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Fibrinous Pericarditis Secondary to Esophageal Ulceration
Fibrinous Pericarditis Secondary to Esophageal Ulceration * GERALD E. MUEHSAM, M.D. Brooklyn, New York Most frequently, fibrinous pericarditis is associated with such Illnesses as rheumatic fever, tuberculosis, sepsis, uremia and scarlet fever. More uncommonly, the entity of so-called idiopathic pericarditis is recognized when no primary etiology is present.t> In addition, fibrinous pericarditis may occasionally result from infectious processes in contiguous structures, especially those of pleural and mediastinal location. . Fibrinous pericarditis, secondary to esophageal ulceration, however, is rare, and a review of the literature of the last 15 years fails to show any mention of it. It is for that reason that this case is considered of sufficient interest to be reported. Our patient presented in addition an extra-renal uremia, which was a puzzling point of clinical differential diagnosis. Case Report: The patient was a 54 year old white male, who for one year prior to admission complained of dysphagia, which had caused him to sub81.st almost entirely on a l1quid diet. Six to eight weeks before adm1ss1on he began to complain of weakness and aching in the lower extremities, with several episodes of stumbllng and falling. One week prior to adm1ss1on he fell, fracturing his right fibula. This was accom panied by a transient episode of aphasia. Two days prior to admission he became increasingly weak , and was in shock when admitted on November 12, 1950. At that time, the blood pressure was imperceptible, and the pulse weak and thready. Typical signs of shock were noted. There was a to-and-fro friction rub audible over the precordium and left sternal border. The patient was treated with the intravenous administration of whole blood, glucose and saline, totalltng between 3,000 and 5,000 cc. of fluids dally , with the addition of Nor-Epinephrine. This was continued untll November 16, 1950, when his blood pressure maintained itself without treatment. During the course of his entire hospital illness his rectal temperature fluctuated between 99 and 101 degrees Fahrenheit, and the urinary output was considered adequate. The EKG showed non-specific T wave changes, suggestive of subacute pericardial disease.
"From the Laboratory Service , Brooklyn Veterans Administration Hospital, Brooklyn 9, New York. Sponsored by the Veterans Administration and published with the approval of the Chief Medical Director. The statements and conclusions published by the author are a result of his own study and do not necessar1ly reflect any op1n1on or pollcy of the Veterans Administration. 356
Vol.XXD
FIBRINOUS PERICARDITIS
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On November 12, 1950 the WBC was 6,950, with a shift to the left, and a RBC of 4.1 million. The BUN level on November 12, 1950 was 140.0 mgm. per cent. It dropped steadlly untll on November 18, 1950, one day before death, it was 32.5 mgm. per cent. The C02 combining power was 27.7 Vol. per cent on November 12, 1950, but by November 17, 1950 had returned to 60 Vol. per cent. The urine on three different occasions showed the spec1f1c gravity to vary between 1.014 and 1.020, with a consistently negative sugar and albumin reaction, and occasional WBC in the sediment. The Kahn test was negative. His condition maintained a steady course for two and a half days, but on November 19, ' 1950 he again lapsed into shock, and died shortly thereafter. Autopsy Findings : (Positive findings only) . Gross Findings : The heart weighed 500 Gms . The visceral and parietal pericardia were fused by moderately firm grey-pink shaggy adhesions, which could be severed without difficulty. There was no pericardial fluid. The remainder of the heart showed no sign1f1cant gross changes. The esophagus had a bright red to grey mottled mucosal surface. Six em. above the gastro-esophageal junction was an oval ulcer, measuring 1.5 by 1.0 em. in diameter, with its long axis parallel to the course of the
FIGURE 1: Showingfibrinous pericarditis with granulation tissue at its base, no infUtration of epicardial f~t.
358
GERALD E. MUEHSAM
Sept., 1952
esophagus. The ulcer had a punched-out margin, and a smooth greywhite base. The wall of the esophagus in this area measured 8 mm. in thickness, as compared to 3-4 mm. elsewhere. Other pertinent pathologic findings included: Chronic passive congestion of the lungs, liver and spleen; slight bilateral straw colored pleural effusion; edema of the tracheal wall; advanced arteriosclerosis of the aorta and coronary arteries; fat replacement of the liver and chronic and acute cystitis. . Microscopic Findings : The epicardial surface of the heart was covered by wide zones of fibrin, which had been partially organized by granulation tissue at the base. The subepicardial zones contained scattered lymphocytes and histiocytes, and the epicardial fat showed no evidence of pathologic change (Figure 1). The esophagus showed a deep ulcer, lined by granulation tissue, and below it, extensive fibrous connective tissue replacement of the esophageal wall. The wall of the esophagus and periesophageal connective tissue contained scattered collections of lymphocytes, plasma cells, histiocytes and occasional polymorphonuclear neutrophlles. The esophageal vessels here showed moderate intimal thickening by connective tissue . The uninvolved esophageal mucosa contained scattered foci of gastric glands. Discussion
The esophagus is a hollow viscus whose walls consist of mucosa, submucosa and muscularis; it lacks the serosal coat ordinarily present in the remainder of the gastro-intestinal tract. The muscularis is surrounded by loose and dense connective tissue, which connects it with the surrounding structures.! The pericardial sac, however, is composed of relatively tough dense fibrous connective tissue. It is thus understandable that an inflammatory process within the esophagus may extend into the mediastinum, without spreading into the contiguous pericardium. Despite the close proximity of the latter, the dense pericardial structure, under most circumstances, acts as an effective barrier. It is only with certain more powerful agents causing esophageal perforation that the pericardium is directly involved, and a number of instances of this kind have been reported. Foreign bodies, particularly fish and fowl bones,4 .5 as well as malignant growths of the esophagus" are occasionally referred to in the literature as directly causing esophageal perforation and subsequent inflammatory involvement of the pericardium. The esophageal lesion in our case, however, was of considerable duration, the patient having complained of increasing dysphagia for approximately one year, and it is likely that SUfficiently long exposure to an otherwise relatively minor trauma caused the above mentioned barrier to break down. In addition a retro-grade lymphatic spread might be considered.
Vol . XXII
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The etiology of the esophageal ulcer is open to speculation. One explanation is that of ingestion of caustic liquids, a feasible possibility in view of the patient's vague alcoholic history; another, the presence of gastric type glands lining the esophageal mucosa, which may have given rise to peptic ulceration of the esophagus.r-' SUMMARY A case of fibrinous pericarditis secondary to esophageal ulceration is presented, and some of the reasons for its infrequent occurrence are discussed.
RESUMEN
Se presenta un caso de pericarditis fibrinosa secundaria a una ulceraci6n esoragtca y se discuten algunas de las razones que explican su rareza. RESUME
L'auteur rapporte un cas de pericardite sero-nbnneuse consecutive Ii une ulceration de l'oesophage. II expose les raisons de la rarete d 'un tel fait. 1 2 3 4 5 6 7 8 9
REFERENCES Tice : "Practice of Medicine," W. F. Prior Co., Inc., Hagerstown, Md., VI, page 117, 1947. Pohl, Arnold W.: "Acute Pericarditis: Report of Eight Cases in Which the Etiology was 'Non -specific' or 'Cryp tic'," Ann. Int. Med., 32:935,1950. Gray's Anatomy, 23rd Edition : Lea and Febiger, Phlla., Pa ., 1936. Holinger, Paul H.: "Complications of Esophageal Perforation," Ann. oto. Rhin. and Laryng., 50:681, 1941. Massias, C. and Hao, N. D.: "A Case of Putrid Pericarditis Following Gangrenous Esophagitis Due to Fishbone," Bull. et mem o Soc. med . d. hop. de Paris, 64:460, 1948. Clinical Pathologic Case Record: "Epidermoid Carcinoma of Esophagus with Extension to Pericardium-Acute Purulent Pericarditis," Delaware State Med. Jour., 22:148, 1950. Hellmann : "Twenty-six Proven Cases of Peptic Esophageal Ulcers," Quoted by Walther Fischer in F. Henke and O. Lubarsch: "Handbuch der speziellen pathologischen Anatomie und Histologie," Julius Springer , Berlin, Vol. 4, part 1, page 109, 1926. Bockus, H. L.: "Gastro-enterology," W. B. Saunders co.. PhUa., Pa., and London, Vol. I, 131, Chapter XII, 1944. Chamberlin, D. T.: "Peptic Ulcer of the Esophagus," Lahey Clinic Bull., 2:59, 1940.
"From the Laboratory Service , Brooklyn Veterans Administration Hospital, Brooklyn 9, New York. Sponsored by the Veterans Administration and published with the approval of the Chief Medical Director. The statements and conclusions published by the author are a result of his own study and do not necessar1ly reflect any op1n1on or pollcy of the Veterans Administration. 356
Vol.XXD
FIBRINOUS PERICARDITIS
357
On November 12, 1950 the WBC was 6,950, with a shift to the left, and a RBC of 4.1 million. The BUN level on November 12, 1950 was 140.0 mgm. per cent. It dropped steadlly untll on November 18, 1950, one day before death, it was 32.5 mgm. per cent. The C02 combining power was 27.7 Vol. per cent on November 12, 1950, but by November 17, 1950 had returned to 60 Vol. per cent. The urine on three different occasions showed the spec1f1c gravity to vary between 1.014 and 1.020, with a consistently negative sugar and albumin reaction, and occasional WBC in the sediment. The Kahn test was negative. His condition maintained a steady course for two and a half days, but on November 19, ' 1950 he again lapsed into shock, and died shortly thereafter. Autopsy Findings : (Positive findings only) . Gross Findings : The heart weighed 500 Gms . The visceral and parietal pericardia were fused by moderately firm grey-pink shaggy adhesions, which could be severed without difficulty. There was no pericardial fluid. The remainder of the heart showed no sign1f1cant gross changes. The esophagus had a bright red to grey mottled mucosal surface. Six em. above the gastro-esophageal junction was an oval ulcer, measuring 1.5 by 1.0 em. in diameter, with its long axis parallel to the course of the
FIGURE 1: Showingfibrinous pericarditis with granulation tissue at its base, no infUtration of epicardial f~t.
358
GERALD E. MUEHSAM
Sept., 1952
esophagus. The ulcer had a punched-out margin, and a smooth greywhite base. The wall of the esophagus in this area measured 8 mm. in thickness, as compared to 3-4 mm. elsewhere. Other pertinent pathologic findings included: Chronic passive congestion of the lungs, liver and spleen; slight bilateral straw colored pleural effusion; edema of the tracheal wall; advanced arteriosclerosis of the aorta and coronary arteries; fat replacement of the liver and chronic and acute cystitis. . Microscopic Findings : The epicardial surface of the heart was covered by wide zones of fibrin, which had been partially organized by granulation tissue at the base. The subepicardial zones contained scattered lymphocytes and histiocytes, and the epicardial fat showed no evidence of pathologic change (Figure 1). The esophagus showed a deep ulcer, lined by granulation tissue, and below it, extensive fibrous connective tissue replacement of the esophageal wall. The wall of the esophagus and periesophageal connective tissue contained scattered collections of lymphocytes, plasma cells, histiocytes and occasional polymorphonuclear neutrophlles. The esophageal vessels here showed moderate intimal thickening by connective tissue . The uninvolved esophageal mucosa contained scattered foci of gastric glands. Discussion
The esophagus is a hollow viscus whose walls consist of mucosa, submucosa and muscularis; it lacks the serosal coat ordinarily present in the remainder of the gastro-intestinal tract. The muscularis is surrounded by loose and dense connective tissue, which connects it with the surrounding structures.! The pericardial sac, however, is composed of relatively tough dense fibrous connective tissue. It is thus understandable that an inflammatory process within the esophagus may extend into the mediastinum, without spreading into the contiguous pericardium. Despite the close proximity of the latter, the dense pericardial structure, under most circumstances, acts as an effective barrier. It is only with certain more powerful agents causing esophageal perforation that the pericardium is directly involved, and a number of instances of this kind have been reported. Foreign bodies, particularly fish and fowl bones,4 .5 as well as malignant growths of the esophagus" are occasionally referred to in the literature as directly causing esophageal perforation and subsequent inflammatory involvement of the pericardium. The esophageal lesion in our case, however, was of considerable duration, the patient having complained of increasing dysphagia for approximately one year, and it is likely that SUfficiently long exposure to an otherwise relatively minor trauma caused the above mentioned barrier to break down. In addition a retro-grade lymphatic spread might be considered.
Vol . XXII
FIBRINOUS PERICARDITIS
359
The etiology of the esophageal ulcer is open to speculation. One explanation is that of ingestion of caustic liquids, a feasible possibility in view of the patient's vague alcoholic history; another, the presence of gastric type glands lining the esophageal mucosa, which may have given rise to peptic ulceration of the esophagus.r-' SUMMARY A case of fibrinous pericarditis secondary to esophageal ulceration is presented, and some of the reasons for its infrequent occurrence are discussed.
RESUMEN
Se presenta un caso de pericarditis fibrinosa secundaria a una ulceraci6n esoragtca y se discuten algunas de las razones que explican su rareza. RESUME
L'auteur rapporte un cas de pericardite sero-nbnneuse consecutive Ii une ulceration de l'oesophage. II expose les raisons de la rarete d 'un tel fait. 1 2 3 4 5 6 7 8 9
REFERENCES Tice : "Practice of Medicine," W. F. Prior Co., Inc., Hagerstown, Md., VI, page 117, 1947. Pohl, Arnold W.: "Acute Pericarditis: Report of Eight Cases in Which the Etiology was 'Non -specific' or 'Cryp tic'," Ann. Int. Med., 32:935,1950. Gray's Anatomy, 23rd Edition : Lea and Febiger, Phlla., Pa ., 1936. Holinger, Paul H.: "Complications of Esophageal Perforation," Ann. oto. Rhin. and Laryng., 50:681, 1941. Massias, C. and Hao, N. D.: "A Case of Putrid Pericarditis Following Gangrenous Esophagitis Due to Fishbone," Bull. et mem o Soc. med . d. hop. de Paris, 64:460, 1948. Clinical Pathologic Case Record: "Epidermoid Carcinoma of Esophagus with Extension to Pericardium-Acute Purulent Pericarditis," Delaware State Med. Jour., 22:148, 1950. Hellmann : "Twenty-six Proven Cases of Peptic Esophageal Ulcers," Quoted by Walther Fischer in F. Henke and O. Lubarsch: "Handbuch der speziellen pathologischen Anatomie und Histologie," Julius Springer , Berlin, Vol. 4, part 1, page 109, 1926. Bockus, H. L.: "Gastro-enterology," W. B. Saunders co.. PhUa., Pa., and London, Vol. I, 131, Chapter XII, 1944. Chamberlin, D. T.: "Peptic Ulcer of the Esophagus," Lahey Clinic Bull., 2:59, 1940.