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Upper Airway Obstruction

Jos e C. Yataco, MD Atul C. Mehta, MD
Critical Care Pearls
Upper airway obstruction (UAO) is a life-threatening emergency that requires prompt diagnosis and treatment. Severe UAO can be surprisingly asymptomatic at rest if it develops gradually. Sudden clinical deterioration is unpredictable. Patients with possible UAO must never be sedated until the airway is secured. Minimal sedation may precipitate acute respiratory failure. Achievement of airway patency in total airway obstruction and reestablishment of ventilatory airflow is the first and foremost goal of the treating physicians. Critical care physicians must be aware that pharmacologic interventions (epinephrine, steroids, and heliox) provide temporary support but cannot significantly improve mechanical UAO. Bronchoscopy constitutes the most accurate diagnostic tool and frequently provides the best way to correct UAO. Cricothyroidotomy is the surgical intervention of choice to reestablish airflow when medical interventions have failed.

pper airway obstruction (UAO) is one of the most serious emergencies faced by critical care physicians. Early diagnosis followed by restoration of airflow is essential to prevent cardiac arrest or irreversible brain damage that occurs within minutes of complete airway obstruction (1,2). Although a long list of causes may be responsible for acute UAO, management must begin almost immediately after recognition of the problem. If there is an actual or potential obstruction sufficient to cause ventilatory or oxygenation impairment, an intervention to secure the airway is indicated by whatever
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method appropriate at the time. No single method is suitable in all instances; selection depends on the assessment of the circumstances (1-3). The timing of the intervention, medical, or surgical, is determined based on the condition of the patient. In practice, an elective procedure before acute decompensation is always preferable.

Etiology and Pathogenesis

For purposes of this chapter, upper airway is considered to represent the conducting

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passages extending from the nose or mouth to the main carina (Figure 37-1). UAO may be functional or anatomic and may develop acutely or subacutely. Relapsing polychondritis constitutes a good example of functional UAO caused by lack of a firm cartilaginous structure to support the tracheal wall. Squamous cell carcinoma of the larynx represents an anatomic example of UAO. Narrowing of the upper respiratory tract has an exponential effect on airflow because

linear airflow is a function of the fourth power of the radius (2-4). Although UAO occurs at any level of the upper respiratory tract, laryngeal obstruction has a particular importance because the larynx is the narrowest portion of the upper airway. The narrowest portion of the larynx is at the glottis in adults and the subglottis in infants (5). Some infections such as parapharyngeal or retropharyngeal abscesses and Ludwig angina (mixed infection of floor of the

Palatine tonsil Tongue Oral pharynx Retropharyngeal space Root of tongue Geniohyoid muscle Mylohyoid muscle Submandibular space Vallecula Epiglottis Hypophyarynx Vocal cord Thyroid cartilage Larynx Cricoid cartilage Trachea

Sternum

Figure 37-1 Anatomy of the upper airway. (Adapted from Aboussouan L, Stoller JK. Diagnosis and management of upper airway obstruction. Clin Chest Med. 1994;15:35-53; with permission.)

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mouth) can be associated with severe soft tissue swelling causing UAO. The differential diagnosis of UAO is wide and varies by age group and by clinical setting. Table 37-1 summarizes the most common causes of airway obstruction. Figures 37-2 and 37-3 show examples of benign and malignant causes of UAO.

Clinical Signs and Symptoms

In a conscious patient, signs and symptoms of UAO include marked respiratory distress, altered voice, dysphagia, odynophagia, the hand-to-the-throat choking sign, stridor, facial swelling, prominence of neck veins, absence of air entry into the chest, and tachycardia. In an

Figure 37-2 Tracheal amyloidosis causing narrowing of the distal trachea.

Table 37-1 Differential Diagnosis of Upper Airway Obstruction According to Etiology

Traumatic causes Laryngeal stenosis Airway burn Acute laryngeal injury Facial trauma (mandibular or maxillary fractures) Hemorrhage Infections Suppurative parotitis Retropharyngeal abscess Tonsillar hypertrophy Ludwigs angina Epiglottitis Laryngitis Laryngotracheobronchitis (croup) Diphtheria Iatrogenic causes Tracheal stenosis post-tracheostomy Tracheal stenosis post-intubation Mucous ball from transtracheal catheter Foreign bodies Vocal cord paralysis Tumors Laryngeal tumors (benign or malignant) Laryngeal papillomatosis Tracheal stenosis (caused by intrinsic or extrinsic tumors) Angioedema Anaphylactic reactions C1 inhibitor deficiency Angiotensin-converting enzyme inhibitors

Figure 37-3 Extrinsic compression of the trachea caused by intrathoracic malignancy. unconscious or sedated patient, the first sign of airway obstruction may be inability to ventilate with a bag-valve mask after an attempt to open the airway with a jaw-thrust maneuver. After a few minutes of complete airway obstruction, asphyxiation progresses to cyanosis, bradycardia, hypotension, and irreversible cardiovascular collapse (1-3). Occasionally, UAO can develop slowly and is confused with reactive airway disease. However,

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the obstructive noise or stridor is thought to be a specific for UAO. Stridor is heard during the entire respiratory cycle but typically intensifies during inspiration and is usually more prominent above the neck. The presence of stridor indicates severe airway obstruction (airway passage <5 mm) but unfortunately does not help to specify its nature or location (4).

the radiology suite for scanning need to be carefully considered.

Spirometry
Spirometry can be used in the patient with gradual and mild symptoms of UAO. It is relatively insensitive and has no role in the management of a patient with acute respiratory distress (3,4). Analysis of the flow-volume loops may be helpful suggesting the location and functional severity of the obstruction (Figure 37-4 A-D).

Investigations
The most important diagnostic tool if UAO is suspected is a quick history and physical examination. Many times, management of a patient with UAO must start simultaneously with the diagnostic process. It is useful to separate patients with potential UAO into those with severe symptoms and impending respiratory failure and those with a more indolent course and less severe symptoms. It is important to understand that airway resistance varies inversely with the fourth power of the radius at the point of UAO, and that small changes in the underlying pathology may dramatically worsen respiratory airflow.

Bronchoscopy
Rigid or flexible bronchoscopy with direct visualization is the most effective tool in establishing diagnosis and frequently provides the best way to correct UAO. The rigid bronchoscope can be used in the emergency setting to secure the airway by carefully passing it through the stenotic segment. Flexible bronchoscopy can be used to establish the diagnosis as well deliver treatment including laser therapy, photoresection, electrocautery electrosurgery, balloon bronchoplasty, and tracheal stenting once the airway has been secured and the patient stabilized (2,3). It is important to have a secured airway or the immediate means to have one because flexible bronchoscopy can worsen UAO to a critical level.

Plain Chest and Neck Radiographs

Plain neck and chest films may be useful as screening tests by identifying tracheal deviation, extrinsic compression, or radiopaque foreign bodies. Lateral neck radiographs are considered insensitive and may result in unnecessary delay in securing the airway (1,4).

Management
Establishing a secure and patent airway is the most important goal in the resuscitation of a patient with acute UAO. A quick evaluation considering age group, history, physical examination, and clinical circumstances helps determine the site and cause of obstruction, the severity of the obstruction, and the need to establish an airway urgently. In the outpatient setting the most common cause of UAO is obstruction of the larynx with a foreign body. Heimlich maneuver is recommended for relief of the airway obstruction in adults and children one to eight years of age. A

Computed Tomography
Computed tomography (CT) can be important in investigating UAO in the stable patient or in the unstable patient with an already secured airway. High-resolution CT of neck and chest can help identify intrinsic and extrinsic tumors, vascular structures, and foreign bodies. It can also provide information on the degree and extension of airway compromise in UAO (1,4). However, the risks and benefits of transporting such a patient to

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10 Expiration 5

10

5 Airflow, L/ S Expiration

Airflow, L/ S

Inspiration

Inspiration

10

10 100 Lung volume, % VC 0

A
10

B
10

100

Lung volume, % VC

Expiration 5 Airflow, L/ S Airflow, L/ S 5 Expiration

Inspiration 5

Inspiration 5

10

10 100 Lung volume, % VC 0

100

Lung volume, % VC

Figure 37-4 Flow-volume curves in upper airway obstruction. (A) indicates the normal contour of the inspiratory and expiratory curves; (B) With variable intrathoracic obstruction (e.g., tracheomalacia within the thorax), obstruction is marked during exhalation with marked truncation of the expiratory curve; (C) With variable extrathoracic obstruction (e.g., collapse of tracheal cartilage in the neck following trauma), obstruction is more marked during inspiration; (D) Finally, with fixed obstructions (e.g., tracheal stenosis), both the inspiratory and expiratory curves are markedly truncated. (Adapted from Hall JB, Schmidt GA, Wood LD, eds. Principles of Critical Care. New York: McGraw-Hill; 1992; with permission.)

subdiaphragmatic abdominal thrust can force air from the lungs; this may be sufficient to create an artificial cough and expel a foreign body from the airway. Repeat abdominal thrusts may be needed to clear the airway. Several medical and surgical approaches are available in the management of UAO including oropharyngeal airways, endotra-

cheal intubation (transnasally or orally), tracheotomy, cricothyroidotomy, fiberoptic intubation, racemic epinephrine, corticosteroids, heliumoxygen mixtures, laser therapy, bronchoscopic dilation, and airway stenting (Table 37-2). The selection of the intervention will depend on the cause of UAO and the urgency to obtain a secure airway.

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Table 37-2 Interventions in Upper Airway Obstruction

Medical Interventions Heimlich maneuver (suspected foreign body aspiration) Oropharyngeal airways Endotracheal intubation (transnasally or orally) Racemic epinephrine Corticosteroids Heliumoxygen mixture Surgical or Bronchoscopic Interventions Fiberoptic intubation Cricothyroidotomy Tracheostomy Laser/electrocautery/balloon dilation Airway stenting

Racemic Epinephrine
Racemic epinephrine is usually used in circumstances when the patient with a partial UAO is still conscious and able to ventilate, and vasoconstriction is desired to decrease mucosal edema. Racemic epinephrine administered by means of a nebulizer has been proven to be effective in treating croup (laryngotracheobronchitis) in the pediatric population decreasing morbidity, mortality, and hospital stay (6). Conversely, racemic epinephrine is not effective in the treatment of epiglottitis and may be deleterious (7). Racemic epinephrine also is used to treat postextubation laryngeal edema, which has been reported to occur from 2.3% to 6.9% (8). The typical case is that of a patient, breathing easily for the first two or three hours, followed by the gradual progression of dyspnea, inspiratory stridor, and increased work of breathing. In this situation repeat racemic epinephrine treatments can be used as a temporary measure until the acute swelling and inflammation subsides. These patients should remain in the intensive care unit under careful observation until it is confirmed that the UAO has resolved or greatly improved.

reducing airway edema. Randomized trials have confirmed the usefulness of corticosteroids in the treatment of croup with decreases in the need for intubation and hospital stay (9). However the treatment of epiglottitis with steroids is controversial and often contraindicated (5). Experimental studies in animals have shown that corticosteroids given at the time of extubation decrease capillary dilatation and permeability as well as edema formation and inflammatory cells infiltration. The preventive use of steroids for postextubation laryngeal edema is until now widely accepted. However, a placebo controlled, double-blind, multicenter study showed that dexamethasone does not prevent laryngeal edema after tracheal extubation, regardless of intubation duration (8-10).

Heliox
Heliox, a heliumoxygen gas mixture, is effective in reducing the work of breathing by decreasing airway resistance to turbulent flow in the density-dependent pressure drop across the airway obstruction. Heliox has been used in several conditions including postextubation laryngeal edema, tracheal stenosis or extrinsic compression, status asthmaticus, and angioedema (11,12). To be effective, the heliumoxygen ratio must be at least 70:30. Unfortunately, most patients with UAO also have lung disease with varying degrees of hypoxemia preventing the use of heliox at effective concentrations. Although the work of breathing and dyspnea improves to some degree with the use of heliox, the mechanical obstruction is still in place. The use of heliox in patients with severe UAO should only be used to provide temporary support pending definitive diagnosis and management.

Endotracheal Intubation
In most cases of UAO, the patency of the upper airway can be reestablished with endotracheal intubation after rapid assessment of the patients airway anatomy. Evaluation of

Corticosteroids
Corticosteroids have been used to treat UAO because of their potential beneficial effect in

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mouth opening (>40 mm), dentition, cervical spine mobility (flexion-extension), thyromental distance (normal is >3 finger breadths) and the function of the temporomandibular joints are key to subsequent success and avoidance of complications (13,14). Orotracheal intubation under direct visualization with a laryngoscope is the most commonly used route for emergency intubations. In patients with distorted airway anatomy or suspected cervical spine injury, fiberoptic bronchoscopy can be used to guide the intubation. The endotracheal tube is positioned over a bronchoscope; the operator introduces the fiberoptic bronchoscope into the patients mouth or nose and advances it through the vocal cords into the trachea. The endotracheal tube is then advanced over the bronchoscope. A prompt and successful intubation in a patient with UAO allows restoration of adequate ventilation and oxygenation and the performance of further diagnostic and therapeutic procedures.

roidotomy be converted to formal tracheotomy if longer than 72 hours of use is anticipated. Tracheostomy is probably the last option available to establish an airway in acute UAO. Laryngeal trauma is a relative contraindication to cricothyroidotomy and laryngotracheal intubation; it is the only indication for emergency tracheostomy. This procedure is time-consuming and requires expertize and attention to detail. Comparison of emergent versus elective tracheotomy reveals a twofold complication rate in the former because of the time spent on isolating the trachea as a result of commonly occurring bleeding (13,15). Cricothyroidotomy has a higher success rate than tracheostomy; it also has better patient neurologic outcome based primarily on less time required for the procedure (11). Overall, patients requiring an emergency surgical airway have a relatively high mortality (15).

Laser Therapy
Carbon dioxide or neodymium:yttrium-aluminum-garnet (Nd:YAG) laser therapy can be used to treat intraluminal tracheobronchial lesions once the UAO has been stabilized with a secure airway. Although the onset of airway compromise is usually gradual, some patients remain asymptomatic despite airways that are only two to three millimeter in diameter. These patients only develop dyspnea on exercise or when complete blockage results from mucus, bleeding, or inflammation with swelling. Laser therapy can be used to excise tracheal webs, to treat benign obstructive lesions, or as palliative therapy for malignant tracheobronchial lesions.

Surgical Interventions
Overall, emergency laryngotracheal intubation is effective in approximately 97% of cases (13). Thus, a surgical airway is needed in only 3% of such emergencies. The need for an immediate surgical airway must be evaluated considering the potential difficulties associated with emergency intubation. In cases of UAO the surgical airway is considered emergently in cases of laryngotracheal trauma, foreign body lodged in the pharyngolaryngeal area, or severe anatomic deformity caused by trauma. When surgical airway management is required, cricothyroidotomy is the procedure of choice in the emergency setting; it is faster (average 30 sec), simpler, and more likely to be successful than tracheotomy. Intraluminal diameter of the trachea is narrowest at the level of the cricoid; there is concern that prolonged use of a cricothyroidotomy may cause subglottic injury and lead to subglottic narrowing. It is recommended that cricothy-

Tracheal Stenting
Tracheal stents placed using either rigid or flexible bronchoscopy can be helpful to maintain a patent airway in patients with tracheal obstruction caused by benign or malignant conditions. Airway resection and reconstruction provide the definitive correction, but

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many patients have unresectable disease. For these patients, therapeutic bronchoscopy provides rapid palliation that can be lifesaving and improve quality of life. Benign lesions can be managed with dilation, with or without laser resection. Malignant lesions often require core out of the tumor with a rigid bronchoscope followed by laser, photodynamic therapy, brachytherapy, cryotherapy, or electrocautery. Airway stents are a valuable adjunct to these techniques and can provide prolonged palliation from an unresectable recalcitrant benign stenosis or rapidly recurrent endoluminal tumor. Neither silicone nor the available metal stents conform to all the ideal characteristics desired for an endobronchial stent. The silicone stent has the advantages of being easily repositioned or removed, causing minimal granulation, and being inexpensive. Its disadvantages are the need for rigid bronchoscopy and general anesthesia, reduced inner diameter, and the potential for being dislodged or distorted (16,17). The expandable metal stent has the advantages of being easily delivered with flexible bronchoscopy, having minimal migration, and conforming well to the anatomy of the airway. The major disadvantage is that it is permanent and can cause significant granulation tissue within the stent (17). Because of the intrinsic problems associated with airway stents, regardless of type, it is important to remember that these patients require lifelong management and are at risk for development of stent obstruction or migration. In one series, 41% of patients required additional endoscopic interventions to maintain airway patency. In patients with benign disease and normal life expectancy (e.g., relapsing polychondritis) a much higher percentage of patients require further interventions (16,17).

monary condition (18-20). There are two types of postobstructive pulmonary edema. Type I follows a sudden, severe airway obstruction such as postextubation laryngospasm, epiglottitis, croup, strangulation, choking, and hanging. Type I is associated with any cause of acute UAO. Type II pulmonary edema develops after surgical relief of long-term UAO. Reported causes include tonsillectomy and removal of upper airway tumors. Postobstructive pulmonary edema usually occurs within one hour of a precipitating event but it has reported to occur up to six hours later. The exact pathogenesis is unclear but the current theory is that young patients are able to generate extremely high negative intrathoracic pressure, which increases venous return, decreases cardiac output, and causes fluid transudation into the alveolar space. The cause of type II postobstructive pulmonary edema is less clear, but it appears that the obstructing lesion produces a modest level of positive endexpiratory pressure (PEEP) and increases end-expiratory lung volume. The sudden removal of this PEEP may then lead to interstitial fluid transudation and pulmonary edema (20). The treatment of postobstructive pulmonary edema is supportive with supplemental oxygen, intubation, and application of low levels of PEEP (5 cm H2O). The role of diuretics in this setting is unclear. Most patients respond promptly to appropriate treatment and have full recovery.

Summary
Upper airway obstruction is a potentially fatal emergency faced by critical care physicians. It can be caused by myriad conditions that will require a particular treatment after appropriate diagnosis. Regardless of the specific cause, the patient with UAO must be carefully monitored in the ICU for impending respiratory failure. A secure and patent airway should be established if clinical deterioration is seen. Pharmacologic interventions have limited

Complications Pulmonary Edema

Postobstructive pulmonary edema is the sudden onset of edema following UAO without evidence of any other underlying cardiopul-

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Stridor suggestive of UAO

Quick history and physical examination Gradual onset and mild symptoms Selection of appropriate ancillary studies: Bronchoscopy CT upper airway Spirometry

Impending respiratory failure

Urgent establishment of patent airway Is ET intubation possible? Direct or fiberoptic intubation Crycothyroidotomy vs Tracheotomy

Yes

No

Figure 37-5 Algorithm for management of upper airway obstruction. (CT = computed tomography; ET = endotracheal; UAO = upper airway obstruction.)

usefulness in the setting of acute mechanical UAO. The critical care physician must be competent in the full range of airway access procedures. Overall, patients requiring an emergency surgical airway have a poor neurological outcome and higher mortality. Figure 37-5 gives an algorithmic approach to management of UAO.

REFERENCES
1. Jacobson S. Upper airway obstruction. Emerg Med Clin North Am. 1989;7:205-17. 2. Khosh MM, Lebovics RS. Upper airway obstruction. In: Parrillo JE, Dellinger RP, eds. Critical Care Medecine. St. Louis: Mosby; 2001:808-25. 3. King EG, Sheehan GJ, McDonell TJ. Upper airway obstruction. In: Hall JB, Schmidt GA, Wood LD, eds. Principles of Critical Care. New York: McGraw-Hill; 1992:1710-8. 4. Aboussouan L, Stoller JK. Diagnosis and management of upper airway obstruction. Clin Chest Med. 94119;5:35-53.

5. Dickison AE. The normal and abnormal pediatric airway. Recognition and management of obstruction. Clin Chest Med. 87819;5:83-96. 6. Quan L. Diagnosis and treatment of croup. Am Fam Physician. 92419;6:747-55. 7. Kissoon N, Mitchell I. Adverse effects of racemic epinephrine in epiglottitis. Pediatr Emerg Care. 85119;143-4. 8. Darmon JY, Rauss A, Dreyffus D, et al. Evaluation of risk factors for laryngeal edema after tracheal extubation in adults and its prevention by dexamethasone. Anesthesiology. 1992;77:245-51. 9. Kairys SW, Olmstead EM, OConnor GT. Steroid treatment of laryngotracheitis: a metaanalysis of the evidence from randomized trials. Pediatrics. 1989;83:683-93. 10. McCulloch TM, Bishop MJ. Complications of translaryngeal intubation. Clin Chest Med. 1991;12:507-21. 11. Boorstein JM, Boorstein SM, Humphries GN, et al. Using heliumoxygen mixtures in the emergency management of acute upper airway obstruction. Ann Emerg Med. 1989;18:688-90. 12. Curtis JL, Mahlmeister M, Fink JB, et al. Heliumoxygen gas therapy. Chest. 1986;90: 455-7.

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13. Feller-Kopman D. Acute complications of artificial airways. Clin Chest Med. 2003;24:445-55. 14. Steinert R, Lullwitz E. Failed intubation with case reports. HNO. 1987;35:439-42. 15. Goldberg J, Levy PS, Morkovin V, Goldberg JB. Mortality from traumatic injuries: a casecontrol study using data from the national hospital discharge survey. Med Care. 1983;21: 692-704. 16. Wood DE, Liu YH, Vallieres E, et al. Airway stenting for malignant and benign tracheobronchial stenosis. Ann Thorac Surg. 2003;76: 167-74.

17. Saad CP, Murthy S, Krizmanich G, Mehta AC. Self-expandable metallic airway stents and flexible bronchoscopy: long term outcome analysis. Chest. 2003;124:1993-9. 18. Kanter RK, Waichko I. Pulmonary edema associated with upper airway obstruction. Am J Dis Child. 1984;138:356. 19. Wilms D, Shure D. Pulmonary edema due to upper airway obstruction in adults. Chest. 88919;4:1090-2. 20. Van Kooy MA, Gargiulo RF. Postobstructive pulmonary edema. Am Fam Physician.2000; 62:401-4.