Case Report

High Altitude induced Ortner’s Syndrome Col SS Panwar*, Lt Col AK Mehta+, Surg Cdr RK Verma#, Sqn Ldr B Mukherji** MJAFI 2004; 60 : 182-183

Introduction rtner’s syndrome, a clinical entity first described by Ortner over a hundred years ago, is characterised by hoarseness of voice due to left recurrent laryngeal nerve palsy secondary to cardiac disease [1]. Although Ortner originally described this cardiovocal syndrome in association with mitral stenosis, it is now a recognised complication of a number of cardiac conditions. A series of rare cases of Ortner’s syndrome induced by high altitude pulmonary hypertension, a hithertofore unreported aetiology, which presented at a tertiary referral hospital are reported here.


Case Report-1 A 25 year old serving soldier in good general health developed hoarseness of voice few days after induction to a high altitude forward post at a height of 18000 feet. The onset of hoarseness was sudden without any history of fever, cough, upper respiratory infection, odynophagia, gastroeosophageal reflux or any difficulty in breathing. There was no history of any systemic disease or tuberculosis. He was treated symptomatically as a case of laryngitis, with antibiotics and antihistamines without any relief. His hoarseness continued to persist and after a delay of over two months he was referred for ENT consultation. Clinical examination revealed a left vocal cord palsy with the cord immobile in paramedian position. The rest of larynx and laryngopharynx was normal. Throat, nasal, postnasal and aural examination was also normal. The general and systemic examination was unremarkable. He was investigated to detect the cause of vocal cord palsy. Haematological, serological and biochemical investigations were normal. Chest radiograph showed mild cardiomegaly. Radiographs of skull base and neck were normal. Detailed cardiovascular examination including echocardiography showed normal chamber dimensions, however, there was tricuspid regurgitation and pulmonary regurgitation and the right ventricular systolic pressure was raised, suggesting a diagnosis of pulmonary hypertension. He was diagnosed as a case of Ortner’s syndrome. Since his major complaint was of dysphonia he was subjected to thyroplasty for symptomatic relief of his vocal disorder. Case Report - 2 A 22 year old serving soldier was posted to a high altitude *

post at 19000 feet in October 2001. One month later he developed hoarseness of voice along with cough and pain on left side of chest. Few days later he developed haemoptysis. He was evacuated to a forward hospital where examination of cardiovascular system revealed a loud second heart sound in the pulmonary area, however there were no murmurs or gallop. Electrocardiography showed T wave inversion in right chest leads. He was treated as a case of high altitude pulmonary hypertension. His symptoms of cough, haemoptysis and chest pain regressed but there was no relief in the hoarseness. He was referred for ENT consultation. Examination revealed left vocal cord palsy. All other ENT and systemic examination was normal. All haematological, biochemical and radiological investigations were normal. Echocardiography confirmed pulmonary arterial hypertension. He was thus diagnosed as a case of high altitude related Ortner’s syndrome. Individual was subjected to thyroplasty to correct the dysphonia after laryngeal electromyographic confirmation of absence of reinnervation. Case Report -3 A 20 year old serving soldier in apparent good health developed sudden hoarseness 8 days after induction to a high altitude forward post. Few days later he developed pain and burning sensation in right great toe. He was diagnosed as a case of chillblains of great toe along with laryngitis and was treated symptomatically. The condition of his toe improved, however the hoarseness continued to persist. ENT consultation done later revealed left vocal cord immobile in paramedian position. All other ENT examination and systemic examination was normal. Chest radiograph showed cardiomegaly, ECG and echocardiography confirmed a diagnosis of pulmonary hypertension. Since all other investigations including endoscopy were normal, he was confirmed to be a case of Ortner’s syndrome following high altitude pulmonary hypertension. He was managed conservatively, his hoarseness improved over a period of time due to compensatory movement of right vocal cord.

Discussion The left vagus nerve emerges through the middle compartment of the jugular foramen and runs within the carotid sheath together with the carotid artery and internal jugular vein. In the root of the neck it passes in front of the artery and enters the mediastinum. It then

Senior Advisor (ENT), Army Hospital (R & R), Delhi Cantt, +,#Classified Specialist (ENT), **Medical Officer (ENT), Command Hospital (Western Command), Chandimandir.

Ortner’s Syndrome


descends parallel to the trachea and crosses the arch of aorta deep to the left superior intercostal vein. The left recurrent laryngeal nerve branches off the vagus as it crosses the arch of aorta, it hooks around the ligamentum arteriosum medial to the arch and then ascends in the groove between trachea and oesophagus to enter the larynx behind the cricothyroid joint [2]. Lesions affecting the left vagus nerve or its recurrent laryngeal branch can occur anywhere from the lower motor neuron through jugular foramen, neck, mediastinum to level of aortic arch. Neoplasms account for upto 44% of all vocal cord palsies [3]. The most common lesions are those of lungs, thyroid and oesophagus. Upto 20% of left recurrent laryngeal nerve palsies are caused by surgical trauma of thyroidectomy or cardiac surgery. Idiopathic recurrent laryngeal nerve palsy accounts for a further 20%. The remaining result from cardiovascular, inflammatory or neurological disorders. Ortner originally described a cardiovocal syndrome of left recurrent laryngeal nerve palsy associated with mitral stenosis. However, it is now a recognised complication of a number of conditions including atrial septal defects, patent ductus arteriosus, pulmonary hypertension and aortic aneurysm. The palsy results from the recurrent laryngeal nerve being compressed between the pulmonary artery and the aorta or aortic ligament as a result of enlargement of one or more of these structures due to cardiopulmonary pathology [4].

The cause of pulmonary hypertension at high altitude is not exactly understood. At high altitudes there may be a breakdown of fibrinolytic enzyme systems upsetting the equilibrium between fibrin formation and dissolution, fibrin is thus deposited in the alveolar capillaries, branches of pulmonary arteries and also in the intra alveolar spaces, this results in increased pulmonary vascular resistance leading to right ventricular hypertrophy which may lead to cardiac failure. Vocal cord palsies resulting from cardiac diseases if detected early are reversible following treatment of the underlying cardiac disease [5]. It is essential to recognise this presentation of hoarseness of voice as an early indicator of pulmonary hypertension. Early recognition of this cause of cardiovocal Ortner’s syndrome and induction of prompt treatment of the causative pulmonary hypertension can save the vocal cord from permanent damage. References 1. Bahl DV. Ortner’s syndrome. Case report. Indian Heart Journal 1979;31:176-89. 2. Last RJ. Last’s anatomy, 9 th ed. Churchill Livingstone, Edinburgh, London : 261. 3. Macgregor FB. Vocal cord palsy. A re-evaluation of investigations. J Laryngol Otol 1994;108:193-6. 4. Nakao M. Left recurrent laryngeal nerve palsy. J. Laryngol Otol 1997;38:190-97. 5. Chen L, Lee C. Ortner’s syndrome. J Cardiology 1996;23:34554.

Erratum Please refer Answers to MCQs published in Jan 2004 issue of MJAFI at page 94. For Answer 2-d, read 2-b. The error is regretted.

MJAFI, Vol. 60, No. 2, 2004

High Altitude induced Ortner's Syndrome.

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