Clinical Pearls & Morning Reports
Published November 13, 2019
Substantial advances have been made in preventive medicine, our understanding of the pathophysiology of acute upper-airway obstruction, and surgical and anesthetic technologies, but management of the obstructed airway remains one of the most challenging emergencies in clinical medicine. Read the Review Article here.
Q: What neoplasms may be associated with acute upper-airway obstruction?
A: Neoplasms can lead to acute upper airway obstruction. The most common intrinsic neoplasms associated with airway obstruction are glottic and supraglottic cancers, most often squamous-cell carcinomas. They are often caused by smoking and alcohol abuse, which act synergistically. In rare instances, thyroid cancers invade the airway, leading to both an extrinsic compression effect and an intrinsic narrowing related to intraluminal disease.
Q: How does Ludwig’s angina cause upper-airway obstruction?
A: Patients with Ludwig’s angina have bilateral infection of the sublingual and submandibular spaces that is characterized by submental and submandibular induration, cellulitis, and a swollen and tender floor of mouth, all of which result in a posteriorly displaced tongue. This displacement ultimately leads to obstruction at the oropharyngeal and supraglottic levels and can be life-threatening. The most common causes of Ludwig’s angina are dental infections, followed by sialadenitis, peritonsillar abscess, abscess involving the parapharyngeal space, traumatic injuries to the oral cavity, and mandibular fractures.
A: Approximately 15% of patients with burn injuries have inhalation injury, which, along with the total body-surface area of the burn, is an important independent predictor of mortality. Patients with inhalation injuries tend to have long-term laryngological complications. Consequent to local inflammation and edema, patients may have granulation tissue, scarring, webbing, vocal-cord immobility, stenosis, and laryngeal hyperfunction. The subglottis is particularly sensitive, and patients with inhalation injuries have an earlier onset and more severe stenosis than those whose subglottic stenosis is due to other causes. The earlier onset and greater severity associated with subglottic stenosis in these patients have led to calls for earlier use of tracheostomy.
A: Angioedema is characterized as recurrent, nonpitting, nonpruritic swelling of the deep layers of the skin and mucosal tissues. It may be hereditary, acquired, drug induced, or idiopathic. Hereditary angioedema, an autosomal dominant condition, results from deficiency of the C1 esterase inhibitor, which may reflect inadequate levels (type I) or function (type II). A recent change in guidelines recommends that patients carry on-demand treatment for hereditary angioedema at all times and consider short-term prophylaxis before undergoing procedures that can induce an attack. The revised guidelines recommend consideration of on-demand treatment (with self-dosing of a C1 esterase inhibitor) for all attacks, treatment of attacks affecting the upper airway, early treatment, and initiation of treatment with a C1 inhibitor — either ecallantide (a kallikrein inhibitor) or icatibant (a bradykinin receptor antagonist). The consensus guidelines recommend screening children from families with a history of hereditary angioedema and all offspring of an affected patient. Because the diagnosis is often delayed, a low threshold for screening in the emergency department is recommended, particularly in patients with a family history of angioedema.