Chapter 34. Upper Airway Obstruction

• Suspected upper airway obstruction(UAO) constitutes a medical emergency. The immediate bedside consultation of a clinician experienced in the management of this condition is indicated.
• The initial evaluation of UAO is focused on determining the severity and suspected site of the obstruction. Arterial desaturation is a late manifestation; better indicators of severity include stridor, poor air movement, accessory muscle use, abnormal mentation or agitation, tachycardia, hypertension, and pulsus paradoxus.
• Infections represent important causes of oropharyngeal and hypopharyngeal UAO and include Ludwig angina, peritonsillar abscess, and infections of the retropharyngeal and lateral pharyngeal spaces. Otolaryngology consultation is indicated. Depending on the initial site of infection, spread to other critical sites (e.g., the mediastinum) may occur.
• While intubation is not always required in adults with epiglottitis, management in an ICU is mandatory, and intubation equipment and a tracheostomy tray should be at the bedside.
• Bacterial infections of the larynx are life-threatening. Causative organisms includeStaphylococcus aureus, Streptococcus pneumoniae, Haemophilus influenzae, andCorynebacterium diphtheriae.
• Laryngospasm and laryngeal edema are important causes of postextubation stridor. Prophylactic corticosteroids have not shown a benefit in preventing postextubation stridor. A short (48 hours) course of corticosteroids is reasonable to treat established cases of laryngeal edema.
• Long-term intubation may result in a variety of problems related to the upper airway, including endotracheal tube obstruction from secretions, vocal cord injury, subglottic stenosis, and tracheal stenosis.
• Risk factors for foreign body aspiration in adults include diminished level of consciousness; impaired swallowing mechanism or diminished upper airway sensation as a result of neuromuscular disorder, prior cerebrovascular accident, or advanced age; and inability to chew food properly because of poor dentition.
• All suspected traumatic laryngeal injuries should be evaluated promptly to reduce the immediate risk of UAO, as well as to prevent long-term sequelae such as subglottic stenosis.
• Early laryngoscopic examination of the upper airway is crucial in the evaluation of burn patients with suspected inhalation injury. The risk of UAO increases throughout the first 24 hours.
• Functional upper airway obstruction may occur in patients who exhibit abnormal glottic closure during inspiration and/or expiration. There is a high risk of coincident asthma, complicating the evaluation of such patients.
• Angioedema may result from allergy, hereditary or acquired disorders of the complement cascade, direct release of histamine from mast cells from nonallergic mechanisms (e.g., opiates), and from angiotensin-converting enzyme inhibitors.
• Angioedema from angiotensin-converting enzyme inhibitors may occur at any time during the course of therapy.
• Helium-oxygen mixtures reduce the density-dependent pressure required to drive airflow across obstructing upper airway lesions, and may stabilize patients with UAO pending definitive therapy.
• Prompt evaluation and management of suspected UAO may prevent subsequent complications including cardiac arrest, anoxic brain injury, and negative pressure pulmonary edema.

There are few medical conditions that are as rapidly and predictably lethal as the loss of upper airway patency. Because of the relative infrequency with which upper airway obstruction (UAO) is encountered by most physicians, opportunities to acquire significant clinical experience are limited. This, combined with the frequently subtle presentation of upper airway obstruction and the clinician's inability to visualize the upper airway in its entire extent through routine physical examination, may hamper diagnosis of this condition until a crisis results. This chapter describes an approach to diagnosing and treating UAO as it presents in adults. While certain infections of the head, neck, and upper respiratory tract are considered here as they relate to UAO, the specific approach to their management is considered in greater detail in Chap. 54. A high index of suspicion for UAO, combined with early consultation of anesthesia and otolaryngology services, is critical to the successful management of this condition.

The upper airway comprises air-conducting passages that begin at the mouth or nose and end at the mainstem carina.1,2 The thoracic inlet divides the upper airway into the intrathoracic and extrathoracic airways. The extrathoracic airways are further divided into the nasopharynx, oropharynx, hypopharynx, larynx, and extrathoracic trachea. Air inspired through the nose passes through the nasal cavities and enters the nasopharynx after exiting the nose by way of the posterior nares. Airflow proceeds inferiorly through the nasopharynx, passes posterior to the soft palate, and enters the oropharynx. Closure of the soft palate allows inspiration of air through the mouth. Air passes inferiorly through the oropharynx to the hypopharynx, which begins just superior to the hyoid bone, and passes the epiglottis, thereby entering the larynx.

The larynx is constructed of a cartilaginous skeleton consisting of the thyroid, cricoid, and arytenoid cartilages (Fig. 34-1). This skeleton surrounds the vocal cords, the movements of which are controlled by the intrinsic muscles of the larynx, with their innervation arising from the left and right branches of the recurrent laryngeal nerve. An exception to this rule is the innervation of the cricothyroid muscle, which arises from the superior laryngeal nerve. This nerve also supplies sensation to the epiglottis and vestibular folds (false cords), which lie superior to the true vocal cords. The larynx is divided into the supraglottic portion, the glottis, and the subglottic portion. The glottis contains the structures within the plane of the true vocal cords and is located at the midpoint of the thyroid cartilage. The supraglottic region extends from the epiglottis to just above the true vocal cords, while the subglottic region lies between the vocal cords and the lower border of the cricoid cartilage.

The trachea lies between the inferior border of the cricoid cartilage and the main carina, and is 10 to 13 cm in length in adults. The extrathoracic trachea is typically 2 to 4 cm long, and comprises the segment that lies between the cricoid cartilage and the thoracic inlet. The normal trachea has roughly the same coronal as sagittal diameter. Normal coronal tracheal diameter is 13 to 25 mm in men and 10 to 21 mm in women.

This chapter will focus on disorders of the extrathoracic upper airway because of this region's greater importance to the topic of UAO.

While obstruction may occur at any point in the upper airway, laryngeal obstruction is most problematic because the airway is narrowest at this point. The glottis is the narrowest region in adults, while the subglottic region is the narrowest in infants. The basis for which seemingly minor reductions in the cross-sectional area of the upper airway have important effects on airflow is presented below.

Alveolar ventilation is accomplished through the bulk flow of fresh gas down to the terminal bronchioles, at which point the cross-sectional area of the airways becomes so large that the forward velocity of gas molecules becomes negligible, and diffusive flow occurs.3 Airflow may be laminar, transitional, or turbulent. Laminar flow consists of orderly streams of gas arranged in lines parallel to the airway. At higher flow rates and at branch points flow may become transitional, with gas eddies that break away from the parallel streams. Turbulent flow is the most disorganized pattern, and occurs at high flow rates. The Reynolds number (Re) is a dimensionless number that derives from the ratio of inertial to viscous forces and allows prediction of whether flow will be laminar or not:

where r is the radius of the tube, v is the average gas velocity, d is the gas density, and μ is the gas viscosity. Values less than 2000 predict laminar flow, values between 2000 and 4000 predict transitional flow, and values greater than 4000 predict turbulent flow. The driving pressure for laminar flow is proportional to the flow rate and inversely related to the fourth power of the radius, among other factors. Thus a relatively minor decrease in the radius of a tube like the upper airway causes a large increase in the driving pressure necessary to achieve the same flow rate. Turbulent flow as occurs in a rough tube like the larynx and trachea requires greater driving pressure than laminar flow, being proportional to the density of the gas and the square of the flow rate. Inhalation of a low-density gas such as helium therefore decreases the driving pressure required for airflow through two mechanisms: reducing the Reynolds number, thereby increasing the proportion of flow that is laminar; and decreasing the density-dependent driving pressure where turbulent flow exists.4

The clinical implications of these principles are as follows: (1) Upper airway obstructing lesions, once symptomatic, can progress rapidly to a crisis with relatively small increases in size and consequent reduction in the size of the airway lumen; (2) while awaiting definitive treatment of the upper airway obstruction, inhalation of a low-density gas mixture such as helium-oxygen may stabilize the patient by decreasing the driving pressure required for a given airflow.

Upper airway obstructing lesions may limit inspiratory flow, expiratory flow, or both, depending on the site and nature of the lesion. Flow-volume loops obtained by spirometry are useful for understanding the physiology of different sites of upper airway obstruction.5

Variable Extrathoracic Obstruction

During normal inspiration the intrathoracic airways dilate, while the extrathoracic airways tend to collapse as the increase in gas velocity causes a fall in intraluminal pressure (Bernoulli effect). As gas velocity increases past an obstructing lesion, this effect is increased, causing flow limitation, with a reduction in peak inspiratory flow and a flattening of the inspiratory limb of the flow volume loop. In contrast, during forced expiration the intraluminal pressure is positive relative to the atmosphere, preserving expiratory flow. These lesions occur above the thoracic inlet and include bilateral vocal cord paralysis, paradoxical movement of the vocal cords, and tracheomalacia of the extrathoracic airway.

Variable Intrathoracic Obstruction

During forced expiration the intrathoracic airways have a tendency to narrow as a result of airway compression and the Bernoulli effect. This leads to a reduction in peak expiratory flow and a flattening of the expiratory limb of the flow volume loop. Inspiratory flow, in contrast, is preserved as lung expansion increases the radius of the airway at the site of the obstructing lesion. Common causes of variable intrathoracic obstruction include low tracheal tumors and tracheomalacia of the intrathoracic airway.6

Fixed Upper Airway Obstruction

Fixed upper airway obstruction occurs when airflow at the site of obstruction is insensitive to the effects of the respiratory cycle because the lesion imparts rigidity to the walls of the affected area. Affected patients have reductions in peak inspiratory and expiratory flow, while the flow volume loop depicts flattening of the inspiratory and expiratory limbs. Examples of this disorder include subglottic stenosis and some tumors.

Patients presenting with upper airway obstruction may complain of a variety of symptoms including hoarseness, stridor, hemoptysis, dysphagia, odynophagia, drooling, and swelling of the neck or face. Dyspnea is typically exacerbated by exercise, and in the case of certain diseases—for example, anterior mediastinal tumors—by the supine position. In many cases prior evaluations have yielded a diagnosis of asthma or chronic obstructive pulmonary disease. While certain disorders such as epiglottitis have very acute presentations, at times symptoms have developed so insidiously that the patient has habituated to the condition, and has few or no complaints.

If time permits, initial evaluation should include a history of the present illness, focusing on the duration of symptoms and any associated oropharyngeal, gastrointestinal, or constitutional symptoms, along with a history of prior upper aerodigestive tract disorders, recent dental problems or procedures, and smoking. Physical examination is directed toward localizing the site of the lesion.7 Inspiratory stridor generally indicates a lesion at or above the level of the glottis, while biphasic stridor (stridor present during both inspiration and expiration), which is usually higher in pitch, suggests a lesion at the subglottic or tracheal level. The presence of stridor indicates a severe degree of narrowing, typically to ≤6 mm. Supraglottic lesions may cause a muffling of the voice, while oral abscesses may cause a “hot potato voice” (i.e., the speech of someone who has a hot potato in his mouth). Hoarseness accompanies unilateral vocal cord paralysis. An oral examination should be performed, unless epiglottitis is suspected and skilled airway personnel are not present. The submental and submandibular regions should be palpated, along with the neck and cervical and supraclavicular lymph nodes.

The first priority in encountering a patient with suspected UAO is to determine the severity of obstruction. When the obstruction is severe and loss of the airway is feared, the airway should be secured by an experienced operator. Arterial desaturation is an extremely late sign of UAO in the patient with normal lungs, and often heralds a catastrophe. This is illustrated by the difficulty normal, untrained individuals have in achieving arterial desaturation during breath holding. Similarly, arterial blood gases provide little information beyond that obtained through the bedside assessment of an experienced clinician. Better indicators of severe airway obstruction include stridor, poor air movement, accessory muscle use, abnormal mentation or agitation, tachycardia, hypertension, and pulsus paradoxus. All patients with newly diagnosed UAO of more than trivial severity should be monitored in an ICU until treatment can be initiated or clinical stability can be determined.

If UAO is suspected but there is no immediate risk of losing the airway, further evaluation may employ a range of techniques, depending on the suspected diagnosis. Spirometry is useful in the elective evaluation of subacute to chronic UAO; however, because the airway must be narrowed to ≤8 mm in order to affect the flow volume loop, spirometry is relatively insensitive. Inspection of the flow volume loop for flattening of the inspiratory or expiratory limb is the most reliable spirometric indication of UAO, particularly when done by an experienced reader. Poor effort may mimic UAO. The report of patient effort by the technician and the reproducibility of the loops are useful in distinguishing poor effort from UAO. Spirometry may fail to detect even significant degrees of UAO in patients with severe chronic obstructive pulmonary disease.

Plain chest radiographs may demonstrate tracheal deviation from masses arising in the mediastinum or neck. Lateral neck films may suggest the diagnosis of croup or epiglottitis. Computed tomography (CT) is extremely useful in evaluating suspected tumors of the upper airway, and in characterizing the extent of upper airway soft tissue infections. Three-dimensional reconstruction is useful in identifying fixed anatomic abnormalities of the upper airway, such as tracheal stenosis, and in following the response to therapy.8 However, dynamically determined disorders such as tracheomalacia require direct visualization.

Endoscopic evaluation may be flexible or rigid. Rigid endoscopy is useful in the management of suspected foreign body aspiration. Flexible endoscopy may be performed via the oropharyngeal or nasopharyngeal route.

Nasal and Nasopharyngeal Causes

Benign and malignant masses of the nose and nasopharynx constitute important sources of morbidity, and occasionally, mortality. However, because ventilation can usually be maintained via the oropharyngeal route in these cases, they will not be discussed here.

Oropharyngeal Causes

Infectious Causes

Infectious etiologies represent relatively common causes of upper airway obstructing lesions. Ludwig angina is an infection of the submandibular space.9 The source of infection is usually a second or third mandibular molar tooth, with causative organisms representing typical oral flora: streptococci, staphylococci, and anaerobes. Gram-negative organisms should be considered as potential etiologies in patients with altered oral flora, such as immunocompromised patients and recipients of broad-spectrum antibiotics. Airway obstruction may result from elevation and posterior displacement of the tongue and supraglottic edema. The infection may extend to the lateral and retropharyngeal spaces, and subsequently along the carotid sheath and to the mediastinum.

Affected patients present with dysphagia, neck swelling (“bull neck”) and stiffness, trismus, drooling, and brawny induration of the floor of the mouth. Occasionally, crepitus of the submandibular area is present. Tooth pain or a history of recent tooth extraction is usual, but not invariable. While not all patients with Ludwig angina need to undergo endotracheal intubation or tracheostomy, the decision to observe the airway rather than secure it should not be made lightly, and should be made after consultation with an otolaryngologist. If intubation is deemed necessary, placement via a flexible fiberoptic approach may be useful in decreasing the risk of laryngospasm during the procedure. Treatment consists of antibiotic therapy, and in some patients, surgical drainage. Obviously, any infected teeth should be extracted.

Lymphatic drainage from the oropharynx, teeth, maxillary sinuses, and ears passes through the retropharyngeal space, predisposing it to infections from the ear, nose, and throat.10 While the space itself contains no vital structures, infection may extend into the mediastinum or epidural space, or provoke atlantoaxial dislocation. Whereas this condition usually follows an upper respiratory tract infection, pharyngitis, or otitis media in children, in adults the more common antecedent problems are odontogenic infection or procedures, or oral trauma. Patients present with throat and neck pain, and may have drooling or symptoms of upper airway obstruction. On occasion, infection may spread to the retropharyngeal space from the prevertebral space, such as with tuberculosis of the spine (Pott disease). The diagnosis may be made through a lateral neck radiograph; however, CT is advisable for helping define the boundaries of infection. Importantly, physical examination may fail to reveal any posterior pharyngeal swelling, highlighting the need for a high index of suspicion for this condition and further investigation via endoscopy or imaging. Treatment consists of antibiotics directed at oral flora (streptococci, staphylococci, anaerobes, and in some patients, gram-negative organisms), airway stabilization, and surgical exploration.

Because the lateral pharyngeal space is bounded by the retropharyngeal and submandibular spaces, it serves as a means of transmitting infections from diverse sources, as suggested previously. Again, infections in this space are typically treated with a combination of antibiotics and surgical drainage.

Peritonsillar abscesses are located between the tonsil and the superior constrictor muscle of the pharynx. Affected patients are typically young adults and have a history of prior tonsillitis; not surprisingly, Streptococcus species are most commonly isolated, along with other oral organisms. Presenting symptoms include sore throat, trismus, and voice change. Despite the prevalence of this disorder, there are several aspects of management that remain controversial.11 While steroids are occasionally administered to patients with peritonsillar abscess, there are no studies to support or refute their efficacy. Both needle aspiration and open abscess drainage with tonsillectomy (“quinsy tonsillectomy”) have been advocated as initial treatment, and both are effective. Complications include UAO and rarely, thrombophlebitis of the internal jugular vein, a condition known as Lemierre syndrome. This condition is usually associated with Fusobacterium necrophorum, but other oral flora may be responsible. Bacteremia and septic emboli may result. The role of anticoagulation in Lemierre syndrome is controversial.

Occasionally, tonsillar enlargement from infectious mononucleosis may be so significant as to obstruct the airway. Management consists of close observation of the airway in a monitored setting, and the administration of corticosteroids.

Other Causes

Angioedema from a variety of causes can involve the tongue and hypopharynx and threaten airway patency both above and at the level of the larynx. This disorder is discussed below along with other disorders of the larynx. Stevens-Johnson syndrome and toxic epidermal necrolysis are rare vesiculobullous diseases that involve the skin and mucous membranes. Affected patients may develop bullae and edema of the upper airway mucosa, leading to obstruction. Causes typically include medications (with antibiotics, nonsteroidal anti-inflammatory medications, and anticonvulsants frequently being implicated), infections, and malignancies. Depending on their location, facial fractures may lead to UAO through local swelling and a loss of support for the tongue and/or facial skeleton. While oral neoplasms are common, patients typically present for evaluation before the airway can be compromised. Obstructive sleep apnea is a form of chronic UAO that is exhibited only during sleep, and is considered in greater detail in Chap. 109.

Laryngeal Causes

Infectious Causes

Supraglottitis, or infection of the supraglottic portion of the larynx, may cause life-threatening UAO primarily through involvement of the epiglottis. Vaccination against Haemophilus influenzae has successfully decreased the number of cases of epiglottitis in children caused by this organism. As a result, adults comprise a greater proportion of all cases of epiglottitis. In addition to H. influenzae, Streptococcus pneumoniae, Staphylococcus aureus, Haemophilus parainfluenzae, and anaerobes all have been implicated as causes of epiglottitis. Because most physicians who treat adults will work a lifetime without seeing a single patient with the acute onset of sore throat go on to develop UAO, the diagnosis may be missed. The classic presentation is that of a patient sitting upright and leaning forward, drooling; however, these signs may not be present initially. An additional clue is the rapid onset and severity of odynophagia. Signs of toxicity, such as fever and tachycardia, may be present. Otolaryngology and anesthesiology consultation should be obtained if the diagnosis is suspected, while an oral examination should be performed extremely carefully, if at all. The approach to diagnosis depends on the patient's overall clinical status. While lateral films of the neck may reveal the diagnosis, a negative examination does not exclude epiglottitis. A fiberoptic examination can often be performed carefully via the nasopharyngeal route, but should be performed only by a person experienced in treating this problem, preferably a seasoned otolaryngologist or anesthesiologist. Visualization of a swollen, cherry-red epiglottis confirms the diagnosis. This examination is preferentially performed in the operating room, or at a minimum with all necessary airway personnel and equipment available. Although many adults with epiglottitis may be managed with antibiotics and observation in the ICU, the potential for acute airway obstruction should always be considered to be extremely high.12,13 A tracheostomy tray should be at the bedside, and all relevant airway personnel—anesthesia as well as otolaryngology—should be alerted to the patient's condition and location. At no time should the patient be sent unaccompanied to another location in the hospital. While blood cultures may on occasion reveal the etiology, in most cases the specific organism is not identified, and antibiotic treatment is empirical. The response to treatment is typically prompt.

Infections of the larynx may be caused by viruses, bacteria, or fungi. Laryngotracheitis in children (croup) is usually caused by a viral infection, and UAO may result. While viral infections of the larynx are rarely serious in adults, bacterial laryngotracheitis can be life-threatening. Because the causative organisms include Staphylococcus aureus, Streptococcus pneumoniae, and Haemophilus influenzae, pneumonia may be present as well. Corynebacterium diphtheriae should always be considered in the differential diagnosis despite the relative infrequency with which it is currently encountered in the United States. In particular, nonimmunized persons and those individuals who have not received a booster in the past 10 years are at risk. Diphtheria is also more frequently encountered in communities with low immunization rates, as in some Native American communities. Diphtheria commonly presents initially as tonsillitis and pharyngitis. Subsequent spread inferiorly may cause laryngitis, although occasionally the larynx is the only site of involvement. Clinical manifestations include fever, sore throat, malaise, headache, and vomiting. Physical examination may reveal a tenacious gray or black membrane overlying involved sites, and cervical lymphadenopathy may be present. Delays in treatment increase the likelihood of systemic complications from circulating toxin, such as myocarditis, neuritis, and nephritis. Death occurs in 5% to 10% of cases, either from systemic effects of diphtheria toxin or from UAO, the latter occurring more commonly in infants. Treatment includes antibiotics and equine antitoxin, which can be obtained through the Centers for Disease Control and Prevention. Sensitivity to horse serum should be assessed prior to administration of the antitoxin, and desensitization should be performed as necessary. Because infection does not ensure immunity, immunization is indicated after recovery.14

Fungal laryngotracheitis may be caused by Candida albicans, histoplasmosis, blastomycosis, and coccidioidomycosis. In addition to fever and sore throat, affected patients may develop dyspnea and voice change from vocal cord nodules and/or vocal cord fixation. The diagnostic approach depends on the presentation, as other sites of involvement—for example, pulmonary infiltrates—may be present. Respiratory papillomatosis is caused by human papillomavirus types 6 and 11, and is manifested by multiple—sometimes innumerable—papules in the larynx and trachea.

Iatrogenic and Traumatic Causes

Related to Endotracheal Intubation

A variety of upper airway problems can follow endotracheal intubation and are listed in Table 34-1. Several of these problems merit further discussion here. Laryngospasm consists of uncontrolled glottic closure, and respiratory distress with inability to ventilate the patient may result. It can be provoked by a variety of stimuli, including stimulation of the glottic aperture and/or superior laryngeal nerve during intubation, medications including general anesthetics and opioids, and the presence of secretions or blood in the upper airway. Careful suctioning of the mouth and endotracheal tube prior to extubation may reduce the likelihood of laryngospasm after extubation, in addition to improving pulmonary toilet. When laryngospasm occurs, gentle mask ventilation with 100% oxygen should be performed. If the laryngospasm fails to break and ventilation is not possible, the short-acting paralytic succinylcholine may be administered followed by mask ventilation or endotracheal intubation. It should be emphasized that in the ICU, laryngeal edema is a much more likely cause of postextubation stridor than laryngospasm.

Long-term endotracheal intubation may cause a variety of injuries to the upper airway. Fortunately, current endotracheal tube cuffs have a higher volume and lower pressure than were used a number of years ago, decreasing problems related to long-term intubation. Whether or not an individual patient will develop subglottic or tracheal stenosis is difficult to predict. While duration of intubation has been shown in some studies to be correlated with laryngeal or tracheal stenosis, the relationship is not strong. Similarly, while increased tube caliber, frequency of insertion, the severity of respiratory failure, female gender, and the presence of diabetes or immunocompromise have all been suggested as exacerbating factors, the data on this topic are inconsistent.1 The decision to perform a tracheostomy therefore depends on the expected duration of need for an artificial airway, and the extent to which conversion to tracheostomy will facilitate other aspects of care; for example, liberation from mechanical ventilation, or recovery from more proximal upper airway injury or toxic therapy (e.g., surgery or irradiation for neoplasm). In general, the usual recommendation of considering tracheostomy for all patients intubated for 2 to 3 weeks who are not likely to recover soon is a prudent one. As mentioned previously, possibility of subglottic or tracheal stenosis should be considered when encountering breathless patients who have undergone long-term intubation previously. In such cases, the diagnosis of UAO may easily be overlooked. Voice change and stridor are clues to the diagnosis. CT of the upper airway with three-dimensional reconstruction can be very useful in such cases, if patient stability permits.

Endotracheal tube obstruction from secretions may be an insidious cause of UAO that may progress occasionally to a circumstance in which ventilation becomes impossible. Its occurrence may be prevented through frequent suctioning. The development of obstructed respiratory system mechanics—a high peak to plateau airway pressure gradient—in a patient without a history of obstructive lung disease, or in the absence of wheezing, suggests the diagnosis. While difficulty passing a suction catheter is highly suggestive, we have removed endotracheal tubes that are nearly completely occluded through which a suction catheter was able to be passed. If time permits, bronchoscopic examination quickly establishes the diagnosis. Chap. 36 outlines the approach to high peak airway pressures in further detail; here, we stress that prompt removal of the endotracheal tube, with manual mask ventilation of the patient while awaiting reintubation, can be lifesaving.

Stridor has been reported to occur following 2% to 16% of extubations in the ICU, with laryngeal edema most frequently responsible.15 Limited investigations in adults do not support the prophylactic administration of corticosteroids in order to reduce the incidence of reintubation.16 Even if corticosteroids are effective at reducing laryngeal edema, the low incidence of reintubation for this disorder in adults means that an extraordinary number of patients would have to be treated in order to demonstrate a benefit in reducing this occurrence. For this reason, a randomized controlled trial of corticosteroids to treat patients with postextubation stridor is not likely to be performed. Our practice is to administer a short (48 hours) course of parenteral corticosteroids such as dexamethasone in such cases. More important is notification of relevant airway personnel and close observation; aerosolized racemic epinephrine may be useful in decreasing laryngeal edema through local vasoconstriction.

Other Traumatic Injuries

Aspirated foreign bodies lodge in the upper airway much less commonly in adults than in children.17 Still, asphyxiation may follow foreign body aspiration in adults, while large objects aspirated into the esophagus can occasionally obstruct the upper airway. Risk factors in adults include diminished level of consciousness; impaired swallowing mechanism or diminished upper airway sensation as a result of neuromuscular disorder, prior cerebrovascular accident, or advanced age; and inability to chew food properly because of poor dentition. Food particles and medical or dental appliances are most frequently aspirated. Symptoms include cough and dyspnea, and stridor may be present. Chest radiography or lateral films of the neck may reveal the diagnosis. In the case of impending respiratory arrest, the Heimlich maneuver may be lifesaving. Otherwise, the patient should undergo endoscopy in most cases with a rigid endoscope. Flexible fiberoptic endoscopy is generally inadvisable for foreign body removal because the airway cannot be protected if the object lodges in the glottis during removal; however, experienced operators may elect to attempt removal in carefully selected patients.

Upper airway injury may result from inhalation of toxic chemicals, or more commonly from thermal injury. Upper airway burn injury should be suspected whenever a patient has survived a fire or explosion in an enclosed space, and when chemicals or plastics have burned. Physical examination findings that suggest the presence of upper airway injury include the presence of burns or soot on the face, singed nasal hairs, erythema of the oropharynx, and hoarse voice. Sometimes the external signs are relatively mild despite significant inhalation injury. Thus any patient suspected of incurring inhalation injury should undergo fiberoptic laryngoscopy. Affected patients may experience life-threatening UAO from airway edema and mucosal sloughing anytime from initial presentation to 24 hours later. In addition, upper airway edema may be exacerbated by the considerable amount of fluids required to resuscitate patients with extensive burns.18 When the airway needs to be secured, endotracheal intubation is preferred over tracheostomy because of the higher incidence of tracheal stenosis associated with the latter therapy when performed in burn patients. Because corticosteroids increase the incidence of infectious complications and may increase mortality when administered to burn patients, we do not recommend their use here.

Traumatic neck injury may directly injure the larynx.7 Such an injury should be suspected whenever there are ecchymoses or tenderness over the thyroid or cricoid cartilages. In addition to pain, patients may have stridor, hoarseness, and hemoptysis. Cervical spine injury should be excluded, while endotracheal intubation must be done with care to avoid exacerbating any existing injury. Stabilization of the neck and avoidance of neck extension during airway manipulation are mandatory. In a crisis, tracheostomy may be necessary to establish an airway. The evaluation and treatment of laryngeal injury is beyond the scope of this review.

There are a number of iatrogenic causes of UAO. A hematoma in the neck may cause UAO through direct compression, as may rarely occur following surgery. Inadvertent carotid artery puncture during central line placement may cause a rapidly expanding hematoma with airway compromise, particularly if the patient has a bleeding diathesis. Recurrent laryngeal nerve injury may occur during neck dissection or cardiac surgery and cause vocal cord paralysis. While unilateral vocal cord paralysis does not by itself embarrass respiration because the contralateral cord has full mobility, bilateral vocal cord paralysis typically requires surgery.

Miscellaneous Causes

Functional UAO may result from abnormal closure of the vocal cords during inspiration, expiration, or both. Affected patients often have a history of frequent treatment for severe “asthma” exacerbations, at times even undergoing intubation. We have witnessed patients with this condition who exhibit significant pulsus paradoxus and respiratory acidosis during attacks mimicking status asthmaticus. Physical examination is revealing in that stridor is heard. If the patient is intubated, the respiratory system mechanics are normal, and wheezing is not heard. Complicating the diagnosis is the fact that a significant portion of patients with this condition also have asthma, which may be severe.19 Spirometry may show flattening of the inspiratory limb of the flow volume loop, indicating a variable extrathoracic obstruction. The diagnosis is confirmed when laryngoscopy reveals abnormal vocal cord closure, particularly during inspiration. Unfortunately, laryngoscopy may be normal, particularly between attacks, and frequently the diagnosis must be made on clinical grounds. While psychiatric disorders and a history of abuse have been reported to be present in a number of cases, these findings are not invariable, and a loss of regulation of normal reflexes controlling the laryngeal muscles has been postulated.20 Treatment involves speech therapy and treatment of any underlying psychiatric disorder.

Neoplasms are important causes of laryngeal obstruction, with squamous cell carcinoma being the most common malignancy of the larynx. Risk factors include tobacco and alcohol use, and patients may present with hoarseness or hemoptysis.21 The diagnosis is typically established through a combination of direct visualization and CT. The evaluation and management of tumors of the head and neck is beyond the scope of this review.

As mentioned previously, bilateral vocal cord paralysis invariably results in UAO, although the presentation is often delayed.22 Previous thyroidectomy is often responsible for the condition, although malignancy, neck irradiation, neck trauma, and prior intubation are additional causes.

Several systemic diseases are associated with upper airway obstructing lesions.23 Airway involvement in Wegener granulomatosis is common, although frequently subclinical. Manifestations include ulcerations, mass lesions from proliferating granulation tissue, and circumferential narrowing, particularly in the subglottic region. Treatment typically involves a combination of immunosuppression—usually prednisone and cyclophosphamide—and surgery. Tracheostomy is frequently necessary when subglottic stenosis is severe.

Rheumatoid arthritis presents several potential problems where the upper airway is concerned. Arthritis of the temporomandibular joint may limit the degree to which the mouth can be opened, frustrating attempts at oral intubation. Cervical spine arthritis, particularly of the atlantoaxial joint, should be considered a serious impediment to manipulation of the cervical spine. In particular, neck extension may lead to catastrophic cervical spinal cord injury when significant atlantoaxial disease is present. When patients with rheumatoid arthritis develop hoarseness, vocal cord nodules or cricoarytenoiditis are frequently responsible. The latter is often associated with significant pain. Over time, the vocal cords may fuse in the midline.24 While treatment with systemic and intralesional corticosteroids is the rule, surgical removal of the arytenoids or tracheostomy may be necessary. Of note, cricoarytenoiditis occurs infrequently in patients with systemic lupus erythematosus, although in affected patients the presentation is more acute, and the response to steroid therapy is more gratifying.25

While pulmonary involvement in sarcoidosis is extremely common, laryngeal disease is relatively rare. When present, it is usually the supraglottic region that is affected, and on occasion upper airway patency may be threatened. Treatment includes a combination of intralesional and systemic steroids. Relapsing polychondritis is manifest as recurrent inflammation of the cartilages of the ears, nose, larynx, trachea, and joints. Half of affected patients have respiratory tract involvement. UAO may result initially from airway edema, subsequently from increased collapsibility from dissolution of cartilage, and later from fibrosis and fixed stenosis. Amyloidosis affecting the larynx and trachea is rare, and presents as firm nodules that may coalesce and cause UAO.

Angioedema

Angioedema is a typically intense, painless swelling of a localized body area caused by leakage of plasma into the affected tissues, and preferentially involving the face, tongue, larynx, gastrointestinal tract, and extremities. Except in the case of angiotensin-converting enzyme inhibitor–associated angioedema, this leakage typically derives either from mast cell–stimulated histamine release or from activation of the complement system. Mast cell histamine release may occur following IgE-mediated hypersensitivity reactions such as those due to severe food allergies, as well as in response to certain substances—such as codeine, aspirin, and iodinated contrast media—that directly stimulate histamine release. Treatment of histamine-mediated angioedema includes histamine blockade (both H1- and H2-receptor blockers are given), corticosteroids, and if the airway is compromised or hemodynamic instability is present, epinephrine.

There are several diseases of the complement cascade that result in angioedema. They can be generally classified according to whether they are hereditary or acquired. Hereditary angioedema (HAE) is an autosomal dominant disease characterized by recurrent episodes of angioedema of the skin, upper airway, and gastrointestinal tract.26 Attacks may be provoked by dental surgery or general anesthesia. Type I HAE is the most common form and is caused by decreased production of C1 esterase inhibitor. Patients with type II HAE have functionally impaired C1 esterase inhibitors. Corticosteroids, antihistamines, and epinephrine are generally considered to be ineffective in acute attacks in patients with HAE, but should not be withheld until the diagnosis is secured. Purified C1 esterase inhibitor concentrate seems to be both effective and safe in treating exacerbations of HAE, but is not widely available outside of Europe.27 Fresh frozen plasma infusion may be considered as a means of administering C1 esterase inhibitor, but carries the potential risk of paradoxical worsening of angioedema through C4-mediated tissue damage. Generally, this treatment is reserved as a means of preventing angioedema in patients undergoing major surgical or dental procedures, when C1 esterase inhibitor is not available. Attenuated androgens and antifibrinolytic agents are used as prophylactic therapy. Although the latter is somewhat less effective, they are useful alternatives to androgens in children.

Acquired angioedema (AAE) is associated with autoimmune disorders, lymphoproliferative diseases, various carcinomas, and a number of chronic infections such as those caused by human immunodeficiency virus and hepatitis B and C viruses. Affected patients have circulating antibodies directed either against specific immunoglobulins expressed on B cells or against C1 esterase inhibitor. There is some evidence that antihistamines, corticosteroids, and epinephrine are somewhat more effective in treating AAE than HAE.

Immunosuppressive therapy may prevent attacks by decreasing autoantibody production. Some patients respond to attenuated androgens, although usually not if antibodies to C1 esterase inhibitor are present. Antifibrinolytic agents may be tried if androgens are ineffective.

Some patients experience recurrent angioedema, yet have no known cause. Most such patients also have urticaria. The evaluation of these patients is beyond the scope of this review.

Angioedema occurs in a small fraction (0.1% to 0.5%) of patients receiving angiotensin-converting enzyme inhibitors (ACEIs). Still, because of the widespread use of these agents, a significant percentage of all cases of UAO are caused by ACEIs. Attacks typically occur shortly after initiation of therapy, but may occur years later. The angioedema seems to respond poorly if at all to treatment with corticosteroids, antihistamines, and epinephrine; although studies demonstrating the efficacy of these agents are lacking, they are frequently administered anyway. The pathophysiology is unclear; although accumulation of bradykinin has been implicated as the cause, the occurrence of angioedema in some patients who have been switched from ACE inhibitors to angiotensin receptor antagonists, which do not inhibit the catabolism of bradykinin, raises questions about the mechanisms by which each agent causes angioedema.28 We believe that angiotensin receptor antagonists should be used in patients who have had a prior episode of angioedema attributed to ACEI therapy only when there is no other reasonable alternative.

The most important aspect of managing a patient with suspected UAO is to immediately summon to the bedside a clinician experienced in the management of such patients. Once a significant UAO has been diagnosed, early involvement of anesthesia and otolaryngology services is crucial. The approach to management varies considerably depending on the site, severity, and tempo of UAO; while patients with slowly progressive or easily treatable causes of UAO may be managed expectantly, signs of impending respiratory arrest dictate that the airway be secured immediately. The presence of an experienced clinician is also important in ensuring that inappropriately aggressive interventions do not take place, such as attempts at intubation by an inexperienced operator with inadequate equipment and backup. In such cases, attempts to secure the airway may in fact precipitate a catastrophe. Because each patient requires an individual approach to management, explicit recommendations are difficult. Following is a discussion of available techniques for treating patients with UAO.

General Stabilizing Measures

If the patient has normal mentation and is able to speak, attempts can be made at stabilizing a severe UAO with noninvasive means pending definitive treatment. Because the pressure required to drive airflow across the upper airway depends in part on the density of the gas, the inhalation of a low-density inert gas such as helium in combination with oxygen has the effect of reducing the work of breathing. In fact, helium-oxygen mixtures have been shown to decrease the transdiaphragmatic pressure swings and the pressure-time index of the diaphragm, as well as improve comfort, in a group of patients with postextubation stridor.29 The proportion of inhaled gas that can be administered as helium is obviously limited by the need to maintain an adequate arterial saturation. On the other hand, mixtures comprising less than 70% helium are of little to no benefit.

We have used noninvasive positive pressure ventilation in some patients with UAO, particularly those who have postextubation stridor and significantly increased work of breathing. While no controlled trials exist to support its use, we believe this therapy may have a role in preventing respiratory muscle fatigue, and occasionally reintubation in this setting. Conceivably, inspiratory positive airway pressure reduces the work of breathing by unloading the inspiratory muscles, while expiratory positive airway pressure may help to “splint” any collapsible segment of the upper airway in a manner similar to that seen in its use in obstructive sleep apnea.30 We caution that this treatment should only be used in carefully selected patients. In particular, the decision to defer intubation in favor of noninvasive ventilation may allow the UAO an opportunity to progress to a point at which intubation becomes more difficult, if not impossible. Similarly, this approach should not take the place of intubation when the UAO is critical and expected to progress (e.g., in the case of an upper airway infection or tumor awaiting definitive therapy, such as surgery or radiation). We believe an additional role for noninvasive ventilation is in the stabilization of the patient with UAO while relevant airway personnel and equipment can be assembled, and a consensus reached among the medical team—anesthesia, otolaryngology, and the critical care service—as to the best approach to securing the airway.

Securing the Airway

When time permits, and the UAO is known to be severe, the opportunity to perform awake fiberoptic intubation in a controlled manner is invaluable. The unconscious patient with UAO who is unable to be ventilated should first undergo a head-tilt or jaw thrust maneuver to advance the mandible and relieve any obstruction from the tongue base in the hypopharynx. In patients with suspected cervical spine injury, the jaw thrust may be performed without the head-tilt maneuver. Placement of an oral airway also facilitates ventilation when the UAO is proximal. If these measures are unsuccessful, the obstruction is likely to be more distal. Direct laryngoscopy with an anterior commissure laryngoscope and gum bougie introducer often permits successful passage of a small endotracheal tube over the bougie introducer and through the glottis. In situations in which the glottis cannot be well visualized, placement of a laryngeal mask airway may be useful. Subsequent fiberoptic tube placement can then be performed through this device. Depending on operator experience, the esophagotracheal Combitube, which is a dual-lumen tube with an open tracheal cannula and a blind esophageal end that is designed for emergency resuscitation by personnel lacking advanced airway management skills, may serve a similar purpose. Ventilation is performed between two inflated balloons, one in the oropharynx and one in the esophagus. This device should not be used when there is known hypopharyngeal or esophageal pathology, or when time permits an attempt to secure the airway by an experienced otolaryngologist or anesthesiologist. Depending on the level of obstruction, ventilation may still not be possible despite successful insertion of either the laryngeal mask airway or the esophagotracheal Combitube.31

If the airway cannot be effectively secured with an endotracheal tube, a surgical airway is indicated. Emergency cricothyrotomy is performed by first making a 1-cm horizontal incision just above the superior border of the cricoid, which can be found 2 to 3 cm below the thyroid notch.32 The cricothyroid membrane is then slit in the midline with the blade directed inferiorly so as to avoid damaging the vocal cords. If the blade is passed too deeply, entry into the esophagus is possible. The hole is then widened with a blunt instrument to allow passage of a small tube or cannula for ventilation. Complications include vocal cord injury, esophageal perforation, and later, subglottic stenosis. While jet ventilation via needle cricothyrotomy utilizing a 14-gauge angiocath may allow adequate ventilation of the patient pending definitive therapy, the frequency of complications is high and operator experience with this technique is typically limited.

The best approach to securing an obstructed upper airway is best determined through a multidisciplinary approach involving the critical care team, anesthesia, and otolaryngology. Available techniques for securing the airway are discussed in greater detail in Chap. 35.

The Decision to Extubate

Deciding when to extubate a patient with an UAO is often difficult. The presence of the endotracheal tube makes an assessment of upper airway patency difficult. Sometimes improvement in the UAO is suggested by the overall clinical course; for example, if a patient was intubated for a borderline indication in the setting of a soft tissue infection, a significant reduction in facial and neck swelling may indicate that the UAO has improved to the point where extubation is safe. Similarly, complete resolution of lip, tongue, and hypopharyngeal swelling from angioedema is often accompanied by resolution of laryngeal edema. However, care must be taken in such circumstances. It is frequently useful to perform a “cuff leak” test. After scrupulous oral and endotracheal suction, the endotracheal tube cuff is deflated. If a patient is unable to pass air around the tube, its removal may not be tolerated, particularly if the tube is small (i.e., 6.0 or 6.5 mm). When the patency of the airway is in question, it is useful to pass a tube changer through the endotracheal tube prior to its removal. The tube changer allows repassage of an endotracheal tube through the glottis and into the trachea if reintubation is required. Careful consultation with anesthesia and otolaryngology services prior to making a decision to extubate is important, and all necessary equipment and personnel should be at the bedside in marginal cases.

Some studies have suggested that quantification of the cuff leak, either by volume or by percentage of total tidal volume, may predict the occurrence of postextubation stridor in patients not intubated for UAO. Because the rate of reintubation in such cases is low and the benefit of steroids uncertain, it is not clear whether this practice should be generally employed, particularly if it results in more patients remaining intubated for longer periods.

Short of cardiac arrest, the most feared complication of UAO is anoxic brain injury. Negative-pressure pulmonary edema may also occur.33 This condition typically occurs in patients with severe UAO, in whom several mechanisms act synergistically to promote its development. First, the patient generates extremely negative pleural pressures during inspiration attempting to overcome the UAO. This promotes venous return and a shift of the interventricular septum to the left, decreasing left ventricular preload. At the same time, left ventricular afterload is dramatically increased by the fall in intrathoracic pressure, as well as by catecholamine-induced systemic hypertension. These events cause a transfer of blood volume from the systemic to the pulmonary circulation. Here, pulmonary capillary transmural pressure is elevated because of reduced interstitial pressure and possibly elevated capillary pressure, the latter from increased blood volume and pulmonary vascular tone from hypercapnia and hypoxia. This rise in capillary transmural pressure causes pulmonary edema. On occasion, the edema fluid in such patients has been noted to be pink or blood-tinged, possibly from red blood cell leakage caused by high transmural pressures across disrupted alveolar-capillary membranes.