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Hemorrhagic Cardiac Tamponade: A Clinicopathologic Correlation
Cardiovascular Clinics Hemorrhagic Cardiac Tamponade: A Clinicopathologic Correlation LYLE J. OLSON, M . D . , Resident in Cardiology*; WILLIAM D. EDWARDS, M . D . , Department of Pathology; BYRON A. OLNEY, M . D . , Division of Cardiovascular Diseases and Internal Medicine; THOMAS A. ORSZULAK, M . D . , Section of Thoracic and Cardiovascular Surgery; MIGUEL JOSA, M . D . , Resident in Thoracic Surgery*t Staphylococcus aureus pericarditis and recurrent episodes of hemorrhagic cardiac tamponade developed in a 31-year-old man. He later died of exsanguination and at autopsy was found to have a ruptured infective pseudoaneurysm of the aortic arch. When hemorrhagic pericardial effusions of undetermined cause are encountered, the heart and great vessels should be evaluated as potential sources of the hemorrhage.
Catastrophic hemopericardium with cardiac tamponade most commonly occurs as a complication of acute myocardial infarction or acute aortic dissection, and subsequent rupture of the heart or ascending aorta leads to the rapid accumulation of blood within the poorly distensible pericardial sac. Subacute or chronic hemopericardium, however, may occur when blood oozes slowly into the cavity, and clinical cardiac tamponade may then develop gradually and episodically. This process may occur during the early stage of cardiac or aortic rupture or may occur in the setting of pericarditis as the visceral and parietal pericardial surfaces scrape each otherwith each heartbeat and cause erosion of the underlying richly vascular granulation tissue.1"4 We report a case of recurrent hemorrhagic cardiac tamponade associated with both bacterial pericarditis and an infective pseudoaneurysm of the aortic arch. REPORT OF CASE In July 1979, a previously healthy 31-year-old man had the onset of sharp stabbing pain in the upper chest and lower neck region which worsened with changes in posture. The man had sought medical attention when the pain had become more severe and associated with a fever (temperatures to 40°C). His local physician had prescribed penicillin and then carbenicillin (both orally), and the patient was subsequently admitted to his local *Mayo Graduate School of Medicine, Rochester, Minnesota. tCurrent address: West Roxbury, Massachusetts.
hospital because of persistent fever and chest pain. The patient had no history of chest trauma. At the time of admission, the hemoglobin concentration was 14.5 g/dl and the leukocyte count was 14,600/mm 3 with 72% neutrophils. Radiographic studies of the chest and soft tissues of the neck and esophagus revealed no abnormalities. Despite parenterally administered antibiotic therapy (6 g of cephalothin and 240 mg of gentamicin daily), the patient continued to have rigors and hectic fevers (temperatures to 40°C). On the fourth hospital day, 2 weeks after the onset of symptoms, he suddenly became hypotensive, had two syncopal episodes, and was found to have a prominent paradoxical pulse. Echocardiography demonstrated a large pericardial effusion, but three attempts at pericardiocentesis were unsuccessful. Cardiac tamponade was diagnosed, and the patient was then transferred to our institution. At the time of transfer, two blood cultures were growing unidentified gram-positive cocci. On admission, the patient was alert, cooperative, and comfortable. He was extremely obese (height, 175 cm; weight, 136 kg). He had a temperature of 39°C, a pulse of 120 beats/min, and a blood pressure of 140/70 mm Hg with an intense paradoxical pulse. Two splinter hemorrhages and one Roth spot were observed. The jugular venous pressure was normal. The heart sounds were distant, and no murmurs were heard. A soft midsystolic sound was considered to be of pericardial origin. No external source of infection was evident. Pertinent laboratory findings included a hemoglobin
Address reprint requests to Dr. W. D. Edwards. Mayo Clin Proc 59:785-790, 1984
785
786
HEMORRHAGIC CARDIAC TAMPONADE
Mayo Clin Proc, November 1984, Vol 59
concentration of 16 g/dl and a leukocyte count of 11,600/mm 3 with 82% segmented neutrophils and 5% banded neutrophils. The serum creatinine concentration was 2.0 mg/dl, and serum creatine kinase was normal. Urinalysis revealed 2 + protein, 4 leukocytes, 2 + granular casts, and occasional epithelial and hyaline casts. A chest roentgenogram revealed cardiac enlargement, increased pulmonary vascularity, and clear lungs. Diffuse ST-segment elevation on an electrocardiogram was consistent with pericarditis. A pericardial effusion was also detected by two-dimensional echocardiography; however, no valvular abnormalities were evident. On the day of admission, the hemodynamic values obtained were consistent with cardiac tamponade (Table 1). Pericardiocentesis resulted in improved hemodynamics even though only 90 ml of bloody fluid could be removed. Analysis of the pericardial fluid revealed a negative Gram stain, 3,558 cells with 99% neutrophils, pH 7.8, protein 2.8 g/dl, and glucose 50 mg/dl. Table 1.—Clinical Hemodynamics* Location
Pressure (mm Hg)
Right atrium (mean) Right ventricle Pulmonary artery Pulmonary artery wedge (mean)
28 51/30 40/29 29
»Cardiac index, 1.9 L/min/m2.
Cultures of blood and pericardial fluid grew Staphylococcus aureus (ß-lactamase positive), as did the two prior cultures from the home hospital. The source of the infection, however, remained elusive. The patient was treated intravenously with oxacillin (12 g daily) and became free of pain, although he continued to have daily temperature elevation to 39°C and daily blood cultures positive for 5. aureus. Intracardiac pressures were normal, as assessed by hemodynamic monitoring, and no paradoxical pulse was noted. Two-dimensional echocardiography was done twice more in an attempt to search for possible cardiovascular sources of the staphylococcal bacteremia and pericarditis. No cardiovascular sources of infection could be demonstrated. Technical factors related to the patient's obesity, however, made the echocardiographic studies suboptimal. On the sixth hospital day, the patient suddenly became hypotensive and syncopäl. A pronounced paradoxical pulse was evident, and hemodynamics were consistent with cardiac tamponade once again. The patient was supported with isoproterenol hydrochloride (Isuprel) and fluid volume replacement and underwent emergency surgical exploration.
A primary anterolateral incision was made in the left side of the chest, and 300 ml of serosanguineous fluid was removed from the left pleural space. The pericardium was opened, and 900 ml of serosanguineous fluid and 250 ml of clotted blood were evacuated. The parietal pericardium and epicardium appeared severely inflamed but nonpurulent. Blood was oozing into the pericardial cavity, but no specific bleeding sites could be identified. A partial pericardiectomy was performed, an anteroinferior pericardial w i n d o w was created, and drainage tubes were placed in the pericardial and pleural cavities. The excised pericardium showed nonspecific fibrinohemorrhagic inflammation microscopically. Pericardial cultures obtained at operation were positive for 5. aureus. On the seventh hospital day, antibiotic therapy was changed to vancomycin (1 g every 12 hours) after susceptibility testing indicated a relative organism tolerance to oxacillin. By the following day, blood cultures were negative, and the patient was free of pain, hemodynamically stable, and febrile only to 38°C. On the ninth hospital day, however, he suddenly lost consciousness. Immediate resuscitative measures were unsuccessful. When the chest was opened for direct cardiac massage, the pericardial and left pleural cavities were found to be filled with bright red blood, consistent with a sudden massive exsanguinating hemorrhage. Further efforts at resuscitation were unsuccessful. AUTOPSY FINDINGS The pertinent findings at autopsy, other than septic renal infarctions, were limited to the thorax. The surgical pericardial window was patent. The pericardial and left pleural blood had been removed during the attempted resuscitation, but the apposing visceral and parietal pericardial surfaces were still lined by a nonpurulent fibrinohemorrhagic exudate (Fig. 1 through 3). The heart was enlarged (450 g) by mild biventricular hypertrophy, but no evidence of myocardial infarction or cardiac rupture was found. When saline was flushed through the pulmonary veins and left-sided cardiac structures, fluid gushed into the pericardial cavity through a defect (0.5 by 1.1 cm) along the pericardial reflection, between the ascending aorta and the superior vena cava (Fig. 1). Along the right lateral border of the aortic arch, just inferior to its brachiocephalic branches, was an irregular defect (1.7 by 2.1 cm) that led into a large sausageshaped infective pseudoaneurysm (1.9 by 2.2 by 6.7 cm) (Fig. 1 and 2). Its ragged orifice and superior extension partially obstructed the innominate and left common carotid arteries near their origin, whereas the inferior extension of the pseudoaneurysm abutted the pericardial
Mayo Clin Proc, November 1984, Vol 59
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Fig. 1. Infective pseudoaneurysm of aortic arch. A, Along pericardial reflection {dashed line), between aorta (Ao) and superior vena cava (SVC), pseudoaneurysm has ruptured (white probe) into pericardial cavity. B, Aorta has been opened to demonstrate orifice of pseudoaneurysm (An) along right lateral aortic wall, adjacent to ostium of innominate artery (*). AV = aortic valve; LV = left ventricle; MV = mitral valve; PT = pulmonary trunk; RA = right atrium; RV = right ventricle.
reflection. This latter site, which was apparently the source of the pericardial infection and chronic hemorrhage, had ruptured into the pericardial cavity. Microscopically, the wall of the aortic pseudoaneurysm was formed by active fibrovascular granu lation tissue that was variably lined by sheets of neutrophils, clotted blood, necrotic debris, and also colonies of gram-positive cocci (Fig. 3). Further inspection of the thoracic organs failed to reveal a source for the aortic infection. Neither the atypical congenitally bicuspid aortic valve nor the other cardiac valves were the site of active healed endocarditis, and we found no evidence of myocarditis or myocardial abscess. Aortic and coronary atherosclerosis was minimal and not associated with ulceration or mural thrombosis. The lungs were free of bronchopneumonia or abscesses, and we could identify no primary infective process of the thoracic cage or extrathoracic structures.
DISCUSSION Staphylococcal bacteremia, pericarditis, and tamponade were recognized well before the patient's death. Despite multiple two-dimensional echocardiographic studies and surgical exploration, no source for the bacteremia, pericarditis, and tamponade could be established. These procedures were limited by the patient's extreme obesity. Not until postmortem examination was the sequence of events that led to exsanguination apparent. On the basis of the autopsy findings, the aortic arch was considered the site of a primary 5. aureus aortitis. Extension of the necrotizing process resulted in a raggededged aortic perforation and the subsequent development of an expanding pseudoaneurysm, the wall of which was formed by infected and necrotic para-aortic soft tissues. A burrowing expansion of the pseudoaneurysm, at the site of contact with the pericardial reflection, apparently produced a small communication
788
HEMORRHAGIC CARDIAC TAMPONADE
Mayo Clin Proc, November 1984, Vol 59
Fig. 2. Infective pseudoaneurysm of aortic arch. A, Diffuse fibrinohemorrhagic nonsuppurative pericarditis. B, Close-up view of aortic cross section seen in A. The orifice (*) into pseudoaneurysm has ragged edges that partially obstruct ostia of innominate (/A) and left common carotid (/.CCA) arteries. C, Another cross section through aorta, showing orifice (between the black arrows), extent (dashed line), and site of rupture (white arrow) of pseudoaneurysm. LIV = left innominate vein; ISA = left subclavian artery. For explanation of other abbreviations, see Figure 1.
Fig. 3. A, Photomicrograph of wall of pseudoaneurysm, showing active granulation tissue with inflammatory infiltrate, ß, Photomicrograph of pericardium, showing fibrinohemorrhagic pericarditis. (Hematoxylin and eosin: A, x90; B, x35.)
Mayo Clin Proc, November 1984, Vol 59
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Table 2.—Autopsy Cases of Active Infective Aortitis (Mayo Clinic, 1940 to 1983)* Aortic site Ascending Arch Descending thoracic Abdominal
Age (yr) and sex 41 31 67 71 56 63 67 68 71
M Mt M F F F M M M
Rupture
Primary infection
Organism
No Yes Yes Yes Yes Yes Yes Yes Yes
Infective aortic and mitral endocarditis Aortitis with pseudoaneurysm Aortitis Colonic carcinoma with pericolic abscess Aortitis Aortitis* Aortitis* Aortitis* Aortitis*
Staphylococcus (probably aureus) S. aureus S. aureus, Aerobacter aerogenes Clostridium septicum Streptococcus hemolyticus Salmonella infantis Bacteria, unspecified Gram-positive cocci Bacteria, unspecified
'Excluding syphilitic aortitis and infected aortic sinus aneurysms or congenital anomalies. tCurrent case. *lnfection of an atherosclerotic aneurysm.
with the pericardial cavity and resulted in an infective, but nonpurulent, fibrinohemorrhagic pericarditis with recurrent tamponade. When the friable thrombonecrotic wall of the pseudoaneurysm finally burst and formed a large aortopericardial fistula, death was caused by exsanguination because the surgical pericardial window was widely patent and cardiac tamponade could not occur. In retrospect, two unusual features of the patient's presentation can be explained by this hypothetical sequence of events. First, his illness, characterized by fever, chest pain, and recurrent tamponade, spanned a period of 4 weeks. This finding is in contrast to the typical course of bacterial pericarditis which is precipitous in onset and usually less than 6 days. 5 Second, pericardial tamponade developed twice preoperatively, with virtually instantaneous appearance of symptoms. Tamponade associated with an expanding effusion of infectious pericarditis may appear rapidly but generally is more slowly progressive. Therefore, the early symptoms of the patient seem to have been caused by an aortitis near the aortic arch, with subsequent formation of a pseudoaneurysm during a period of several weeks. The pseudoaneurysm then eroded along a fistulous tract into the pericardial space and produced pericarditis and tamponade. Thrombosis and thrombolysis within the fistulous tract may explain the recurrent nature of the tamponade. The patient's presentation was that of bacterial pericarditis with tamponade. Previous publications indicate that bacterial pericarditis is rarely a primary infection. 5,6 An intrathoracic surgical procedure, other primary infections (especially of adjacent intrathoracic structures), or compromised host defense mechanisms usually coexist with or precede the appearance of bacterial pericarditis. 5,6 Aside from severe obesity, however, our patient had no known health problems, and he had no readily
apparent primary focus of infection other than the infective aortic pseudoaneurysm. Therefore, the patient's bacterial pericarditis was presumed secondary to a primary infective aortitis. Why the primary aortic infection occurred, however, is not clear. Infective aortitis is usually caused by Staphylococcus or Salmonella7 and characteristically occurs in elderly men with atherosclerosis. In the Mayo Clinic experience of nine autopsy cases (Table 2), six of the patients were men, six were older than 60 years, and the process was primary in seven. In this series, infection of atherosclerotic aneurysms occurred only in the abdominal aorta. In the current case, a primary infective aortic pseudoaneurysm was associated with secondary staphylococcal fibrinohemorrhagic pericarditis and recurrent hemorrhagic cardiac tamponade. When a pericardial effusion of undetermined cause is grossly hemorrhagic, the heart and great vessels should be evaluated for potentially treatable or potentially lethal sources of bleeding. Twodimensional echocardiography is a valuable tool for assessment of the great vessels, but adequate visualization of the aortic arch is obtained in less than 80% of studies in which a suprasternal transducer position is used.8 With current technology, computed tomography of the thorax is the best method of evaluating the great vessels and the pericardium; therefore, in cases such as this one, in which the source of the hemopericardium is not apparent, computed tomography is recommended. Once a mycotic aneurysm of the aortic arch has been diagnosed, resection is necessary but may be complicated by subsequent graft infection; furthermore, operative mortality is high. REFERENCES 1. Anderson MW, Christensen NA, Edwards JE: Hemopericardium complicating myocardial infarction in the absence of cardiac rupture: report of three cases. Arch Intern Med 90:634-645, 1952
790
2. 3. 4.
5.
HEMORRHAGIC CARDIAC TAMPONADE
Cobel FL, Visudh-Arom K, Edwards JE: Pseudoaneurysm of the left ventricle leading to recurrent pericardial hemorrhage. Chest 59:23-27, 1971 Baldwin JJ, Edwards JE: Uremic pericarditis as a cause of cardiac tamponade. Circulation 53:896-901, 1976 Ofori-Krakye SK, Tyberg Tl, Ceha AS, Hammond CL, Cohen LS, Langou RA: Late cardiac tamponade after open heart surgery: incidence, role of anticoagulants in its pathogenesis and its relationship to the postpericardiotomy syndrome. Circulation 63:1323-1328, 1981 Rubin RH, Moellering RC Jr: Clinical, microbiologic and therapeutic aspects of purulent pericarditis. Am J Med 59:68-78, 1975
Mayo Clin Proc, November 1984, Vol 59
6. 7. 8.
Klacsmann PC, Bulkley BH, Hutchins GM: The changed spectrum of purulent pericarditis: an 86 year autopsy experience in 200 patients. Am J Med 63:666-673, 1977 Bennett DE: Primary mycotic aneurysms of the aorta: report of case and review of the literature. Arch Surg 94:758-765, 1967 Bansal RC, Tajik AJ, Seward JB, Offord KP: Feasibility of detailed two-dimensional echocardiographic examination in adults: prospective study of 200 patients. Mayo Clin Proc 55:291-308, 1980
Catastrophic hemopericardium with cardiac tamponade most commonly occurs as a complication of acute myocardial infarction or acute aortic dissection, and subsequent rupture of the heart or ascending aorta leads to the rapid accumulation of blood within the poorly distensible pericardial sac. Subacute or chronic hemopericardium, however, may occur when blood oozes slowly into the cavity, and clinical cardiac tamponade may then develop gradually and episodically. This process may occur during the early stage of cardiac or aortic rupture or may occur in the setting of pericarditis as the visceral and parietal pericardial surfaces scrape each otherwith each heartbeat and cause erosion of the underlying richly vascular granulation tissue.1"4 We report a case of recurrent hemorrhagic cardiac tamponade associated with both bacterial pericarditis and an infective pseudoaneurysm of the aortic arch. REPORT OF CASE In July 1979, a previously healthy 31-year-old man had the onset of sharp stabbing pain in the upper chest and lower neck region which worsened with changes in posture. The man had sought medical attention when the pain had become more severe and associated with a fever (temperatures to 40°C). His local physician had prescribed penicillin and then carbenicillin (both orally), and the patient was subsequently admitted to his local *Mayo Graduate School of Medicine, Rochester, Minnesota. tCurrent address: West Roxbury, Massachusetts.
hospital because of persistent fever and chest pain. The patient had no history of chest trauma. At the time of admission, the hemoglobin concentration was 14.5 g/dl and the leukocyte count was 14,600/mm 3 with 72% neutrophils. Radiographic studies of the chest and soft tissues of the neck and esophagus revealed no abnormalities. Despite parenterally administered antibiotic therapy (6 g of cephalothin and 240 mg of gentamicin daily), the patient continued to have rigors and hectic fevers (temperatures to 40°C). On the fourth hospital day, 2 weeks after the onset of symptoms, he suddenly became hypotensive, had two syncopal episodes, and was found to have a prominent paradoxical pulse. Echocardiography demonstrated a large pericardial effusion, but three attempts at pericardiocentesis were unsuccessful. Cardiac tamponade was diagnosed, and the patient was then transferred to our institution. At the time of transfer, two blood cultures were growing unidentified gram-positive cocci. On admission, the patient was alert, cooperative, and comfortable. He was extremely obese (height, 175 cm; weight, 136 kg). He had a temperature of 39°C, a pulse of 120 beats/min, and a blood pressure of 140/70 mm Hg with an intense paradoxical pulse. Two splinter hemorrhages and one Roth spot were observed. The jugular venous pressure was normal. The heart sounds were distant, and no murmurs were heard. A soft midsystolic sound was considered to be of pericardial origin. No external source of infection was evident. Pertinent laboratory findings included a hemoglobin
Address reprint requests to Dr. W. D. Edwards. Mayo Clin Proc 59:785-790, 1984
785
786
HEMORRHAGIC CARDIAC TAMPONADE
Mayo Clin Proc, November 1984, Vol 59
concentration of 16 g/dl and a leukocyte count of 11,600/mm 3 with 82% segmented neutrophils and 5% banded neutrophils. The serum creatinine concentration was 2.0 mg/dl, and serum creatine kinase was normal. Urinalysis revealed 2 + protein, 4 leukocytes, 2 + granular casts, and occasional epithelial and hyaline casts. A chest roentgenogram revealed cardiac enlargement, increased pulmonary vascularity, and clear lungs. Diffuse ST-segment elevation on an electrocardiogram was consistent with pericarditis. A pericardial effusion was also detected by two-dimensional echocardiography; however, no valvular abnormalities were evident. On the day of admission, the hemodynamic values obtained were consistent with cardiac tamponade (Table 1). Pericardiocentesis resulted in improved hemodynamics even though only 90 ml of bloody fluid could be removed. Analysis of the pericardial fluid revealed a negative Gram stain, 3,558 cells with 99% neutrophils, pH 7.8, protein 2.8 g/dl, and glucose 50 mg/dl. Table 1.—Clinical Hemodynamics* Location
Pressure (mm Hg)
Right atrium (mean) Right ventricle Pulmonary artery Pulmonary artery wedge (mean)
28 51/30 40/29 29
»Cardiac index, 1.9 L/min/m2.
Cultures of blood and pericardial fluid grew Staphylococcus aureus (ß-lactamase positive), as did the two prior cultures from the home hospital. The source of the infection, however, remained elusive. The patient was treated intravenously with oxacillin (12 g daily) and became free of pain, although he continued to have daily temperature elevation to 39°C and daily blood cultures positive for 5. aureus. Intracardiac pressures were normal, as assessed by hemodynamic monitoring, and no paradoxical pulse was noted. Two-dimensional echocardiography was done twice more in an attempt to search for possible cardiovascular sources of the staphylococcal bacteremia and pericarditis. No cardiovascular sources of infection could be demonstrated. Technical factors related to the patient's obesity, however, made the echocardiographic studies suboptimal. On the sixth hospital day, the patient suddenly became hypotensive and syncopäl. A pronounced paradoxical pulse was evident, and hemodynamics were consistent with cardiac tamponade once again. The patient was supported with isoproterenol hydrochloride (Isuprel) and fluid volume replacement and underwent emergency surgical exploration.
A primary anterolateral incision was made in the left side of the chest, and 300 ml of serosanguineous fluid was removed from the left pleural space. The pericardium was opened, and 900 ml of serosanguineous fluid and 250 ml of clotted blood were evacuated. The parietal pericardium and epicardium appeared severely inflamed but nonpurulent. Blood was oozing into the pericardial cavity, but no specific bleeding sites could be identified. A partial pericardiectomy was performed, an anteroinferior pericardial w i n d o w was created, and drainage tubes were placed in the pericardial and pleural cavities. The excised pericardium showed nonspecific fibrinohemorrhagic inflammation microscopically. Pericardial cultures obtained at operation were positive for 5. aureus. On the seventh hospital day, antibiotic therapy was changed to vancomycin (1 g every 12 hours) after susceptibility testing indicated a relative organism tolerance to oxacillin. By the following day, blood cultures were negative, and the patient was free of pain, hemodynamically stable, and febrile only to 38°C. On the ninth hospital day, however, he suddenly lost consciousness. Immediate resuscitative measures were unsuccessful. When the chest was opened for direct cardiac massage, the pericardial and left pleural cavities were found to be filled with bright red blood, consistent with a sudden massive exsanguinating hemorrhage. Further efforts at resuscitation were unsuccessful. AUTOPSY FINDINGS The pertinent findings at autopsy, other than septic renal infarctions, were limited to the thorax. The surgical pericardial window was patent. The pericardial and left pleural blood had been removed during the attempted resuscitation, but the apposing visceral and parietal pericardial surfaces were still lined by a nonpurulent fibrinohemorrhagic exudate (Fig. 1 through 3). The heart was enlarged (450 g) by mild biventricular hypertrophy, but no evidence of myocardial infarction or cardiac rupture was found. When saline was flushed through the pulmonary veins and left-sided cardiac structures, fluid gushed into the pericardial cavity through a defect (0.5 by 1.1 cm) along the pericardial reflection, between the ascending aorta and the superior vena cava (Fig. 1). Along the right lateral border of the aortic arch, just inferior to its brachiocephalic branches, was an irregular defect (1.7 by 2.1 cm) that led into a large sausageshaped infective pseudoaneurysm (1.9 by 2.2 by 6.7 cm) (Fig. 1 and 2). Its ragged orifice and superior extension partially obstructed the innominate and left common carotid arteries near their origin, whereas the inferior extension of the pseudoaneurysm abutted the pericardial
Mayo Clin Proc, November 1984, Vol 59
HEMORRHAGIC CARDIAC TAMPONADE
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Fig. 1. Infective pseudoaneurysm of aortic arch. A, Along pericardial reflection {dashed line), between aorta (Ao) and superior vena cava (SVC), pseudoaneurysm has ruptured (white probe) into pericardial cavity. B, Aorta has been opened to demonstrate orifice of pseudoaneurysm (An) along right lateral aortic wall, adjacent to ostium of innominate artery (*). AV = aortic valve; LV = left ventricle; MV = mitral valve; PT = pulmonary trunk; RA = right atrium; RV = right ventricle.
reflection. This latter site, which was apparently the source of the pericardial infection and chronic hemorrhage, had ruptured into the pericardial cavity. Microscopically, the wall of the aortic pseudoaneurysm was formed by active fibrovascular granu lation tissue that was variably lined by sheets of neutrophils, clotted blood, necrotic debris, and also colonies of gram-positive cocci (Fig. 3). Further inspection of the thoracic organs failed to reveal a source for the aortic infection. Neither the atypical congenitally bicuspid aortic valve nor the other cardiac valves were the site of active healed endocarditis, and we found no evidence of myocarditis or myocardial abscess. Aortic and coronary atherosclerosis was minimal and not associated with ulceration or mural thrombosis. The lungs were free of bronchopneumonia or abscesses, and we could identify no primary infective process of the thoracic cage or extrathoracic structures.
DISCUSSION Staphylococcal bacteremia, pericarditis, and tamponade were recognized well before the patient's death. Despite multiple two-dimensional echocardiographic studies and surgical exploration, no source for the bacteremia, pericarditis, and tamponade could be established. These procedures were limited by the patient's extreme obesity. Not until postmortem examination was the sequence of events that led to exsanguination apparent. On the basis of the autopsy findings, the aortic arch was considered the site of a primary 5. aureus aortitis. Extension of the necrotizing process resulted in a raggededged aortic perforation and the subsequent development of an expanding pseudoaneurysm, the wall of which was formed by infected and necrotic para-aortic soft tissues. A burrowing expansion of the pseudoaneurysm, at the site of contact with the pericardial reflection, apparently produced a small communication
788
HEMORRHAGIC CARDIAC TAMPONADE
Mayo Clin Proc, November 1984, Vol 59
Fig. 2. Infective pseudoaneurysm of aortic arch. A, Diffuse fibrinohemorrhagic nonsuppurative pericarditis. B, Close-up view of aortic cross section seen in A. The orifice (*) into pseudoaneurysm has ragged edges that partially obstruct ostia of innominate (/A) and left common carotid (/.CCA) arteries. C, Another cross section through aorta, showing orifice (between the black arrows), extent (dashed line), and site of rupture (white arrow) of pseudoaneurysm. LIV = left innominate vein; ISA = left subclavian artery. For explanation of other abbreviations, see Figure 1.
Fig. 3. A, Photomicrograph of wall of pseudoaneurysm, showing active granulation tissue with inflammatory infiltrate, ß, Photomicrograph of pericardium, showing fibrinohemorrhagic pericarditis. (Hematoxylin and eosin: A, x90; B, x35.)
Mayo Clin Proc, November 1984, Vol 59
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Table 2.—Autopsy Cases of Active Infective Aortitis (Mayo Clinic, 1940 to 1983)* Aortic site Ascending Arch Descending thoracic Abdominal
Age (yr) and sex 41 31 67 71 56 63 67 68 71
M Mt M F F F M M M
Rupture
Primary infection
Organism
No Yes Yes Yes Yes Yes Yes Yes Yes
Infective aortic and mitral endocarditis Aortitis with pseudoaneurysm Aortitis Colonic carcinoma with pericolic abscess Aortitis Aortitis* Aortitis* Aortitis* Aortitis*
Staphylococcus (probably aureus) S. aureus S. aureus, Aerobacter aerogenes Clostridium septicum Streptococcus hemolyticus Salmonella infantis Bacteria, unspecified Gram-positive cocci Bacteria, unspecified
'Excluding syphilitic aortitis and infected aortic sinus aneurysms or congenital anomalies. tCurrent case. *lnfection of an atherosclerotic aneurysm.
with the pericardial cavity and resulted in an infective, but nonpurulent, fibrinohemorrhagic pericarditis with recurrent tamponade. When the friable thrombonecrotic wall of the pseudoaneurysm finally burst and formed a large aortopericardial fistula, death was caused by exsanguination because the surgical pericardial window was widely patent and cardiac tamponade could not occur. In retrospect, two unusual features of the patient's presentation can be explained by this hypothetical sequence of events. First, his illness, characterized by fever, chest pain, and recurrent tamponade, spanned a period of 4 weeks. This finding is in contrast to the typical course of bacterial pericarditis which is precipitous in onset and usually less than 6 days. 5 Second, pericardial tamponade developed twice preoperatively, with virtually instantaneous appearance of symptoms. Tamponade associated with an expanding effusion of infectious pericarditis may appear rapidly but generally is more slowly progressive. Therefore, the early symptoms of the patient seem to have been caused by an aortitis near the aortic arch, with subsequent formation of a pseudoaneurysm during a period of several weeks. The pseudoaneurysm then eroded along a fistulous tract into the pericardial space and produced pericarditis and tamponade. Thrombosis and thrombolysis within the fistulous tract may explain the recurrent nature of the tamponade. The patient's presentation was that of bacterial pericarditis with tamponade. Previous publications indicate that bacterial pericarditis is rarely a primary infection. 5,6 An intrathoracic surgical procedure, other primary infections (especially of adjacent intrathoracic structures), or compromised host defense mechanisms usually coexist with or precede the appearance of bacterial pericarditis. 5,6 Aside from severe obesity, however, our patient had no known health problems, and he had no readily
apparent primary focus of infection other than the infective aortic pseudoaneurysm. Therefore, the patient's bacterial pericarditis was presumed secondary to a primary infective aortitis. Why the primary aortic infection occurred, however, is not clear. Infective aortitis is usually caused by Staphylococcus or Salmonella7 and characteristically occurs in elderly men with atherosclerosis. In the Mayo Clinic experience of nine autopsy cases (Table 2), six of the patients were men, six were older than 60 years, and the process was primary in seven. In this series, infection of atherosclerotic aneurysms occurred only in the abdominal aorta. In the current case, a primary infective aortic pseudoaneurysm was associated with secondary staphylococcal fibrinohemorrhagic pericarditis and recurrent hemorrhagic cardiac tamponade. When a pericardial effusion of undetermined cause is grossly hemorrhagic, the heart and great vessels should be evaluated for potentially treatable or potentially lethal sources of bleeding. Twodimensional echocardiography is a valuable tool for assessment of the great vessels, but adequate visualization of the aortic arch is obtained in less than 80% of studies in which a suprasternal transducer position is used.8 With current technology, computed tomography of the thorax is the best method of evaluating the great vessels and the pericardium; therefore, in cases such as this one, in which the source of the hemopericardium is not apparent, computed tomography is recommended. Once a mycotic aneurysm of the aortic arch has been diagnosed, resection is necessary but may be complicated by subsequent graft infection; furthermore, operative mortality is high. REFERENCES 1. Anderson MW, Christensen NA, Edwards JE: Hemopericardium complicating myocardial infarction in the absence of cardiac rupture: report of three cases. Arch Intern Med 90:634-645, 1952
790
2. 3. 4.
5.
HEMORRHAGIC CARDIAC TAMPONADE
Cobel FL, Visudh-Arom K, Edwards JE: Pseudoaneurysm of the left ventricle leading to recurrent pericardial hemorrhage. Chest 59:23-27, 1971 Baldwin JJ, Edwards JE: Uremic pericarditis as a cause of cardiac tamponade. Circulation 53:896-901, 1976 Ofori-Krakye SK, Tyberg Tl, Ceha AS, Hammond CL, Cohen LS, Langou RA: Late cardiac tamponade after open heart surgery: incidence, role of anticoagulants in its pathogenesis and its relationship to the postpericardiotomy syndrome. Circulation 63:1323-1328, 1981 Rubin RH, Moellering RC Jr: Clinical, microbiologic and therapeutic aspects of purulent pericarditis. Am J Med 59:68-78, 1975
Mayo Clin Proc, November 1984, Vol 59
6. 7. 8.
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