Vocal Cord Paralysis Associated with Pulmonary Emboli

ROBERT E. ALBERTINI

508 Subsequent to this, the patient had an uneventful course and bretylium was stopped on the 12th postoperative day. The patient was discharged on June 27, 1970 on 400 mg of quinidine every six hours, digoxin 0.25 mg daily and isosorbide dinitrate (Isordil). Since then, he has been doing well on digoxin, furosemide (Lasix ) 40 mg daily, warfarin, isosorbide dinitrate and quinidine 300 mg every six hours and has remained free of arrhythmia until now, a total follow-up period of 14 months. DISCUSSION

Association of ventricular tachycardia with ventricular aneurysm is now well documented.v" Various antiarrhythmic drugs have been used for controlling this arrhythmia. Recently, bretylium tosylate" and artificial pacingt-" have shown promising results in selected cases of resistant ventricular tachycardia. The exact mechanism by which ventricular aneurysm contributes to the production and intractability of the ventricular tachycardia is not clear. As suggested by Ritter et al, 2 establishment of circus movement around the aneurysmal orifice may playa role. As we already know, ischemic dead and fibrosed tissue may help in establishing reentry phenomenon by creating an area of relative refractoriness and decrimental conduction and it can also act as an independently firing ectopic pacemaker site by being protected from depolarization due to entrance block. 9 Ventricular arrhythmia in our case was not precipitated by acute myocardial infarction as evidenced by serial ECG and enzyme studies. These two cases add to the literature that postmyocardial infarction, ventricular aneurysms may contribute to the refractoriness of ventricular tachycardia and the successful outcome obtained here suggests that the aneurysmal resection could be the logical procedure for intractable recurrent ventricular tachycardia. REFERENCES

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Couch OA: Cardiac aneurysm with ventricular tachycardia and subsequent excision of aneurysm. Circulation 20:251253, 1959 Ritter ER: Intractable ventricular tachycardia due to ventricular aneurysm with surgical cure. Ann Intern Med 71:1155-1157,1969 Hunt D, Sloman G, Westlake G: Ventricular aneurysmectomy for recurrent tachycardia. Br Heart J 31 :264-266, 1969 Thind GS: (Letters and comments) . Ann Intern Med 72:603-604, 1970 Maloy WC: Arrants JE, Sowell BF, Hendrix GH: Left ventricular aneurysm of uncertain etiology with recurrent ventricular arrhythmias. New Eng J Med 285:662, 1971 Macalpin RN, Zalis EG, Kivowitz CF: Prevention of recurrent ventricular tachycardia with oral bretylium tosylate. Ann Intern Med 72:909-912, 1970 DeSanctis RW, Kastor JA: Rapid intracardiac pacing for treatment of recurrent ventricular tachyarrhythmias in the absence of heart block. Am Heart J 76: 168-172, 1968 McCallister BD, McGoon DC, Connolly DC: Paroxysmal ventricular tachycardia and fibrillation without complete heart block. Am J Cardiol 18:898-903, 1966 Han J: Mechanisms of ventricular arrhythmias associated with myocardial infarction. Am J CardioI24:800-813, 1969

Vocal Cord Paralysis Associated with Pulmonary Emboli* Robert E. Albertini, M.D. oo

The first reported case of left vocal cord paralysis caused by pulmonary embolization is presented. The apparent mechanism was compression of the recurrent laryngeal nerve against the aorta by a dilated, tense pulmonary artery, enlarged as a result of embolic vascular obstruction. Perfusion lung scanning should be a part of the evaluation of patients with paralysis of the left vocal cord, when recurrent pulmonary embolization is a possibility. vocal cord paralysis occurring as an indirect conL eftsequence of cardiovascular disease was first recog-

nized in 1897 when Ortner! described this finding in association with mitral stenosis. Other causes which have been well documented since that time include hypertensive" and coronary heart disease.v" aortic aneurysm," atrial septal defeet,"-" patent ductus arteriosus," and Eisenmenger's complex."? This report concerns a patient with left vocal cord paralysis associated with recurrent pulmonary emboli, a previously unreported cause. CASE REPORT

A 46-year-old housewife was admitted to the Geisinger Medical Center complaining of hoarseness for two months. She had noted easy fatigability and dyspnea on exertion for several years and had recently experienced recurrent episodes of mild chest pain. Three pregnancies, the first at age 28, had been complicated by thrombophlebitis involving the left lower extremity. As a consequence, this limb had remained larger than the right for many years, although the patient had noted no further acute symptoms suggesting active phlebitis. At the age of 32 she had had an intracranial venous thrombosis which required a subtemporal decompression. Positive findings on physical examination included obvious hoarseness and central cyanosis. The left vocal cord was paralyzed. There was a prominent left parasternal systolic outthrust, and auscultation disclosed accentuation of the pulmonic component of the second heart sound and a loud presystolic gallop. The entire left lower extremity was considerably larger than the right, and there were minimal signs of deep thrombophlebitis in the left calf. On arterial blood gas analysis, the P02 was 37 mm Hg, oxygen saturation 66 percent, PC02 40 mm Hg, pH 7.38. Chest fllm (Fig 1) showed an enlarged pulmonary outflow tract, rapid tapering of the pulmonary vessels, and no parenchymal lesions. Electrocardiogran gave normal findings. Numerous sputum examinations were negative for malignant cells, acid-fast bacilli and fungi. The main pulmonary artery could not be successfully catheterized, but right ventricular pressure was found to be increased to 61 mm Hg. "From the Department of Medicine, Geisinger Medical Center, Danville, Pennsylvania. ""Resident, Internal Medicine. Reprint requests: Dr. Albertini, Geisinger Medical Center, Danville 17821

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VOCAL CORD PARALYSIS AND PULMONARY EMBOLI

FIGURE 1. Chest film showing an enlarged pulmonary outflow tract, rapid tapering of the pulmonary vessels and no parenchymallesions. Direct laryngoscopy revealed a paralyzed left vocal cord with no intrinsic abnormality. Bronchoscopy, esophagoscopy, and barium swallow studies were normal. Lung scan (Fig 2) showed multiple perfusion defects bilaterally. The patient was treated with anticoagulant drugs. DISCUSSION

Many explanations have been advanced concerning the pathogenic relationship between cardiovascular disease and left vocal cord paralysis. Ortner's initial report stressed the significance of an enlarged left atrium compressing the recurrent laryngeal nerve against the aortic arch.' Other investigators have attributed nerve injury

to; enlarged lymph nodes in the triangle formed by the pulmonary artery, aortic arch and ligamentum arteriosum;' traction on the nerve by the aorta drawn caudally by a greatly hypertrophied right ventricle; inflammation of tissue surrounding the left recurrent laryngeal nerve; and compression of the nerve between the aorta and a greatly enlarged ductus artenosus.v More recent theory has centered on an enlarged pulmonary artery as the common mechanism of nerve injury. In reported cases studied by cardiac catheterization, pulmonary hypertension has been a constant finding. ll . l 3 Radiographic'? and postmortem studies'< and observations at thoracotomy1 2 , 1 3 , 1 5 have supported the concept that the left recurrent laryngeal nerve is compressed between an enlarged, tense, main or left pulmonary artery and the aorta at the ligamentum arteriosum. Three cases of primary pulmonary hypertension with associated left vocal cord paralysis have been reported. 16 • 1 8 None of these has had documented pulmonary emboli; however, perfusion lung scans were not done. Primary pulmonary hypertension is rare, but pulmonary embolism is quite common. Why then has vocal cord paralysis in a patient with pulmonary embolism not been previously reported? The most likely explanation is that only the relatively uncommon situation of multiple and recurrent emboli over a protracted period will permit the development of sustained pulmonary hypertension sufficient to produce chronic dilatation of the pulmonary artery and entrapment of the nerve. Massive acute embolism will cause arterial dilatation, but should cord paralysis develop it would probably go unobserved in the midst of the many striking symptoms and signs attendant on that event. Moreover, it may be necessary to have both a dilated pulmonary trunk and a strategically located lymph node or ligamentum arteriosum as suggested by Dolowitz and Lewis." It seems likely that recurrent pulmonary emboli were responsible for some of the cases of vocal cord paralysis termed idiopathic (1019 percent) in three previously reported series totaling 622 patients. 19 • 2 l In a patient with left vocal cord paralysis of undetermined cause, it is necessary to look for pulmonary hypertension and dilatation of the main pulmonary trunks. Since recurrent pulmonary emboli can clearly produce these changes, perfusion lung scanning should be performed as a part of the evaluation of the patient with left vocal cord paralysis, when recurrent pulmonary embolization is a possibility. ACKNOWLEDGMENT; The assistance of Frederick L. Jones, jr., M.D., F.C.C.P. of the Pulmonary Division, Department of Medicine, is gratefully acknowledged. REFERENCES

Ortner N: Recurrenslahmung bei Mitral-stenose. Wien Klin Wschr 10:753-755, 1897 2 Diefenbach WCL: Left vocal cord paralysis with hypertensive heart disease. New Eng J Med 240:419-420, FIGURE 2. Perfusion lung scan (posterior view) showing multiple perfusion defects bilaterally.

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3 King FH, Hitzig WM, Fishberg AM; Recurrent laryngeal

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paralysis in left ventricular failure. Am J Med Sci 188: 691-697, 1934 Tashneck AB: Left recurrent laryngeal nerve paralysis in patient with arteriosclerotic heart disease. Southern Med J, 46:718-719, 1953 Zelman S, Nice GW: Recurrent left laryngeal nerve paralysis in atherosclerotic heart disease. JAMA 149: 12911292, 1952. Huppler EG, Schmidt H, Devine KD, et aI: Causes of vocal cord paralysis. Proc Staff Meet Mayo Clin 30:518521, 1955 Erlanger H, Levine SA: Atrial septal defect: A report of two cases in which there was recurrent laryngeal nerve paralysis. Am Heart J 26:520-527, 1943 Dolowitz DA, Lewis CS: Left vocal cord paralysis associated with cardiac disease. Am J Med 4:856-862, 1948 Mead KC: Persistent patency of the ductus arteriosus. JAMA 50:2205-2210, 1910 Talley JD, Fowler K: Tetralogy of Fallot with hypoplasia of dextroposed aorta. Am J Med Sci 191:618-626, 1936 Camishion RC, Gibbon JH, Pierucci L, et al: Paralysis of the left recurrent laryngeal nerve secondary to mitral valve disease: Report of two cases and literature review. Ann Surg 163:818-827, 1960 Fife R, Miur A: Laryngeal paralysis associated with mitral stenosis. (Ortner's syndrome): Report of two cases. Glasgow Med J 36:164-167,1955 Malcomson K, Hillman LM: Ortner's syndrome. Guy Hosp Rep 105:307-319, 1956 Fetterolf G, Norris GW: The anatomical explanation of the paralysis of the left recurrent laryngeal nerve found in certain cases of mitral stenosis. Am J Med Sci 141:625638, 1911 Ari R, Harvey WP, Hufnagel CA: Etiology of hoarseness associated with mitral stenosis: Improvement following mitral surgery. Am Heart J 50:153-160,1955 Brinton WD: Primary pulmonary hypertension. Br Heart J 12:305-311, 1950 Soothill JF: A case of primary pulmonary hypertension with paralyzed left vocal cord. Guy Hosp Rep 100:232237, 1951 Bohme Von H, Bohme G: Das Ortner-Syndrome. Munchen Med Wschr 104:681-687, 1962 Parnell FW, Brandenburg JH: Vocal cord paralysis: A review of 100 cases. Laryngoscope 80: 1036-45, 1970 Clerf LH: Unilateral vocal cord paralysis. JAMA 151:900903, 1953 Goff WF: Letter to the Editor. JAMA 212:1378-1379, 1970

Meandering Right Pulmonary Vein Simulating the Scimitar Syndrome* Lawrence R. Goodman, M.D.,oO Ahmed Jamshidi, M.D.,t and Elorencio A. Hipona, M.D.t

°From the Department of Medicine, Cardiovascular Laboratory, Bridgeport Hospital, Bridgeport, Connecticut and the Department of Radiology, The Boston City Hospital, Boston. ··Resident in Radiology, Boston University Medical Center. tAssistant Clinical Professor in Pediatrics, Yale University School of Medicine; Director, Cardiovascular Laboratory, Bridgeport Hospital. ~Associate Professor of Radiology, Harvard Medical School.

Reprint requests: Dr. Hipona, Department of Radiology, Boston City Hospital, Boston 02118

GOODMAN, JAMSHIDI, HIPONA A 51-year-old woman presented with clinical and chest x-ray film findings simulating partial anomalous pulmonary venous return below the diaphragm (scimitar syndrome). Angiography, however, revealed the sclmi" vein turned cephalad at the diaphragm and drained into the left side of the left atrium. It is postulated that the abnormal left atrial drainage is via persistent thebeslan veins.

O

n frontal chest x-ray film, a large pulmonary vein running caudad and medially along the right heart border to the diaphragm is referred to as a scimitar sign. This commonly indicates partial anomalous pulmonary venous return to the inferior vena cava or low right atrium. Associated findings in the scimitar syndrome include displacement of the heart to the right, abnormal segmentation of the right lung, hypoplastic right hemithorax and hypoplastic right pulmonary artery. Varicosities of the pulmonary veins or arteriovenous malfonnations may cause a scimitar-like vein adjacent to the right border.' -s This communication describes a patient whose condition simulated the classic scimitar syndrome except that the right pulmonary vein, after a meandering course, drained into the left atrium rather than the inferior vena cava. CASE REPORT

A 51-year-old woman was admitted to the Bridgeport Hospital for episodes of coughing small amounts of bright red blood every several weeks over a 20-year period. The last episode had been three weeks prior to admission. These episodes were associated with difficult breathing when lying in the left lateral decubitus position. For the last 15 years, the patient had had multiple episodes of right-sided pleurisy, fever and productive cough. Recurrent asthmatic attacks required use of bronchodilators. X-ray fllms of this period described a large tubular density over the right mid-lung, as well as right pleural thickening. Past medical history revealed one bout of hematemesis about 12 years previously. This was believed due to a "stomach ulcer." Physical examination was unremarkable except for dullness and decreased breath sounds at the right base. Frontal chest x-ray fllm (Fig lA) revealed dextroposition of a normal-sized heart. There was pleural thickening at the right base. A 9 mm diameter vessel was seen adjacent to the right heart border. The main right pulmonary artery appeared small. On the lateral film (Fig IB) the 9 mm vessel was seen posteriorly overlapping the vertebral column. Apparently, continuous with this vessel was a 12 mm vessel coursing upward and forward to the upper posterior heart border. Right anterior oblique examination confirmed their continuity. Angiography (Fig 2A) showed the right main pulmonary artery to be smaller than the left. A lingular artery was present on the right (mirror image circulation). The levophase (Fig 2B, C) demonstrated the posterior vessel (described above) drained the entire right lung toward the diaphragm. Instead of piercing the diaphragm, it was continuous with the larger mid-thoracic vessel. This vein drained cephalad, crossed the mediastinum and entered the left side

CHEST, VOL 62, NO.4, OCTOBER, 1972