1 Hypoventilation Syndromes

The ASA Closed Claims Project found that 4% of 1175 closed claims resulted from critical respiratory events in the PACU. The highest proportion was attributed to inadequate ventilation, and many of these patients died or suffered brain damage.³¹

Many clinical conditions may give rise to postoperative ventilatory failure. A multicenter, prospective survey in France that looked at almost 200,000 general anesthetics administered between 1978 and 1982 found that postoperative respiratory depression accounted for 27 of 85 respiratory complications that were life-threatening or had serious sequelae. These complications were responsible for seven deaths and five cases of hypoxic encephalopathy.³² A respiratory rate of less than 8 breaths/min was observed by PACU nurses among 0.2% of 24,000 patients after general anesthesia.²²

Hypoventilation may be mediated centrally at the level of the upper motor neuron, anterior horn cell, lower motor neuron, neuromuscular junction, or respiratory muscles. Clinical correlates include central sleep apnea, carotid endarterectomy,³³ medullary injuries, demyelinating disorders, direct injury to peripheral nerves, poliomyelitis, Guillain-Barré syndrome, motor neuron disease, myasthenia gravis, and botulism. Hypoventilation may result from the loss of lung or pleural elasticity, diaphragmatic splinting caused by abdominal pain or distention, thoracic deformities such as kyphoscoliosis, or multifactorial entities such as morbid obesity and severe chronic obstructive pulmonary disease. Rarely, hypercapnia results from excess carbon dioxide production or a marked increase in physiologic dead space.

The residual effects of anesthetic drugs contribute to inadequate postoperative ventilation.^34–36 It may be aggravated by incomplete reversal of neuromuscular blockers,³⁷ hypocalcemia or hypermagnesemia, or the administration of other drugs, including antibiotics, local anesthetics, diuretics, and calcium channel blockers, which may potentiate neuromuscular blockade.

2 Hypoxemic Respiratory Failure

A review of the many causes of postoperative hypoxemia is beyond the scope of this chapter, but it can occur because of hypoventilation, a low inspired oxygen concentration, ventilation-perfusion mismatch, right-to-left shunting, increased oxygen consumption, diminished oxygen transport, or rarely, an impairment of oxygen diffusion. These events are more likely in some clinical situations because of preexisting medical conditions or anesthetic and surgical interventions. If sufficiently severe, there may be a requirement for continuous positive airway pressure (CPAP) or reintubation and mechanical ventilation.

3 Inability to Protect the Airway

ICU or postoperative patients may be unable to protect the airway because of preexisting obtundation, neurologic injury, or the effects of residual anesthesia. In the latter case, it may be possible to temporize by turning patients on their sides, altering their positions (head up or head down) or by reversing residual medications with antagonists. These measures may not restore airway competency, and lack of resolution may necessitate reintubation.

4 Failure of Pulmonary Toilet

Inadequate clearance of pulmonary secretions may result from a depressed level of consciousness with impaired airway reflexes, overproduction of secretions, alteration of sputum consistency leading to inspissation and plugging, impaired mucociliary clearance, or inadequate neuromuscular reserve. These problems may result in atelectasis or pneumonia with attendant hypoxemic respiratory failure. Alterations in pulmonary mechanics may also lead to hypercapnia, necessitating reintubation.

5 Inadvertent Extubations

Inadvertent extubations may result from movement of or by the patient with an inadequately secured tracheal tube. Intraoperatively, this may occur in the prone position, when the airway is shared with the surgeon, when the head and neck are extended, when draping obscures the view, or when drapes adhere to the endotracheal tube (ETT) or circuit and are carelessly removed. In the ICU, extubation may occur when the patient is repositioned for a radiograph or routine nursing care. Patients insufficiently sedated are at greater risk for deliberate self-extubation,³⁸ but those more heavily sedated are more likely to require reintubation.³⁹ Fastidious attention to securing and supporting the ETT and breathing circuit is essential. Self-extubation may occur during emergence from anesthesia, when the patient is confused, agitated, and distressed, which promotes premature extubation. In the ICU, it may not be possible to know whether a self-extubation is accidental or deliberate, but many of these patients require reintubation,⁴⁰ are more likely to exhibit post-extubation stridor, and may need multiple intubation attempts, increasing the likelihood of esophageal intubation and death.^41–43

6 Entrapment

The tracheal tube may become entrapped due to an inability to deflate the cuff,^44,45 or there may be difficulties with the pilot tube.^46,47 Difficulties include a crimped pilot tube, a defective pilot valve, and fixation of the tracheal tube by Kirschner wires,⁴⁸ screws,⁴⁹ ligatures,⁵⁰ or entanglement with other devices.^51,52 Entrapment can also occur during a percutaneous tracheostomy.⁵³ Mechanical obstruction of an entrapped tube is a life-threatening complication. Partial transection of the tracheal tube by an osteotome during a maxillary osteotomy has resulted in the partially cut tube forming a barb that caught on the posterior aspect of the hard palate.⁵⁴ One report of tube entrapment with fatal consequences involved a Carlens tube that was inadvertently sutured to the pulmonary artery.⁵⁵ Lang and colleagues recommended routine intraoperative testing for tracheal tube movement when fixation devices are used in proximity to the airway.⁴⁹ Uncertainty about tube movement should prompt fiberoptic examination before emergence from general anesthesia.

7 Hypertension and Tachycardia

Transient hemodynamic disturbances accompany extubation in most adults. These responses may be prevented by deep extubation,⁵⁶ insertion of a laryngeal mask airway (LMA) before emergence, or attenuated by concurrent medication.^57–59 Most healthy patients not on antihypertensive agents or other cardioactive drugs exhibit increases in heart rate and systolic blood pressure of more than 20% in association with extubation.⁶⁰ After coronary artery bypass surgery, these changes tend to be transient, lasting 5 to 10 minutes, and they usually are not associated with electrocardiographic evidence of myocardial ischemia.⁶¹ Coronary sinus lactate extraction measurements, however, indicate that among patients with poor cardiac function, extubation may be associated with myocardial ischemia.⁶² Patients with inadequately controlled hypertension, carcinoid, pheochromocytoma, hypertension associated with pregnancy, or hyperthyroidism may be expected to display even greater increases in blood pressure in response to tracheal extubation. The specific strategies needed to attenuate these usually transient changes are dictated by the clinical context. The strategies, which are not universally effective, include the use of intracuff,^63–65 intratracheal,⁶⁶ or intravenous lidocaine^61,67,68; beta-blockers^60,69–71; dexmedetomidine^72,73; and nitrates.

8 Intracranial Hypertension

Tracheal intubation and suctioning are associated with a rise in intracranial pressure. Extubation probably is associated with comparable or even greater increases in intracranial pressure. There is evidence, albeit contradictory, that intravenous and endotracheal lidocaine attenuate this effect.^74,75

9 Intraocular Pressure

Madan and colleagues compared the intraocular pressure changes of tracheal intubation and extubation in children with and without glaucoma.⁷⁶ They observed significantly greater increases 30 seconds and 2 minutes after deep extubation compared with the corresponding times after uncomplicated intubations. These differences were seen in both groups of children. It is likely that significant increases in intraocular pressure observed after deep extubation would have been even higher had extubation occurred after recovery of consciousness. Lamb and coworkers observed similar effects of extubation on intraocular pressure in adults and commented that this increase could be prevented by using an LMA rather than a tracheal tube.⁷⁷

10 Coughing

Coughing on emergence from general anesthesia is virtually ubiquitous, particularly when an ETT is used.⁷⁸ No difference between smokers and nonsmokers is observed. Although coughing is a protective reflex, it can be particularly troublesome in the setting of ophthalmologic, neurologic, oropharyngeal, and neck surgery.

Several strategies have been proposed to minimize coughing, including deep endotracheal extubation, primary use of or conversion to an LMA,^57,79,80 use of the sedative dexmedetomidine,⁷³ intravenous or topical application of a local anesthetic to the vocal folds, and use of intracuff lidocaine.^63,65,67,81 However, coughing on emergence is common and relatively benign for most patients.

The emergence of severe acute respiratory syndrome (SARS) and the high prevalence of drug-resistant droplet or airborne diseases in some locales make coughing potentially hazardous to the airway manager. In 2003, Toronto was the North American epicenter for SARS, and coughing assumed life-threatening proportions for medical personnel.^82–87 Patients with cough, fever, and pulmonary infiltrates were dangerous, and coughing on emergence was not protective, but rather posed a threat by dispersing infectious respiratory droplets on those in the patient’s vicinity. The strategies adopted at that time have been largely relaxed, although they may again become necessary when new risks threaten patients and care providers.

11 Laryngeal Edema

Several of the complications of endotracheal intubation do not become apparent until after extubation occurs.⁸⁸ Glottic or tracheal injury may occur despite a good laryngeal view or during awake fiberoptic intubation.^89–91 Anatomic or functional laryngeal problems are more likely to develop as a consequence of a difficult or prolonged intubation attempts.²² Possible airway injuries include laryngeal edema, laceration, hematoma, granuloma formation, vocal fold immobility, and dislocation of the arytenoid cartilages.⁹²

Glottic edema has been classified as supraglottic, retroarytenoidal, and subglottic.⁹³ Supraglottic edema may result in posterior displacement of the epiglottis, reducing the laryngeal inlet and causing inspiratory obstruction. Retroarytenoidal edema restricts movement of the arytenoid cartilages, limiting vocal cord abduction on inspiration. Subglottic edema, a particular problem in neonates and infants, results in swelling of the loose submucosal connective tissue that is confined by the non-expandable cricoid cartilage. In neonates and small children, this is the narrowest part of the upper airway, and small reductions in diameter result in a significant increase in airway resistance. In children, laryngeal edema is promoted by a tight-fitting ETT, traumatic intubation, intubation longer than 1 hour, coughing on the tracheal tube, and intraoperative alterations of head position.⁹⁴ Koka and coworkers found an incidence of 1% among children younger than 17 years. Laryngeal edema should be suspected when inspiratory stridor develops within 6 hours of extubation. Management of laryngeal edema depends on its severity. Treatment options include head-up positioning, supplemental humidified oxygen, racemic epinephrine, helium-oxygen administration, reintubation, and tracheostomy.

Clinical studies of children and adults that evaluated the role of prophylactic corticosteroids in the prevention of post-extubation stridor have yielded contradictory findings.^95–98 In the setting of adult ICUs, a large, multicenter, prospective, randomized, double-blind trial of methylprednisolone (20 mg administered 12 hours before and every 4 hours until extubation) versus placebo found that steroids significantly reduced post-extubation laryngeal edema (11 of 355 versus 76 of 343, P < 0.0001) and required reintubation due to laryngeal edema (8% versus 54%, P = 0.005). Laryngeal edema was defined by any two of stridor, inspiratory prolongation, and use of accessory muscles. It was classified as severe if reintubation was required within 36 hours. Laryngoscopy was not performed unless reintubation was required. Factors associated with a greater risk of laryngeal edema included female sex, shorter height, larger-diameter ETT, admission for trauma, and shorter duration of intubation. The absence of pretreatment with methylprednisolone was associated with a hazard ratio of more than 8.⁹⁹ It is possible that the benefits of steroids are restricted to high-risk populations and require administration of multiple doses.^{100, 101} Contradictory findings may relate to risk factors in the study populations and variability of dosage regimens.

An alternative classification has been proposed for laryngotracheal injury after prolonged intubation.^102–104 Immediate post-extubation airway obstruction results from glottic and subglottic granulation tissue, which may swell on removal of the ETT. Posterior glottic and subglottic stenosis due to contracting scar tissue results in increasing obstruction weeks or months after extubation. Benjamin found that fiberoptic evaluation or laryngoscopy with the tube in situ was of limited value.¹⁰² An ETT obscures the view of the posterior glottis and subglottis. These lesions were best identified using rigid telescopes with image magnification during general anesthesia. This approach permitted anticipation of problems and development of a management strategy.

12 Laryngospasm

Laryngospasm is believed to be a common cause of post-extubation airway obstruction, particularly in children.¹⁰⁵ Even in adults, Rose and colleagues found that it accounted for 23.3% of critical postoperative respiratory events, although the diagnosis was presumptive.¹⁰⁶ Olsson and Hallen observed an increased incidence among patients presenting for emergency surgery, those requiring nasogastric tubes, and patients undergoing tonsillectomy, cervical dilation, hypospadias correction, oral endoscopy, or excision of skin lesions.¹⁰⁵ A variety of triggers are recognized, including vagal, trigeminal, auditory, phrenic, sciatic, and splanchnic nerve stimulation; cervical flexion or extension with an indwelling ETT; or vocal cord irritation from blood, vomitus, or oral secretions.¹⁰⁷ A risk assessment questionnaire was used in a study to prospectively evaluate almost 10,000 children undergoing general anesthesia. A positive history of nocturnal dry cough, exertional wheezing, or more than three wheezing episodes in the prior 12 months was associated with a fourfold increase in the risk of laryngospasm in the PACU and a 2.7-fold increased risk of airway obstruction during surgery or in the PACU.¹⁰⁸ Twice as many children were managed with an LMA than an ETT, and an equal number had their devices removed awake and asleep. The depth of anesthesia at the time of device removal did not influence the incidence of laryngospasm.

Laryngospasm involves bilateral adduction of the true vocal folds, vestibular folds, and aryepiglottic folds that outlasts the duration of the stimulus. This is protective to the extent that it prevents aspiration of solids and liquids. It becomes maladaptive when it restricts ventilation and oxygenation. The intrinsic laryngeal muscles are the main mediators of laryngospasm, and they include the cricothyroids, lateral cricoarytenoids, and thyroarytenoid muscles. The cricothyroid muscles are the vocal cord tensors, an action mediated by the SLN. Management of laryngospasm consists of prevention by either extubating at a sufficiently deep plane of anesthesia or awaiting recovery of consciousness.⁵⁶ Potential airway irritants should be removed and painful stimulation should be discontinued. If laryngospasm occurs, oxygen by sustained positive pressure may be helpful, although this may push the aryepiglottic folds more tightly together.¹⁰⁹ Larson described a technique of applying firm digital pressure anteriorly directed to the “laryngospasm notch” between the ascending mandibular ramus and the mastoid process and observed that this technique is rapid and highly effective.¹¹⁰ Very small doses of a short-acting neuromuscular blocker with or without reintubation may be necessary.^111,112

13 Macroglossia

Massive tongue swelling may complicate prolonged posterior fossa surgery performed with the patient in the sitting, prone, or park bench position.^113–116 It is also seen with very steep or prolonged Trendelenburg positioning, hypothyroidism, acromegaly, lymphangioma, idiopathic hyperplasia, metabolic disorders, amyloidosis, cystic hygroma, neurofibromatosis, rhabdomyosarcoma, sublingual or submandibular infections, and chromosomal abnormalities such as the Beckwith-Wiedemann syndrome.¹¹⁷

The most common and dramatic presentation of macroglossia results from angioedema.¹¹⁸ It can be congenital or acquired. Hereditary angioedema results from a deficiency of C1 esterase inhibitor; acquired C1 esterase deficiency is associated with histamine release, a physical stimulus, or most commonly, a reaction to angiotensin-converting enzyme inhibitors or angiotensin receptor blockers.^118,119 Although involvement of the tongue is the most obvious manifestation, the uvula, soft tissues, and larynx may also be involved.

In the ICU setting, macroglossia may be seen as a complication of extreme volume overloading or tongue trauma, particularly when it is further complicated by a coagulopathic state. If this occurs or progresses after extubation, it can lead to partial or complete airway obstruction, making reintubation necessary but difficult or impossible.¹¹⁴ Lam and Vavilala postulate that positioning in most cases results in venous compression leading to arterial insufficiency and subsequent reperfusion injury.¹¹⁵ Alternatively, local compression may cause venous or lymphatic obstruction with resultant immediate and typically milder tongue swelling. The latter form is less severe but more apparent, and extubation is likely to be postponed.

14 Laryngeal or Tracheal Injury

Airway injuries, such as lacerations, edema, arytenoid dislocation, and vocal fold paralysis, may occur from the lips to the distal trachea. The lip or tongue may become entrapped between the laryngoscope blade and the mandibular teeth, resulting in swelling or bleeding, although this is unlikely to be severe enough to complicate extubation. The glottis may be injured as a result of insertion of a round tube through a triangular opening. The trachea can be lacerated or penetrated by the ETT or its introducer or by ischemic compression by the cuff on the tracheal mucosa. Palatopharyngeal injuries have been described as a consequence of blind insertion of an ETT during video laryngoscopy.^120–127 Although these injuries are not often apparent at the time of laryngoscopy, they have been managed conservatively and should not complicate extubation. The epiglottis can be downfolded during intubation, but the consequences of downfolding, even if prolonged, are unknown.¹²⁸

Laryngeal injuries accounted for 33% of all airway injury claims and 6% of all claims in the ASA Closed Claims Project database.¹²⁹ They range from transient hoarseness to vocal fold paralysis. Even when direct laryngoscopy provides a satisfactory glottic view or intubation is facilitated by fiberoptic instrumentation,^89,91 airway injury can occur and go unsuspected until after the ETT is removed. Airway injuries are presumed to be less likely if intubation is easy, but analysis of the ASA Closed Claims Project revealed that 58% of airway trauma and 80% of laryngeal injuries were associated with intubations that were not difficult.^129,130 Judging from the findings of the Closed Claims Project, difficult intubations were more likely to result in pharyngeal and esophageal than tracheal injuries.

Vocal fold immobility may result from injury to the recurrent laryngeal nerve or the arytenoid cartilages.^92,131–139 Arytenoid immobility has resulted from seemingly uneventful Macintosh and McCoy direct laryngoscopy,^137,140 double-lumen tube insertion, and lightwand intubation.¹³⁴ The mechanism of this injury is uncertain. It may be a consequence of a subluxation or a hemarthrosis with subsequent resolution or fixation. Prolonged or stressful contact between the ETT and the posteromedial aspects of the vocal cords, arytenoids, or posterior commissure may result in ulceration of the perichondrium, which heals with fibrous adhesions that produce an immobile glottis. This complication may be more common than the literature indicates.^92,141 Persistent post-extubation hoarseness, a breathy voice, and an ineffective cough should prompt assessment by an otolaryngologist. The diagnosis is confirmed by endoscopic visualization of an immobile vocal cord associated with a rotated arytenoid cartilage.⁸⁸ If the diagnosis is made early, before the onset of ankylosis, it may be possible to manipulate the arytenoid back into position.

Vocal fold paralysis results from injury to the vagus or one of its branches (i.e., recurrent laryngeal nerve [RLN] or external division of the superior laryngeal nerve [ex-SLN]) and may resemble arytenoid dislocation or ankylosis. Differentiation may require palpation of the cricoarytenoid joints under anesthesia or laryngeal electromyography.⁸⁸ When vocal fold paralysis occurs as a surgical complication, it is usually associated with neck, thyroid, or thoracic surgery. The left RLN can also be compressed by thoracic tumors, aortic aneurysmal dilatation, left atrial enlargement, or during closure of a patent ductus arteriosus. Occasionally, a surgical cause cannot be implicated. Cavo and coworkers postulated that an overinflated ETT cuff might result in injury to the anterior divisions of the RLN.¹⁴²

The RLN supplies all of the intrinsic laryngeal muscles except the cricothyroid, the true vocal cord tensor, which is innervated by the ex-SLNs. Unilateral ex-SLN injury results in a shortened, adducted vocal fold with a shift of the epiglottis and the anterior larynx toward the affected side. This produces a breathy voice but no obstruction and usually resolves within days to months. Bilateral ex-SLN injury causes the epiglottis to overhang, making the vocal folds difficult to visualize. If seen, they are bowed. This produces hoarseness with reduction in volume and range but no obstruction. Unilateral RLN injury causes the vocal fold to assume a fixed paramedian position and produces a hoarse voice. There may be a marginal airway with a weak cough. Bilateral RLN injury results in both vocal folds being fixed in the paramedian position and inspiratory stridor, often necessitating a surgical airway.¹⁴³

Pharyngeal, nasopharyngeal, and esophageal injuries include perforation, lacerations, contusions, and infections. These injuries may be associated with difficult laryngoscopy or intubation, but they may also result from the blind passage of a gum elastic bougie,¹⁴⁴ nasogastric tube,¹⁴⁵ nasotracheal tube,¹⁴⁶ suction catheter, esophageal stethoscope transesophageal echo probe, or temperature probe.¹⁴⁷ Penetrating injuries can communicate with the esophagus, resulting in a tracheoesophageal fistula, or with the mediastinum, which may go unrecognized and result in mediastinitis, retropharyngeal abscess, and death.¹³¹ After a brief intubation, soft tissue injuries resulting in airway obstruction are more likely to result from edema or hematoma than infection. Most of the described injuries do not significantly complicate extubation. Laryngeal and tracheal stenoses are serious complications, but they are rarely evident at the time of extubation.

15 Airway Injury

Burn patients can have intrinsic and extrinsic airway injuries. Circumferential neck involvement is an example of an extrinsic injury. Smoke inhalation or thermal injuries are examples of intrinsic injuries. Burn patients are at particular risk of requiring reintubation. They can have bronchorrhea, impaired mucociliary clearance and local defenses, laryngeal and supraglottic edema, increased carbon dioxide production, and progressive acute respiratory distress syndrome. Carbon monoxide may also diminish their level of consciousness and the ability to protect their airway. It may be difficult to secure the tracheal tube because of involvement of the adjacent skin, and burn victims may be agitated or uncooperative, increasing the risk of unintended extubation.¹⁴⁸ Kemper and coworkers reported their management of 13 burn patients younger than 15 years, 7 of whom exhibited post-extubation stridor. Patients treated with helium-oxygen mixtures had lower stridor scores than patients treated with an air-oxygen mixture.¹⁴⁹ They found that 11 of 30 extubated burn victims required treatment for stridor after extubation, consisting of racemic epinephrine, helium-oxygen, reintubation (n = 5), or tracheostomy (n = 1). The absence of a cuff leak was considered to be the best predictor of failure, with a sensitivity of 100% and a positive predictive value of 79%.¹⁴⁹

A variety of conditions may lead to airway edema severe enough to result in post-extubation stridor. It occurred in 2% to 37% of ICU patients after “prolonged intubation.”¹⁵⁰ A test was sought to predict patients with sufficient airway swelling to compromise safe extubation. The cuff-leak test was initially proposed for children with croup.¹⁵¹ The concept is that marked airway swelling is likely if air does not escape around the deflated ETT cuff when the ETT is occluded as the patient exhales. The cuff-leak test was the best predictor of successful extubation in a pediatric burn and trauma unit, and although sensitive, it was not specific for predicting stridor, necessitating reintubation in 62 adults.^152,153

The test has been refined by evaluating cuff-leak volume as the difference between inspiratory and expiratory tidal volumes during assist-control ventilation after cuff deflation.^41,154 Two studies found the cuff-leak volume could predict post-extubation stridor. In one study, 8 of 45 patients exhibited stridor, 4 of whom required reintubation.¹⁵⁴ In the other study involving 88 adult medical ICU patients, 6 patients exhibited stridor, 3 of whom required reintubation.⁴¹ They observed a significantly smaller cuff leak in patients who subsequently developed stridor, concluding that this measurement was the best predictor of the presence or absence of stridor. However, a study of 561 consecutive cardiothoracic patients who were extubated within 24 hours (median, 12 hours) defined a the cuff leak as the difference between the inspired and expired tidal volumes during assist-controlled ventilation. None of the (20) patients with leaks <110 mL developed stridor whereas one patient with a leak of 350 mL did and required reintubation. This led the investigators to conclude that the quantitative cuff-leak test was not reliable in this patient population.¹⁵⁵

In another study involving 110 trauma victims, cuff leaks of less than 10% had a 96% specificity for predicting post-extubation stridor or the need for reintubation.¹⁵⁶ De Bast and colleagues studied 76 adults in a combined medical-surgical ICU.¹⁵⁷ An equal number of patients had been intubated for more or less than 48 hours. Assist-control ventilation was reinstituted after cuff deflation, and the percentage of cuff leak was determined. Receiver operating characteristic (ROC) curves yielded a cutoff value of 15.5% cuff leak to equalize the false positives and false negatives for reintubation due to laryngeal edema, but this study was relatively small. Among patients intubated for more than 48 hours, only 2 of 22 with large-volume leaks and 6 of 16 with small-volume leaks required reintubation for laryngeal edema.

Kriner and colleagues evaluated the cuff-leak test for its ability to predict post-extubation stridor among 462 adult patients intubated for longer than 24 hours.¹⁵⁰ They evaluated the two thresholds previously described; a positive test was defined as a cuff-leak volume of 110 mL or less or of 15.5% or less of the exhaled tidal volume. Ten of 82 patients with leak volumes of 110 mL or less developed post-extubation stridor, and 10 of 380 with larger leaks developed post-extubation stridor, giving a positive predictive value for stridor of 0.12 and negative predictive value of 0.97. The sensitivity and specificity of the test under these conditions were 0.50 and 0.84, respectively.¹⁵⁰ With leak volumes of 15.5% or less, 7 of 48 patients developed post-extubation stridor, and 13 of 414 patients with volumes greater than 15.5% developed stridor, yielding positive and negative predictive values of 0.15 and 0.97, respectively. The sensitivity and specificity of this test for post-extubation stridor were 0.35 and 0.91, respectively. The prevalence of post-extubation stridor was 20 of 462. Seven of these patients required reintubation; 15 were managed with racemic epinephrine or helium-oxygen mixtures, or both, and 2 of the 15 failed, requiring intubation. The investigators concluded that neither threshold adequately predicted post-extubation stridor or could justify delaying extubation.

The reported variability of post-extubation stridor (2% to 37%) results in part from inconsistent diagnostic criteria,¹⁵⁰ but undoubtedly there are many other factors at play. Factors increasing the risk of post-extubation stridor include longer duration of intubation,¹⁵⁰ trauma and burns,^{14,148,154,158} pediatric age group,¹⁵⁸ female gender,^95,97,150 traumatic or emergent intubations, periods of hypotension, agitation, persistent attempts at phonation, inadequate ETT fixation, aggressive tracheal suctioning, highly positive fluid balance, low plasma oncotic pressure, gastroesophageal reflux, increased ETT diameter, and the presence of a nasogastric tube.^95,97,150

In summary, it appears that despite the intuitive appeal of the cuff-leak test, neither the qualitative nor quantitative test adequately predicts adult patients who will develop stridor after extubation.^150,155,159 It did not predict where patients were likely to require reintubation. Deem argued that absence of a cuff leak might result in an unnecessary delay of extubation, whereas a large cuff leak might produce false reassurance that there will be no difficulties.¹⁵⁹ At least in adults, the value of this test is uncertain.

16 Postobstructive Pulmonary Edema

Severe airway obstruction from any cause may complicate extubation and lead to postobstructive pulmonary edema, also called negative-pressure pulmonary edema.¹⁶⁰ This edema occurs when a forceful inspiratory effort is made against an obstructed airway (i.e., Mueller maneuver), often a closed glottis, generating large negative intrapleural pressures that promote venous return. The increase in venous pressure is aggravated by a lowered alveolar pressure, resulting in transudation of fluids into the pulmonary interstitium and alveoli. It may also result in a rightward shift of the interatrial and interventricular septa, raising left atrial and ventricular pressures. Some instances may be complicated by a permeability defect with exudative fluid and inflammatory cells.^161–166

Postobstructive pulmonary edema usually occurs in adult patients with upper airway tumors, severe laryngospasm, or rarely, bilateral vocal cord palsy,¹⁶⁷ whereas in children, it occurs most commonly as a complication of croup or epiglottitis.¹⁶⁸ The onset may be within minutes of the development of airway obstruction. It typically resolves with relief of the obstruction and supportive treatment for pulmonary edema.¹⁶⁶

1 Laryngoscopic Surgery

Mathew and colleagues looked at 13,593 consecutive PACU admissions from 1986 through 1989.²¹ Twenty-six (0.19%) of these patients required reintubation while in the PACU; seven of them had undergone ear, nose, and throat procedures. Of the seven patients, three had laryngeal edema, one was obstructed from a large thyroid, two bled at the operative site, and one developed postobstructive pulmonary edema after a tonsillectomy.

Patients undergoing laryngoscopy and panendoscopy (i.e., laryngoscopy, bronchoscopy, and esophagoscopy) are at an increased postoperative risk for airway obstruction and are approximately 20 times as likely to require reintubation as patients undergoing a wide variety of other surgical procedures.²⁰ Reviewing the records of 324 diagnostic laryngoscopies and 302 panendoscopies, Hill and colleagues found that patients who had undergone laryngeal biopsy were at the greatest postoperative airway risk. Thirteen (5%) of 252 patients required reintubation, most within 1 hour of extubation. Twelve of 13 had undergone laryngeal biopsy. Most of these patients had chronic obstructive pulmonary disease, and their need for reintubation was attributed largely to this.

Robinson prospectively studied 183 patients who had 204 endoscopic laryngeal procedures.¹⁷¹ Seven patients had tracheostomies before or after their surgery because of high-risk airways. Two of the remaining patients developed postoperative stridor; one required reintubation, and the other required a delayed tracheostomy. Indirect laryngoscopy carried out 4 to 6 hours after surgery revealed mucosal hemorrhage or laryngopharyngeal swelling in 32% of cases. Because the patients undergoing tracheostomy were not described, it is possible that the low incidence of reintubation resulted from an aggressive approach to preemptive tracheostomy.

2 Thyroid Surgery

A variety of airway-related injuries can be associated with thyroidectomies, including SLN and RLN injuries, wound hematoma, and tracheomalacia. Lacoste and colleagues retrospectively reviewed the records of 3008 patients who underwent thyroidectomies between 1968 and 1988.²⁷ The RLN had been identified intraoperatively in 2427 of these patients. Indirect laryngoscopy was performed on the third or fifth postoperative day. The RLN was damaged in 0.5% of patients with benign goiters and 10.6% of patients with thyroid cancer. RLN injury produces hoarseness, persistent coughing with phonation, and risk of aspiration. Unilateral RLN palsy was observed in 1.1% of patients. Three patients had bilateral RLN palsy and required tracheostomy. Six of a total of 16 deaths during the first 30 postoperative days were attributed to respiratory complications. One death occurred after failed intubation due to a deviated, constricted trachea. A second death was attributed to difficulties performing a tracheostomy. Two deaths resulted from aspiration or pneumonia, possibly related to RLN dysfunction.

SLN injury is more challenging to diagnose. It produces dysphonia and vocal fatigue, particularly in the higher registers. In a 5-year, multicenter study involving 42 centers and almost 15,000 thyroid operations, the diagnosis was suspected in 3.7% and confirmed in 0.4% of patients.¹⁷²

Local hemorrhage or hematoma occurs postoperatively in 0.1% to 1.6% of patients undergoing thyroid surgery and in 0.36% of the patients cared for by Lacoste and colleagues.^27,172–174 These complications occurred 5 minutes to 3 days postoperatively. Re-exploration within the first day was required only twice. Airway obstruction may result from significant laryngeal and pharyngeal edema, and wound evacuation may be of limited value in the relief of airway obstruction.^173,175,176 It may result from or be aggravated by ligature slippage, coughing, vomiting,¹⁷⁴ coagulopathies, and reoperation.¹⁷³ The prophylactic placement of surgical drains likely reduces the incidence of this complication. Wound evacuation may result in significant improvement; however this is not always the case. If time permits or intubation fails, wound evacuation should be considered.¹⁷⁶ Laryngeal edema may persist after the wound has been evacuated, necessitating postoperative intubation.

Tracheomalacia is rarely diagnosed after thyroidectomies, even in patients with significant retrosternal tracheal compression, although it may exist subclinically.^177–181 Although symptoms, computed tomography (CT), and pulmonary function test results make it easy to recognize airway compression preoperatively, tracheomalacia may be difficult to predict or even detect from the surgical field, and it does not become apparent until after the ETT is removed and spontaneous ventilation has resumed.¹⁸²

3 Carotid Artery Surgery

Neck swelling or hematoma formation after carotid endarterectomy may be relatively common. The New York Carotid Artery Surgery (NYCAS) study analyzed 9308 procedures performed between 1998 and 1999 at 167 hospitals.¹⁸³ A hematoma was identified in 5% of patients, substantially increasing the risk of death (OR = 4.30; 95% CI, 2.72 to 5.00) and stroke (OR = 3.89; 95% CI, 2.82 to 5.38). Hematoma occurrence reported in the literature ranges from 1.2% to 12%, depending on the definition used.¹⁸³ The overall rate of wound hematomas in the North American Symptomatic Carotid Endarterectomy Trial (NASCET), involving 1415 patients was 7.1%, 3.9% of which cases were considered to be mild (i.e., no delay in discharge), 3.0% were moderate (i.e., delay in discharge), and 0.3% were severe (i.e., permanent functional disability or death). The moderate and severe cases required re-exploration or wound evacuation (3.3%). Hematoma contributed to the death of four patients.¹⁸⁴ When wound hematomas are identified by a comparison of preoperative and postoperative CT scans, it occurs far more frequently (26%).¹⁸⁵ The postoperative reintubation or exploration rate is 1% to 3.3%.^184,186

Kunkel and colleagues described 15 patients who developed wound hematomas after carotid endarterectomy.¹⁸⁷ Eight of these were evacuated under local anesthesia. In six of seven cases in which general anesthesia was induced before opening the wound, difficulties arose with airway management, resulting in two deaths and one patient with severe neurologic impairment. O’Sullivan and coworkers reported a similar experience for six patients with airway obstruction after carotid endarterectomy.¹⁸⁸ Stridor was not relieved by wound evacuation. Administration of muscle relaxants made manual mask ventilation and tracheal intubation virtually impossible due to marked glottic or supraglottic edema. Cyanosis and extreme bradydysrhythmias or asystole occurred in four patients. The providers endorsed Kunkle’s recommendation for wound evacuation but thought that much of the airway compromise was caused by edema from venous or lymphatic congestion. They emphasized that the outward appearance may lead to an underestimation of the situation’s gravity. Voice changes are early signs of danger and may be relatively subtle. Rapid clinical deterioration can occur after stridor develops.¹⁸⁹

Studies by Carmichael and colleagues provided additional evidence for the role of swelling and bleeding in a small but elegant study. They compared the CT scans of 19 patients before and after carotid endarterectomy surgery.¹⁸⁵ Clinically, 1 patient had severe swelling, 4 had moderate swelling, and 3 had mild swelling, but 10 were deemed normal. However, postoperative CT scans demonstrated significant swelling of the retropharyngeal space and a reduction of the anteroposterior and transverse airway diameter, particularly at the level of the hyoid. Compared with preoperative CT scans, the calculated volume reduction averaged 32% ± 7% for extubated patients. The scans revealed a wound hematoma estimated to be greater than 10 mL (range, 44 to 94 mL) in 5 of 19 patients. Patients who remained intubated postoperatively showed a significantly greater volume reduction of 62% ± 9% (P < 0.025). Those remaining intubated as a result of swelling had contralateral extension of the swelling. These observations may help to explain why opening the wound frequently fails to provide benefit in many patients. Nonetheless, it may be difficult to clinically differentiate bleeding from swelling. After radiologic demonstration of swelling, the same group evaluated the benefits of prophylactic dexamethasone but failed to demonstrate any clinical benefit.¹⁹⁰

A 10-year, retrospective review of 3224 carotid endarterectomies performed at The Mayo Clinic revealed that 44 (1.4%) patients required wound exploration within 72 hours of surgery, despite the nonreversal of heparin.¹⁹¹ In two patients, re-exploration occurred before the initial extubation. The decision to re-explore was made in the PACU for 7 patients; the remaining 35 were identified in the ICU or ward. Only one patient required a surgical airway when direct laryngoscopy failed in the ICU. Several techniques were initially employed: awake bronchoscopic intubation (15 of 20 of which were successful), direct laryngoscopy after induction (13 of 15 were successful), and awake direct laryngoscopy (5 of 7 were successful). When awake bronchoscopy failed, direct laryngoscopy was successful whether the patient was awake (3 of 3) or asleep (2 of 2). When direct laryngoscopy initially failed after induction in two patients, it succeeded after opening the incision. When awake direct laryngoscopy failed, one patient required a surgical airway; in the other, direct laryngoscopy succeeded after opening the incision. Despite the size of this series, it is not possible to draw conclusions about which techniques are most successful. Success likely depends on the skill and judgment of the airway manager. It is also possible that this study differed from the other studies in that the decision to re-explore was made earlier and patients had less airway distortion.

Several nerve injuries can result from carotid artery surgery or the anesthetic technique. The range reported in the literature is 3% to 23%, although most of these cases resolve within 4 months of surgery.¹⁹² In the NYCAS study, cranial nerve palsies occurred in 514 (5.5%) of 9308 patients and involved, in descending order, the hypoglossal nerve (170), producing tongue deviation to the operative side; a branch of the facial nerve (126), resulting in lip or facial droop; the glossopharyngeal nerve (41); a branch of the vagus, which may involve the RLN and produce vocal cord paresis (31); the trigeminal nerve (19); a branch of the cervical plexus (10); or more than one nerve group (117).¹⁸³

Bilateral vocal cord and bilateral hypoglossal nerve palsies have been described after staged, bilateral carotid endarterectomies.^24,25 In the latter case, the first procedure, performed under regional anesthesia, had been complicated by a wound hematoma, resulting in numbness over the anterior neck and diminished sensation in the C2 and C3 distribution. The subsequent endarterectomy, done 4 weeks later under deep cervical plexus block with subcutaneous infiltration, caused intraoperative airway obstruction and asystole. The airway was secured, but repeated attempts at extubation resulted in persistent obstruction due to bilateral hypoglossal nerve palsy. In another case, performed under cervical plexus block, the patient developed bilateral vocal cord paralysis that required intubation and subsequent tracheotomy. It is suspected that she had a previously unrecognized contralateral vocal cord palsy from a prior thyroidectomy.¹⁹³ In this case, the vocal cord dysfunction was co-incident with retraction of the carotid sheath—although it can also be induced by a cervical plexus block—but it raises the importance of the preoperative assessment of patients who have had prior head and neck surgery.

4 Cervical Surgery

Cervical spine procedures may be followed by airway-related complications, including vocal cord paralysis and airway obstruction. Vocal cord dysfunction was seen in 5% of 411 patients undergoing anterior cervical discectomy and fusion.¹⁹⁴ Stridor was observed in one patient with bilateral vocal cord paralysis who required a tracheostomy. Fifteen of 17 patients had recovered by 12 months. One additional patient had recovered by 15 months, and the remaining patient was lost to follow-up.

Emery and colleagues studied the records of 133 patients who underwent cervical corpectomies with arthrodesis between 1974 and 1989.²⁶ The patients had undergone an anterior approach to achieve a three-level vertebral body and disc resection with bone grafting. This surgical approach requires tracheal and esophageal retraction toward the opposite side to permit exposure. Drains were placed, and all patients were immobilized by a halo vest or a rigid head-cervical-thoracic orthosis. They identified seven patients (5.3%) who required postoperative reintubation, and although they did not compare these patients with those not requiring reintubation, they attempted to identify common features that increased the risk of postoperative airway compromise. Three patients were immediately reintubated in the operating room, and four were reintubated 12 to 91 hours postoperatively. Severe hypopharyngeal swelling was observed at reintubation in four of seven patients and possibly in a fifth. Five of the seven reintubations had no serious sequelae; these patients were extubated within 2 to 8 days. One patient required a cricothyroidotomy, but delay resulted in hypoxic encephalopathy and death. Another patient was reintubated but developed and succumbed to severe adult respiratory distress syndrome. The investigators think that preexisting pulmonary disease, moderate or severe preoperative myelopathy, extensive multilevel decompression with prolonged surgery, and tissue retraction were risk factors for postoperative airway obstruction, but there were no controls.²⁶ They recommended 1 to 3 days of elective intubation postoperatively, a cuff-leak test, and direct laryngoscopy at extubation.

Venna and Rowbottom reviewed the records of 180 patients who had undergone a variety of cervical surgical procedures.²⁸ Based on the Emery study, they had made the decision to keep high-risk patients intubated until they met specified criteria, including a demonstrable cuff leak and the absence of significant airway edema on laryngoscopy. The average time to extubation was 33.5 hours. Despite the delay and the aforementioned criteria, 12 patients (6.6%) demonstrated post-extubation stridor and breathing difficulties, and 5 (2.7%) required reintubation. Two patients required tracheostomy, and two deaths were attributed to airway obstruction and unsuccessful reintubation.

Sagi and coworkers conducted a retrospective chart review of 311 anterior cervical procedures in an effort to identify the factors associated with airway complications.¹⁹⁵ In this series, 19 (6.1%) of patients had airway complications, but only 6 (1.9%) required reintubation. Most of these complications were attributed to pharyngeal edema. Risk factors included increased intraoperative bleeding, prolonged surgery (>5 hours), and exposure of more than three vertebral bodies, particularly when they included C2, C3, or C4. Reviewing the literature, these investigators identified an airway complication rate of 2.4% (from 1615 cases), 35 of whom required reintubation or tracheostomy. On average, those requiring reintubation did so at 24 hours.

Epstein and coworkers developed a collaborative protocol involving the neurosurgeon and anesthesiologist. Their objective was avoidance of reintubations.¹⁹⁶ Although their study enrolled only 58 patients, they required high-risk, lengthy procedures involving several cervical levels and significant blood loss. All patients remained electively intubated overnight and underwent fiberoptic airway examination before considering extubation. Most patients were extubated the day after surgery, but three remained intubated until day 7. Only one patient required reintubation. This reintubation rate was essentially the same as that observed by Emery and colleagues,²⁶ but Epstein’s cohort appeared to undergo higher-risk surgery.

In an effort to better understand the mechanism of postoperative airway obstruction, Andrew and Sidhu compared the soft tissue changes on the preoperative and postoperative cervical spine radiographs of 32 consecutive patients after a one- or two-level anterior cervical discectomy and fusion.¹⁹⁷ They found that the swelling was maximal at the C3-C4 level, corresponding to the area where Emery observed pharyngeal edema. None of their patients experienced dyspnea despite mean differences of 9.4 mm (95% CI, 7.41 to 11.09 mm) to 10.7 mm (95% CI, 7. 8.82 to 12.58 mm) between the preoperative and postoperative radiographs at C3 and C4, respectively. It appears that this area is most vulnerable, regardless of the level operated on. Compared with Sagi’s study, these patients underwent much shorter and more limited procedures.

Extubation criteria after anterior cervical spine surgery were discussed at length in the Society for Airway Management online Forum in 2011. The groups who perform this surgery frequently tend to extubate most of their patients at the conclusion of surgery, except when the blood loss is high (e.g., >500 mL), the surgery is prolonged (e.g., >5 hours), the operation involves more than three levels, the airway was difficult or expected to be difficult, or comorbidities exist, such as severe cervical myelopathy, obesity, and obstructive sleep apnea (OSA). Patients with multiple risk factors are cared for in an ICU and are extubated over an airway exchange catheter (AEC) (personal communication from C.A. Hagberg, SAM Forum, February 2011).

Patients undergoing posterior cervical surgery may face the risk of macroglossia and significant retropharyngeal and hypopharyngeal swelling, which may be aggravated by fixation of the cervical spine and make intubation more difficult.¹⁹⁸ There is a low probability (1.1% to 1.7%) that reintubation will be required,^196,198 but accomplishing this may be very difficult.

5 Maxillofacial Surgery and Trauma

Maxillary and mandibular surgery produces conspicuous and often worrisome swelling. Anxiety regarding postoperative care may be heightened by limited airway access, fear that airway intervention may disrupt the surgical repair, and anecdotal reports of near misses or actual fatalities. Because many of these patients are young and otherwise healthy and are undergoing elective surgery for functional or cosmetic improvement, there may be concerns about litigation. It is speculative about whether this results in more or less aggressive care.

Although these concerns demand special attention, deaths rarely occur. In a review of 461 perioperative deaths reported to the Ontario, Canada, coroner between 1986 and 1995, the investigators found only one death associated with orthognathic surgery, although they were unable to determine how many such cases had been performed (see “In Vivo Studies”).¹⁹⁹ They were unable to identify nonlethal complications. Meisami and others performed magnetic resonance imaging (MRI) approximately 24 hours after maxillary or mandibular surgery in 40 patients.²⁰⁰ Despite the significant facial swelling seen in almost all the patients, none exhibited soft tissue swelling from the base of the tongue to the glottis.

Complete airway obstruction after elective orthognathic surgery has been reported. Dark and colleagues described a case involving a young woman who underwent seemingly uneventful mandibular and maxillary osteotomies with submental liposuction.²⁰¹ Immediately after extubation, she developed airway obstruction requiring reintubation. Repeated fiberoptic examination and CT showed severe and extensive edema from the tongue to the trachea, which was maximal at the level of the hyoid. By the fourth postoperative day, a cuff leak was detected, and the patient was successfully extubated over a tube exchanger. Hogan and Argalious described a patient in whom maxillomandibular advancement was performed for OSA.²⁰² The procedure lasted 9 hours, during which he received 7200 mL of crystalloid and 500 mL hetastarch. He remained intubated overnight, and after demonstrating adequate spontaneous ventilation and a cuff leak, he was extubated (over a 19-F AEC). Extubation was immediately followed by clinical evidence of airway obstruction, and he was reintubated. The obstruction was attributed to fractured hardware and a hematoma in the piriform fossa that caused extrinsic compression. This could easily have resulted from periglottic edema. The investigators concluded that patients undergoing this type of surgery face a high risk of airway complications and recommended nasopharyngolaryngoscopy before extubation.

Clinical assessment of airway edema is unreliable,²⁰⁰ and studies indicate that the cuff-leak test is neither sufficiently sensitive nor specific to determine when to extubate these patients. Endoscopic assessment may help to identify patients who harbor occult clots (i.e., “coroner’s clot”) behind the soft palate or adjacent to the glottis, but it may miss or itself give rise to troublesome bleeding.

Maxillofacial injuries often result from unrestrained occupants of motor vehicles encountering an unyielding dashboard, windshield, or steering wheel. Gunshot wounds or physical altercations also cause maxillofacial injury. Airway obstruction is a primary cause of morbidity and mortality in these patients, and many die before they reach the hospital.²⁰³ Those with less life-threatening injuries are likely to present with a full stomach, and many have associated head and neck injuries, lacerations, loose or avulsed teeth, intraoral fractures, and fractures extending into the paranasal sinuses, into the orbit, or through the cribriform plate. They may also have an unstable cervical spine or damage to the neural axis. Injuries to the lower face raise the possibility of a laryngeal fracture. Intermaxillary fixation may be part of the surgical plan, necessitating a nasal intubation or a surgical airway. Timing of tracheal extubation is complex and must take into consideration factors such as the patient’s level of consciousness, ability to maintain satisfactory gas exchange, coagulation status, and integrity of protective airway reflexes. Attention must be paid to the difficulties originally encountered in securing the airway and an evaluation of whether reintubation would be easier or more difficult after surgery and resuscitation. Most of the trauma literature about airway management addresses intubation and offers little help with extubation, making cooperation between the anesthesiologist,^204,205 surgeon, and critical care physician essential. Intermaxillary fixation requires wire cutters to be immediately available and personnel to know which wires to cut. A flexible bronchoscope, provisions for an emergency surgical airway, and the required expertise should be immediately available at the time of extubation. Alternatives include prophylactic tracheotomy, submental intubation,^206–208 nasal intubation, and bronchoscopic airway evaluation performed before extubation,²⁰⁹ although assessment may be limited to supraglottic structures and exclusion of tube entrapment. Ideally, extubation should be accomplished in a reversible manner, permitting supplemental oxygenation, ventilation, and reintubation if needed (see “Extubation Strategies”).

6 Deep Neck Infections

Infections involving the submandibular, sublingual, submental, prevertebral, parapharyngeal, and retropharyngeal spaces are significant airway management challenges, whether intubation is achieved for surgical drainage or for protection during medical management. In expert hands, bronchoscopy-assisted intubation can often be achieved.²¹⁰ When this is unsuccessful or constitutes a significant risk of rupturing the abscess, a surgical airway before incision and drainage may be called for.²¹¹ Potter and colleagues retrospectively compared the outcomes of 34 patients in whom a tracheotomy was performed with 51 patients who remained intubated after surgical drainage.²¹² All patients had undergone surgical drainage for impending airway compromise and required airway support postoperatively. It was not always evident to the investigators why a particular strategy was chosen, and these groups were not likely identical. Airway loss occurred more commonly in the intubated patients, but this characteristic was not statistically significant. Two deaths occurred, one resulting from an unintended extubation and the other from post-extubation laryngeal edema and an inability to reestablish the airway. The latter patient had a cuff leak before extubation, and signs of obstruction developed 30 minutes after the ETT was removed. Surgical drainage rarely results in immediate airway improvement, and reintubation or emergent placement of a surgical airway, if required, may be complicated by edema, tissue distortion, and urgency.

7 Posterior Fossa Surgery

Posterior fossa surgery can cause injury to cranial nerves, bilateral vocal cord paralysis, brainstem or respiratory control center injury, and macroglossia.^{114,115,167,213–216} Because the nerve roots may be very close to the operative site, the resultant injuries may be bilateral, extensive, and transient or permanent. Gorski and coworkers suggested that tolerance of the ETT and the absence of a gag reflex on oral suctioning should arouse suspicion of such an injury.²¹⁴ Howard and colleagues described a patient with a recurrent choroid plexus papilloma involving the fourth ventricle.²¹⁵ Preoperatively, the patient displayed bulbar dysfunction. His extubation on the first postoperative day was complicated by complete airway obstruction, hypoxia, and a seizure. Laryngoscopy performed after neuromuscular blockade revealed mildly edematous vocal cords. After reintubation and elective tracheostomy, fiberoptic examination showed the vocal folds in a neutral position. Nocturnal ventilation and tracheostomy were still required at 1 and 3 months, respectively. This patient demonstrated central apnea and bulbar dysfunction with hypoglossal paralysis and unopposed vocal fold adduction.

Artru and colleagues described a patient with a cerebellar mass, severe papilledema, and bulbar signs.²¹³ Despite recovery of consciousness and strength, the patient remained apneic and required ventilatory support for 7 days. The investigators cautioned that the dorsal pons and medulla are the sites of the cardiovascular and respiratory centers that control hemodynamics and ventilation. The area is also host to several cranial nerve nuclei. Damage to these areas can result from edema, disruption, ischemia, or compression and may cause a loss of respiratory drive or airway obstruction.

Dohi and coworkers described a patient who developed bulbar signs, including bilateral vocal cord paralysis after excision of a recurrent cerebellopontine angle tumor.¹⁶⁷ Negative-pressure pulmonary edema developed as a consequence of a bilateral, presumably central RLN injury, and a tracheostomy was required until recovery 3 months later. During the initial intubation, the glottis could not be seen by direct laryngoscopy, and blind intubation was performed. The details of three subsequent unsuccessful extubations and reintubations were not described. Trials of extubation in a patient known to be a difficult (direct) laryngoscopy case are life-threatening and cannot be justified. A tracheostomy was performed, and vocal cord function recovered after 3 months.

Early vocal cord evaluation after extubation has been advocated along with the involvement of a neurosurgeon, otolaryngologist, speech therapist, and intensivist to manage patients who have developed laryngeal dysfunction.²¹⁶ A tracheostomy and an enteral feeding tube may be needed. A more preemptive approach (described later in more detail) involves flexible laryngoscopic assessment through a supraglottic airway (SGA) after removal of the ETT.

8 Stereotactic Surgery and Cervical Immobilization

Stereotactic neurosurgical and neuroradiologic procedures are finding increasing applications. When head frames are used, they may impede access for SGA placement or laryngoscopy. Similarly, patients in cervical immobilization devices for spinal cord protection may undergo high-risk surgical procedures.¹¹⁶ Careful planning for their extubation is critical because reintubation may be difficult, and rapid surgical access may be virtually impossible. Full recovery of strength and consciousness, persistence of respiratory drive, the presence of a cuff leak, preservation of protective reflexes, and absence of significant tongue swelling are the essential prerequisites for extubation. Postoperative seizures, vomiting, elevated intracranial pressure, and neurologic obtundation may make extubation particularly hazardous. Several of the strategies described subsequently should be given serious consideration in managing these patients.

9 Tracheal Resections

Patients with moderate or severe tracheal stenosis may come for surgical tracheal resection. These patients usually have tracheal stenosis or tracheomalacia, often caused by prolonged intubation or occasionally caused by a retrosternal mass. Some patients may have compromised preoperative respiratory function. After an end-to-end anastomosis, the surgeon may elect to place a “guardian suture” from the chin to the chest, maintaining the head and neck in flexion and thereby minimizing traction on the suture lines (Fig. 50-1).^217,218 The preference is for early extubation to avoid positive pressure, coughing, and presence of a foreign body in the airway.^217–221 A cough-free extubation is highly desirable, as is avoidance of a need for reintubation, which if required could prove very challenging.

Figure 50-1 This patient has undergone a cricotracheal resection. Cervical extension is restricted by a chin-to-chest guardian suture. The patient has been extubated, and a laryngeal mask airway has been introduced before reversal of neuromuscular blockade or awakening. This reduces coughing on emergence, allowing gradual recovery and assessment of spontaneous respiratory function while minimizing the potential distraction of the surgical anastomosis. It also provides the optimal means of performing flexible laryngobronchial examination under controlled conditions.

(Courtesy of Patrick Gullane, MD, University Health Network, Toronto, Ont.)

10 Palatoplasty

A variety of surgical procedures have been employed to treat OSA, including uvulopalatopharyngoplasty, midline glossectomy, mandibular advancement, limited mandibular osteotomies with genioglossal advancement, and hyoid bone suspension.²²² Pepin and colleagues published a critical analysis of the literature on the risks and benefits of surgical treatment of snoring and OSA.²²³ They identified “at least five deaths” after uvulopalatopharyngoplasty and found that few studies had adequate numbers to allow conclusions to be drawn regarding their outcomes. Less than one half of the studies commented on the frequency of complications. A retrospective review of 101 uvulopalatopharyngoplasties identified an early postoperative respiratory complication rate of 10%.²²⁴ Ten of 11 patients required reintubation, and 1 death resulted from airway obstruction.

Uvulopalatopharyngoplasty was introduced to deal with retropalatine collapse. However, in approximately one half of the adult patients with OSA, obstruction occurs at the retrolingual pharynx. Tongue suspension is one of several approaches introduced to manage the latter group of patients.²²⁵ The procedure involves placement of an anchoring screw in the genial tubercle and attachment of a suture through the base of the tongue. Szokol described a morbidly obese patient with OSA in whom this procedure was performed.²²² Laryngoscopy and bag-mask ventilation had been difficult. At the conclusion of the procedure, the patient was fully awake, was able to sustain a head lift for 5 seconds, demonstrated a negative inspiratory pressure of 40 cm H₂O, and was extubated. Stridor was observed immediately, and bag-mask and laryngeal mask ventilation were ineffective. Attempts to reintubate the patient were unsuccessful, necessitating a cricothyroidotomy. Subsequent direct laryngoscopy showed a markedly swollen epiglottis and grossly edematous laryngeal and hypopharyngeal tissues. The patient developed negative-pressure pulmonary edema, and a tracheostomy was performed 2 days later because of persistent swelling. Tracheal decannulation occurred uneventfully 2 weeks later. The physicians speculated that airway manipulation during the surgery was the cause of this patient’s swelling. They did not consider that the swelling might have resulted from or at least been aggravated by repeated attempts at laryngoscopy.

Palatoplasty, alone or in combination with other procedures, may be performed on patients with cleft palates or other congenital abnormalities. In one study, 14 (5.7%) of 247 patients undergoing palatoplasty had postoperative airway problems, 12 of whom required reintubation. One half of the patients experiencing complications had Pierre Robin sequence; three of the patients required reintubation 24 to 48 hours postoperatively.²²⁶

1 Paradoxical Vocal Cord Motion

Paradoxical vocal cord motion (PVCM) is the quintessential example of a situation wherein reintubation will be required. Intubation is not more difficult; extubation is the challenge. This uncommon and poorly understood condition is frequently mistaken for refractory asthma or recurrent laryngospasm.^227–229 The diagnosis is both overlooked and overused, leading to confusion.²³⁰ It also is called vocal cord dysfunction, Munchausen stridor, psychogenic stridor, factitious asthma, pseudoasthma, and irritable larynx syndrome.^230,231 Normal vocal cord motion involves inspiratory abduction and 10% to 40% adduction on expiration. With PVCM, adduction of the true vocal cords occurs on inspiration or expiration, or both. The false vocal cords and the posterior laryngeal wall may further contribute to the airway obstruction.^231–234 This condition may be associated with psychosocial disorders, stress, exercise, gastroesophageal reflux, irritant exposure, or airway manipulation. Pulmonary function tests show normal expiratory but flattened inspiratory flow loops. It is important to differentiate this condition from asthma, laryngospasm, anaphylaxis, angioedema, gastroesophageal reflux, and vocal cord paralysis. The incidence of PVCM is unknown.

Harbison and coworkers described two patients who had post-extubation stridor after thyroidectomies.²³⁵ This is a particularly challenging situation with a complex differential diagnosis, especially because one of the patients had unilateral vocal cord paralysis preoperatively. In that patient, post-extubation stridor developed 24 hours postoperatively and could be observed while awake and asleep. Fiberoptic examination under sedation showed paradoxical motion of the mobile cord. She was managed successfully with speech therapy. They speculated that these cases might have resulted from surgical manipulation of the RLN during the thyroidectomies.

Hammer and colleagues described a 32-year-old woman with recurrent episodes of stridor,²³⁶ sometimes associated with cyanosis, despite normal flow-volume loops and pulmonary function tests. The diagnosis of PVCM was made endoscopically and managed with relaxation techniques. After preoperative sedation, topical lidocaine, and bilateral SLN blocks, she underwent an awake fiberoptic intubation. At the conclusion of surgery, extubation was performed after she was fully awake, but sustained inspiratory stridor ensued, resulting in reintubation. A subsequent attempt the next day confirmed inspiratory vocal fold adduction, and a tracheostomy was required for 58 days. In the absence of features predicting a challenging intubation, there seems little justification for awake intubation, and it may contribute unnecessarily to an anxiety disorder.

PVCM imposes no special requirements for intubation. The abnormality is functional rather than anatomic. Appropriate management depends on having the correct diagnosis, which requires clinical suspicion and endoscopic confirmation of inspiratory adduction of the vocal cords. Adequate oxygenation, consideration of CPAP or helium-oxygen administration, positioning, reassurance, and support may suffice, although sedation may be required after the diagnosis is confirmed. Speech therapy, psychotherapy, hypnosis, and reassurance may be helpful in the long-term management,²³⁷ but such is not always the case.²²⁷ Some reports have recommended electromyographically guided botulinum toxin injection into the thyroarytenoid muscle for recalcitrant cases. The optimal anesthetic management of these patients is unknown. Regional anesthesia avoids airway intervention, but it does not ensure that a condition that may be stress related will not occur. Familiarity with this condition, calm reassurance when there is prior suspicion, and perhaps deep extubation seem prudent.

2 Parkinson’s Disease

Susceptibility to aspiration is common among patients with Parkinson’s disease and is the most common cause of death. Dysphonia, most frequently hypophonia, occurs in approximately 70% to 90% of patients with Parkinson’s disease.^238,239 Video stroboscopic findings include laryngeal tremor, vocal fold bowing, and abnormal glottic opening and closing.²³⁹ Several neurodegenerative diseases, including multiple system atrophy, have some features in common with Parkinson’s disease, including dysphonia, and these patients may exhibit bilateral abductor vocal fold paresis. Typically, symptoms in patients with Parkinson’s disease progress insidiously, are not recognized by the patient, and may be associated with nocturnal stridor. These features resemble those of OSA identified by polysomnography. Many of these patients may benefit from nocturnal CPAP or bi-level positive airway pressure (BiPAP).²³⁸

Blumin and Berke described seven patients, only one of whom presented for surgery. This patient underwent a transurethral prostate resection under general anesthesia, and 2 weeks after surgery, he returned with biphasic stridor that necessitated an emergent tracheostomy. It is unclear whether there was a relationship between the surgery or anesthesia and subsequent airway obstruction.

Patients with multiple system atrophy have daytime hypoxemia associated with abnormal laryngopharyngeal movements, including obstruction at the arytenoids, epiglottis, base of the tongue, and soft palate. The significance of these problems is unclear, but they may contribute to complications after extubation.²⁴⁰

Vincken and colleagues studied 27 patients with extrapyramidal disorders.²⁴¹ Twenty-four had flow-volume loops, many of which demonstrated saw-toothed oscillations, even in the absence of respiratory symptoms. They observed oscillations with rhythmic (4 to 8 Hz) or irregular movements of the glottis and supraglottic structures. Ten patients exhibited intermittent upper airway obstruction. Four patients had stridor or dyspnea. The investigators believed that the upper airway was the primary site of involvement. In a subsequent report, they observed symptomatic improvement with levodopa despite persistence of the oscillatory pattern on flow-volume loops.²⁴² Inspiratory and expiratory flows after levodopa increased from 1.40 to 3.50 L/sec and 0.95 to 5.05 L/sec, respectively. Bronchodilators provided no additional benefit. This case may have important implications for the perioperative management of patients with Parkinson’s disease.

Easdown and colleagues described a patient with Parkinson’s disease who had a respiratory arrest 60 hours after surgery.²⁴³ Before that event, the patient had episodic desaturation, labored breathing, and progressive hypercapnia in the absence of tremor or rigidity. Treatment with bronchodilators produced no benefit, and his condition improved immediately after intubation. With the ETT, compliance and resistance appeared normal. This patient’s levodopa or carbidopa had not been resumed postoperatively, and the investigators speculated that this caused or contributed to upper airway obstruction. Because most patients with Parkinson’s disease are elderly and may have comorbidities that can make the diagnosis uncertain, it is important to consider involvement of the upper airway and the dramatic effect withdrawal and reinstatement of medications can have on their clinical course. This concern is reinforced by a case report describing a patient who developed airway obstruction and acute respiratory acidosis requiring intubation preoperatively because five doses of his antiparkinsonian medications were withheld while he was being fasted.²⁴⁴ Easdown and colleagues emphasized the importance of continuing these medications, and avoidance of dopamine antagonists throughout the perioperative period.²⁴³

Backus and colleagues described a patient with long-standing Parkinson’s disease who became aphonic, developed stridor, and suffered respiratory arrest shortly after taking cough medication.²⁴⁵ Complete upper airway obstruction recurred with vocal fold apposition immediately after extubation. Four days later, the patient extubated herself with no further complications. The investigators interpreted this spontaneous laryngospasm as a manifestation of Parkinson’s disease. Others have observed upper airway dysfunction, airflow limitation, and bilateral abductor vocal cord paralysis in association with Parkinson’s disease. The first episode might not have been spontaneous but instead a consequence of aspiration of the cough medicine. Nonetheless, there remains a possibility that these patients are more prone to laryngospasm, whether spontaneous or induced by glottic stimulation.

Liu and coworkers described airway obstruction during induction of anesthesia.²⁴⁶ Despite being unable to visualize the larynx, they attributed the obstruction to laryngospasm. The obstruction resolved with awake, blind nasal intubation but recurred 24 hours later on extubation. At that point, fiberoptic examination showed inspiratory vocal fold adduction, necessitating reintubation. It is unclear whether they were observing manifestations of Parkinson’s disease or PVCM, but extubation was uneventful 24 hours later after increasing the dosage of levodopa or carbidopa.

Parkinson’s disease is a common disorder, but only 13 cases of stridor have been attributed to it.²³⁹ The pathogenesis of upper airway obstruction is unknown. It may be mediated by the basal ganglia and nucleus ambiguus. A similar phenomenon involving esophageal spasm has been associated with Parkinson’s disease. One theory invokes laryngeal hypertonicity, which may be triggered by copious secretions.

3 Rheumatoid Arthritis

In patients with rheumatoid arthritis, the airway manager needs to be concerned about three joint areas: the cervical spine, the temporomandibular joint (TMJ), and the cricoarytenoid joint.²⁴⁷ Autopsy studies suggest that 30% to 50% of patients with rheumatoid arthritis have significant cervical spine involvement. Cervical subluxation has been identified clinically in 43% to 86% of these patients and may represent a serious neurologic risk during intubation with flexion or extension.^{145,247–249} The spectrum of cervical involvement ranges from ligamentous destruction with subluxation and impaction to extreme limitations in the range of motion because of fibrosis and ankylosis. These patients may have a narrowed glottic aperture, limited mouth opening due to involvement of the TMJs, micrognathism, laryngeal deviation, and cricoarytenoid and cricothyroid involvement.^250,251 Kohjitani and colleagues retrospectively described four patients undergoing bilateral TMJ replacement; three had glottic erythema and swelling on endoscopy, three had OSA, and three experienced laryngospasm at intubation and after extubation.²⁵¹ TMJ involvement may result in loss of ramal height and micrognathia with or without ankylosis and associated OSA.

Cricoarytenoid arthritis and its consequences have long been recognized in the anesthesia and general medical literature.^252–256 Although rheumatoid arthritis is the most common cause of this condition, it also may be associated with bacterial infections, mumps, diphtheria, syphilis, tuberculosis, Reiter’s syndrome, ankylosing spondylitis, systemic lupus erythematosus, gout, progressive systemic sclerosis, and other conditions.²⁵⁷ The cricoarytenoid joint has a synovial lining and bursa. Its mobility is vital for speech, respiration, and protection from aspiration. Inflammatory changes may include effusion, pannus formation, joint erosion, and ankylosis, any of which may compromise the joint’s functions. Its involvement may be unsuspected or mistaken for asthma until intubation or after extubation and may necessitate a surgical airway.^258,259 Dysphonia, dyspnea, or stridor should raise suspicion of this possibility. Complete airway obstruction is a well-described but uncommon complication, despite involvement of the cricoarytenoids in 26% to 86% of patients with rheumatoid arthritis.^251,259 Laryngoscopy may reveal a rough and thick mucosa with narrowing of the vocal chink. Although airway obstruction occurs most commonly in patients with long-standing rheumatoid arthritis with polyarticular and systemic involvement, laryngeal stridor has been described as the sole manifestation of this disease.²⁶⁰

Keenan and coworkers described tracheal scoliosis, which consisted of tracheal deviation, laryngeal rotation, anterior angulation, and vocal fold adduction seen fiberoptically and on CT scans.²⁵⁵ It was presumed to result from the loss of vertical height and asymmetrical bony erosions.

Wattenmaker and colleagues studied patients with rheumatoid arthritis undergoing posterior cervical spine procedures.²⁵⁰ Their primary objective was to compare the perioperative airway complications seen in rheumatoid arthritis patients when intubation was performed by direct laryngoscopic or flexible bronchoscopy. Retrospectively reviewing 128 consecutive posterior cervical procedures, upper airway obstruction characterized by stridor occurred in 9 of 128 patients, 1 of 70 patients intubated with bronchoscopic guidance, and 8 of 58 patients intubated otherwise (i.e., direct laryngoscopy or blind nasotracheal technique). Five patients (all in the nonbronchoscopic group) required emergency reintubation that proved to be very difficult, with two near fatalities and one death. Although the two groups were similar with regard to age, gender, American Rheumatology Association classification, ASA physical status, duration of surgery and anesthesia, fluid balance, and postoperative immobilization, there were significant differences in time to extubation. Seven of the patients could not be intubated by flexible bronchoscopy and were therefore intubated by a nonfiberoptic technique. The patients were not randomized to different methods; criteria for the method of intubation and techniques were not described; all patients were intubated awake; and the study was carried out over an 11-year period.²⁶¹ Although it is not possible to draw firm conclusions from this study, there was a high incidence (7%) of post-extubation stridor and difficult or failed reintubations, regardless of the intubation technique.

Patients with rheumatoid arthritis qualify as higher-risk extubation cases because they may have a fixed or unstable cervical spine, TMJ ankylosis, difficult intubations by direct or flexible laryngoscopy, and increased risk of post-extubation airway obstruction. Several investigators have recommended postponing extubation until the patient is wide awake. Unfortunately, this provides increased protection against nothing other than laryngospasm and aspiration. The prevailing wisdom is that patients with limited mouth opening and a potentially unstable cervical spine should be intubated with a flexible bronchoscope.²⁵⁰ This method involves blind passage of the ETT through the cords, which may be traumatic,^91,261 particularly in the face of preexisting cricoarytenoid arthritis. Regional anesthesia should be considered as an alternative to general anesthesia when appropriate. When intubation cannot be avoided, proposed extubation strategies include a preemptive tracheostomy or a method that increases the reversibility of extubation. Neither strategy has been prospectively evaluated in this population.

4 Tracheomalacia

Tracheomalacia is a dynamic airway obstruction resulting from loss of the cartilaginous tracheal support. This results in the posterior membranous wall bulging anteriorly when the intratracheal pressure is reduced or the intrathoracic pressure is increased.¹⁴¹ Although rare, it should be considered when the patient has dyspnea on exertion with difficulty clearing secretions and a seal-like, incessant cough.^141,262

Patients frequently are misdiagnosed with asthma and fail to respond to escalating therapy. Pulmonary function tests (i.e., forced expiratory volume at 1 second, forced vital capacity, and peak expiratory flow) show severely diminished expiratory flow with relative preservation of the inspiratory flow. The diagnosis may be confirmed fiberoptically during spontaneous breathing. Tracheomalacia may be congenital²⁶³ or result from vascular compression,²⁶⁴ an intrathoracic goiter,²⁶⁵ chronic obstructive pulmonary disease, or prolonged intubation. The latter may be caused by ETT cuff-induced erosion of the tracheal cartilage with or without extension to the membranous trachea.

The severity of the dynamic obstruction is proportional to the expiratory force. It may be unapparent during quiet breathing but disabling in a distressed patient. Positive pressure or bypassing the lesion with a tracheal tube provides temporary relief while further management options are considered. They may include medical management, surgical resection, or placement of a stent.²⁶² Additional suggestions for the extubation of a patient with suspected tracheomalacia are described later.

Relapsing polychondritis is an example of extensive tracheobronchomalacia. It is a rare, multisystem disease characterized by episodic inflammation of cartilaginous structures resulting in tissue destruction.^262,266 Laryngeal and tracheal tract involvement occurs in approximately one half of patients. It usually occurs early in the course of the disease and may manifest as hoarseness, nonproductive cough, shortness of breath, and stridor. Upper airway obstruction is usually diffuse and may progress to involve the glottis, subglottic area, trachea, and bronchial cartilages. Histologically, there is evidence of perichondral inflammation and replacement of cartilage by fibrous tissue that manifests as inflammatory swelling and progressive destruction of cartilage. The clinical manifestations range from bronchorrhea and recurrent pneumonia to airway collapse. Medical management consists of steroids, nonsteroidal anti-inflammatory drugs, and immunosuppressant agents, but their benefit varies. Surgical management consists of external airway splinting or self-expanding metallic stents. These patients may present for bronchoscopy, tracheostomy, tracheal or nasal reconstruction, aortic valve replacement, or stent placement.^{264,267–271} Airway collapse after extubation should be anticipated and may be temporarily dealt with by CPAP.^272,273

5 Obstructive Sleep Apnea Syndrome

In the ASA Closed Claims Project analysis of adverse respiratory events, 65 of the 156 perioperative events involved obese patients; for the claims specifically related to extubation, 12 of the 18 were obese, and 5 of these patients had been diagnosed with OSA.² OSA correlates positively with age and obesity, both of which are becoming increasingly prevalent. The pathophysiology and perioperative airway management of OSA in obese patients has been comprehensively reviewed.^274–276 Many surgical patients have undiagnosed or untreated OSA. OSA syndrome is associated with an increased risk of gastroesophageal reflux, difficult mask ventilation^276–278 and laryngoscopic intubation,^279–282 and accelerated arterial oxygen desaturation.^276,283 The risk of airway obstruction after surgery is increased for patients with OSA; life-threatening post-extubation obstruction occurred in 7 (5%) of 135 patients.^279,284 Rapid desaturation, difficult mask ventilation, and difficult direct laryngoscopy make this a particularly high-risk setting.²⁸⁵ The ASA practice guidelines for the management of patients with OSA provided limited guidance beyond a strong recommendation that they be fully awake and that the airway manager verify that neuromuscular blockade is completely reversed before extubation. If possible, extubation and recovery should be carried out in the lateral or semi-upright position,²⁸⁶ nasal CPAP should be available or routinely implemented, and consideration should be given to extubation over a tube exchanger.^{274,276,280,284,287} These strategies have been associated with better outcomes, and anecdotal comparisons are compelling, but they have not been subjected to controlled, randomized trials, and they were not addressed by the ASA Task Force.

6 Laryngeal Incompetence

Laryngeal function may be disturbed for at least 4 hours after tracheal extubation.²⁸⁸ Immediately after extubation, 8 (33%) of 24 patients aspirated swallowed radiopaque dye; 5 showed radiologic evidence of massive aspiration. Four hours after extubation, 4 (20%) of 20 patients aspirated dye; 3 had massive aspirations. At 24 hours, the rate was reduced to 5%. In this study, patients had been intubated for 8 to 28 hours during and after cardiac surgery. Although the investigators did not observe a relationship between duration of intubation (8 to 28 hours) and aspiration, it is unclear whether the presumed laryngeal incompetence occurs after brief intubation or is more common and severe with prolonged intubation. The mechanism of laryngeal incompetence was postulated to be primarily sensory because patients who aspirated dye did not cough.

Residual neuromuscular paralysis is a common problem in postoperative patients and may result in hypoventilation, hypoxemia, pharyngeal and laryngeal dysfunction, or increased pulmonary aspiration.^264,289 Pharyngeal function was impaired in conscious volunteers receiving a continuous infusion of vecuronium and resulted in laryngeal penetration of contrast medium proportional to the degree of blockade.²⁹⁰ Relaxation of the upper esophageal sphincter was also observed. None of the volunteers coughed or had respiratory symptoms. Berg and colleagues found a higher incidence of postoperative pulmonary complications (i.e., pulmonary infiltrate or atelectasis associated with cough, sputum, or shortness of breath) among patients randomly assigned to receive a long-acting or intermediate-acting neuromuscular blocker.²⁹¹ It is intriguing to speculate on how residual neuromuscular blockade may contribute to laryngeal incompetence.

7 Pulmonary Aspiration of Gastric Contents

Although more patients are being diagnosed with gastroesophageal reflux, the diagnosis of perioperative pulmonary aspiration has not increased.^292,293 Aspiration is estimated to complicate 1 of 2000 to 3000 general anesthetics and was responsible for only 3 of 156 perioperative events in the ASA Closed Claims Project review.^2,293,294 Nonetheless, it is the leading cause of pneumonia in the ICU and a common cause of acute respiratory distress syndrome.²⁹⁵ Many of these cases are ventilator-associated pneumonia and occur with the ETT in situ. Factors predisposing a surgical patient to aspiration include emergency surgery, pain, obesity, narcotics, nausea, ileus, bowel obstruction, pregnancy, some surgical positions, depressed level of consciousness, inadequate depth of anesthesia, postoperative drowsiness, and residual neuromuscular blockade. Despite the ubiquity of these conditions, perioperative aspiration is not commonly identified. Before intubation, difficult bag-mask ventilation may result in gastric distention, which may be further complicated if laryngoscopy proves difficult because it may delay securing the airway. Repeated laryngoscopic attempts may cause edema, thereby increasing glottic resistance. Aspiration may also result from obtundation or conditions that impair vocal cord apposition (e.g., vocal cord paralysis, laryngeal incompetence, residual neuromuscular blockade, granulomas). Aspiration can cause serious morbidity and death.^292–295

Although most incidents of aspiration seem to occur at induction, many occur during maintenance and recovery from anesthesia.²⁹⁶ Numerous strategies have been described to reduce the risk at induction, but relatively little information is available on how best to prevent this later. Premature extubation, postoperative nausea, delayed gastric emptying, residual neuromuscular blockade, relaxation of the esophageal sphincters, decreased level of consciousness, gagging on an ETT, supine recovery, and impaired laryngeal competence may make emergence from anesthesia and tracheal extubation as problematic as induction. A kinked or clamped nasogastric tube may promote regurgitation and aspiration. Evidence-based recommendations on an extubation strategy to reduce aspiration are not available. It would seem logical to minimize the contributing factors: postoperative nausea and vomiting, residual neuromuscular blockade, decreased level of consciousness and associated diminished protective airway reflexes, and gastric evacuation. We do not know whether gastric decompression reduces aspiration; a well-seated i-gel SGA²⁹⁷ or ProSeal LMA may or may not offer some protection from aspiration.^298–300 With the current information, it is not appropriate to recommend the elective use of these devices in a patient at increased risk for aspiration.

1 Tracheal Tube Exchangers

The most basic commercial tube exchangers are the Sheridan T.T.X. (Hudson Respiratory Care Inc. [RCI], Temecula, CA) (Fig. 50-4) and the JEM Endotracheal Tube Changer (Instrumentation Industries Inc., Bethel Park, PA). The T.T.X. devices are available in four ODs (2.0-, 3.3-, 4.8-, and 5.8 mm) and two lengths (56 and 81 cm). The smallest can be inserted into tracheal tubes with IDs as small as 2.5 mm. A longer, 100-cm endobronchial exchanger (Sheridan E.T.X.) is available for exchanging double-lumen tubes. They are firm—Shore hardness of 85, the same durometer measurement as the CAEC and Cardiomed International’s Endotracheal Ventilation Catheter (ETVC)—although thermolabile and therefore subject to softening with heat. They are frosted to minimize drag and have a radiopaque stripe and distance markings. They have no side holes or connectors. An alternative product, the Sheridan JETTX Exchanger, is a longer device (100 cm), but it is available in only a single OD that is suitable for ETTs greater than 6.5-mm ID. It incorporates a proximal slip-fit connector that can be connected by a Luer-Lok to a jet ventilator. As with the T.T.X., there is only a single, distal end hole.

Figure 50-4 The tracheal tube exchanger (Sheridan T.T.X., Hudson RCI) is a simple catheter with no proximal or distal modifications. These devices are available in four diameters and two lengths. If the device is to be used for ventilation, it must be adapted by the user. There are no distal side ports, which makes jet injection potentially hazardous.

(From Cooper RM: The difficult airway–II. Anesthesiol Clin North Am 13:683–707, 1995.)

The JEM devices are available in nine sizes and are compatible with ETTs from 2.5- to 7.5-mm ID (JEM 325 to 400). These are single-use, high-density, polyethylene devices without proximal connectors or distal side holes.

2 Cook Airway Exchange Catheters

Cook Critical Care has developed a family of hollow stylets known as CAECs (Fig. 50-5A). They are available in 8.0-, 11-, 14-, and 19-F sizes, corresponding to 2.7-, 3.7-, 4.7-, and 6.3-mm ODs, respectively. They can be used to exchange ETTs with IDs of 3, 4, 5, and 7 mm, respectively. The 8-F CAEC is 45 cm long, and the others are 83 cm long. The devices are radiopaque, have distance markings between 15 and 30 cm from the distal end, and have two distal side holes and an end hole. Proximally, two types of connectors are secured and released by a patented Rapi-Fit adapter (see Fig. 50-5B). They provide a 15-mm connection or a Luer-Lok jet ventilation attachment and were designed for rapid removal and reattachment while the tracheal tube is being off-loaded and replaced. The length and IDs (1.6 to 3.4 mm) make manual ventilation with a resuscitation bag possible but useful only for short periods because resistance is very high. The Luer-Lok jet Rapi-Fit connector allows jet ventilation, but the paucity of distal side holes potentially increases catheter whip and the risk of barotrauma.³³³

Figure 50-5 The Cook airway exchange catheters are available in four diameters and two lengths. They are radiopaque and have distance markings at each centimeter throughout the working length. A, The proximal Rapi-Fit adapter, the middle section, and the distal end of a flexible-tip exchange catheter (available only on the double-lumen exchange catheter). Notice that there are two distal side holes and one end hole. B, Two Rapi-Fit adapters: a Luer-Lok jet adapter (right) and a 15-mm connector (left).

(Courtesy of Cook Critical Care, Bloomington, IN.)

Atlas and Mort examined the relationship between the diameter of the two larger CAECs and tolerance, as well as the ability to phonate and cough.³³⁴ It is unclear whether their patients were randomly assigned to specific sizes of catheters. Phonation and discomfort were similar in both groups, with only 3 of 101 patients experiencing significant discomfort. Cough effort tended to be reduced with the larger CAEC, but this did not achieve significance. Atlas and colleagues also looked at a larger tube exchanger (JEM 400 Endotracheal Tube Changer, Instrumentation Industries Inc.), which they reasoned would have a higher degree of success as a tube exchanger. This device has an OD of 6.35 mm and is said to be stiffer. They adapted the JEM 400 using the Rapi-Fit connector from the CAEC 19-83 to enable jet ventilation.³³⁵ This device, like the Sheridan JETTX, has only a single end-hole and is not recommended for jet ventilation.

Mort evaluated the concept of reversible extubation in patients with difficult airways.³³⁶ From an institutional database, he identified patients who were extubated in the operating room, PACU, or ICU with a CAEC. The tube exchanger was left in place until the need for reintubation was considered unlikely. Over a 9-year period, 354 patients qualified. Two groups emerged: those who required reintubation while the AEC was still in place and another group who required reintubation within 7 days but after the AEC had been removed. Airway-related complications were compared for the two groups. The AEC dwell time was a mean of 3.9 hours (range, 5 minutes to 72 hours). Of 354 patients, 288 were extubated in the ICU and had previously required three or more laryngoscopic attempts or alternative devices to achieve intubation. Comparing the overall success rate in the two groups, 47 of 51 patients in the AEC group were successfully reintubated, 87% on the first attempt. The four failures in this group resulted from inadvertent removal of the AEC in three; one patient was rescued with an intubating LMA and flexible bronchoscope. Mild (SpO₂ < 90%) and severe hypoxia (<70%) were experienced by three and four patients, respectively. Of the 37 patients requiring reintubation without an AEC, the first pass success rate was only 14%, with mild and severe hypoxia in 50% and 19%, respectively; three or more laryngoscopy attempts in 28 of 36 patients; and the need for a rescue device in 32 of 36 patients.³³⁶ In all cases, reintubation was attempted by a member of an anesthesia airway team: an attending anesthesiologist or a resident under direct supervision. Although reintubation over an AEC does not guarantee first-pass success, this strategy was strikingly more effective (87% versus 14% first-pass success) and had far fewer life-threatening complications.

3 Arndt Airway Exchange Catheter

The Arndt Airway Exchange Catheter (Cook Critical Care), a radiopaque exchange catheter, consists of an extrastiff Amplatz guidewire with positioning marks, a Rapi-Fit adapter, a bronchoscopic port, and a distally tapered 14-F (4.7-mm-OD), 70-cm-long AEC. It was designed for the exchange of LMAs, endobronchial tubes, and ETTs (Fig. 50-6). Bronchoscopy is performed through the existing airway device. The flexible end of the Amplatz guidewire is introduced through the working channel of the bronchoscope and under visual control and is advanced to the level of the carina. The bronchoscope is removed over the wire, taking care that it is neither advanced nor withdrawn. The Arndt AEC is advanced over the guidewire to the appropriate depth, determined by aligning the distance markings on the airway device with that of the AEC. The original airway is carefully removed, and its replacement is advanced over the AEC.³⁰⁹

Figure 50-6 The Arndt Airway Exchange Catheter Set (Cook Critical Care, Bloomington, IN) consists of a bronchoscopic adapter, a stiff Amplatz guidewire, a tapered airway exchange catheter, and two Rapi-Fit adapters. The adapter permits continuation of positive pressure ventilation while a bronchoscope is introduced through the original endotracheal tube (ETT). The guidewire is inserted through the bronchoscope’s working channel, and the original ETT and bronchoscope are withdrawn. A tapered exchange catheter is advanced over the guidewire, and it may be connected with a 15-mm or jet Rapi-Fit adapter to provide ventilation. The replacement ETT is then advanced over the exchange catheter.

4 Endotracheal Ventilation Catheter

Cardiomed’s Endotracheal Ventilation Catheter (Lindsay, Ontario, Canada) is made of a hybrid plastic (Fig. 50-7). It is 85 cm long and has a 4-mm OD (12 F) and 3-mm ID. It has a radiopaque stripe along its entire length and distance markings at 4-cm intervals. Proximally, it has a male hose barb with a threaded adapter welded into the catheter. These attachments have been constructed to prevent restriction of the catheter’s ID. The threaded adapter connects to an easily removed Luer-Lok adapter. Distally, it is blunt ended with one end hole and eight helically arranged side holes to minimize catheter whip and jet ventilation pressures. Unpublished studies by the manufacturer found no significant softening over time at body temperature. This is desirable for a product that may remain in situ and be required to serve as a stylet. A metal guidewire is available to provide additional stiffness, but we have not found this to be necessary.

Figure 50-7 The Endotracheal Ventilation Catheter (ETVC) is available in one length (85 cm) with an outside diameter of 4 mm. It is nonthermolabile and has a radiopaque stripe along its length. There are distance markings every 4 cm. A, Proximally, there is a welded, barbed, plastic connector with a threaded Luer-Lok adapter for jet ventilation. B, Distally, there is a blunt end hole with eight helically arranged side holes, which minimize catheter whip and reduce the jet injection pressure.

The ETVC was designed to facilitate reversible extubation.³³⁷ We have used it in at least 600 patients, the first 202 of whom has been reported.³³⁸ Although the ETVC had been used to facilitate reintubation, this was not required in most cases. In the original series, reintubation or tube exchange was performed in 32 (16%) of 202 cases, a rate that was very similar to that reported by others.³³⁹ In both series, the ETVC³³⁸ and the CAEC³³⁹ were used primarily to maintain airway access. In the original publication, the ETVC was used for oxygen insufflation (31 patients), jet ventilation (45 patients), and post-extubation capnography (54 patients).³³⁸

Reintubation was successful in 20 (91%) of 22 attempts. One failure occurred with a softer prototype. The second failure resulted when an inexperienced and unsupervised operator attempted a tube exchange. Difficulty was occasionally encountered advancing the ETT through the glottis, similar to that experienced when using an FOB to intubate.³⁴⁰ Tongue retraction with a laryngoscope blade should always be attempted when possible. ETT rotation or the use of an ETT such as the Parker Flex-Tip (Parker Medical, Boulder, CO) may prove useful. Because the ETVC has a relatively small OD, use of a smaller-diameter ETT is recommended.

Oxygen insufflation was achieved by connecting the male component of the ETVC to an oxygen flowmeter with 1 to 2 L/min flow rate, which was titrated to the arterial saturation. Jet ventilation is discussed later.

Complications included barotrauma, intolerance, unintended dislodgment, and tracheal perforation. Intolerance occurred in 2 of 202 patients (typically because of carinal irritation) and in 1 patient recently recovered from status asthmaticus. Intolerance should prompt reassessment of the depth of insertion. If the depth is clinically or radiographically appropriate, and the ETVC (or other AEC) continues to be required, tolerance usually can be achieved by instilling lidocaine through the device. Most patients, including those with reactive airways, have tolerated the ETVC without difficulty. Dislodgement occurred when the ETVC was inadequately secured or the patient “tongued” the catheter out. Proper fixation is essential (see Fig. 50-3). Tracheal or bronchial perforation with different instrumentation has been described.^325,326 In our case, it occurred in a patient with obstructing, proliferative tracheal papillomatosis and a chronic tracheostomy. A rigid prototype catheter was inserted alongside the tracheostomy, penetrating the posterior tracheal wall. Jet ventilation resulted in fatal barotrauma. Aspiration and laryngospasm have not been observed.

1 Visually Assisted Tube Exchange

It is difficult to imagine a safer or more secure confirmation of a tube exchange than seeing one tube replace another. This is not always possible, but it sometimes may be achieved by combining techniques, such as indirect laryngoscopy (video laryngoscopy) with a tube exchanger, thereby providing security, visual verification, and a means of correcting difficulties with tube advancement.

The recently discontinued WuScope (Achi Corp., Fremont, CA, and Asahi Optical, Tokyo, Japan) has been used to exchange double-lumen tubes and conventional ETTs in patients with difficult airways.^344–346 The WuScope provided a good glottic view in a morbidly obese patient with adult respiratory distress syndrome and permitted insertion of a suction catheter anterior to the existing nasotracheal tube. The nasotracheal tube was withdrawn, and the replacement oral ETT was easily advanced over the suction catheter with minimal interruption of mechanical ventilation. We think that a visually direct tube exchange with a WuScope, Bullard Scope (Circon, Santa Barbara, CA), Upsher UltraScope (Mercury Medical, Clearwater, FL), or video laryngoscope is preferable to blind passage of an ETT over a flexible bronchoscope or tube exchanger. A hollow tube exchanger, however, would have permitted oxygen insufflation or jet ventilation had desaturation or difficulties with tube advancement occurred. A supraglottic view (in contrast to the infraglottic view provided by a flexible bronchoscope) of the exchange enables identification and correction of an ETT impingement or the outward migration of the exchange catheter.³⁴⁷

The concept of visually direct tube exchange was assessed retrospectively in a population in whom no view of the larynx could be obtained by direct laryngoscopy.³⁴⁸ Using one of three indirect laryngoscopes—the Glidescope (Verathon Medical, Bothell WA), Airtraq (Prodol Meditec, Vizcaya, Spain), or McGrath Series 5 (Aircraft Medical, Edinburgh, Scotland)—in conjunction with an AEC, 51 exchanges were performed. Four of the cases involved a double-lumen tube converted to a conventional ETT or a nasal to oral conversion. Thirty-seven patients had previously difficult intubations requiring multiple attempts or a rescue technique. Most of the patients were obese or morbidly obese and had a positive fluid balance of more than 10 L over the previous 4 days. The intention of the study was not to compare the specific devices but rather to evaluate the advantages of visually directing the tube exchange. Mort reported that this was achieved on the first attempt in 47 of 49 patients.³⁴⁸ In the two failures, use of the Glidescope video laryngoscope afforded an excellent view of the AEC migrating cephalad, allowing rapid reintubation with a styletted ETT. He pointed out that had the tube exchange been performed blindly, the replacement would have failed, with potentially serious consequences. Others have made similar observations.^349,350 These findings and our personal experiences are consistent with Mort’s recommendations.

2 Conversion from Nasal to Oral Intubation

Blind or bronchoscopically assisted nasal intubation is sometimes performed when oral approaches are difficult or unsuccessful. The nasal tube may have to be converted to an oral one because of complications or the intended surgery. Whenever possible, this should be done under visual control, assisted by a flexible bronchoscope,³⁵¹ rigid fiberoptic device, or video or optical laryngoscope.^344,348 The more anatomically or physiologically challenging the patient, the more compelling the case for including a tube exchanger.

Gabriel and Azocar described a patient in halo fixation in whom the connector was detached and the nasotracheal tube was advanced deeper into the trachea.³⁵² The tube was then grasped close to the uvula with forceps and digitally extracted through the mouth. Novella used a Sheridan T.T.X. to convert a nasal to an oral tube in a patient with Klippel-Feil syndrome who first underwent orthognathic surgery and subsequent septorhinoplasty.³⁵³ After completion of orthognathic surgery, the T.T.X. was inserted into the nasal tracheal tube, and the latter was withdrawn. The T.T.X. was then grasped with two Magill forceps; the caudal one was used to stabilize the catheter, and the cephalad one was used to withdraw the proximal end out of the mouth. An oral tube was then railroaded over the T.T.X. Cooper described a similar maneuver in a patient in whom oral fiberoptic intubation could not be accomplished, but fiberoptic nasal intubation was achieved.³⁵⁴ He passed an ETVC through the existing nasal tube and removed the latter. The ETVC was then stabilized with caudal Magill forceps and withdrawn through the mouth with the cephalad forceps. Oxygen insufflation was provided through the ETVC, which was then used to thread an oral tube into the trachea. In this case, oxygen desaturation was avoided, although the procedure was easily and quickly accomplished.

3 Conversion from Oral to Nasal Intubation

During efforts to convert from an oral to a nasal tracheal tube, Sumiyoshi and coworkers used negative-pressure ventilation during the tube exchange.³⁵⁵ Their patient was in a halo and chest cast due to a cervical injury, and laryngoscopy had been unsuccessful. An attempt to introduce a 4.8-mm FOB adjacent to the existing tube (with a tube exchanger through it) was unsuccessful. A subsequent effort involved a 3.5-mm FOB and a 7-F METTRO using negative pressure to achieve ventilation. A smaller, hollow tube exchanger might have been successful and could have avoided the risk of negative-pressure pulmonary edema resulting from an ETT and FOB occupying a small glottic opening.³⁵⁶ Smith and Fenner performed an oral to nasal conversion using a 4.0-mm-OD, flexible bronchoscope, which they inserted through the glottis and anterior to an oral tube.³⁵⁷ The oral tube was withdrawn, and a nasal tube was advanced over the FOB. Many of the difficulties in performing a tube exchange can be avoided with the use of indirect (fiberoptic or video) laryngoscopes, ideally in combination with AECs.

4 Conversion from Supraglottic Airways to Endotracheal Tubes

A discussion of the conversion of various SGAs to ETTs is beyond the scope of this chapter, but the process is addressed elsewhere. Whenever possible, this conversion should be facilitated by visual guidance, using direct laryngoscopy or an indirect technique. These techniques include the use of a flexible bronchoscope and Aintree catheter or a video laryngoscope.^358,359

5 Changing Tracheostomy Tubes

A tracheostomy tube may need to be replaced because of tube damage, such as cuff rupture, occlusion with secretions, or conversion to another type or size of tracheostomy tube. If the tracheostomy was recently performed, the tissue is friable. In patients in whom a false passage has been created during the original procedure, in those with poor tissue integrity, or those highly dependent on supplemental oxygen, exchanging the tracheostomy tube can be difficult and fraught with complications. The Weinmann Tracheostomy Exchange Set (Cook Critical Care) (Fig. 50-8), consists of a Ciaglia Blue Rhino tracheostomy dilator, a CAEC, Rapi-Fit adapter, and two loading dilators (26 and 28 F). The 45-cm-long exchange catheter is passed through the tracheostomy tube to be replaced; its cuff is deflated, and the tube is removed over the exchange catheter. The replacement tracheostomy tube and its loading dilator are placed over the AEC, which is connected to the Rapi-Fit adapter, permitting ventilation as required. The loading catheter and tracheostomy catheter are advanced using the AEC as a guide. If stomal dilatation is required, the set is equipped with Ciglia Blue Rhino dilators (32 to 38 F).³⁶⁰ The only description of this device advocates jet ventilation and high-flow oxygen insufflation. AEC insertion must be atraumatic, confirmed with a carbon dioxide (CO₂) tracing, and the depth verified to ensure it is not beyond the carina. Only the amount of oxygen (O₂) required to prevent significant oxygen desaturation should be supplied.

Figure 50-8 Weinmann Tracheostomy Exchange Set.

(Courtesy of Cook Critical Care, Bloomington, IN.)