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Postoperative Left Vocal Cord Dysfunction Caused by Ortner’s Cardiovocal Syndrome

Hebl, James R. MD; Rose, Steven H. MD; Narr, Bradly J. MD; Rorie, Duane K. MD, PhD

doi: 10.1097/00000539-200104000-00050
Case Report: Case Report

Department of Anesthesiology, Mayo Clinic and Foundation, Rochester, Minnesota

December 7, 2000.

Address correspondence to James R. Hebl, MD, Department of Anesthesiology, Mayo Clinic, 200 First St. Southwest, Rochester, MN, 55905. Address e-mail to

IMPLICATIONS: Postoperative hoarseness is a complication of endotracheal intubation. However, etiologies unrelated to surgical or anesthetic events may also be involved in this common postoperative condition. Ortner’s cardiovocal syndrome is the development of unilateral vocal cord paralysis secondary to abnormal cardiac or pulmonary anatomy. This syndrome should be considered as a potential cause of postoperative hoarseness in patients with identified risk factors preoperatively.

Postoperative hoarseness is a complication of endotracheal intubation. Important etiologies may include airway instrumentation with resultant edema, granuloma or nodule formation, hematoma, arytenoid dislocation, and vocal cord paralysis (1). However, the development of unilateral vocal cord paralysis postoperatively may also be caused by abnormal cardiac and/or vascular anatomy induced by specific disease states. Several disease-induced changes in cardiovascular and pulmonary anatomy cause impaired conduction through the left recurrent laryngeal nerve (2–6). We present such a case that occurred postoperatively in a patient with left atrial enlargement secondary to mitral regurgitation and significant pulmonary hypertension whose injury was initially attributed to endotracheal intubation for a surgical procedure.

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Case Report

An 80-yr-old man with a history of compensated congestive heart failure, chronic atrial fibrillation, and mitral regurgitation, 10 years after mitral valve repair, presented for abdominal exploration after a 2-day history of right lower quadrant pain and hematochezia. The presumptive diagnosis was diverticulitis. The preoperative electrocardiogram showed atrial fibrillation with a ventricular rate of 71 bpm, nonspecific ST-T wave abnormality, and a prominent U wave. A chest radiograph demonstrated previous sternotomy, marked cardiomegaly, and a tortuous aorta.

After an IV induction of anesthesia with thiopental and succinylcholine, the trachea was intubated easily and uneventfully with an 8.5-mm oral endotracheal tube. Excellent visualization of the vocal cords indicated normal appearance and symmetrical relaxation bilaterally. There was no documentation of previous trauma or other related complications. A nasogastric tube and esophageal stethoscope were also placed without difficulty after intubation. Maintenance anesthesia included isoflurane, morphine, and cisatracurium in an oxygen/air mixture. The 3.5-h intraoperative course was without problems, and the trachea was extubated 30 min after arrival in the recovery room.

Twenty-four hours after completion of the surgical procedure, the patient was admitted to the intensive care unit because of increasing shortness of breath, tachypnea, and moderate hypoxemia. A chest radiograph demonstrated marked cardiac enlargement with prominent pulmonary vasculature and bilateral pleural effusions. Hemodynamic monitoring revealed pulmonary artery pressures of 50/20 mm Hg with a pulmonary artery occlusion pressure of 25 mm Hg. Transthoracic echocardiography at that time demonstrated “Grade III/IV mitral regurgitation with enormous left atrial enlargement.” A diagnosis of congestive heart failure exacerbation was made, and the patient was diuresed. On the third postoperative day, the patient noted difficulty with his voice and hoarseness which was unchanged at the time of his discharge from the hospital on the twelfth postoperative day.

On Postoperative Day 21, the patient was evaluated by an otorhinolaryngologist because of persistent hoarseness. He was diagnosed with “paramedian paralysis of the left vocal cord, possibly secondary to recent intubation.” He continued to be treated as an outpatient for repeated exacerbations of his congestive heart failure over the next several weeks. Ten weeks after his surgical exploration and diverticular resection, the patient returned to his preoperative weight, and was believed to be normovolemic. At 5 mo postoperatively, he continued to note hoarseness, though improving, and was reevaluated by an otorhinolaryngologist. This follow-up examination revealed “satisfactory adduction of both vocal cords and near resolution of symptoms.” The patient has remained normovolemic and with minimal hoarseness since that time.

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Ortner’s cardiovocal syndrome is a clinical entity manifested by hoarseness caused by an impaired ability of the left recurrent laryngeal nerve to transmit impulses to laryngeal musculature because of stretching or impingement of the nerve from disease-induced changes in cardiac or great vessel anatomy. It was first described in 1897 by Ortner (7) in patients with left atrial enlargement secondary to mitral valve stenosis. Subsequently, it has been reported to occur in a variety of cardiopulmonary disease states, including thoracic aortic aneurysms, patent ductus arteriosus, primary pulmonary hypertension, atrial and ventricular septal defects, Eisenmenger’s syndrome, and recurrent pulmonary embolism (2–6). The incidence of left vocal cord paralysis in patients with disease-induced changes in cardiac and vascular anatomy is infrequent. However, patients with mitral stenosis tend to be at increased risk, demonstrating frequencies of 0.6% to 5%(8). Although our patient did not have mitral stenosis, he did have significant mitral regurgitation with left atrial enlargement in addition to pulmonary hypertension.

Ortner deduced that, in the presence of mitral stenosis, the enlarged left atrium pushed the laryngeal nerve upward compressing it against the aortic arch resulting in ischemic injury and degeneration of nerve fibers. However, subsequent anatomic and radiographic studies have made Ortner’s original theory less plausible than other possibilities according to some investigators. Fetterolf and Norris (9) used cadaveric studies to demonstrate that the distance between the aorta and pulmonary artery within the aortic window is only 4 mm. Therefore, they concluded that the primary mechanism of injury must include compression of the left recurrent laryngeal nerve between the left pulmonary artery and aorta at this location. This theory was further supported by Ari et al. (10) when they found the left recurrent laryngeal nerve being compressed between an enlarged left pulmonary artery and aorta near the ligamentum arteriosum in two patients with mitral stenosis and hoarseness who were undergoing mitral commissurotomy. Ancillary factors that may contribute to the primary mechanism of injury include mediastinitis, pericarditis, lymphadenopathy and scarring within the aortic window, and anatomic variations of the left bronchus and ligamentum arteriosum (8). The natural history of the disorder generally results in resolution of symptoms if there is early detection and correction or treatment of the underlying cardiovascular etiology.

In summary, postoperative hoarseness has many potential causes. These include those with anesthetic implications, such as laryngeal trauma during laryngoscopy, extreme head rotation, flexion, or extension, excessive or asymmetrical endotracheal cuff inflation, prolonged intubation, concomitant esophageal stethoscope or nasogastric tube use, or transesophageal echocardiography probe placement. Additional causes include direct surgical trauma, preexisting neuropathies, or medical conditions such as Ortner’s cardiovocal syndrome. Differentiating factors among these potential etiologies may be difficult to elicit. However, the majority of “anesthetic-related” causes of postoperative hoarseness are generally evident immediately after extubation, and are resolved within four to six weeks (11,12).

In the present case, our patient did not complain of hoarseness until the third postoperative day, and continued for nearly six months. This chronological time frame coincides with the patient’s significant mitral regurgitation and severe pulmonary hypertension that occurred three days postoperatively during an exacerbation of his congestive heart failure. In the absence of direct surgical trauma and apparent anesthetic complications, we believe factors related to the patient’s cardiopulmonary status contributed significantly to the onset and subsequent resolution of his left vocal cord palsy. Although this may seemingly be a rare postoperative event, early recognition and rapid treatment or correction of the underlying cardiac or vascular anomaly is critical to a successful recovery. Therefore, we believe anesthesia providers should be aware of Ortner’s cardiovocal syndrome as a potential cause of postoperative hoarseness. This syndrome may especially be relevant in patients who have a history of mitral stenosis or regurgitation with associated left atrial enlargement and pulmonary hypertension. Consideration must also be given to informing the patient preoperatively that vocal cord dysfunction may occur postoperatively if these risk factors are known to be present.

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