Fig. 18.1
Benjamin’s and Inglis’ classification of laryngeal clefts. Type 1: Interarythenoid defect, type 2: extending partially into the cricoid cartilage, type 3 complete seperation of the cricoid cartilage extending with possible extension into the tracheoesophageal wall. Type 4: common tracheoesophagus with possible extension to the carinal level (From Pezzettigotta SM et al (2008) Laryngeal Cleft. Otolaryngol Clin North Am 41 (2008) 913–933. Used with permission)
Laryngeal webs are rare congenital or acquired malformation in which abnormal fibrous tissue forms anteriorly between two structures within the larynx. They are staged type 1–4 depending on the degree of severity using either Cohen’s [18] or Benjamin’s [19] classification (Fig. 18.2). They are most frequently congenital, with associated anomalies (mostly cardiac, or deletion of 22q11 chromosome) in 51 % of patients [18], but can be acquired following a surgical procedure, intubation, or infection. Webs can extend from the supra- to the subglottic area. Their definitive treatment is difficult, as vocal cords tend to form fibrosis and granulation tissue following surgery.
Fig. 18.2
Cohen’s and Benjamin’s classification of laryngeal webs. Type 1: 35 % or less of the glottis is involved. Type 2: 35–50 %, Type 3: 50–75 %, Type 4: more than 75 % with extension to the subglottic area. In Type 2 and 3, may extend into the subglottis and result in subglottic stenosis. (From Otolaryngol Clin North Am 41 (2008) 877–888. Used with permission)
Vocal cord paralysis is the second most common cause of inspiratory stridor, accounting for 15–20 % of cases. It can be idiopathic, secondary to central nervous system immaturity, due to a compression of midbrain structures by either a Chiari malformation [20] or any lesion occupying space in the cranium and causing a partial herniation of midbrain structures through the foramen ovale [21]. Unilateral palsy can be seen after head and neck or cardiac surgery. Proper evaluation of the condition is best done without an endotracheal tube in place. These patients may require a tracheostomy.
18.5 Subglottic and Tracheal Pathologies
Subglottic stenosis (SGS) is most frequently caused by endotracheal intubation in the neonatal period. It happens at the level of the cricoid cartilage which is the narrowest point of the pediatric airway. The incidence has decreased in the past 30 years; however, a recent prospective study found that 11.38 % of patients had some degree of stenosis after intubation [22]. Length of intubation and need for additional sedation appeared to be key factors for the development of SGS. The congenital form of SGS is rare, accounting for no more than 10 % of cases. Depending on the severity of the narrowing, these patients will undergo a variety of treatments: observation and repeat examination, balloon dilatation, laser therapy, laryngotracheoplasty, cricoid split, or partial cricotracheal resection. Not infrequently a tracheotomy will be done to insure unobstructed breathing and allow healing after a complex corrective surgery. In the general pediatric population, anesthesiologists should have a high index of suspicion if an infant cannot be intubated with an age-appropriate endotracheal tube. The four-grade Cotton-Myers classification of SGS is based on the relation between the biggest size of endotracheal tube fitting the airway and the expected size of the tube calculated for age [23].
Infantile hemangiomas are the most common benign vascular tumors in children and proliferate rapidly in the first year of life. There seems to be an increased risk of laryngeal hemangioma associated with a “beard” distribution of cutaneous lesions. Left untreated the mortality associated with subglottic hemangiomas can be as high as 50 %. Lesions can be found in any part of the airway where they may extrinsically compromise air entry or grow inside structures, including the trachea. It is a common differential diagnosis in infants presenting with progressive stridor and undergoing diagnostic bronchoscopy. Patients with head and neck hemangiomas should undergo a workup for PHACES (Posterior fossa brain malformations, Hemangiomas of the face, Arterial Cerebrovascular abnormalities, Eye abnormalities, and Sternal defects.). The use of propranolol has been recently reported to have significant effects by decreasing the size of the lesions [24]. For a recent up to date review, see [25]
Tracheomalacia is caused by either the altered structure of the tracheal tissue architecture or by secondary factors like external compression or inflammatory response to various insults. It causes variable degrees of respiratory distress due to the exaggerated collapse of the airway typically during expiration. Bronchoscopic observation during spontaneous ventilation (functional bronchoscopy) is used to evaluate the extent and severity of collapsus; however, there is yet no standardized way to classify the severity. Tracheomalacia might be underdiagnosed in children, some patients being wrongly labeled as asthmatics. Most patients needing more careful follow-up have an associated esophageal atresia or an anomaly of the aortic arch or the supra-aortic vessels causing extrinsic compression [26, 27]. In some instances, an aortopexy will allow decompression of the trachea, but a conservative approach is usually indicated in the first 18 months of age [28]. Extrinsic compression of the tracheal tree can also be caused by a mediastinal mass and a neck mass from tumoral or cystic origin and treated according to the diagnosis.
Congenital distal tracheal stenosis represents only 0.3–1.6 of all laryngotracheal lesions and is often accompanied by cardiovascular, gastrointestinal, and pulmonary comorbidities. While patients presenting minimal symptoms can be observed as the stenotic area may grow to a normal size, those having more severe symptoms will undergo surgery. A variety of tracheoplasty techniques may be used: costochondral grafting, resection with end-to-end anastomosis, or slide tracheoplasty [29]. Options for anesthetic airway management include intubation with the cuff passed in the stenotic area, selective split endotracheal tube with one side in each mainstem bronchus, selective intubation, bilateral jet ventilation, and cardiopulmonary bypass [30, 31].
18.6 Anesthetic Management
18.6.1 Emergency Airway Rescue
Situations of airway rescue with impending complete obstruction are emergencies during which the anesthesiologist must work in close collaboration with the otolaryngologist. A variety of airway devices must be available: oro- and nasopharyngeal airways, appropriate sized supraglottic devices [32], various laryngoscope blades of sizes 00 and 0, intubation aids like the family of devices labeled as videolaryngoscopes, and fiber-optic tracheoscopes. The presence of the otolaryngologist is mandatory in order to establish an emergency surgical airway if needed. Induction of anesthesia should be cautious and progressive. The presence of midfacial deformities or various types of mandibular hypoplasia and macroglossia may impair proper bag and mask ventilation at a very early stage of induction. Inhalational induction probably remains the first choice of many anesthesiologists for induction of anesthesia keeping in mind that the anesthetic administration is more likely to be interrupted while the airway is secured or when the surgeon is working. TIVA with short-acting agents like propofol and remifentanil allows a progressive deepening of anesthetic state, maintenance of spontaneous respiration, and relatively rapid reversal of anesthesia when stopped. An excellent review on the topic has been published by Sims and von Ungern-Sternberg [33].
18.6.2 Anesthesia for Diagnostic and Therapeutic Procedures
Most patients presenting with a symptomatic airway problem will be first evaluated with bedside FFE. Even in an awake patient, a good overall evaluation of the airway down to the level of the glottis can be made, and some pathologies can be identified for further evaluation under anesthesia. Subsequently, patients are brought to the OR for detailed visual characterization of obstructive structures and pathologies, as well as a precise evaluation of the functional mechanics of the airway, ideally and most of the time during spontaneous breathing. Precise evaluation in that context is very challenging for the anesthesiologist as the depth of anesthesia needs to be precisely reached and maintained for the performance of very stimulating procedures like rigid bronchoscopy or airway suspension while spontaneous breathing is maintained. Moreover, during the same diagnostic session, the depth of anesthesia might have to change significantly as the patient may require, for example, deep levels for rigid bronchoscopy followed by very light levels of anesthesia in order to observe the glottis structure behavior in a “sleep-like” state.
A variety of ventilation techniques may be used depending on the context, the nature, and the extent of the obstruction and the level of comfort of the anesthesiologist. In a recent retrospective study on the anesthetic management for subglottic stenosis, Knights et al. found no difference in the outcome between eight different airway management techniques [34].
Extubation of neonatal intensive care patients after prolonged intubation is often made in the operating room because of the significant frequency of immediate reintubation in a sometimes difficult context. In our institution, this is done under general anesthesia and spontaneous breathing with a flexible endoscope in situ to observe the laryngeal area.
Patients with TBAO and pathologies of the upper airway and supraglottic area need careful induction as they might obstruct quite early. Their ability to maintain some airway patency during anesthesia is useful to help determine the need for further intervention, for example, tongue-lip adhesion.
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