Show Summary Details
Page of

Upper airway obstruction in the critically ill 

Upper airway obstruction in the critically ill
Chapter:
Upper airway obstruction in the critically ill
Author(s):

Edmond Cohen

DOI:
10.1093/med/9780199600830.003.0079
Page of

PRINTED FROM OXFORD MEDICINE ONLINE (www.oxfordmedicine.com). © Oxford University Press, 2021. All Rights Reserved. Under the terms of the licence agreement, an individual user may print out a PDF of a single chapter of a title in Oxford Medicine Online for personal use (for details see Privacy Policy and Legal Notice).

date: 28 October 2021

Key points

  • Partial upper airway obstruction (UAO) may progress to complete obstruction.

  • UAO should be managed by personnel trained to manage airway crises using a supraglottic device, by performing tracheal intubation and, if necessary, by establishing a surgical airway.

  • Do not burn any bridges! Sedatives, neuromuscular blocking drugs or airway manipulation may precipitate complete airway obstruction.

  • Airway management devices must be immediately available before attempting any airway manipulation.

  • UAO that develops gradually may not be obvious in a patient at rest. Sudden clinical deterioration is unpredictable. Noisy breathing is better than silence and no breathing.

Presentation

In a conscious patient, upper airway obstruction (UAO) may present as respiratory distress, stridor, dyspnoea, altered voice, cyanosis, cough, decreased or absent breath sounds, wheezing, the hand-to-the-throat choking sign in the case of a foreign body, facial swelling, and distended neck veins. Respiratory depression must be avoided to prevent cardiac arrest and anoxic brain injury. Partial airway obstruction may be mild, as in snoring or nasal congestion, or may be more severe, perhaps requiring the use of airway adjuncts. Complete UAO is usually managed by prompt intubation, but in some situations a surgical airway is life-saving [1]‌.

Causes of upper airway obstruction

Although obstruction can occur at any level of the upper respiratory tract, laryngeal obstruction is especially important because the glottis is the narrowest portion of the upper airway (UA) [2]‌. UAO may be anatomical or functional, and may develop acutely or subacutely (Box 79.1).

The presence of stridor is ominous. Stridor is a noisy inspiration caused by turbulent gas flow in the UA and is common during airway obstruction [3]‌. Stridor indicates a serious airway emergency because it can progress rapidly to complete UAO. It is important to establish the aetiology of stridor and determine whether the obstruction can be safely treated by positive pressure mask ventilation or requires tracheal intubation.

Upper airway obstruction during anaesthesia

The induction of general anaesthesia is accompanied by a decrease in UA muscle tone and possibly even airway collapse. UAO may occur depending on the airway’s calibre and shape, extraluminal tissue pressure and airway wall compliance [4]‌. Light sedation offers some protection against obstruction by maintaining muscle tone, whereas deep sedation is associated with muscle relaxation and lack of arousability, which may result in UAO. During anaesthesia, airway maintenance requires active intervention either by mask ventilation or tracheal intubation until the patient regains the ability to spontaneously maintain a patent airway.

Common causes of UAO during anaesthesia include:

  • Laryngospasm following tracheal extubation due to an irritable airway (common among smokers). Initial treatment is positive pressure ventilation, but sometimes a small dose of succinylcholine (~20 mg iv) may be necessary to break the laryngospasm.

  • Residual neuromuscular block despite the administration of reversal agents. Patients with impaired renal function require special attention because of their decreased ability to clear drugs.

  • Residual opioid medications can cause respiratory depression and UAO in the post-anaesthesia care unit (PACU).

Obstructive sleep apnoea

Obstructive sleep apnoea (OSA) patients are at increased risk of developing UAO. Factors that act to narrow the airway and predispose to OSA are similar to those that predispose to UAO under anaesthesia [5]‌. These include increasing age, male gender distribution of body fat, obesity, increased neck circumference (>17 inches), macroglossia, retrognathia, and maxillary constriction [6]. Loud snoring suggests the presence of a narrow floppy airway that causes recurrent episodes of partial or complete UAO, apnoea, and hypoxaemic episodes during sleep [7].

With sleep, sedation or anaesthesia, upper airway collapsibility increases as a result of a reduction in pharyngeal dilator muscle activation, loss of the stimulatory effect of wakefulness, reduction in respiratory drive, and depression of negative pressure reflexes. In normal individuals without anatomic compromise, the upper airway is robust and patency is not significantly compromised. However, in individuals with anatomically vulnerable airways, these changes can precipitate partial or complete upper airway obstruction [8]‌.

Many OSA patients use a continuous positive airway pressure (CPAP) machine to maintain airway patency during sleep. CPAP titrated to the patient’s need should be readily available for use in the peri-operative period. The American Society of Anesthesiologists (ASA) has published guidelines for the identification and management of patients with OSA [8]‌.

Obesity

Obese patients often have a ‘bull neck’, macroglossia, and/or redundant folds of pharyngeal tissue, rendering them difficult-to-intubate and at increased risk of developing UAO. Mask ventilation may be challenging because of difficulty in maintaining a patent airway, decreased chest wall compliance, decreased FRC, and a high risk of aspiration. If tracheal intubation is not planned, a supraglottic airway device can be effective. If tracheal intubation is planned, adequate pre-oxygenation, and rapid sequence induction with cricoid pressure is recommended. If there is any concern about securing the airway safely, an awake fibre optic intubation is recommended.

Airway polyps

Polyps may occur anywhere in the upper airway and lead to partial or complete UAO. Vocal cord granulomas and polyps may result from traumatic intubation, vocal cord irritation from tracheal tube movement, or from lubricants. Patients with laryngeal papillomatosis may require frequent laser treatments to eradicate the papillomas.

Thyroid goitre

A large thyroid goitre can compress the trachea and, over time, cause tracheomalacia. A retrosternal goitre may exert pressure on the trachea causing partial airway obstruction. The CT scan should be reviewed preoperatively to assess the extent of any tracheal obstruction. If compression is severe, mask ventilation is challenging in these patients, who may progress to complete UAO. If the lesion is anterior to the trachea, the airway obstruction can worsen when the patient is placed supine for induction of general anaesthesia. In such cases, an awake fibre optic intubation would probably be best for the patient’s safety. A potential complication of thyroidectomy is uni- or bi-lateral recurrent laryngeal nerve injury, which can result in uni- or bi-lateral vocal cord paralysis. Careful evaluation of the airway (vocal cord movement) following tracheal extubation is therefore crucial [9]‌. Finally, UAO may result from post-thyroidectomy bleeding in the PACU. If this is suspected, immediate re-opening of the surgical incision to relieve the extrinsic tracheal pressure can be life-saving.

Mediastinal masses

When a patient presents with an anterior mediastinal mass, careful evaluation of the degree of tracheal compression is critical. Some cases are associated with superior vena cava obstruction syndrome. Difficulty breathing when supine or pulmonary function tests showing an obstructive pattern, is cause for concern. Close interaction with the surgeon and review of the CT scan are essential when planning management. Anaesthesia is needed primarily for diagnostic biopsies, staging of neoplasms, and (occasionally) for relief of acute airway obstruction [10]. Use of short-acting agents, small doses of opioids, and adequate post-operative pain management should allow the patient to be tracheally extubated when fully awake. Maintaining spontaneous ventilation is preferable. A rigid bronchoscope should be immediately available in case complete airway obstruction develops. Turning the patient to the lateral position decreases pressure on the airway. If the tracheal obstruction is severe, a tracheal stent placed under sedation can provide some protection prior to the induction of general anaesthesia.

Epiglottitis

Epiglottitis can occur in adults, but is less symptomatic than in children because the adult airway is larger [11]. Management is challenging because the swollen epiglottis can act as a valve mechanism and obstruct the airway. For any surgical intervention, awake fibre optic intubation is the safest approach. These patients should not be paralysed prior to securing the airway because that would only exacerbate the degree of UAO.

Damage from endotracheal intubation

Acquired subglottic stenosis is a complication of long-term tracheal intubation. Tracheal tube complications are usually due to incorrect size, over-inflated cuff, traumatic or multiple intubations, and movement of the tube due to inadequate analgesia and sedation. Cooper and Grillo [12] studied tracheal stenosis at the cuff site and found that the main cause was the pressure exerted by the cuff. Cuff pressures >30 mmHg (> 4 kPa) cause mucosal ischaemia by exceeding mucosal capillary perfusion pressure. The ischaemic area can develop chondritis and granulation tissue, then heal by fibrosis, leading to progressive tracheal stenosis. Most cases of post-extubation stridor resolve with appropriate medical interventions, such as racemic epinephrine or corticosteroids. Fibre optic bronchoscopy may reveal the formation of soft granulation tissue that can often be treated by the use of the CO2 laser. In clinical practice, if a patient fails extubation for 2 weeks, an elective tracheostomy should be performed to avoid the development of tracheal stenosis.

Acquired vocal-cord paralysis or dysfunction

Vocal cord paralysis may be uni- or bi-lateral. The most common cause is damage to the recurrent laryngeal nerve (RLN) leading to transient or permanent cord paralysis. Damage to the RLN can result from a laryngeal, thyroid, or Pancoast tumour and from neck or mediastinal surgery. On spontaneous inspiration, the flaccid vocal cord becomes adducted across the midline, creating inspiratory airflow obstruction. UAO may result from vocal cord adduction during inspiration. It presents as acute attacks of dyspnoea, stridor or wheeze, and complaints about tightness at the neck. Tracheomalacia, in contrast, presents as airway obstruction during exhalation because of lack of support from the tracheal rings. Tracheomalacia is a condition in which there has been a weakening of the cartilaginous structures of the trachea [13]. Typical causes are rheumatic (polychondritis), infectious, secondary to external beam radiation, and secondary to trauma or surgery. In all these cases of UAO, the best treatment is to apply gentle positive pressure ventilation with a face mask. This may temporarily overcome the obstruction until a more definitive solution can be established.

Clinical evaluation of uao

Airway resistance varies inversely with the fourth power of the radius at the point of UAO, and small changes in the underlying pathology may dramatically worsen respiratory airflow. Based on the patient’s history and physical examination, it is useful to separate patients with potential UAO into those with severe symptoms and impending respiratory failure who require immediate intervention, from those with a more gradual course and less severe symptoms.

Plain X-ray and CT scan

Plain neck and chest films are useful screening tests that identify tracheal deviation, extrinsic compression, or presence of a foreign body. Computed tomography (CT) can be important in investigating UAO in a patient who is haemodynamically stable or in one who is unstable, but whose airway has already been secured. A CT scan focused on the airway evaluates the entire airway with thinner ‘cuts’. If thicker cuts are used, one can underestimate, or miss the site of stenosis or obstruction. High-resolution CT of the neck and chest helps identify intrinsic and extrinsic tumours, vascular structures, and foreign bodies, as well as provides information on the degree and extent of airway compromise in UAO [14]. The risks and benefits of transporting such a patient to the radiology suite for examination must be carefully considered and a person qualified in airway management should accompany the patient.

Pulmonary function testing

Spirometry is useful in patients with gradual onset and mild symptoms of UAO. Flow-volume loops may identify the location and functional severity of the obstruction. Spirometry has no role in the management of a patient with acute respiratory distress [15]. The flow-volume loop shows an obstructive pattern. The flow-volume loop in a patient with fixed UAO shows flattening of the inspiratory and the expiratory phases. The test is performed with the patient upright and is repeated in the supine position to assess the degree of tracheal compression from an intrathoracic mass. The main purpose is to evaluate is the degree of airflow obstruction. It is an effort-dependent test and, therefore, requires the patient’s cooperation.

Rigid and flexible bronchoscopy with direct visualization

Bronchoscopy is the primary procedure in the diagnostic work-up of tracheal stenosis and is key in defining the characteristic features, extent, and location of the stenosis. Bronchoscopy is performed with the patient awake and breathing spontaneously following adequate airway topicalization. A rigid bronchoscope should be available for emergency use to secure the airway by carefully passing it through the stenotic segment. Flexible bronchoscopy is useful to establish the diagnosis and deliver treatments including laser therapy, electrocautery, electrosurgery, balloon dilatation, and metal stenting once the airway has been secured and the patient stabilized [16]. Light sedation may be used. Dexmedetomidine infusion is useful because respiratory drive is maintained. Performing a fibre optic bronchoscopy in a conscious patient enables examination of vocal cord function and determination if RLN damage is present. It also permits the evaluation of dynamic airway collapse with respiration.

Management

In all cases of UAO, a rapid evaluation considering age group, history, physical examination, and clinical circumstances helps determine the site, cause, and the severity of the obstruction, and the urgency for establishing an airway. An actual or potential obstruction that impairs ventilation must be immediately addressed. If obstruction is near-complete, mask ventilation or a supraglottic airway device (e.g. laryngeal mask airway (LMA)) may alleviate the obstruction, otherwise prompt tracheal intubation may be life-saving. Management of UAO can be pharmacological or interventional (i.e. supraglottic device, tracheal tube, or a surgical airway).

Pharmacological management

Racemic epinephrine

Racemic epinephrine is used in patients with partial UAO who are conscious and breathe spontaneously. Racemic epinephrine administered by nebulizer is effective by inducing vasoconstriction, which decreases mucosal oedema. Racemic epinephrine is also used to treat laryngeal oedema following extubation. The typical case is a patient, breathing easily for the first 2–3 hours, followed by the gradual progression of dyspnoea, inspiratory stridor, and increased respiratory effort. In this situation, racemic epinephrine can be used as a temporizing measure until the acute swelling and inflammation subside. These patients should be carefully monitored in the ICU until there is confirmation that the UAO has resolved, or at least greatly improved.

Corticosteroids

Corticosteroids, such as dexamethasone are used to treat UAO because of their effect in reducing airway oedema. Corticosteroids given at the time of tracheal extubation decrease capillary dilatation and permeability, oedema formation, and inflammatory cell infiltration. Randomized trials have confirmed the efficacy of corticosteroids in the treatment of croup, decreasing the need for intubation and hospital stay. Although the prophylactic use of steroids for post-extubation laryngeal oedema is widely accepted, one placebo-controlled, double-blind, multicentre study reported that dexamethasone does not prevent laryngeal oedema after tracheal extubation, regardless of duration of intubation [17].

Heliox

The low density of a helium–oxygen (heliox) gas mixture decreases the work of breathing by decreasing airway resistance to turbulent gas flow across the obstruction. Heliox has been useful in the treatment of post-extubation laryngeal oedema, tracheal stenosis or extrinsic compression, status asthmaticus, and angioedema [18]. Benefit is temporary because the obstruction remains until relieved. To be effective, the helium–oxygen ratio must be at least 70:30%, which limits its use in patients who cannot tolerate a low FiO2.

Tracheal intubation and tracheostomy

In most cases of UAO, the airway can be established with tracheal intubation. If the airway is difficult, many video laryngoscopes are commercially available to facilitate the intubation, otherwise fibrescopic intubation may be necessary. If an airway cannot be established, a surgical airway via cricothyrotomy, tracheostomy, or retrograde intubation should be performed. The method of intervention should be individualized for each patient. The intervention chosen will depend on the aetiology of UAO and the urgency with which the airway must be secured.

The surgical airway-securing procedures require special expertise. Comparison of emergent versus elective tracheostomy reveals a two-fold complication rate in the former due to time spent isolating the trachea as a result of bleeding.

Laser therapy

Carbon dioxide or neodymium-doped yttrium-aluminium-garnet (Nd:YAG) laser therapy is used to treat intraluminal tracheobronchial lesions once the UAO has been stabilized and an airway secured. Although the onset of airway compromise is usually gradual, some patients remain asymptomatic despite airways that are only 2–3 mm in diameter. These patients only develop dyspnoea on exercise or when complete obstruction results from mucus, bleeding, inflammation, or swelling. It is easy to underestimate the risk of progression to a complete UAO. Laser therapy can be used to excise tracheal webs, treat benign obstructive lesions, or as palliative therapy for malignant tracheobronchial lesions [19].

Tracheal dilatation and stenting

Stents are usually placed following dilatation and maintain airway patency in patients with tracheal obstruction from benign or malignant conditions. A stent supports the airway wall against collapse or external compression, and impedes extension of tumour into the airway lumen. Rigid bronchoscopy is used to place a silicone stent or a flexible bronchoscope to deploy a metal stent. They are used either in the preparation for a more definitive resection procedure or palliative to alleviate the tracheal compression. If an intraluminal tumour is significant enough to cause UAO, it can be managed with laser therapy, photodynamic therapy, brachytherapy, or electrocautery.

The management of UAO is summarized in Fig. 79.1. Whatever the aetiology, a patient with UAO must be carefully monitored in an intensive care unit for impending respiratory failure [20].

Fig. 79.1 Clinical approach to upper airway obstruction.

Fig. 79.1 Clinical approach to upper airway obstruction.

References

1. Hagberg C, Georgi R, Krier C, et al. (2005). Complications of managing the airway. Best Practice & Research Clinical Anaesthesiology, 19, 641–59.Find this resource:

2. Dickison AE. (1987). The normal and abnormal pediatric upper airway. Recognition and management of obstruction. Clinical Chest Medicine, 5, 83–96.Find this resource:

3. Renz V, Hern J, Tostevin P, Hung T, and Wyatt M. (2000). Functional laryngeal dyskinesia: an important cause of stridor. Journal of Laryngology & Otology, 114, 790–2.Find this resource:

4. Eastwood PR, Szollosi I, Platt PR, et al. (2002). Collapsibility of the upper airway during anesthesia with isoflurane. Anesthesiology, 97, 786–93.Find this resource:

5. Malhotra A, Huang Y, Fogel R, et al. (2006). Aging influences on pharyngeal anatomy and physiology: the predisposition to pharyngeal collapse. American Journal of Medicine, 119, 9–14.Find this resource:

6. Young T, Peppard PE, and Taheri S. (2005). Excess weight and sleep disordered breathing. Journal of Applied Physiology, 99, 1592–9.Find this resource:

7. Hillman DR, Platt PR, and Eastwood RP. (2010). Anesthesia, sleep, and upper airway collapsibility. Anesthesiology Clinics, 28(3), 443–55.Find this resource:

8. Gross JB, Bachenberg KL, and Benumof JL. (2006). American Society of Anesthesiologists Task Force on perioperative management of patients with obstructive sleep apnea: practice guidelines for the perioperative management of patients with obstructive sleep apnea. Anesthesiology, 104, 1081–91.Find this resource:

9. Graham, GW, Unger, BP, and Coursin DB. (2000). Perioperative management of selected endocrine disorders. International Anesthesiology Clinics, 38(4), pp. 31–67.Find this resource:

10. Conacher ID. (2003). Anaesthesia and tracheobronchial stenting for central airway obstruction in adults. British Journal of Anaesthesia, 90, 367–74.Find this resource:

11. Ames WA, Ward VM, Tranter RM, and Street M. (2000). Adult epiglottitis: an under-recognized, life-threatening condition. British Journal of Anaesthesia, 85, 795–7.Find this resource:

12. Cooper JD and Grillo HC. (1969). The evolution of tracheal injury due to ventilatory assistance through cuffed tubes: a pathologic study. Annals of Surgery, 169, 334–48.Find this resource:

13. Cansiz H, Yener M, Tahamiler R, et al. (2008). Preoperative detection and management of tracheomalacia in advanced laryngotracheal stenosis. B-ENT 4, 163–7.Find this resource:

14. Boiselle PM and Ernst A.(2002). Recent advances in central airway imaging. Chest, 121, 1651–60.Find this resource:

15. Culver BH. (2004). Pulmonary function and exercise testing. In: Albert RK, Spiro SG, and Jett JR (eds) Clinical Respiratory Medicine, 2nd edn, pp. 117–28. Philadelphia, PA: Elsevier Saunders.Find this resource:

16. Shapshay SM and, Valdez TA. (2001). Bronchoscopic management of benign stenosis. Chest Surgery Clinics of North America, 11, 749–68.Find this resource:

17. Klassen TP, Craig WR, Moher D, et al. (1998). Nebulized budesonide and oral dexamethasone for treatment of croup: a randomized controlled trial. Journal of the American Medical Association, 279,7 1629–32.Find this resource:

18. Boorstein JM, Boorstein SM, Humphries GN, et al. (1989). Using helium–oxygen mixtures in the emergency management of acute upper airway obstruction. Annals of Emergency Medicine, 18, 688–90.Find this resource:

19. Bolliger CT, Sutedja TG, Strausz J, et al. (2006). Therapeutic bronchoscopy with immediate effect: laser, electrocautery, argon plasma coagulation and stents [comment]. European Respiratory Journal, 27, 1258–71.Find this resource:

20. Wood DE, Liu YH, Vallieres E, et al. (2003). Airway stenting for malignant and benign tracheobronchial stenosis. Annals of Thoracic Surgery, 76, 167–74.Find this resource: