Extubation and Reintubation of the Difficult Airway

Postextubation stridor

Several of the complications of tracheal intubation may not be apparent while the patient remains intubated. Although anatomic or functional laryngeal problems are more likely to develop as a consequence of multiple, prolonged, or blind intubation attempts, glottic or tracheal injury may also occur despite a good laryngoscopic view or during awake bronchoscopic intubation. Airway injuries may range from those that are subtle and reversible to the more extreme that necessitate reintubation. They include laryngeal edema, ulceration, laceration, hematoma, granuloma formation, vocal fold immobility, tracheal and esophageal perforation, and subluxation or dislocation of the arytenoid cartilages. Reports often omit details regarding the ETT size, cuff type, methods of cuff inflation, laryngoscopist, or clinical context. A recent systematic review detailed the findings of 21 publications involving over 6000 patients restricted to prospective studies involving adults undergoing elective surgical procedures with postoperative laryngeal examination. The incidence of edema ranged from 9% to 84% and was identified in the following locations in decreasing prevalence: arytenoid, interarytenoid, vocal folds, Reinke’s space, postcricoid, and unspecified locations. The study did not specify whether any patients required reintubation despite identifying some with arytenoid subluxation and vocal cord paralysis. Most of the injuries were short lived, resolving without intervention; however, 4% to 5% of the injuries were classified as moderate to severe. Presumably, patients requiring emergent or prolonged intubation are more susceptible to laryngeal injury.

Upper airway edema is a pathologic diagnosis, suggested by postextubation stridor resulting in turbulent flow due to decreased caliber of the airway lumen. The resultant increased work of breathing (WOB) may culminate in respiratory failure. The reported incidence of postextubation respiratory failure associated with stridor in ICU populations ranges from 1.8% to 31%. Recognition of patients at risk of failing extubation due to airway edema is challenging and has involved inspection, the cuff leak test, and ultrasonography (USG). Management of airway edema depends on its severity. This may involve the use of a lower-density helium/oxygen blend (heliox), aerosolized epinephrine, or reintubation.

The cuff leak test has been advocated as a tool to predict postextubation stridor. The test can be performed in a variety of ways with results of variable predictive value. Essentially, the test determines the adequacy of airflow around an occluded ETT after the cuff is deflated. It can be performed qualitatively by simply listening during exhalation, or quantitatively by comparing the difference between inspiratory tidal volume and the average expiratory volume. The sensitivity and specificity of this test will depend upon the cutoff value chosen, but other factors undoubtedly come into play, such as compliance of the respiratory system and the mechanical forces the patient is able to generate. The presence of a leak reduces the likelihood of postextubation stridor and subsequent need for reintubation. ^, Patients with postextubation stridor required reintubation in 18% of cases compared with 7.9% of patients without stridor. Reintubation was usually required within a median of 2 hours (range 1–6) in those with stridor, compared with 20 hours in those without (3–43 hours). Although the cuff leak test is recommended in higher-risk patients, it has “limited diagnostic power” with moderate sensitivity and excellent specificity. A quantitative test is more discriminating, but performance depends upon the selected cutoff value (leak volume) and the population being studied. If no cuff leak is identified, deferral of extubation might be prudent until conditions improve, especially if the airway is anatomically challenging or the patient is physiologically marginal.

USG can be used to better define the amount of space between the vocal cords and the ETT. This space was found to be significantly less in patients who subsequently develop postextubation stridor, though the sensitivity and specificity of this diagnostic application vary widely across studies. Several studies have compared USG with the cuff leak test ; however, the findings must be interpreted cautiously since so few patients with stridor were included. A large study involving 400 ventilated children, 44 of whom exhibited postextubation stridor, observed significant decreases in the quantitative cuff leak and the ultrasound-measured air column around the ETT in those who subsequently exhibited stridor. The ultrasonographic assessment demonstrated higher sensitivity and specificity. ^, Video-assisted laryngoscopy (VAL) can be used as a tool to record the laryngeal anatomy and clinical progress, but one must be very cautious in using this as a predictive tool of postextubation stridor, as the ability to accurately assess the anatomy is limited while the ETT remains in situ.

It is unlikely that laryngeal edema can be eliminated, but it may be possible to minimize it by attempting to achieve a visually controlled, atraumatic intubation with an appropriately sized ETT, a compliant cuff inflated just sufficiently to achieve a seal (with cuff-pressure manometry), minimizing the duration of intubation, optimizing patient positioning, and timely administration of IV corticosteroids. The benefits of corticosteroids with respect to postextubation stridor and the reintubation rate have been variable and likely depend upon patient selection, the steroid used, the dose, its timing, and when and if the dose is repeated. A meta-analysis of three randomized controlled trials involving patients with no cuff leak found that corticosteroids were associated with a reduced rate of reintubation and postextubation stridor. To be effective, these must be given in adequate doses, sufficiently before and, often enough, following extubation.

As mentioned, in the face of airway swelling or postextubation stridor, temporizing measures, such as head-up positioning, nebulized epinephrine, and heliox may be of some value. The efficacy of NIPPV in the symptomatic patient following extubation will depend upon the severity of the respiratory difficulty and the preexisting factors. Large-scale studies have not looked specifically at patients who fail as a consequence of laryngeal edema. One meta-analysis found that NIPPV had a greater effect on reducing reintubation rates in postoperative patients compared with ICU patients (odds ratio 0.24 [95% CI, 0.12–0.50] vs 0.72 [0.51–1.02]). Another meta-analysis concluded that, compared with standard medical therapy, the risk of reintubation was not significantly reduced by the use of NIPPV. A prospective study comparing NIPPV with standard medical therapy, involving 37 centers in 8 countries, failed to demonstrate benefit with respect to reducing reintubation; in fact, the study was stopped prematurely because of an increased mortality rate in the NIPPV group.

Laryngospasm

Laryngospasm involves bilateral adduction of the true vocal cords, vestibular folds, and/or aryepiglottic folds. This is protective to the extent that it prevents aspiration of solids and liquids; it becomes maladaptive when sustained or restrictive of ventilation and oxygenation. The intrinsic laryngeal muscles are the main mediators of laryngospasm, and they include the cricothyroid, lateral cricoarytenoid, and thyroarytenoid muscles. The cricothyroid muscles are the vocal cord tensors, an action mediated by the superior laryngeal nerve (SLN).

The diagnosis of laryngospasm is based upon visualization of laryngeal and supraglottic closure with inspiratory stridor, paradoxical breathing, and suprasternal retraction. Laryngospasm is believed to be a common cause of postextubation airway obstruction, particularly in children. Even in adults, Rose and colleagues stated that it accounted for 23.3% of critical postoperative respiratory events, although the diagnosis was presumptive. Emergency surgery, nasogastric tubes, and surgery for tonsillectomy, cervical dilation, hypospadias correction, oral endoscopy, or excision of skin lesions appear to be risk factors. The triggers are generally noxious but nonspecific, including vagal, trigeminal, auditory, phrenic, sciatic, and splanchnic nerve stimulation; cervical flexion or extension with an in situ ETT; or vocal cord irritation from blood, vomitus, or oral secretions. A risk assessment questionnaire was used to prospectively study over 9000 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 4-fold 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. In this study, twice as many children were managed with a laryngeal mask airway (LMA) than with 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, although this contradicts conventional teaching.

Nevertheless, it is widely believed that prevention of laryngospasm is best achieved by extubating at a sufficiently deep plane of anesthesia or awaiting recovery of consciousness. 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 together more tightly. Larson described a technique of applying firm digital pressure to the “laryngospasm notch” between the ascending mandibular ramus and the mastoid process, stating that this technique is rapid and highly effective. Very small doses of a short-acting neuromuscular blocking drug (NMBD) with or without reintubation may be necessary. ^, Recently, a case report described the successful use of transnasal humidified rapid-insufflation ventilatory exchange (THRIVE) in a patient with refractory laryngospasm, circumventing the need for reintubation.

Macroglossia

Macroglossia, or severe enlargement of the tongue, can result in airway obstruction and increase the risk of extubation failure. One cause is angioedema, which may be caused by a hereditary or acquired deficiency of C1-esterase inhibitor. These cases are usually recurrent with varying severity; oropharyngeal involvement is less common but can be life-threatening when encountered. Most other cases of angioedema are mediated by mast cells, which release histamine, heparin, leukotriene, and prostaglandin, enhancing capillary permeability and producing tissue edema. It may be triggered by exercise or an allergic reaction to food, latex, or drugs, most commonly to angiotensin-converting enzyme inhibitors or angiotensin receptor blockers, aspirin, or nonsteroidal anti-inflammatory drugs (NSAIDs). ^, Although involvement of the tongue is the most obvious manifestation, the uvula, soft tissues, and larynx may also be affected.

Massive tongue swelling also can complicate prolonged posterior fossa surgery performed with the patient in the sitting, prone, or park bench position and steep or prolonged Trendelenburg positioning. Robotic surgery, coupling extreme Trendelenburg positioning with peritoneal insufflation, can also give rise to facial and airway swelling. Likewise, transoral placement of robotic instrumentation into a confined space may result in compressive injuries to the tongue and other oral structures. Other causes of macroglossia include hypothyroidism, acromegaly, lymphangioma, idiopathic hyperplasia, metabolic disorders, amyloidosis, cystic hygroma, neurofibromatosis, rhabdomyosarcoma, sublingual or submandibular infections, and chromosomal abnormalities such as Beckwith-Wiedemann syndrome.

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. Macroglossia may result from venous or lymphatic compression leading to immediate swelling or arterial insufficiency and subsequent reperfusion injury.

Laryngeal or Tracheal Injury

Airway injuries from the lips to the distal trachea can include lacerations, edema, arytenoid dislocation, and vocal fold damage. The lip or tongue may be compressed between the laryngoscope blade and the maxillary teeth, resulting in swelling or bleeding, although this is unlikely to be severe enough to delay or complicate extubation. The glottis may be injured as a result of the blind advancement of the ETT. This probably results in universal swelling or mucosal erosion of varying degrees to the posteromedial larynx that is largely unrecognized. The trachea can be lacerated or penetrated by the ETT or its introducer or by ischemic compression of the tracheal mucosa by the cuff. Arytenoids may become dislocated during difficult intubation efforts. Palatopharyngeal injuries have been described as a consequence of blind insertion of an ETT during VAL. ^, The epiglottis can be downfolded during placement of an ETT, the consequences of which are unknown. ^, Although these injuries are not often apparent at the time of intubation or SGA placement, they are typically managed conservatively and should not complicate extubation.

Laryngeal injuries accounted for 33% of all airway injury claims and 6% of all claims in the ASA Closed Claims Project database. These range from transient hoarseness to vocal fold paralysis. Even when direct laryngoscopy (DL) provides a satisfactory glottic view or intubation is facilitated by flexible bronchosopy, ^, airway injury can occur and go unsuspected until after the ETT is removed or only when symptoms prompt further investigation. 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 described as difficult. ^, The Closed Claims Project observed that difficult intubations were more likely to result in injuries to the pharynx and esophagus than to the trachea.

Vocal fold immobility can result from injury to the recurrent laryngeal nerve or the arytenoid cartilages. ^{, ,} Arytenoid immobility has resulted from seemingly uneventful DL, double-lumen tube (DLT) insertion, and lighted stylet intubation. In a prospective study involving over 3000 intubations, postoperative hoarseness was observed in approximately half of intubated patients on the day of surgery, persisting to days 3 and 7 in 11% and 0.8% of patients, respectively. ^, Three patients (<0.1%) had arytenoid dislocation, and four had vocal cord paralysis. ^, Arytenoid dislocation is confirmed by endoscopic visualization of an immobile vocal cord associated with a rotated arytenoid cartilage. ^, If the diagnosis is made prior to the onset of ankylosis, it may be possible to manipulate the arytenoid back into position.

Vocal fold paralysis results from injury to the vagus nerve or one of its branches (i.e., the recurrent laryngeal nerve [RLN] or external division of the SLN [ex-SLN]) and may resemble arytenoid dislocation or ankylosis. Differentiation may require palpation of the cricoarytenoid joints under anesthesia or laryngeal electromyography. 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 postulated that an overinflated ETT cuff might result in injury to the anterior divisions of the RLN. ^,

The RLN supplies all 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 weak, breathy voice but no obstruction and usually resolves within days to months. Bilateral ex-SLN injury causes the epiglottis to overhang, and the vocal cords may appear bowed and lacking in tension. This does not produce obstruction. The vocal quality is hoarse with a reduction in volume and range. Unilateral RLN injury causes the affected vocal fold to assume a fixed paramedian position and may produce a hoarse voice or weak cough, though many patients with unilateral vocal cord paralysis are asymptomatic. Bilateral RLN injury results in both vocal folds being fixed in the paramedian position and inspiratory stridor, often necessitating a surgical airway. ^,

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 can heal with fibrous adhesions leading to vocal cord fixation. An otolaryngologist should assess a patient with persistent postextubation hoarseness, a breathy voice, or an ineffective cough.

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 passage of a gum elastic bougie, nasogastric tube, nasotracheal tube, orotracheal tube, suction catheter, esophageal stethoscope, esophageal temperature probe, or transesophageal echocardiogram probe. Penetrating injuries can communicate with the esophagus, resulting in a tracheoesophageal fistula, or with the mediastinum, resulting in mediastinitis, retropharyngeal abscess, or death.

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.

Postobstructive Pulmonary Edema

Severe airway obstruction from any cause and at any anatomic level may complicate extubation by leading to postobstructive pulmonary edema (POPE), also called negative-pressure pulmonary edema. ^, This occurs when a forceful inspiratory effort is made against an obstructed airway (also known as the Mueller maneuver). The most common causes include a closed glottis, occlusive biting on an SGA or ETT, laryngospasm, bilateral vocal cord paralysis, croup, or epiglottitis. A strong inspiratory effort results in large negative intrapleural pressures, promoting venous return. ^, Type I POPE can occur with the onset of obstruction (e.g., laryngospasm, croup, epiglottitis, foreign body aspiration, hanging, biting, or neck hematoma). Type II POPE (reexpansion pulmonary edema) is seen following relief of the obstruction (e.g., chronic partial obstruction from enlarged tonsils, adenoids, or a laryngeal mass). The consequences of the Mueller maneuver include increased venous return, leftward shift of the interatrial and interventricular septa, decreased left ventricular compliance, and elevated pulmonary pressures and flow. The increased negative intrapleural pressure coupled with the increased hydrostatic pressure promotes transudation of fluid, resulting in pulmonary interstitial and alveolar edema.

Perioperatively, Type I POPE most commonly occurs in healthy patients capable of generating large negative intrathoracic pressures when inhaling against airway obstruction caused by occlusive biting on an ETT or SGA. Fortunately, this can be prevented by the routine placement of a bite block prior to awakening. Care must be taken not to place this as the patient is emerging from anesthesia as it may provoke more biting, dental damage, a gag reflex, or regurgitation. An effective bite block might be fashioned from a roll of gauze wrapped by tape with a “tail” to prevent its aspiration.

Type II POPE follows relief of the obstruction and occurs as follows: An expiratory effort opposed by an obstructed airway (i.e., a Valsalva maneuver) reduces venous return and raises intrapleural and alveolar pressures. With relief of the obstruction, the sudden increase in preload elevates the hydrostatic pressures leading to pulmonary edema. This state is exacerbated by circumstances promoting pulmonary vasoconstriction, such as hypothermia, hypercapnia, hypoxia, and adrenergic stimulation.

POPE typically has a rapid onset. The diagnosis should be suspected when tachypnea, crackles, rhonchi, frothy sputum, hypoxemia, and diffuse pulmonary infiltrates are observed following the relief of upper airway obstruction. The diagnosis is supported by the clinical context, exclusion of other more common causes, and more rapid resolution than that typically seen with other causes of pulmonary edema. Other than ensuring airway patency, treatment primarily consists of positive pressure ventilation (including NIPPV); diuresis is only appropriate when there is associated volume overload. ^,