Constrictive Pericarditis John S. Simon, M.D., and James R. Pluth, M.D. ABSTRACT A patient with constrictive pericarditis following an open-heart operation without sepsis is discussed. In the absence of sepsis, it has been widely held that this complication does not develop following an open-heart procedure. The fatal outcome in this patient could have been avoided had such an association been known.
heart compared with films taken one year previously. Echocardiography revealed an enlarged left atrium and the echo pattern of mitral stenosis. On June20,1974, the patient underwent aortic and mitral valve replacement. Cardiac chamber pressures taken at the time of operation revealed left ventricular pressure to be 160/0 mm Hg; aorConstrictive pericarditis has been reported to tic pressure, 160/60; left atrial pressure, 95/20; occur after both open and closed chest trauma right ventricular pressure, 95/15; and right atrial l21. The etiological factor for the development of pressure, 17P. The aortic and mitral valves were constriction is said to be retained blood in the excised and replaced with a 19 mm and a 25 mm pericardial space [31. Postcardiotomy pericar- Bjork-Shiley prosthetic valve, respectively. Total ditis [6] is an occasional complication of open- bypass time was 107 minutes, and hemostasis heart operations, but it has not been known to appeared to be excellent at the completion of the progress to constriction [5]; a review of theliter- procedure. The pericardium was partially closed ature fails to reveal a single case of constrictive to the base of the great vessels with interrupted pericarditis associated with an open-heart oper- silk sutures prior to closure of the sternum. ation in the absence of sepsis. We wish to report The postoperative period was complicated by a patient in whom the diagnosis was not enter- mild hypotension that necessitated support tained mainly because of this widely held view with isoproterenol for the first 36 hours. Total that a constrictive process does not occur after an blood loss was 760 ml for the first postoperative open-heart procedure. day and 120 ml for the second. The remainder of the patient’s convalescence was unremarkable; A 52-year-old woman had been followed at no fever or leukocytosis occurred. She was disthe Mayo Clinic since her first episode of conges- missed from the hospital on the twelfth posttive heart failure in June, 1970. Diuretics and operative day on a regimen of anticoagulants digoxin had controlled her cardiac status until (warfarin, digoxin, and spironolactone with 1973. A modified radical mastectomy for car- hydrochlorothiazide). Her weight at dismissal cinoma of the left breast was performed in 1971, was 51.4 kg. and postoperatively she received a full course of The first month after operation her cardiac radiation therapy. In June, 1974, she returned to status improved. Episodic ataxia and dizziness, the clinic stating that she had noted progressive which had both been present preoperatively, deterioration over the preceding twelve months. were thought to have been aggravated by the Orthopnea was severe, and dyspnea occurred surgical procedure. Four weeks after operation with even minimal conversation. the patient’s weight was 53.2 kg, and a chest The physical examination demonstrated a roentgenogram demonstrated a reduction in blood pressure of 140/60 and ausculatatory evi- cardiac size. Six weeks after operation she had dence of both aortic stenosis and aortic insuffi- developed a cough associated with moderate ciency. The chest roentgenogram disclosed a 1 shortness of breath. The chest roentgenogram cm increase in the transverse diameter of the again showed a small heart, but bilateral pleural effusions were now present. Eight weeks after From the Mayo Graduate School of Medicine, University of the operative procedure the patient was readMinnesota, and the Mayo Clinic, Rochester, MN. mitted to the hospital for evaluation of ataxia, Accepted for publication June 20, 1975. Address reprint requests to Dr. Simon, 3865 Cherry Creek persistent cough, and shortness of breath. She North Dr, Denver, CO 80209. weighed 52.7 kg and on physical examination 440
441 Case Report: Simon and Pluth: Constrictive Pericarditis
was noted to have prominent jugular venous pulsations and a hepatojugular pulse. The liver was palpable and measured 10 cm by percussion. Physical findings of bilateral pleural effusions were present. Prosthetic valve sounds were normal, and there was no gallop rhythm. The serum alkaline phosphatase was 635 U (normal, 30 to 70). Chest roentgenography revealed a small heart, and on this basis it was thought the patient had had ”an excellent postoperative result.” She was dismissed from the hospital on digoxin and diuretic therapy. Twelve weeks after the original operative procedure she died suddenly at home. Postmortem examination showed bilateral pleural effusions of 900 and 1,400 ml. The heart weighed 245 gm. The prosthetic valves were normally seated. The pericardium was markedly thickened and adherent, causing functional constriction. The thickening was very severe in relationship to both vena cava orifices; the peel around the cava was 3 to 4 cm thick and densely fibrous. Microscopical examination disclosed dense scar tissue.
Comment The diagnosis of constrictive pericarditis in this patient would undoubtedly have been suspected antemortem had the patient not had an open-heart operation. It was not considered because of the widely accepted belief that constrictive pericarditis is not a sequela of an aseptic open-heart procedure. Indeed, review of the literature in English and of Mayo Clinic records has failed to produce another case. It is doubtful that the radiation therapy administered in 1971 played any role in the development of the constrictive process. At the time of the surgical procedure neither significant thickening of the pericardium nor adhesions between the pericardial sac and the heart were noted. In addition, the time course for development of pericarditis suggests that the operative procedure, rather than the previous radiation therapy, was the inciting agent. A constrictive process has been reported to occur following both open and closed chest trauma [21. Tuberculous effusions are most commonly associated with constrictive pericarditis, although a similar reaction has been noted
following myocardial infarction. Common to all these entities is retention of blood in the pericardial space. Ehrenhaft and Taber [2] in 1962 demonstrated that constrictive pericarditis can develop following pericardial hemorrhage, although this possibility was first suggested by Diiniel and Puder [l] in 1932. Were this the only factor responsible for development of the constrictive process, one would anticipate chronic constrictive pericarditis to be a frequent OCcurrence after open-heart operations. Perhaps adequate drainage of the pericardial space prevents this from occurring [4], but even so, the cardiac silhouette in many of these patients is enlarged for days to weeks after the surgical procedure. Indeed, delayed tamponade resulting from lysis of a retained blood clot at the time of operation may occur as a complication of the open-heart procedure. It would appear, therefore, either that several factors were responsible for the constrictive process in this patient or that there are other cases of constrictive pericarditis of a less pernicious nature that go undiagnosed after open-heart operations. Persistent heart failure following a corrective cardiac operation suggests the coexistence of myocardiopathy, but as this patient demonstrates, constrictive pericarditis should be considered in the differential diagnosis. Certainly the most important clue to the diagnosis in this patient was the early reduction in heart size, which was out of proportion to the clinical situation. The small heart, pleural effusion, and elevated jugular venous pressure were, in retrospect, obvious clues to the correct diagnosis.
References 1. Diniel G , Puder S: Perikarditis et Neuritis cholesterinea. Virchows Arch [Pathol Anat] 284:853,1932 2. Ehrenhaft JL, Taber RE: Hemopericardium and constrictive pericarditis. J Thorac Cardiovasc Surg 24:355, 1962 3. Schaffer AI: A case of traumatic pericarditis with chronic tamponade and constriction. Am J Cardiol 7:125, 1961 4. Tabatznik 8, Isaacs JP: Postpericardiotomy syndrome following traumatic hemopericardium. Am J Cardiol 7:83, 1961 5. Uricchio JF: The postcommissurotomy (postpericardiotomy) syndrome. Am J Cardiol 12:436, 1963 6. Wood P: Chronic constrictive pericarditis. Am J Cardiol 7:48, 1961
heart compared with films taken one year previously. Echocardiography revealed an enlarged left atrium and the echo pattern of mitral stenosis. On June20,1974, the patient underwent aortic and mitral valve replacement. Cardiac chamber pressures taken at the time of operation revealed left ventricular pressure to be 160/0 mm Hg; aorConstrictive pericarditis has been reported to tic pressure, 160/60; left atrial pressure, 95/20; occur after both open and closed chest trauma right ventricular pressure, 95/15; and right atrial l21. The etiological factor for the development of pressure, 17P. The aortic and mitral valves were constriction is said to be retained blood in the excised and replaced with a 19 mm and a 25 mm pericardial space [31. Postcardiotomy pericar- Bjork-Shiley prosthetic valve, respectively. Total ditis [6] is an occasional complication of open- bypass time was 107 minutes, and hemostasis heart operations, but it has not been known to appeared to be excellent at the completion of the progress to constriction [5]; a review of theliter- procedure. The pericardium was partially closed ature fails to reveal a single case of constrictive to the base of the great vessels with interrupted pericarditis associated with an open-heart oper- silk sutures prior to closure of the sternum. ation in the absence of sepsis. We wish to report The postoperative period was complicated by a patient in whom the diagnosis was not enter- mild hypotension that necessitated support tained mainly because of this widely held view with isoproterenol for the first 36 hours. Total that a constrictive process does not occur after an blood loss was 760 ml for the first postoperative open-heart procedure. day and 120 ml for the second. The remainder of the patient’s convalescence was unremarkable; A 52-year-old woman had been followed at no fever or leukocytosis occurred. She was disthe Mayo Clinic since her first episode of conges- missed from the hospital on the twelfth posttive heart failure in June, 1970. Diuretics and operative day on a regimen of anticoagulants digoxin had controlled her cardiac status until (warfarin, digoxin, and spironolactone with 1973. A modified radical mastectomy for car- hydrochlorothiazide). Her weight at dismissal cinoma of the left breast was performed in 1971, was 51.4 kg. and postoperatively she received a full course of The first month after operation her cardiac radiation therapy. In June, 1974, she returned to status improved. Episodic ataxia and dizziness, the clinic stating that she had noted progressive which had both been present preoperatively, deterioration over the preceding twelve months. were thought to have been aggravated by the Orthopnea was severe, and dyspnea occurred surgical procedure. Four weeks after operation with even minimal conversation. the patient’s weight was 53.2 kg, and a chest The physical examination demonstrated a roentgenogram demonstrated a reduction in blood pressure of 140/60 and ausculatatory evi- cardiac size. Six weeks after operation she had dence of both aortic stenosis and aortic insuffi- developed a cough associated with moderate ciency. The chest roentgenogram disclosed a 1 shortness of breath. The chest roentgenogram cm increase in the transverse diameter of the again showed a small heart, but bilateral pleural effusions were now present. Eight weeks after From the Mayo Graduate School of Medicine, University of the operative procedure the patient was readMinnesota, and the Mayo Clinic, Rochester, MN. mitted to the hospital for evaluation of ataxia, Accepted for publication June 20, 1975. Address reprint requests to Dr. Simon, 3865 Cherry Creek persistent cough, and shortness of breath. She North Dr, Denver, CO 80209. weighed 52.7 kg and on physical examination 440
441 Case Report: Simon and Pluth: Constrictive Pericarditis
was noted to have prominent jugular venous pulsations and a hepatojugular pulse. The liver was palpable and measured 10 cm by percussion. Physical findings of bilateral pleural effusions were present. Prosthetic valve sounds were normal, and there was no gallop rhythm. The serum alkaline phosphatase was 635 U (normal, 30 to 70). Chest roentgenography revealed a small heart, and on this basis it was thought the patient had had ”an excellent postoperative result.” She was dismissed from the hospital on digoxin and diuretic therapy. Twelve weeks after the original operative procedure she died suddenly at home. Postmortem examination showed bilateral pleural effusions of 900 and 1,400 ml. The heart weighed 245 gm. The prosthetic valves were normally seated. The pericardium was markedly thickened and adherent, causing functional constriction. The thickening was very severe in relationship to both vena cava orifices; the peel around the cava was 3 to 4 cm thick and densely fibrous. Microscopical examination disclosed dense scar tissue.
Comment The diagnosis of constrictive pericarditis in this patient would undoubtedly have been suspected antemortem had the patient not had an open-heart operation. It was not considered because of the widely accepted belief that constrictive pericarditis is not a sequela of an aseptic open-heart procedure. Indeed, review of the literature in English and of Mayo Clinic records has failed to produce another case. It is doubtful that the radiation therapy administered in 1971 played any role in the development of the constrictive process. At the time of the surgical procedure neither significant thickening of the pericardium nor adhesions between the pericardial sac and the heart were noted. In addition, the time course for development of pericarditis suggests that the operative procedure, rather than the previous radiation therapy, was the inciting agent. A constrictive process has been reported to occur following both open and closed chest trauma [21. Tuberculous effusions are most commonly associated with constrictive pericarditis, although a similar reaction has been noted
following myocardial infarction. Common to all these entities is retention of blood in the pericardial space. Ehrenhaft and Taber [2] in 1962 demonstrated that constrictive pericarditis can develop following pericardial hemorrhage, although this possibility was first suggested by Diiniel and Puder [l] in 1932. Were this the only factor responsible for development of the constrictive process, one would anticipate chronic constrictive pericarditis to be a frequent OCcurrence after open-heart operations. Perhaps adequate drainage of the pericardial space prevents this from occurring [4], but even so, the cardiac silhouette in many of these patients is enlarged for days to weeks after the surgical procedure. Indeed, delayed tamponade resulting from lysis of a retained blood clot at the time of operation may occur as a complication of the open-heart procedure. It would appear, therefore, either that several factors were responsible for the constrictive process in this patient or that there are other cases of constrictive pericarditis of a less pernicious nature that go undiagnosed after open-heart operations. Persistent heart failure following a corrective cardiac operation suggests the coexistence of myocardiopathy, but as this patient demonstrates, constrictive pericarditis should be considered in the differential diagnosis. Certainly the most important clue to the diagnosis in this patient was the early reduction in heart size, which was out of proportion to the clinical situation. The small heart, pleural effusion, and elevated jugular venous pressure were, in retrospect, obvious clues to the correct diagnosis.
References 1. Diniel G , Puder S: Perikarditis et Neuritis cholesterinea. Virchows Arch [Pathol Anat] 284:853,1932 2. Ehrenhaft JL, Taber RE: Hemopericardium and constrictive pericarditis. J Thorac Cardiovasc Surg 24:355, 1962 3. Schaffer AI: A case of traumatic pericarditis with chronic tamponade and constriction. Am J Cardiol 7:125, 1961 4. Tabatznik 8, Isaacs JP: Postpericardiotomy syndrome following traumatic hemopericardium. Am J Cardiol 7:83, 1961 5. Uricchio JF: The postcommissurotomy (postpericardiotomy) syndrome. Am J Cardiol 12:436, 1963 6. Wood P: Chronic constrictive pericarditis. Am J Cardiol 7:48, 1961
