Upper airway obstruction

1. Description of the problem

What every clinician needs to know

The upper airway is the segment of the airways between the nose or mouth and the carina at the lower end of the trachea. Unlike lower conducting airways, such as the main, lobar and segmental bronchi, the upper airway has no means of collateral ventilation. Hence, any obstruction, whether it be acute, occurring within minutes, or chronic, developing over weeks or months, can be catastrophic.

The upper airway has four compartments: the nose (during nasopharyngeal breathing) and mouth (during oropharyngeal breathing), the pharynx, the larynx and the trachea. Because of their parallel arrangement, the mouth and nose are rarely the site of obstruction except in massive facial trauma.

The upper airway has been divided into the extrathoracic portion of the airway, the segment above the thoracic inlet, and the intrathoracic portion. This anatomic distinction is important to the physiologic assessment of patients suspected of having an upper airway obstruction, as is also the distinction between a dynamic (variable) and anatomical (fixed) obstruction. Clinically significant obstruction may occur at any site along the upper airway; recognition and treatment can be life saving.

Common causes of obstruction of the upper airway include malignancy, infection, inflammatory disorders, trauma, and iatrogenic causes. It appears that malignancy and benign strictures related to previous airway interventions have become more prevalent in recent years. Fortunately, advances in thoracic imaging and endoscopic techniques have led to better recognition of these disorders, and effective palliation and cure are commonplace.

Clinical features

Obstruction of the upper airway may occur acutely and result in respiratory distress and death in minutes. Alternatively, upper airway obstruction may evolve chronically, resulting in progressive dyspnea and exercise intolerance. Chronic obstruction may also result in acute respiratory distress when a critical narrowing of the airway is reached through progression of the primary cause of the obstruction or as a result of mucus plugging or bleeding.

2. Emergency Management

Treatment options for chronic upper airway obstruction

Both benign and malignant diseases of the upper airways may lead to progressive airway obstruction. Management strategies depend on the cause and extent of disease. Ideally, surgical resection of the obstructing lesion(s) should be first considered. However, if the extent of disease does not allow for complete surgical resection, a number of palliative procedures may be used to relieve symptoms and improve short- and long-term outcomes. These include cryotherapy, laser ablation, endoscopic resection, and stent placement.

Treatment of malignant causes of chronic upper airway obstruction

Two common causes of malignant upper airway obstruction include laryngeal and tracheal carcinomas.

Laryngeal carcinoma

The treatment of head and neck tumors depends on proper staging of the disease (extent of local invasion and nodal metastases) and site of the tumor (supraglottic, glottic, or subglottic). These features may be ascertained using computed tomography. For limited disease, both surgery (endoscopic or open resection) and radiation therapy provide comparable results and spare the larynx. For locally advanced disease, surgery, radiation therapy, and chemotherapy have been employed. Organ-sparing approaches are utilized whenever possible.

Tracheal carcinoma

Squamous cell carcinoma is the most common tracheal tumor; the next most common is adenoid cystic carcinoma. Surgical resection is the treatment of choice, whenever possible; surgery provides superior results to primary radiation. Postoperative radiation therapy is often employed, but whether survival is enhanced with its use is unclear. When the obstruction is severe, laser resection and tracheal stenting have been used as a bridge to surgery.

Treatment of benign causes of upper airway obstruction

Benign causes of chronic airway obstruction are numerous and include infectious diseases (eg, tuberculosis, aspergillosis) and chronic inflammatory diseases (eg, sarcoidosis, Wegener’s granulomatosis, relapsing polychondritis).Treatment using antiinfectives or antiinflammatory agents, respectively, is appropriate. However, these conditions may be complicated by development of granulation tissue and fibrosis, and surgical or bronchoscopic procedures may become necessary adjuncts.

Depending on the extent of the lesion, resection of the lesion, resection of the involved section of large airway (eg, with airway stenosis, presence of an inflammatory mass, or an area of tracheomalacia). or tracheal reconstruction using a pericardial or synthetic implant may be warranted.

3. Diagnosis

Acute presentation

The sudden onset of respiratory distress and stridor should suggest an acute upper airway obstruction. However, the causes of upper airway obstruction are numerous, and clinical history is essential in establishing a definitive diagnosis. This axiom is true for patients who develop chronic upper airway obstruction, who are likely to give a history of progressive dyspnea on exertion. A careful assessment of co-morbidities that may predispose to this complication is important.

The major symptom of upper airway obstruction is shortness of breath. When the obstruction is acute, such as with anaphylaxis-induced laryngospasm, sudden dyspnea, or even suffocation, may result. In this circumstance, a variety of causes should be considered including the following:

– Infection (eg, epiglottitis, Ludwig’s angina, croup)

– Aspiration (eg, foreign body)

– Angioedema (eg, allergic, hereditary, drug-induced)

– Iatrogenic (eg, instrumentation, postsurgical)

– Hemorrhage (eg, tumors, blood dyscrasia)

– Inhalation injury (eg, explosion, fire, industrial accident)

– Blunt trauma (eg, motor vehicle accident, physical attack)

– Neuromuscular disease (eg, myasthenic crisis, laryngeal-pharyngeal dystonia)

Subacute – chronic presentation

When upper airway obstruction occurs over time, such as with post-intubation tracheal stenosis, patients first experience dyspnea with exertion. Typically, a significant degree of anatomic obstruction precedes overt symptoms with chronic obstruction. For example, when exertional dyspnea occurs, the airway diameter is likely to be reduced to about 8 mm.

Dyspnea at rest develops when the airway diameter reaches 5 mm. As the mean tracheal diameter measured at the thoracic inlet is 18.2 mm (standard deviation, + 1.2 mm) in men and 15.2 mm (standard deviation, + 1.4 mm) in women, considerable airway compromise may occur before symptoms arise.

When chronic upper airway obstruction is suspected a broad differential diagnosis should be considered:

Infection (eg, tuberculosis, rhinoscleroma)
Tumor (eg, squamous cell carcinoma of larynx and trachea, hamartoma, hemangioma)
Collagen vascular disease (eg, Wegener’s granulomatosis, relapsing polychondritis)
Sarcoidosis
Amyloidosis
Post-intubation (eg, tracheomalacia, tracheal stenosis)
Mediastinal mass (eg, thymoma, lymphadenopathy)
Vascular abnormality (eg, vascular ring, aortic aneurysm)
Esophageal disorder (eg, achalasia, Zenker’s diverticulum)
Laryngeal dysfunction (eg,vocal cord paralysis, vocal cord dysfunction, laryngocoele)
Neuromuscular disease (eg, Parkinson’s disease, bulbar palsy)
Tracheobronchopathia, osteochondroplastica
Idiopathic (eg, subglottic stenosis)

Can the presence of stridor distinguish between upper and lower airway obstruction?

Although it should be easy to distinguish stridor from lower airway sounds, audio recordings from the neck and chest have shown that the sound signals from the asthmatic wheeze and stridor are of similar frequency. This explains why errors in diagnosis may be made and why upper airway obstruction due to a tumor or foreign body is often mistakenly treated as asthma. Certain clinical findings may help distinguish between stridor and wheeze:

The musical sounds of stridor usually occur during inspiration and are heard loudest in the neck. Wheezing, which is characteristic of diffuse lower airway narrowing, occurs predominantly during expiration and gets louder at end-expiration.
Maneuvers that increase flow, such as voluntary hyperventilation induced by panting, accentuate stridor.
Neck flexion may change the intensity of stridor, suggesting a thoracic outlet obstruction.
If the obstructing lesion is below the thoracic inlet, both inspiratory and expiratory stridor may be heard.
The character of a patient’s voice may be a clue to an upper airway obstruction. Hoarseness may be a sign of a laryngeal abnormality. Muffling of the voice without hoarseness may represent a supraglottic process.

What imaging studies will be helpful in making or excluding the diagnosis of upper airway obstruction?

As dyspnea and respiratory distress are the predominant symptoms of both acute and chronic upper airway obstruction, roentgenographic assessment needs to be performed immediately in the stable patient. When anaphylaxis or foreign body aspiration is suspected, immediate treatment is warranted, as a delay for completing radiographic studies may be dangerous and noninformative.

Helpful roentgenographic clues for the diagnosis of upper airway obstruction

In stable patients, lateral views of the neck, as well as standard chest films, should be part of the initial evaluation. Swelling of upper airway structures, such as the epiglottis, aryepiglottic folds, and uvula may be detected on plain radiographs; in addition, foreign bodies, cellulitis, and abscess formation of deep cervical spaces may be seen on lateral views of the neck.

Contrast-enhanced computed tomography (CECT) is usually necessary in the evaluation of acute upper airway obstruction, especially when deep neck infection is suspected; serial scanning may be useful in monitoring the patient’s response to treatment. CECT, coupled with physical examination, has an accuracy of 89% in differentiating a drainable abscess from cellulitis.

Ultrasound is more accurate than CECT in differentiating a drainable abscess from cellulitis in patients with deep neck infection. Ultrasound technology is portable, inexpensive, and avoids exposure to radiation. However, accurate application of the technique and its interpretation are subject to the skill level of the operator.

Magnetic resonance imaging (MRI) provides better soft tissue definition than CECT and avoids exposure to radiation. However, MRI is expensive and time consuming. Magnetic resonance angiography may be useful in evaluating vascular complications of certain causes of upper airway obstruction, such as thrombophlebitis seen in Lemierre’s syndrome, or vascular aneurysms.

Imaging may be useful in identifying unusual complications of upper airway obstruction, eg, a laryngopyocele, which is identified as a fluid-filled or air and fluid-filled density emanating from the laryngeal ventricle and extending superolaterally into the paraglottic fat. Radiographic enhancement demonstrating a thick rim in the structure indicates underlying inflammation.

Radiographic assessment of the patient with suspected chronic upper airway obstruction

CT scanning is the standard imaging modality for evaluation of chronic upper airway obstruction. The technique is highly accurate (sensitivity, 90%-94%) for depicting focal abnormalities in the central airways. However, conventional CT scanning is imprecise in characterizing bronchial abnormalities depicted on bronchoscopy.

The use of multiplanar CT techniques, coupled with three-dimensional reconstructions, provides accurate anatomic delineation of the trachea and larynx. Helical CT scanning incorporates volume averaging techniques during a single breath-hold, thereby eliminating respiratory motion-related artifact. Overlapping thin CT slices can be reconstructed from the raw data, enabling creation of high-quality images.

With recent advances in computer techniques, CT bronchography (or virtual bronchoscopy) and three-dimensional, external renderings of the tracheobronchial tree may be derived from helical CT data. The resulting images are remarkable, high-quality reproductions of airway anatomy. Airway wall thickening, narrowing of the tracheal air column, calcifications, extrinsic compression of the airway, intraluminal lesions, and airway fistulas may be identified.

Three-dimensional images may help surgeons and interventional bronchoscopists select the proper procedures for diagnosis and treatment of upper airway obstruction. Intravenous contrast agent is not needed in assessment of suspected benign lesions; however, use of contrast agent may be useful in distinguishing suspected malignancy from adjacent lymph nodes. Scanning during a dynamic expiratory maneuver may help identify focal airway collapse due to tracheomalacia.

What non-invasive pulmonary diagnostic studies will be helpful in making or excluding the diagnosis of upper airway obstruction?

The diagnosis of acute upper airway obstruction needs to be established and managed immediately. Noninvasive pulmonary diagnostic tests are not indicated in this setting.

The diagnosis of chronic upper airway obstruction may incorporate noninvasive pulmonary function tests

Spirometry, including measurements of maximal inspiratory and expiratory flows, is the most commonly used test. However, the forced vital capacity (FVC) and forced expiratory volume in one second (FEV1) may be normal in upper airway obstruction.

Critical in evaluating pulmonary function tests in the setting of suspected upper airway obstruction is inspection of the configuration of the flow-volume loop (FVL), as described below. The FVL is created by plotting maximal inspiratory and maximal expiratory flows against lung volume. Inspection of the FVL may be helpful in determining the location of upper airway obstruction and in monitoring its response to treatment.

Although the FVL is easily generated and, potentially, very informative, it is not very sensitive in diagnosing upper airway obstruction. The diameter of the upper airway may need to be narrowed to less than 8 mm to produce flow limitation. Therefore, if the FVL is normal, further procedures, such as laryngoscopy or radiographic studies, should be considered when upper airway obstruction is suspected.

What else could it be?

When upper airway obstruction develops slowly, a delay in diagnosis may predispose patients to unnecessary complications, such as bleeding or respiratory failure, and in the case of an upper airway malignancy, to advanced and incurable disease.

When upper airway obstruction occurs acutely, asphyxia and death may result within minutes to hours. Treatment for acute asthma or COPD exacerbation is ineffective.

The symptoms of dyspnea and noisy breathing are identical to those experienced by patients with lower airway diseases, such as asthma and chronic obstructive pulmonary disease (COPD), leading to diagnostic confusion. Since asthma and COPD are considerably more common in the general population, they may be assumed to be the cause of symptoms in patients with undiagnosed upper airway obstruction. Consequently, the diagnosis of upper airway obstruction may be delayed, resulting in possible catastrophic consequences.

4. Specific Treatment

Management of upper airway obstruction, either acute or chronic, depends on the cause. When airway obstruction is acute (within minutes), no testing is warranted, and immediate treatment is mandatory.

When the obstruction evolves over several hours or longer, ancillary studies, such as roentgenograms and blood studies, may be very helpful in targeting therapy. When symptoms of chronic upper airway obstruction progress over months, pulmonary function tests, roentgenographic testing, and endoscopic assessment are helpful in establishing the diagnosis and directing treatment.

Acute upper airway obstruction is a medical emergency that requires prompt intervention. Reactions to allergens (eg, peanuts, medications, bee stings), infections (epiglottitis), or particles and gases (smoke inhalation) may cause acute edema of the throat and larynx. In addition, a foreign body lodged in the throat or larynx may cause acute upper airway obstruction. Treatment consists of interventions designed to restore airway patency, to provide adequate oxygenation and ventilation, and to alleviate the underlying cause.

If there is difficulty establishing a patent airway, endobronchial intubation should be performed, as this is the definitive means of securing the airway and alleviating acute upper airway obstruction. This may be accomplished by performing a standard laryngoscope-guided oral intubation or a blind nasotracheal intubation.

If tongue swelling or pharyngeal soft tissue edema precludes visualization of the vocal cords or placement of an endotracheal tube, emergency tracheostomy should be performed. If a tracheostomy cannot be performed immediately, cricothyroidotomy may provide short-term airway control.

Etiology-specific treatment

1. Aspiration of Food or Foreign Body

Use of the Heimlich maneuver in an individual who suddenly is unable to speak while eating (a so-called, “café coronary”) may relieve the obstruction.

2. Angioedema

Use of corticosteroids, antihistamines, H1 and H2 blockers, and subcutaneous epinephrine may alleviate angioedema due to ACE inhibitors or laryngeal edema due to other agents.

General measures, such as elevating the head of the bed and use of humidified oxygen or a mixture of helium and oxygen (Heliox) may permit sufficient time for medications to decrease airway swelling and improve airway patency.

Heliox is supplied as a tank of compressed gas composed of 80% helium and 20% oxygen. Helium is less dense than nitrogen; consequently, by decreasing turbulent flow in large airways the work of breathing is reduced with Heliox administration. The fraction of inspired oxygen in Heliox may be increased to as much as 40% to address concurrent hypoxemia.

What are the palliative considerations for patients with chronic upper airway obstruction?

Palliative interventions for patients with chronic upper airway obstruction include:

balloon dilatation
airway stenting
laser therapy
electrocautery and argon plasma coagulation
cryotherapy
nocturnal, noninvasive, positive-pressure ventilation

Pathophysiology

Common etiologies of acute upper airway obstruction

Infection (eg, epiglottitis, Ludwig’s angina, croup)

Aspiration (eg, foreign body)

Angioedema (eg, allergic, hereditary, drug-induced)

Iatrogenic (eg, instrumentation, post-surgical)

Hemorrhage (eg, tumors, blood dyscrasia)

Inhalation injury (eg, explosion, fire, industrial accident)

Blunt trauma (eg, motor vehicle accident, physical attack)

Neuromuscular disease (eg, myaesthenic crisis, laryngeal-pharyngeal dystonia)

Etiologies for chronic upper airway obstruction

Infection (eg, tuberculosis, rhinoscleroma)

Tumor (eg, squamous cell carcinoma of larynx and trachea, hamartoma, hemangioma)

Collagen vascular disease (eg, Wegener’s granulomatosis, relapsing polychondritis)

Sarcoidosis

Amyloidosis

Post-intubation (eg, tracheomalacia, tracheal stenosis)

Mediastinal mass (eg, thymoma, lymphadenopathy)

Vascular abnormality (eg, vascular ring, aortic aneurysm)

Esophageal disorder (eg, achalasia, Zenker’s diverticulum

Laryngeal dysfunction (eg, vocal cord paralysis, vocal cord dysfunction, laryngocele)

Neuromuscular disease (eg, Parkinson’s disease, bulbar palsy)

Tracheobronchopathia osteochondroplastica

Idiopathic (eg, subglottic stenosis)

Prognosis

The prognosis in upper airway obstruction depends on the cause, whether the obstruction is acute or chronic or malignant or benign, and the extent of the disease within the airway; in the case of malignancy, the extent of disease beyond the upper airway is also important.

The prognosis is poor with squamous cell carcinoma of the trachea, which carries a 5-year survival of approximately 40% when resectable and 7% when unresectable. The prognosis is generally more favorable when the cause is an infectious or inflammatory disorder.

What's the evidence?

Abu-Hijleh, M, Lee, D, Braman, SS. “Tracheobronchopathia osteochondroplastica: A rare large airway disorder”. Lung. vol. 186. 2008. pp. 353-9. (Discussion of tracheobronchopathia osteochondroplastica [TO], a rare disorder of the airways, characterized by the development of submucosal cartilaginous and bony nodules.)

Bandi, V, Munnur, U, Braman, SS. “Airway problems in patients with rheumatologic disorders”. Crit Care Clin . vol. 18. 2002. pp. 749-65. (A complete review of a spectrum of airway complications seen in patients with rheumatologic diseases.)

Dool, H, Soetekouw, R, van Zanten, M. “Lemierre's syndrome: three cases and a review”. Eur Arch Otorhinolaryngol. . vol. 262. 2005. pp. 651-4. (A nice review of this rare, and if unrecognized, fatal cause of upper airway obstruction. The syndrome is a complication of head and neck infection, most often due to F. necrophorum. The infection involves the lateral pharyngeal space; it may be complicated by suppurative thrombophlebitis of the internal jugular vein and septic emboli to the lungs and joints.)

Ernst, A, Feller-Kopman, D, Becker, HD. “Central airway obstruction”. Am J Respir Crit Care J . vol. 169. 2004. pp. 1278-97. (A state-of-the-art review of the work-up and treatment of patients with obstruction to the central airways. As bronchoscopy is always necessary in the evaluation, the authors carefully describe the procedure and include information on indications, uses, attention to securing the airway, anesthesia, and therapeutic approaches.)

Ernst, A, Rafeq, S, Boiselle, P. “Relapsing polychondritis and airway involvement”. Chest . vol. 135. 2009. pp. 1024-30. (This article presents a chart review of 145 patients with relapsing polychondritis, 21% of whom had airway involvement. Airway problems included subglottic stenosis; focal and diffuse malacia, and focal airway stenosis.)

Gaissert, HA, Burns, J. “The compromised airway: tumors, strictures, and tracheomalacia”. Surg Clin North Am. . vol. 90. 2010. pp. 1065-89. (The surgical treatment of diseases of the upper airway, including tracheal stenosis. Tracheomalacia, and a variety of airway tumors are discussed.)

Guldfred, LA, Lyhne, D, Becker, BC. “Acute epiglotitis: epidemiology, clinical presentation, management and outcome”. J Laryngol Otol . vol. 122. 2008. pp. 818-23. (The clinical presentation and therapy of this infection are reviewed, and the controversies regarding use of corticosteroids and airway management are discussed.)

Kuo, GP, Torok, CM, Aygun, N. “Diagnostic imaging of the upper airway”. Proc Am Thorac Soc . vol. 8. 2011. pp. 40-5. (Use of advanced imaging modalities, including computed tomography and magnetic resonance imaging, in the diagnosis of upper airway diseases is discussed.)

Lee, KS, Boiselle, PM. “Update on multidetector computed tomography imaging of the airways”. J Thorac Imaging. 2010. pp. 112-24. (This review provides an update on the use of advanced techniques of computed tomography scanning for the noninvasive evaluation of the upper airways.)

Morris, MJ, Christopher, KL. “Diagnostic criteria for the classification of vocal cord dysfunction”. Chest . vol. 138. 2010. pp. 1213-23. (This article addresses vocal cord dysfunction caused by paroxysms of glottic obstruction due to vocal cord adduction. The disorder remains a poorly understood and characterized entity.)

Pana, RS, Moonis, G. “Head and neck inflammation and infection”. Radiol Clin North Am . vol. 49. 2011. pp. 165-82. (A review of the important sites, routes of infection, complications, and radiographic signs of neck infections that may affect the upper airways. Important infections, such as epiglottitis, peritonsillar abscess, Ludwig’s angina, retropharyngeal abscess, Lemierre’s syndrome, and necrotizing fasciitis are discussed.)

Simons, FE. “Anaphylaxis pathogenesis and treatment”. Allergy. vol. 66. 2011. pp. 31-4. (This article discusses the mechanisms, triggers, and treatment of anaphylaxis.)

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