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CONSTRICTIVE PERICARDITIS DIJE TO A PQREIGX BODY (NEEDLE) IN THE ~~~I~ARDII~~I BERNARD
OF THE: UKITED STATES
?&ES of constrictive perieardit.is of t,raumatic origin are rure. Glenn1 receiitly reporied a case as a result of a crushing injury to the chest in an automobile accident. M7arburg,2 in an extensive review af the literature, cites three cases of traumatic origin, one of which was of dubious authenticity. Cases have been reported of bullets in the pericardium,3 and migrating fish bones lodging in the pericardium, producing acute fibrinopurulent pericarditis.41 0 However, a review of the literature has failed to reveal any case of chronic constrictive periearditis due to a foreign body. It is, therefore, believed that the foiiowing case of constrict,ive pericarditis caused by the lodgment of a surgical needle in the perica,rdium will be of interest. REPORT
T. B.: a 46-year-old fireman, was admitted to the Veterans FXospital, Bronx, New York, June 23, 1942, with a dia,vosis of “‘cirrhosis of the liver with possible obstruction.” His chief complaint was that he had been losing weight since Christmas of 1941, but, despite that fact, his abdomen continued to be large and occasioned the ridicule of his fellow workers. He feared that he had an abdominal tumor, altho~~gl~ he stated that he did not believe his abdomen had increased in size. In the preceding six months he had lost 30 pounds in weight, e cornplained of an excessive amount of gas, v&i&h was accompanied by belching. He had always been stout; his usual. weight was 220 pounds. Be had an uncomfortable sensation In his abdomen. When he walked rapidly, his “belly shook.” In 1935, while 6ghting a fire, he fell three stories and sustained a fracture of the right knee, the left. forearm, and several ribs on the left side. He was taken to a hospital, and, whi?e undergoing an anesthetic preliminary to correction of the fra,ctt;res, the patient stated that his heart stopped, He was given an injectioYr in the third right intercostal space jn t,he parasteynal line. The needle broke off. An incision was made to recover the needle, but the attempt was unsuccessful. While in the hospital undergoing treatment for his fractures, he was told that pericardial effusion had developed, A physician wished to operate on his heart, but he was dissuaded a,gairist A roentgenogram in the patient’s any operation by another physician. possession, taken in December, 1935, revealed evidence of perieardial effusion. The patient stated that: since the accident, his blood pressure had been low, usually about 88, systolic. He did r;ot co.mplain of shortness Seven years before -__ of breath or pain in the chest on admission. From the Veterans Administration Hospital, New York, N. Y. This paper is published with permission of the Medical Director, is-,x-ation, who assumes no responsibility for the opinions expressed. Received for publication June 10, 1943. 805
he aid have pain in the right side of his chest, but this disappeared completely. In December, 1941, he had an attack of phlebitis in the right leg, and still had occasional swelling of this extremity. He drank about three to four glasses of beer weekly. He never drank wine or hard liquor. This was confirmed by the patient’s wife. Examination disclosed a somewhat undernourished, well-developed, white male, with a protuberant abdomen, who did not appear to be acutely ill. His temperature was 98” F., his respirations, 20, and his weight, lSSl/ pounds. There was no dyspnea or cyanosis in the erect or sitting position. In the supine position, the patient’s face and neck assumed a dusky, cyanotic hue. He didnot become dyspneic. Examination of the fundi disclosed slight retinal arteriosclerosis. The veins of the neck were moderately distended in the erect position; in the supine position they were markedly so. The thorax was of medium size and configuration, and the lungs were normal. There was a 3 cm., linear, postoperative cicatrix in the third right intercostal space in the parasternal line. Heart : The point of maximum intensity of the apex impulse could not be palpated. The heart was not enlarged to percussion, the sounds were muffled, and the second sound was reduplicated at the apex. There were no thrills or murmurs. The blood pressure was 112/76-76. The pulse rate was 92. No appreciable peripheral arteriosclerosis was present. There was no paradoxical pulse, Broadbent’s sign, or systolic retraction at the apex. The abdomen was swollen moderately. A fluid wave was present, and the liver was 11/2 inches below the costal margin, on the right. It was not tender. The spleen was not enlarged. There were no other masses. Extremities: The left arm was 2 inches shorter than the right. There was incomplete ankylosis at the elbow joint, and extension was limited to 165 degrees. Supination was moderately curtailed. There was a 4 by 3 cm. cicatrix over the right knee. Flexion of the right leg at the knee joint was limited to 90 degrees. Laboratory studies: A roentgenogram of the chest (Fig. 1) on June 30, 1942, showed that the heart and lungs were within normal limits. There was evidence of a pleuropericardial adhesion at the base. Two linear densities were seen at the border of the pericardium at the right. These had the appearance of broken fragments of a needle. The roentgenologist said that they appeared to be embedded within the pericardium or myocardium. Fluoroscopic examination revealed marked diminution of the phasic excursions of the heart. The pulsations were feeble. There was no change in the heart size or position with deep inspiration or expiration. Esophageal study with barium showed no definite abnormalities. There was no evidence of esophageal varices. The electrocardiogram (Fig. 2) revealed a diphasic T,; T, was inverted. QRS, was of low voltage, and S, was prominent. The venous pressure measurement, using the direct method, on July 3, 1942, was 33.5 cm. (normal, 4 to 12 cm.). On July 9 the venous pressure was 27.5 cm. The arm-to-tongue time on July 3, 1942, using sodium dehydrocholate, was 18 seconds (normal, 12 to 18 seconds). On J,uly 9 the armto-tongue time was 10 seconds. The arm-to-lung time (ether) on July 3, 1942, was 6 seconds (normal, 4 to 6 seconds). Bromsulfalein test : 5 minutes, S5 per cent; 30 minutes, 5 per cent. The icteric index was 12.5. The van den Bergh was 0.1 mg. The serum albumin was 5.2, the serum globulin, 2.8. There was a mild anemia. Chemically, the blood was normal. The urine was negative. The blood Wassermann and Hahn reactions were negative.
Diagnoses of “‘chronic constrictive pericarditis of traumatic origin7 with enlargement of the liver and ascites, Class III, and foreign body, metallic, right side of the chest” were made. The cause of the constrictive pericarditis was believed to be either the needle in the perieardium or the original trauma, i.e., the fall. Pericardiectomy was recommended. However, the patient wished some time t,o arrange his affairs, and he was discharged July 14,1942.
@I July 22, 1942, the patient entered the Nt. Sinai IHospital, Se&r Pork. City, Surgical Service of Dr. Harold Neuhof.*” On July 23, 1942, abdominal paracentesis was done and 8,000 cc. of straw-colored R:rid were removed. The blood pressure was 105/E%. *I. am indebted went course.
Operation by Dr. Harold Neuhof : Under nitrous oxide, oxygen, and ether, oro-endotracheal anesthesia, an incision was made in the right third intercostal space, in a transpleural approach. Evidence of an old inflammatory process was noted in the intercostal muscles. The right side of the heart was exposed, and the amplit,ude of the cardiac excursions was seen to be distinctly diminished. A large pericardiodiaphragmatic adhesion was seen and divided. The pericardium was thick, indurated, and densely adherent. The epicardium and pericar-
were completely fused over the exposed portion of the hear:. The pericardium over the right side of the heart was dissected away and removed. In the region of the inferior vena eava. the needle was found in two pieces in a dense, fibrous sheath, and removed. No attempt was made to free the left side of the heart. Xnlfathiazole was placed in the operative field. Closed drainage was instiiuted in the right axilla and the chest wound was closed. The patient left the operating room in excellent condition. blood pressure at onset of the operation was 101/64. When the p eardium was opened, the blood pressure rose from &l/45 to 128j80, This rise in blood pressure was maintained throughout the postoperative period, indicating that the heart had heen dfeetively freed. The day after the operation the patient developed a pumlent bronchitis which rapidly progressed to bronchopneumonia. Despite the administration of oxygen, several bronchoscopic procedures, sulfadiazinc, and supportive measures, the patient died on the third no&operative day, July 26, 1942. Death apparently was caused by suppurative bronchopneumonia. The pathologist reported fragments of thickened perieardinm, showing marked fibrosis, with hyalinizaiion and focal lymphocytic inf?ltraLion. The second fragment of pericardium showed the foreign body (needle). An autopsy was not obtained. &urn
A case is presented in which chronic constrictive pericarditis developed six years after the accidental deposition of a portion of a surgical needle in the pericardium. Whites observes that trauma resulting in hemopericardium nmy leave chronic adhesive pericarditis. This is due to fibrosis following organization of the blood. In this case the pathogenesis is probably related 30 two factors: 1. The development of an acute inflammatory process, beginning a.t the site of the needle. This is substantiated by evidence of an old infection of the intercostal muscles along the course of the needle, am?. by the development of a pericardial effusion about two weeks after the injury. 2. Fibrosis due to chronic irritation of the pericardium because of the needle itself. This idea is supported by the fact that the thickening, fibrosis, and induration of the pericardium mere maximal at the locus of the needle. REFERENCES a. Qlenn, E. E.: Traumatic Constrictive Periearditis-Case Report, J. Missour: 34. A. 37: 7, 1940. 8. Warburg, Erik: Subacute and Chronic Pericardial and Myocardial Lesions, Due to Non-Penetrating Traumatic Lesions, Copenhagen, London, 1935, Humphrey Milford. 3. Lower, W. E.: Removal of Bullet From Pericardium, Ann. Surg. 63: 533, 1016. 4. Wilaolm, 9.: Pericarditis Due to Penetrating Foreign Body (Fish-Bone) Case, Nerd. Med. (Hygeia) 4: 3521, 1938. 5 Daleas, B., Joyeux, and Nguyen-Thue-Tung: Fish-Bone Migrated to Perieap dium as Cause of Fatal Periearditis During Pregnazcy, Eev. m&i. franq. d’Ext&me-Orient. 17: 1166, 1039. 5, White, P. D.: IEeart Disease, New York, 1934, The Maernillm Co.