A 39-year-old otherwise healthy man presented to the emergency department (ED) with a 2-month history of hoarse voice and progressive dyspnea on exertion. He reported a preceding flu-like illness with negative COVID-19 testing at the time. Physical examination was notable for a pulse rate of 113 beats/min and a hoarse voice. Bedside nasopharyngoscopy by the ED team demonstrated left vocal cord paresis (Figure 1 , Video E1 [available at http://www.annemergmed.com]). Chest radiography showed marked cardiomegaly (Figure 2 ). Laboratory studies were notable for a pro b-type natriuretic peptide of 2,444 pg/mL. The patient was admitted to the cardiology service with a diagnosis of acute systolic heart failure. Cardiac catheterization demonstrated severe global systolic dysfunction without angiographically apparent coronary artery disease. COVID-19 antibody testing returned positive.
Figure 1.
Flexible nasopharyngoscopy demonstrating left vocal cord paresis (arrow).
Figure 2.
Chest radiograph (posteroanterior) demonstrating marked cardiac enlargement (arrows).
Diagnosis
Ortner syndrome, also known as cardiovocal syndrome. When cardiovascular structures enlarge, they may compress the left recurrent laryngeal nerve, a terminal branch of the vagus nerve, between the aortic arch and pulmonary artery.1 , 2 This space, known as the aortopulmonary window, can be as small as 4 mm.3 The recurrent laryngeal nerves supply motor function to all laryngeal muscles but the cricothyroid muscle. Therefore, the compression of a recurrent laryngeal nerve can lead to unilateral vocal cord paresis and hoarseness.1 After 4 days of medical management for presumed viral-mediated nonischemic cardiomyopathy, this patient was discharged. As an outpatient, he underwent vocal medialization for symptomatic treatment of hoarseness.
Footnotes
For the diagnosis and teaching points, see page 30.
To view the entire collection of Images in Emergency Medicine, visitwww.annemergmed.com.
Supplementary Data
References
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