS) assessment, 168 classification, 168 management, 168–175 symptoms, 168 Congenital web, prevalence, 126 Continuous positive airway pressure (CPAP), 25, 42, 78, 190, 306, 310, 344 Continuous working (CW) mode, laser, 61 Cook exchange catheter, 80, 284 Cordotomy, posterior, 111, 113–114 Cor pulmonale, in laryngomalacia, 101 Corrosive ingestion. See Caustic ingestion Corticosteroids for airway management, 189–190 for postoperative management after SS-PCTR, 309–310 for subglottic haemangioma, 136, 138 Costal cartilage graft (CCG) carving of ACCG, 267 carving of PCCG, 264–265 harvesting, 263–264 suturing technique, 265–267, 269–270 Cotton airway grading system, 87–89, 233 Cotton–Fearon operation, 259 Counselling for LTS inadequate counselling, 351–352 parental, 232, 233, 238–240 Cranio-maxillo-facial anomalies, difficult airway management, 79 Cricoarytenoid ankylosis (CAA), 86–87, 89, 91, 92, 236–238, 249, 262, 265–266, 318 Cricoarytenoid joint, fixation, 86–87, 115, 186, 233, 236, 318, 319, 351 Cricoid cartilage anatomy, 15–16 diameter, 16–18 framework expansion, 259–260 Cricoid framework expansion with graft (LTR), 93, 258–260 without graft (LTP), 259 Cricoid plate, lamina, 11, 13, 14, 47, 87, 93, 113–115, 122,123, 148, 149, 155, 200, 203, 258–266, 269, 270, 280, 282, 283, 288–295, 297, 298, 300, 318, 354, 356 Cricoid split anterior, 183, 190–191, 258 posterior, 93, 111, 114–115, 237, 249, 260–263, 265–266, 269, 270, 280, 282, 283, 294, 300, 317, 349, 352, 355 Cricothyroid joint anatomy, 13 landmark in PCTR, 14 Cricothyroid muscle anatomy, 13 function, 13 Cricothyrotomy for extended PCTR, 93 for PCTR, 93 Cricotracheal resection (CTR). See Partial cricotracheal resection (PCTR) Croup, 119, 121, 133, 135, 304 CT-scan, 3D reconstruction, 32, 38–39, 168
364 Cuff ET tube related tracheal lesions, 323 tracheostomy tube related lesions, 332, 197 Cuneiform cartilage, 9, 11, 15, 103, 113, 151, 153 Cysts bronchogenic, 158, 164 ductal, 141–144, 247–249 saccular, 141–144 treatment, 144 D Decannulation indications, 334 surgical closure, 197, 334–336 Decannulation rates for LTR operation specific, 272, 274 overall, 272, 274 Decannulation rates for PCTR operation specific, 316–317 overall 90, 315–316 Decision making process for PCTR extent of airway resection, 300–302 malacic tracheal segment, 302–303 release manoeuvres, 302 Dehiscence, anastomotic, 195, 239, 280, 283, 297, 299, 302, 305, 312–316, 318, 327, 345, 349, 350 Difficult airway, 1, 32, 46, 56, 78–80, 239, 344 DiGeorge (CATCH 22, Shprintzen) sequence, 127 Dilation, endoscopic balloon dilation, 72 tapered bougies, 71–72, 86, 121, 247–251, 254, 284, 311, 344 Dimensions larynx, 16–18 trachea, 18–19 Diode laser, 60–61, 67 Direct laryngoscopy, 37, 77, 80, 84–85, 233 Direct laryngo-tracheoscopy, 77, 80, 84–85, 233, 234, 310 Disk battery, corrosive injury, 210 Disruption (traumatic) cicatricial sequelae, 208 laryngotracheal, 207–209 supraglottic, 206–207 Double aortic arch, 158, 163 Double-stage LTR (DS-LTR) complications, 271 indications, 235–238 postoperative care, 271 results, 271–274 surgical highlights, 270–271 surgical steps, 262–268 Double-stage PCTR (DS-PCTR) complications, 313–315 indications, 293 postoperative management, 312–313 results, 317 surgical highlights, 297, 300 surgical steps, 293–297 Down syndrome (trisomy 21, mongolism), influence on surgical outcome, 316 Ductal cyst, subglottic, 247–249
Index Dumon stent, 25, 26 Dynamic airway evaluation, 40 Dynamic airway obstruction, 79, 81–84 Dysphagia following PCTR, 319 Dysphonia following PCTR, 318 Dyspnoea following PCTR, 318 E Eliachar stent, 19, 22–23 Emergency airway support, 78–80 Endoscopic airway assessment, 77–93 instrumentation, 45–74 posterior cricoid split + rib grafting, 93, 114–115, 249 report, 86–87, 90 suturing instruments, 50–52 treatment for LTS, 241–254 Endoscopic airway procedure for LTS (primary) anaesthesia for, 242–246 cicatricial subglottic stenosis, 246–247 ductal cyst, 247–249 indications, 246–249 posterior glottic stenosis, 249 subacute lesions of intubation, 249–250 Endoscopic airway procedure for LTS (secondary), 250 Mitomycin-C, 251–254 postoperative optimisation of results, 250–251 Endoscopic anatomy, larynx, 15–16 Endoscopy anaesthetic techniques, 81–85 instrumentation, 45–74 suite, 45, 46, 233 Endotracheal intubation faulty technique, 184 pressure induced injuries, 184–186 Endotracheal stents, 24–26 Endotracheal tube (ETT) diameters, 17 sizes, 16, 17 Energy density (fluence), laser, 59, 61–62 Eosinophilic oesophagitis, 77, 85, 91, 233–234, 239, 240, 351, 354 Epiglottic petiole prolapse (EPP), 301, 350, 355 Epiglottis, anatomy, 15–16 Erbium-YAG laser, 59, 61, 67 Excimer laser, 59, 61, 66 Extended PCTR indication, 292, 293 results, 302, 317–318 surgical highlights, 297 surgical technique, 293–297 Extended PCTR with intussusception of thyrotracheal anastomosis indication, 283, 297 surgical highlights, 300 surgical technique, 297–300 Extrinsic airway compression cardiac anomalies, 164 complete vascular rings, 163 incomplete vascular rings, 161–163 mediastinal masses, 161, 164 treatment, 164–165
365
Index Extubation, after SS-PCTR, 306–309 Ex-utero intrapartum treatment (EXIT), 126 F Facial mask ventilation for airway obstruction, 42 for postoperative management of SS-PCTR, SS-LTR, 306–307, 310 for therapeutic endoscopy, 243, 284 Failure of surgery LTR with CCG, 352 PCTR and tracheal resection, 353–354 False cord retractor (Lindholm), 49, 51, 86–88, 115, 128, 136–137, 192, 219, 246, 249 Family counselling, inadequate counselling, 351–352 Faulty intubation technique, 184 Fibre (wave guide), lasers, 62, 64–65 Fibreoptic endoscope, 53–54 intubation, 79 Fire hazard, lasers, 68–69 Fire prevention, lasers anaesthesia, 68–70 intermittent apnoeic technique, 69 jet ventilation, 70 laser safe tube, 69 spontaneous respiration, 69–70 Fistula acquired tracheo-innominate artery, 329–331 acquired tracheo-oesophageal, 331, 332, 334 congenital tracheo-oesophageal, 165–167 Flexible naso-laryngoscopy. See Transnasal fibreoptic laryngoscopy Flexible scope bronchofibrescope, 53 oesophagoscope, 54 Fluence (energy density), laser, 59, 61–62 Folds aryepiglottic, 15–16, 83, 101–102, 141–142, 144 vocal, 9–11, 15–16, 40, 77 Forceps for bronchoscopy, 54 for oesophagoscopy, 56, 57 Fracture, larynx, 199, 200, 207 Functional endoscopic evaluation of swallowing (FEES), 40 Fusion arytenoids, 208 vocal cords, 20, 93, 280–281, 296, 297, 317–318 G Gastrograffin oesophagram in H-fistula, 40 in LTOC, 149 Gastro-oesophageal reflux (GOR), 42, 43, 91, 99, 100, 110, 148, 155, 167, 186, 233, 234, 238, 306, 316, 318, 351, 354 Gated (chopped) mode, laser, 61, 63, 70, 134, 136, 144, 219, 250 Genetic counselling, 125, 127, 150 Glottis, posterior, 9, 17, 86, 112, 115, 184, 185, 189, 191–193, 249, 298
Glotto-subglottic stenosis, extended PCTR for, 293–300, 317–318 Granulation tissue, postintubation, 191–194 Granulomatous disease (Wegener), 232 G (Opitz Frias) syndrome, 148 H Haemangioma, subglottic, 36, 69, 73, 133–139, 217, 218 Healy–Montgomery T-tube, 19, 21–22, 25 Helical CT-scan, 32, 38–40, 127, 158, 159 Helium–oxygen (Heliox), for postoperative care in PICU, 306, 308–309 High-frequency jet ventilation (HFJV), 245–246, 284–285 Hilar release procedure, 302, 339, 346 Holinger–Benjamin laryngoscope, 48 Holmium-YAG laser, 59 H-type fistula, 166 Human papilloma virus (HPV), in RRP, 218, 220–222 Hyoid bone, 8–10, 14, 201, 206, 262, 286, 300, 301, 302, 355 I Imaging studies, 38–40, 158 Immobility, vocal cords cicatricial, 20, 86–87, 93, 280–281 neurogenic, 37, 49, 84, 86–87, 109–115 Indication for surgery, LTS, 232, 234–236 Indications for endoscopic airway procedure primary endoscopic techniques, 246–250 secondary endoscopic techniques, 250–251 Indol-3 carbinol (I3C), for RRP, 226 Infant, results of PCTR, 317 Inferior thyroid artery, 14, 15 Infrahyoid release, 302–303 Ingestion, caustic, corrosive, 209–214 Inhalation injuries flame burns, 199, 209 larynx, 209 steam burns, 199, 209 trachea, 209 Innervations, larynx, 12–14 Innominate artery compression, 36, 161, 162 erosion, 331 Innominate, subclavian arteries, 14, 15 Instruments bronchoscopes, 18, 52–54 laryngoscopes, 46–52, 79, 101 for microlaryngoscopy, 46, 48–50, 67, 85–90, 101–104, 121, 127, 128, 193–194, 225, 233, 246 oesophagoscopes, 54–55 Intensive care unit, 303–309 Interarytenoid adhesion, 86–87, 89, 188, 192, 234, 237, 249 distance, 9, 11, 17, 18, 22, 23, 86, 115, 130, 131, 155, 249, 251, 264, 280, 294, 356 Interarytenoid muscle anatomy, 11, 12 in treatment of PGS, 86, 263, 294 Interferon therapy, for RRP, 226 Intraluminal oesophageal impedance, 43 Intrinsic laryngeal muscles, 11, 12
366 Intrinsic tracheal anomalies, 158, 167–175 Intubation technique, 184, 186 trauma, 17, 183–186, 189 Ischemic necrosis, glotto-subglottis, 184–186, 189 Isolated posterior glottic stenosis (PGS), 236–238 Isolated subglottic stenosis (SGS) acquired, 181, 285–292 congenital, 92, 119–124, 292 J Jaw lift, 79, 81 Jet ventilation, 70, 224–225, 245–246, 284–285 Juvenile-onset recurrent respiratory papillomatosis (JORRP), 222–223 K Karl Storz laryngoscope, 46–47, 101 Kleinsasser laryngoscope, 47–48, 50, 101 KTP laser. See Potassium titanyl phosphate (KTP) laser L Laryngeal anatomy, 8–18 Laryngeal atresia, 119, 120, 125–131 Laryngeal cleft (LC). See Laryngotracheo-oesophageal cleft (LTOC) Laryngeal cysts ductal, 120, 141–144 saccular, 141–144 treatment, 144 Laryngeal fracture, 199–201, 207 Laryngeal framework, 9–11, 93, 199, 200, 205–207, 261, 265, 281, 300, 352 Laryngeal functions respiration, 19, 31, 35, 81, 101, 222, 224, 231, 243 sphincter, 12, 35, 36, 212 voice, 31, 35, 203, 222–224, 231 Laryngeal innervations, 12–14, 115 Laryngeal morphometry, dimension, 16–18 Laryngeal musculature, 11–12 Laryngeal release procedure, manoeuvre, 7, 8, 14, 15, 287, 301–302, 313, 314, 319, 339, 342, 346, 350 Laryngeal stenosis. See Laryngotracheal stenosis Laryngeal web assessment, 35, 126–127 classification, 125–127 management, 127–131 symptoms, 36, 125, 126 Laryngocele, 33, 141–144 Laryngofissure for arytenoidectomy, pexy, 111, 112 Laryngomalacia (LM) assessment, 100, 101 classification, 100 indication for surgery, 101 pathogenesis, 100 postoperative care, 104–105 prevalence, 97, 99, 100 results, 105 supraglottoplasty, 11, 69, 99–105 surgical intervention, 99, 101 symptoms, 36, 100, 101, 105
Index Laryngoscopes Benjamin/Lindholm, 47–48, 50, 85, 101, 102, 104, 144, 246, 248, 249 Holinger/Benjamin, 48–50, 150 Kleinsasser, 47–50, 101 Parsons, 47–48, 101, 128, 151–153 Laryngoscopy, 32, 37, 49, 77, 79–87, 99, 108, 110, 125, 138, 142, 149, 158, 183, 193, 202–204, 218, 334 Laryngospasm, in caustic injuries, 213 Laryngotracheal decompression, anterior cricoid split, 190–191 Laryngotracheal injury external trauma, 199–214 postintubation, 19, 183–195 Laryngotracheal reconstruction (LTR) historic review, 258–260 indications for, 122, 123 milestones in LTR, 258 postoperative care, 271 reporting system for, 272, 273 results, 271–274 single-stage LTR, 120, 190, 195, 235, 236, 258, 260, 266, 268–272, 274, 305 surgical steps, 261–271 Laryngotracheal stenosis (LTS) indication for surgery, 234–240, 246–251, 325, 326 parental counselling, 231–234, 238–240 preoperative assessment, 231–234, 238–240, 337, 349 Laryngotracheofissure for LTR, 130, 261, 262, 267, 355 for PCTR, 294–295, 297, 298, 300, 355 Laryngotracheo-oesophageal cleft (LTOC), 35, 47, 51, 70, 81, 84, 148–155, 157, 158, 161 Laryngotracheoplasty (LTP), 257, 259, 260–262 Larynx, morphometry, 16–18 Laser hazards eye, 46, 59, 66–67 fire, 45, 68–70 skin, 46, 59, 65–68 Lasers absorption, 59–60, 62, 65 induced accidents, 68, 70, 244 parameters, 45, 56–58, 60–62, 70, 100, 102–104, 112, 137, 138, 151, 152, 219, 248, 249, 251 platforms, 46, 51, 52, 103, 249 principles, 57–58, 68 properties, 58–61, 63, 114, 219 safety, 45, 65–71 tissue interaction, 45, 57–62, 65 wavelength, 58–59, 61, 65, 67, 70 Late complications, tracheostomy A-frame deformity, 196–197, 313, 315, 330, 331, 335, 350 suprastomal collapse and granuloma, 197, 233, 315, 330–331, 334, 350, 354–355 tip of cannula lesions, 330 Lateral approach for arytenoidectomy, pexy, 111 Lateral fixation of vocal cord, endoscopic technique, 113–115 Lavage, bronchoalveolar, 91, 233, 234 Lichtenberger needle carrier, 26, 50–51, 111, 113, 129, 194
367
Index Light delivery systems, lasers articulated arm, 58, 62–64, 102 micromanipulator, 62–64, 102 waveguides, fibres, 64–65 Lindholm–Benjamin laryngoscope, 47–48, 50, 85, 101, 102, 104, 144, 246, 248, 249 Lindholm self-retaining false vocal fold retractor, 51, 85, 86, 88, 128, 136, 192, 246 Long segment congenital tracheal stenosis (LSCTS) aetiology, 167 classification, 168, 169 patch tracheoplasty, 170–171, 175, 346 resection with end-to-end anastomosis, 169–170 slide tracheoplasty, 169, 171–175 symptoms, 168 tracheal autograft, 169, 171–172 tracheal homograft, 169, 175 LT-Mold gauges for endoscopy, 194 gauges for open surgery, 266 stent, 23–25, 93, 130, 131, 208, 211, 213, 235, 237, 242, 261, 266, 267, 269, 297, 299, 300, 311, 312, 353, 356 Lymphatic malformation, 68, 161, 218 M Magnetic resonance imaging (MRI), 32, 38–42, 110, 134, 135, 158, 161, 163, 164, 168, 217, 218 Malacia, trachea primary diffuse, 157–160, 167 secondary localised, 160–165 tracheostoma related, 315, 355 Malformation. See Congenital anomalies Malignant tumours, larynx, 219 Malinckrodt endotracheal tube, 17 Measurements airway stenosis, 7, 84, 86, 87 glottis, 9–11, 130 subglottis, 9–11, 16–18, 21, 267, 288–289, 311 trachea, 16, 18–19 Medialisation, vocal cord, 109 Mediastinal mass, 33, 40, 42, 164 Microcirculation, trachea, 15, 174 Microdebrider instrument, 46, 72–73, 137, 224–225, 227, 242 for recurrent respiratory papillomatosis, 224–225, 227 for subglottic haemangioma, 134, 137 Microlaryngoscopy, suspension, 46, 48–50, 67, 77, 85–87, 101–104, 121, 128–130, 159, 193–194, 225, 233, 234 Micromanipulator, laser, 63–64, 102 Mitomycin-C (MMC), 251–254 dosage, 252 duration of application, 252 indication and contraindications, 253 multiple applications, 253 wound rinsing, 253 Modified Myer–Cotton airway grading system, 89–90, 231, 233, 234 Mongolism (Down syndrome, trisomy 21), influence on PCTR, 316 Monnier LT-Mold, 23–25
Montgomery T-tube complications, 7, 21, 352, 353 stent, 22 Morphometry larynx, 16–18 trachea, 18–19 Mucosal oedema, subglottis, 11, 18 Musculature, larynx, 11–12 Myer–Cotton airway grading system, 85, 87–89, 234, 273, 274 N Nasopharyngeal airway, 70, 78–80 Nasopharyngeal obstruction, 33, 36, 83, 233 Neodymium-YAG (Nd-YAG) laser, 60, 67 Neonate airway dimension, 9–11, 15–19 larynx, 97, 303 Neoplasm larynx and trachea, 158, 164, 217–219 recurrent respiratory papillomatosis, 220–227 subglottic haemangioma, 133–139, 218 Nerve injury recurrent laryngeal nerve, 108, 200, 201, 203, 208, 290, 315, 345, 350, 354 superior laryngeal nerve, 14 Nerve palsy, paralysis complication of PCTR, 353–354 complication of tracheal resection, 353–354 Neuroblastoma, 161, 164 Newborn, infant airway dimension, 9–11, 15–19, 53, 220, 304 larynx, 8–11, 15–19, 102, 128, 142, 170, 181 Noisy infant, child, 33–35, 78, 80–85, 135 Non-invasive ventilation (NIV), 306–309 Nutritional supplement, 109, 212, 226, 306 O Obstructive dyspnoea age related, 31–38 anaesthetic technique for, 40–42 influence of body position, 31, 36 worsening factors, 36 Obstructive sleep apnoea (OSA), 38, 40, 41, 83, 101, 233, 273, 307, 326, 354 Oedema, subglottic mucosa, 9, 11, 18, 189, 204, 309 Oesophageal atresia, 165–167 assessment, 35, 126, 148, 159, 166 management, 166–167 postoperative endoscopies, 167 symptoms, 166 Oesophageal pH-monitoring, 43, 91, 240, 354 Oesophageal stricture, caustic ingestion, 212–214 Oesophago-gastroscope, 54 Oesophagoscopes flexible, 54, 85 Hasslinger, 54, 57 rigid, 54–55, 91, 159, 166, 204 sizes, 54–57 Oesophagoscopy, for caustic ingestion, 210–211
368 Oesophago-tracheal fistula acquired, 197, 331–334 congenital, 165–167 Oesophagram, 40, 147, 149, 158, 166 Omega-shaped epiglottis, 15–16 in laryngomalacia, 101, 103 Opitz Frias (G) syndrome, 147, 148 Optical forceps for bronchoscopy, 53, 54 for oesophagoscopy, 55, 56 P Paediatric intensive care unit (PICU), 3, 16, 17, 19, 104, 110, 136, 138, 186, 187, 209, 239, 258, 270, 271, 303–311, 326, 333, 335, 352 Pallister–Hall syndrome, 147, 148 Papillomatosis. See Recurrent respiratory papillomatosis Paralysis, neurogenic, 37, 49, 77, 85–87, 107 Parental counselling inadequate counselling, 351–352 for LTS, 231–234, 236–240 Parsons laryngoscopes, 47–48, 128, 151–153 Partial cricotracheal resection (PCTR) anaesthesia for, 283–285 extended PCTR, 12, 19, 93, 122, 131, 236, 238–239, 257, 261, 279–283, 293–300, 311–312, 316–317, 355–356 extended PCTR with thyro-tracheal intussusception, 279–280, 297–300 historical review, 282–283 indications, 122–124, 234–237, 283, 292, 300, 352 milestones in PCTR, 282–283 PCTR vs. LTR, 272, 281 simple PCTR, 280, 281, 285–293 single-stage vs. double-stage PCTR, 291–293 surgical highlights for extended PCTR, 297 surgical highlights for extended PCTR with thyrotracheal intussusception, 300 surgical highlights for simple PCTR, 292–293 surgical technique for extended PCTR, 293–297 surgical technique for extended PCTR with thyrotracheal intussusception, 297–300 surgical technique for SS-PCTR, 285–293 Patch tracheoplasty, 170–172, 175, 346 Patient assessment endoscopy workup, 80, 135, 158, 159, 168, 210 general condition, 43–44, 232–233, 351 indication for surgery, 231, 234–239 medical history, 36–37, 231, 232 preoperative planning, 232–234, 239 preparation for surgery, 239–240 timing for surgery, 77, 230, 238–239 Penetrating trauma, neck, 204, 205 Pericardium patch tracheoplasty, 170–171 Perioperative care after LTS general aspects, 304–306 helium–oxygen (heliox) gas mixture, 306, 308–309 non-invasive ventilation (NIV), 306–309 postextubation management, 306–308 Per-nasal endoscopy. See Transnasal fibreoptic laryngoscopy Petiole, epiglottic prolapse, 184, 301, 350, 355 Pharyngeal reflux. See Gastro-oesophageal reflux Pharyngolaryngeal discoordination
Index in laryngomalacia, 104, 149 in LTS, 238, 240, 326 Photodocumentation, 55–57 pH probe study, monitoring, 43 Physical examination, in airway obstruction, 31–33, 37–38, 40, 42, 79 Pierre Robin sequence (retrognathia), 79 Portex endotracheal tube, 16, 17, 27, 104, 193, 270, 285, 327 Posterior cordotomy, 113, 114 Posterior costal cartilage graft, 93, 122–123, 131, 235, 260, 262–266, 269, 270, 272, 280–281, 294–295, 298 Posterior cricoarytenoid muscle, 11–13, 115, 237, 263, 355 Posterior cricoid split endoscopic, 111, 114–115, 237, 249 open surgery, 260–262, 294, 298 Posterior glottic stenosis (PGS) vs. BVCP, 85–89, 108, 233, 234 classification, 86–89, 237–238 endoscopic assessment, 86–87, 88, 89, 92, 93 treatment, 92, 108, 115, 237–238, 249 Posterior glottis commissure adhesion, 86, 88, 188 scarring, 86–89, 235, 265, 283, 294, 356 Postintubation stenosis, 19, 183–194, 199, 315 Potassium titanyl phosphate (KTP) laser, 53, 55, 59–61, 64–65, 67, 137, 167, 217, 219, 225, 331 Power density, lasers, 61, 63, 67, 68, 70, 74, 104, 134, 137, 219 Pre-epiglottic space, in epiglottic prolapse, 301,355 Premature neonate acquired SGS, 120, 123 subglottic diameter, 16–18, 119, 120 Preoperative assessment for LTS airway grading system, 87–90, 234, 351 endoscopic workup, 231–234 indications for surgery, 234–238 medical history, 231, 232, 239 patient’s general condition, 232–233, 239 preoperative planning, 232–234, 239 preparation for surgery, 238–240 timing for surgery, 238–239 Pressure-induced ET injuries, 184 Primary endoscopic airway procedures for cicatricial subglottic stenosis, 246–247 for incipient LTS, 242, 249–250 for posterior glottic stenosis, 249 for subglottic ductal cysts, 247–249 Prismatic light deflector, 52, 54 Propofol, 40, 41, 79, 81, 82, 242–244, 284, 285, 305, 306 Pulmonary artery sling, 39, 161–162, 167, 169, 173 Pulmonary function testing, 43 Pulsed mode, laser, 61–62 superpulse, 60, 62–64, 92, 102 ultrapulse, 45, 60–64, 92, 100, 102, 112–114, 128, 129, 151, 213, 219, 224, 246, 248, 249, 254 Pulse oximeter, 79 R Radiology, evaluation of airway stenosis, 38 Reconstruction, airway, 1, 7, 19–22, 32, 39, 86, 93, 154, 168,172, 173, 195, 204, 209, 229, 238, 240, 249, 251, 257–274, 281, 300, 301, 311, 335 349–352, 354
Index Recurrent laryngeal nerve (RLN) anatomy, 12–14 injury, 13–14, 108, 282, 287, 290, 291, 315, 316, 345, 350, 354 Recurrent respiratory papillomatosis (RRP), 220–227 adjuvant medical therapy, 225–227 aetiology, 218 alpha-2A interferon, 226, 227 Cidofovir, 224, 226–227 clinical course, 221–222 indol-3-carbinol, 225, 226 limited laryngeal disease, 222–224 management, 222–225 moderately invasive disease, 224 pathogenesis, 220 recurrent aggressive disease, 224–225 Reflux. See Gastro-oesophageal reflux Reinnervation procedures for vocal cord paralysis, 109 Remifentanil, 81, 82, 242–244, 284, 285 Resection/anastomosis subglottis, 14, 285–293 trachea, 14, 15, 169–170, 219, 323, 338–346, 353–354 Respiratory cycle, 31–33, 35, 158, 224, 233 Respiratory distress airway support, 78–80 clinical examination, 32–36 degree, 31–33 history, 33, 36–37, 135, 232 Respiratory sounds, 31–33, 37, 233 Restenosis post-LTR, 271 post-PCTR and tracheal resection, 344–345, 353 Results of surgery for LTR, 271–274 for PCTR, 315–319 for tracheal resection, 345–346 Rethi’s procedure, 259 Retractions, in respiratory distress, 32, 82, 121, 135, 158 Retrograde endoscopy, through tracheostoma, 213 Revision surgery causes for, 4, 165, 271, 313–315, 318, 351–355 for LTR, 271, 272, 350–353 for PCTR and tracheal resection, 353–356, 318 Rhabdomyosarcoma larynx, 219 trachea, 164, 219 Right aortic arch, in external tracheal compression, 163 Right atrium, in external tracheal compression, 164 Rigid bronchoscopes in acute airway management, 78–79 instruments, 46, 52–54, 71, 101 sizes, 16, 18, 46, 52–54, 71, 79, 80, 90, 159 Rüsch endotracheal tube, 17, 283, 284, 286 S Saccular cysts, 47, 142–144 Sarcoma larynx, 219 trachea, 164 Savary–Gilliard dilator, 71, 167, 212, 247, 249, 338 Secondary airway lesions (SAL), in laryngomalacia, 100
369 Secondary endoscopic airway procedures, for LTS, 250–251 Sedation, for postoperative care following PCTR, 305, 309, 311 Segmental resection larynx, 15, 285–300 trachea, 15, 338–342, 345–346 Self-expandable metallic airway stents (SEMAS), 24, 25 Sevoflurane, 40, 79, 81, 82, 242, 243, 284 Shapsay’s technique, 92, 234, 247 Shiley cannula, 18, 19 Silicone tube, stent, 20, 25–26, 345 Single-stage reconstruction LTR, 190, 195, 235, 236, 260, 268–272, 274, 305, 352 PCTR, 93, 284–285, 288, 291–292, 300, 305, 309–311, 314, 317, 344, 351–353 Sleep apnoea syndrome. See Obstructive sleep apnoea Slide tracheoplasty, 172–175, 352 cervical, 323, 340–342, 346 Sphincteric function, larynx, 12, 35, 36 Spiral CT-scan, 38, 127, 158, 159 Spontaneous respiration technique, for PCTR, 283, 285 Spot size, laser, 60–65, 70, 92, 102, 113, 128, 144, 213, 219, 246, 248, 249, 251, 254 Stenosis acquired, 183–189, 235, 308, 345, 346 congenital, 93, 119–124, 168, 175, 346 Stent endoscopic fixation, 194 larynx, 19–25 during open surgery, 138, 153, 154, 171, 174, 175, 266, 295, 299, 318 trachea, 24–26 without tracheostomy, 25 Sternohyoid muscle, 8, 114, 154, 155, 287, 302, 303, 329, 331–334 Sternothyroid muscle, 8, 287, 288, 303 Steroids for airway management, 189–190, 193–194, 352 for postoperative care after PCTR, 309, 310 for subglottic haemangioma, 136, 138 Stertor, 33, 34, 36 Stomal stenosis, 195, 197, 354–355 Stoma, trachea closure, 334–336 Storz bronchoscope, 18, 53, 54 Stridor, 32–35, 38, 53, 78, 82, 100, 101, 108, 109, 121, 135, 139, 142, 149, 158, 159, 161, 163, 167, 168, 210, 218, 307, 308, 310, 313, 315, 317 Subclavian artery system, 13, 15, 158, 161–163 Subglottic cyst, 135, 247–249 Subglottic haemangioma (SGH), 133–139 assessment, 135 clinical course, 134–135 endoscopic treatment, 136–137 management, 135–139 medical treatment, 135–136 open surgical treatment, 137–139 prevalence, 97 results of treatment, 138 Subglottic larynx, luminal diameters, 16–17
370 Subglottic lumen, 11, 16–18, 127, 138, 193, 246, 253, 257, 259, 265, 288, 289, 293, 294, 296, 297 Subglottic stenosis (SGS) acquired, 123, 183–189 congenital, 92, 119–124, 268, 327 grading system, 87–90, 234 Subglottiscope, 47, 219 Submucosal capillary plexux, trachea, 14, 15 Superior laryngeal nerve (SLN), 12–14, 300, 302 Superior thyroid artery, 14 Superpulse, laser, 60, 62–64, 92, 102 Supraglottic stenosis, 103, 105, 209, 298, 300–302 Supraglottoplasty, 11, 69, 100–105, 251, 318 Suprahyoid release, 8 Suprastomal collapse, granuloma, 197, 233, 315, 329–331, 334, 354–355 Surgery for LTS, 4–5, 229–230, 238, 239, 257–274, 279–319, 325–336, 337–346 Surgical failure LTR with CCG, 274, 352 PCTR and tracheal resection, 318, 353–355 Suspension microlaryngoscopy (SML), 26, 46, 48–50, 67, 80, 84–90, 101–105, 108, 113, 121, 127–129, 136, 150, 159, 193–194, 205–206, 222–225, 233–234, 247, 250 Synechia, vocal cords, 11, 35, 70, 188, 223, 224–226, 234–236, 248, 262, 265, 266, 273, 295–299, 350, 352 T Tactile feedback, during dilation, 72, 247 Teaching and documentation, 55–57 Telescopes for bronchoscopes, 52–53 for oesophagoscopes, 54–55 Thyroarytenoid muscle, 11, 109, 113, 130 Thyroid ala, 9–11, 111, 114, 130, 138, 144, 191, 200, 201, 204, 260, 262, 289, 294, 296 Thyroid artery inferior, 14–15 superior, 14 Thyroid cartilage anatomy, 9–11, 13, 15–16 fracture, 200–203, 207 Thyrotomy full, 111, 270, 294 partial inferior, 289 Thyro-tracheal anastomosis, 11, 12, 14, 208, 280, 289–291, 313–314, 353 Toddler age group, in caustic injuries, 210 Trachea congenital anomalies, 97, 157–176 diameter, 18, 19 extrinsic compressions, 158, 161–164 intrinsic anomalies, 97, 167–177 length, 19, 169, 172, 339, 346 Tracheal agenesis, atresia, 175–176 classification, 176 treatment, 176 Tracheal anastomosis for acquired tracheal stenosis, 338–340 for congenital tracheal stenosis, 169–170 Tracheal anatomy, 12, 18–19
Index Tracheal anomalies, congenital, 97, 157–176, 323 Tracheal autograft, 169, 171–172 Tracheal blood supply, 14–15, 170, 286–287, 301, 341 Tracheal cleft. See Laryngotracheo-oesophageal cleft (LTOC) Tracheal compression cardiac causes, 161–163 mediastinal masses, 161, 164 vascular anomalies, 160–165 Tracheal deformity A-frame, 196–197, 313, 315, 330–331, 335, 355 localised malacia, 313, 315, 331 Tracheal dilation, 71, 246–248 Tracheal framework, 9–11, 154, 155, 159, 208, 229, 296, 335, 338, 340, 346, 355 Tracheal intubation-faulty technique, 184 Tracheal length recapture, 300–302 Tracheal replacement, 356 Tracheal resection/anastomosis cervical slide tracheoplasty, 323, 340–342, 346 complications, 344–345 indications for, 338 for postintubation stenosis, 337–341, 346 postoperative management, 344 for post-tracheostomy stenosis, 338, 341, 345 results of tracheal resections, 345–346 for stenosis in tracheostomised child, 338, 342–343 surgical highlights for tracheal resection, 342–343 surgical procedure, 338–341 tracheoplasty, 338, 339, 341, 345, 346 Tracheal rupture, 201–203 Tracheal stenosis acquired, 195–197, 323, 340, 345, 346 congenital, 158, 167–175, 346 prevalence, 97 Tracheal stents, 20–22, 24–26 Tracheal surgery, 323, 337–345 Tracheal web, 158, 167 Trachea morphometry, 18–19 Tracheoarterial fistula, 331 Tracheobronchial compression, 158, 161, 164–165 Tracheobronchial dilation, 71–72 Tracheobronchial tree anatomy, 12 dimension, 18–19 Tracheobronchoscopy. See Bronchoscopy, rigid Tracheocutaneous fistula, 335 Tracheo-innominate artery fistula, 323, 330–334 Tracheomalacia primary diffuse, 97, 159–160 secondary localised, 160–163, 233, 234, 302, 303 with tracheo-oesophageal fistula, 165–167 treatment, 164–165 Tracheo-oesophageal fistula (TOF) acquired, 197, 330 congenital, 165–167 tracheo-innominate artery fistula, 331–334 Tracheostomised child challenges facing families, 3–5 challenges facing physician, 3–5 Tracheostomy
371
Index cannula, tube, 19, 91, 160, 195–197, 224, 233, 271, 311, 342 correct placement in impending LTS, 195, 196 indications, 189, 225, 326 related collapse, 233, 315, 330, 331, 334, 335 related stenosis, 196–197, 315, 337, 338, 341 sizes, 19, 196 Tracheostomy closure indications for, 334–336 plugging trial, 334 technique, 335–336 Tracheostomy-related stenosis A-frame tracheal deformity, 196–197, 313, 315, 330–331, 335, 355 suprastomal collapse and granuloma, 315, 330, 334, 354–355 Tracheotomy complications, 329–334 early complications, 329–330 indications for, 326 late complications, 330–334 location, 326–327 operative technique, 327–328 surgical closure of tracheostoma, 335–336 surgical highlights for tracheotomy, 328–329 tracheo-innominate artery fistula, 330–334 tracheo-oesophageal fistula, 332–334 Transglottic stenosis, treatment for, 297–300 Transnasal fibreoptic laryngoscopy (TNFL) asleep, 82–84, 233–234 awake, 80, 83, 100, 108, 233, 234 Transverse interarytenoid muscle, 12, 270, 294 Trauma blunt, 181, 200–209 external, 181, 199–214 penetrating, 181, 200–209 Traumatic laryngeal injuries 199–209 clinical presentation, 203–205 lesion sites, 201–203 management, 205–209 radiological evaluation, 205 Treatment plan, for LTS, 91–93 Trisomy 21 (Down syndrome, Mongolism), 316 T-tube, Montgomery, 20–21, 25, 208, 318, 345, 350, 352, 353 U Ultrafast computed tomography, 38 Ultraflex stent. See Self-expandable metallic airway stents Ultrapulse, laser, 61–64, 102, 112–114, 128, 151, 213, 219, 224, 246, 248, 249, 254 Ultrasonography, in BVCP, 110 Unilateral vocal cord paralysis (UVCP) aetiology, 108 symptoms, 109 treatment, 109 Upper airway resistance (UAR), 40, 41 Upper tracheo-oesophageal fistula, 166 V Vacterl syndrome, 148 Vagus nerve, anatomy, 12–14, 162 Variable airway obstruction
extrathoracic, 34 intrathoracic, 34 Vascular anomalies, 39, 40, 42, 161–163, 173 Vascular malformation, 134 Vascular rings complete, 161, 163 incomplete, 161–163 Vascular sling, left pulmonary artery, 39, 161–163, 167, 169, 173 Vascular supply larynx, 14–15 trachea, 14–15, 169, 171–173, 288, 296, 333, 344, 353 Velocardiofacial syndrome (Shprintzen, DiGeorge), 127 Ventilation, 242–246 apnoeic, 243 controlled, 69, 244 jet, 224, 245–246 spontaneous respiration, 42, 144, 242–243 Ventricule, laryngeal in saccular cysts, 142, 143 Video bronchoscope, 53, 56, 79, 91, 213 monitoring, 57 oesophagoscope, 91, 54 Vocal cord anatomy, 9–11 endoscopic lateralization, 113–114 endoscopic medialization, 109 motion, 40, 70, 81, 114, 243 oedema post-PCTR, 306, 344, 354 Vocal cord paralysis (VCP) bilateral (BVCP), 36–37, 85–88, 109–115, 326 unilateral (UVCP), 35, 36, 108–109, 149 Vocal process, 111–114, 185, 186, 356 Voice after PCTR, 318 W Waveguides (fibers), laser, 62, 64–65 Web, 125–131 assessment, 126–127 classification, 126 management, 127–131 symptoms, 126 vocal cords, 125–131 Wegener’s granulomatosis, 232 Wheezing, 33–35, 159, 163, 164, 167, 168, 313 Wound dehiscence. See Anastomosis, dehiscence Wound healing, 189, 252, 271, 281, 305 X X-ray, 38–40, 127, 135, 149, 158, 168, 309, 311, 328 Y YAG laser. See Neodymium-YAG (Nd-YAG) laser Z Zeitel’s injection needle, 50, 51, 224
