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Pericardial fat necrosis
J
THoRAc CARDIOVASC SURG
1988;95:727-37
Brief communications PericardiaI fat necrosis Daniel A. Stephens, MD,a and Frank Kocab, MD,b
Youngstown, Ohio From the Departments of Surgery' and Pathology," St. Elizabeth Hospital Medical Center, Youngstown, Ohio.
Pericardial fat necrosis has a highly characteristic clinical picture that enables a preoperative diagnosis to be made on clinicalgrounds. Surgical therapy, which remains the treatment of choice for this curable entity, confirms the diagnosis. This report reviews the literature and adds a thirteenth documented case to the previously reported 12 cases. Since the first reported case of pericardial fat necrosis in 1957 by Jackson, Clagett, and Mcljonald,' 11 other cases have been reported in the literature, the most recent being in 1974.2- 10 This infrequently reported entity is associated with a highly characteristic clinical picture and typical roentgenographic findings, which should place pericardial fat necrosis high on the list of differential diagnoses. In the reported cases, the admitting diagnoses were primarily of a major catastrophe, such as myocardial infarction or pulmonary embolism, but were changed to suspected pericardial cyst or pulmonary neoplasm after the clinical picture unfolded. All patients required exploratory thoracotomy for diagnosis and therapy. The prognosis is excellent (no reported mortality), but the cause remains obscure. This article presents the thirteenth documented case of pericardia I fat necrosis and reviews the findings of the previous 12 cases. Case report. A 37-year-old woman was admitted to St. Elizabeth Hospital Medical Center complaining of pain in the right side of the chest. She had been in good physical condition until 2 days before admission, when she had a sudden onset of severe, sharp, "deep-seated" pain in the right anterior part of the chest, without radiation, aggravated by deep inspiration. No history of injury or strenuous activity was noted. Medical history included dilation and curettage, hemorrhoidectomy, ovarian and breast cystectomies, and an episode of "pleurisy," Address for reprints: Daniel A. Stephens, MD, Department of Surgery, St. Elizabeth Hospital Medical Center, 1044 Belmont Ave., P.O. Box 1790, Youngstown, OH 44501.
Fig. 1. Anteroposterior chest roentgenogram with mass in right cardiophrenic angle. which had occurred 5 years previously. She was a gravida I, para I woman with no allergies. She smoked a pack of cigarettes per day and indulged in an occasional alcoholic drink. Her family history was unremarkable. On physical examination, the patient was a well-developed, nonobese white woman in no distress. Temperature was 98.4° F (36.8° C), pulse rate 82 beats/min, respiratory rate 20 breaths/min, and blood pressure 140/82 nun Hg. Height was 5'2 inches and weight was 107Y2 pounds. Significant physical findings included only slight tenderness over the right anterior part of the chest on deep palpation. The lungs were clear. The heart rate was regular and without murmur, rub, or gallop. The remainder of the examination disclosed no abnormalities. Laboratory examination revealed the following values: hemoglobin 14.7 gm/dl, hematocrit 44.4%, and white blood cell count 1O.0/mm3 (68% segmented cells, 24% lymphocytes, 2% eosinophils, and 6% monocytes). The erythrocyte sedimen-
727
7 2 8 Brief communications
The Journal of Thoracic and Cardiovascular Surgery
Fig. 3. Computed axial tomogram of chest showing wellcircumscribed low density area in right cardiophrenic angle extending to chest wall anteriorly. Hounsfield numbers of this area were indicative of fat. Fig. 2. Lateral chest roentgenogram with well-defined soft tissue density, without calcification or cavitation, in low anterior part of chest. tation rate was 63 mm/hr (normal 10 to 20). The activated partial thromboplastin time was 21.4 seconds. The urinalysis report was normal, as were results of the sequential multiple analyzer with computer (SMAC-18). Roentgenographic examination revealed a soft tissue density in the right cardiophrenic angle (Figs. I and 2). The lungs were clear of acute infiltrates and the heart was not enlarged. A tomogram of the chest showed a well-defined soft tissue density at the right cardiophrenic angle extending anteriorly to the chest wall (Fig. 3). The lateral margin was somewhat irregular with a thick strand of increased density running through this area of low density. The rib margins were intact. Hounsfield numbers of this low density area showed values indicative of pericardial fat. An electrocardiogram showed normal sinus rhythm. After admission the chest pain gradually decreased. On the eighth hospital day (with a preoperative diagnosis of pericardial cyst rather than a neoplastic lesion), the patient underwent exploratory thoracotomy. Findings confirmed fat necrosis with inflammation and hemorrhage of the mediastinal and pericardial fat pad. The pathology report showed numerous segments of yellowbrown tissue, the largest measuring 4 by 1.5 by I em. Sections revealed fat lobulations and areas of hemorrhage. A diagnosis of organizing fat necrosis was made. Postoperatively her hospital stay was uneventful, and 7 years later she continues to do well.
Discussion. Pericardial fat necrosis characteristically occurs between 23 and 64 years of age. With some
exceptions, the patient is a moderately obese man or woman who complains of the sudden onset of low anterior chest pain that is pleuritic in nature. No history of antecedent infectious process or trauma is noted. In two patients heavy activity was temporally related to the onset of the pain." The chest pain may radiate to the axilla or the shoulder and is characteristically selflimited. Pain may be intermittent, lasting initially for 3 days to a week, only to recur after a few to several days, usually with less intensity. If untreated, the duration of the pain may exceed a year." Some patients receive partial relief from pain by resting. Associated dyspnea is frequent. Occasionally, the patient may be pale, diaphoretic, and in shock on admission.' ) The cause of pericardial fat necrosis is unknown. It has been reported in cases of severe pancreatitis" in association with fat necrosis elsewhere. None of the 13 patients had a causally related medical condition. In two patients a pedicle was found," and torsion with ischemic necrosis has been implicated as causative. Two patients had episodes of straining and lifting, and a Valsalva maneuver with increased intrathoracic pressure has been postulated." Six of the patients were mildly to moderately obese. Point tenderness over the fifth or sixth rib anteriorly was noted in three patients, and three patients had a low-grade fever." A friction rub was present in two individuals. Laboratory examinations were noncontributory. Mild
Volume 95 Number 4
Brief communications
April 1988
729
REFERENCES
leukocytosis or an elevated erythrocyte sedimentation rate was present occasionally. Results of other investigations, including amylase and the SMAC-18, were normal. Electrocardiographic abnormalities were seen in only two patients; one had a pattern of resolving pericarditis" and the other had a right bundle branch block. 10 In all patients plain roentgenogram showed a juxtacardiac mass in the anterior costophrenic angle on the side of the pain, more commonly on the left side. The computed tomographic scan showed a well-defined soft tissue density, compatible with fat, in the anterior cardiophrenic angle. Immediately after the onset of pain, the initial appearance has mimicked symptoms of angina or frank myocardial infarction, pulmonary embolus, pericarditis, or pleurisy. The patients have undergone confirmatory enzyme evaluations, serial electrocardiograms, ventilation/perfusion scans, and even pulmonary angiograms. After the appearance of the mass, usually within 2 to 3 days after the onset of pain, diagnoses have included pericardial cyst or pericardial or pulmonary neoplasm. Further investigation at this point has been to undertake plain chest or computed tomograms, bronchoscopic examinations, thoracentesis, and cytologic washings. After a nondiagnostic workup, the patient has undergone exploratory thoracotomy, which has revealed pericardial fat pad necrosis in varying stages of evolution, depending on the timing of the operation. The mass has varied in size from 2 to more than 8 em. The necrotic tissue is generally easily removed during the operation. The pathologic features are typical of fat necrosis elsewhere in the body, including that seen in the epiploic appendices and breast.': 8 Gross and microscopic findings are dependent on the age of the lesion. 12 Early lesions are characterized by hemorrhagic necrosis, which progresses to central liquefactive necrosis. A dense fibrous scar eventually forms or the lesion becomes encapsulated as a pigmented, calcified nodule. Histologically, early lesions form a central focus of necrotic fat cells encompassed by macrophages with intense neutrophilic infiltration. Within days, fibroblastic proliferation occurs, vascularity increases, and a chronic inflammatory infiltrate appears. The necrotic fat cells gradually give way to a central focus filled with lipid-laden macrophages. Foreign body giant cells appear, along with calcium salts and hemosiderin pigment. Finally the lesion resolves into scar tissue or is walled off by a dense collagenous capsule. Postoperatively, the patients do well.
Damage to the posterolateral wall of the left ventricle was found in eight of approximately 700 sheep undergoing mitral valvular replacement as part of animal model studies of bioprosthetic valves. The damage consisted of left ventricular aneurysms in five animals, subacute rupture of the left ventricle in one, acute left ventricular laceration in one, and endocardial scarring in one. Six of the eight bioprostheses were bovine pericardial valves, including five low-profile valves and one standard valve;
We would like to thank Carole F. Klingler for her secretarial and editorial assistance.
Address for reprints: Michael Jones, MD, Building 10, Room 2N244, National Institutes of Health, Bethesda, MD 20892.
I. Jackson RC, Clagett OT, McDonald JR. Pericardial fat necrosis: report of three cases. J THORAC SURG 1957; 33:723-9.
2. Kasserman WHo Pericardial fat necrosis: an unusual entity. J THORAC SURG 1958;35:689-91. 3. Chester MH, Tully JB. Acute pericardiaI fat necrosis. J THoRAe CARDIOVASC SURG 1959;38:62-6. 4. Perrin MB. PericardiaI fat necrosis. Can J Surg 1960; 4:76-8.
5. Kyllonen KEJ, PerasaloO. Acute pericardialfat necrosis. Acta Chir Scand 1961;122:275-7. 6. Chipman CD, Aikens RL, Nonamaker EP. Pericardia! fat necrosis. Can Med Assoc J 1962;86:237-9. 7. Kyllonen KEJ. A case of pericardiaI fat necrosis simulating tumor of the lung. Acta Chir Scand 1964;128:77880.
8. Behrendt DM, Scannell JG. Pericardial fat necrosis: an
unusualcase of severe chest pain and thoracic "tumor." N Engl J Med 1968;279:473-5. 9. Wychulis AR, Connolly DC, McGoon DC. Pericardial cysts, tumors, and fat necrosis. J THORAC CARDIOVASC SURG 1971 ;62:294-300. 10. Webster MW, Bahnson HT. Pericardial fat necrosis: case report and review. J THORAC CARDIOVASC SURG 1974;67: 430-3. II. Cannon JR, Pitha JV, Everett MA. Subcutaneous fat necrosis in pancreatitis. J Cutan Pathol 1979;6:501-6. 12. Robbins SL, Cotran RS, Kumar V. Pathological basis of disease. Philadelphia: WB Saunders, 1984:1168.
Ventricular aneurysms and other lesions produced by the struts of bioprosthetic valves implanted in sheep Michael Jones, MD, Elling E. Eidbo, BA, E. Rene Rodriguez, MD, Victor J. Ferrans, MD, PhD, and Richard E. Clark, MD, Bethesda. Md. From the Surgery and Pathology Branches, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Md.
THoRAc CARDIOVASC SURG
1988;95:727-37
Brief communications PericardiaI fat necrosis Daniel A. Stephens, MD,a and Frank Kocab, MD,b
Youngstown, Ohio From the Departments of Surgery' and Pathology," St. Elizabeth Hospital Medical Center, Youngstown, Ohio.
Pericardial fat necrosis has a highly characteristic clinical picture that enables a preoperative diagnosis to be made on clinicalgrounds. Surgical therapy, which remains the treatment of choice for this curable entity, confirms the diagnosis. This report reviews the literature and adds a thirteenth documented case to the previously reported 12 cases. Since the first reported case of pericardial fat necrosis in 1957 by Jackson, Clagett, and Mcljonald,' 11 other cases have been reported in the literature, the most recent being in 1974.2- 10 This infrequently reported entity is associated with a highly characteristic clinical picture and typical roentgenographic findings, which should place pericardial fat necrosis high on the list of differential diagnoses. In the reported cases, the admitting diagnoses were primarily of a major catastrophe, such as myocardial infarction or pulmonary embolism, but were changed to suspected pericardial cyst or pulmonary neoplasm after the clinical picture unfolded. All patients required exploratory thoracotomy for diagnosis and therapy. The prognosis is excellent (no reported mortality), but the cause remains obscure. This article presents the thirteenth documented case of pericardia I fat necrosis and reviews the findings of the previous 12 cases. Case report. A 37-year-old woman was admitted to St. Elizabeth Hospital Medical Center complaining of pain in the right side of the chest. She had been in good physical condition until 2 days before admission, when she had a sudden onset of severe, sharp, "deep-seated" pain in the right anterior part of the chest, without radiation, aggravated by deep inspiration. No history of injury or strenuous activity was noted. Medical history included dilation and curettage, hemorrhoidectomy, ovarian and breast cystectomies, and an episode of "pleurisy," Address for reprints: Daniel A. Stephens, MD, Department of Surgery, St. Elizabeth Hospital Medical Center, 1044 Belmont Ave., P.O. Box 1790, Youngstown, OH 44501.
Fig. 1. Anteroposterior chest roentgenogram with mass in right cardiophrenic angle. which had occurred 5 years previously. She was a gravida I, para I woman with no allergies. She smoked a pack of cigarettes per day and indulged in an occasional alcoholic drink. Her family history was unremarkable. On physical examination, the patient was a well-developed, nonobese white woman in no distress. Temperature was 98.4° F (36.8° C), pulse rate 82 beats/min, respiratory rate 20 breaths/min, and blood pressure 140/82 nun Hg. Height was 5'2 inches and weight was 107Y2 pounds. Significant physical findings included only slight tenderness over the right anterior part of the chest on deep palpation. The lungs were clear. The heart rate was regular and without murmur, rub, or gallop. The remainder of the examination disclosed no abnormalities. Laboratory examination revealed the following values: hemoglobin 14.7 gm/dl, hematocrit 44.4%, and white blood cell count 1O.0/mm3 (68% segmented cells, 24% lymphocytes, 2% eosinophils, and 6% monocytes). The erythrocyte sedimen-
727
7 2 8 Brief communications
The Journal of Thoracic and Cardiovascular Surgery
Fig. 3. Computed axial tomogram of chest showing wellcircumscribed low density area in right cardiophrenic angle extending to chest wall anteriorly. Hounsfield numbers of this area were indicative of fat. Fig. 2. Lateral chest roentgenogram with well-defined soft tissue density, without calcification or cavitation, in low anterior part of chest. tation rate was 63 mm/hr (normal 10 to 20). The activated partial thromboplastin time was 21.4 seconds. The urinalysis report was normal, as were results of the sequential multiple analyzer with computer (SMAC-18). Roentgenographic examination revealed a soft tissue density in the right cardiophrenic angle (Figs. I and 2). The lungs were clear of acute infiltrates and the heart was not enlarged. A tomogram of the chest showed a well-defined soft tissue density at the right cardiophrenic angle extending anteriorly to the chest wall (Fig. 3). The lateral margin was somewhat irregular with a thick strand of increased density running through this area of low density. The rib margins were intact. Hounsfield numbers of this low density area showed values indicative of pericardial fat. An electrocardiogram showed normal sinus rhythm. After admission the chest pain gradually decreased. On the eighth hospital day (with a preoperative diagnosis of pericardial cyst rather than a neoplastic lesion), the patient underwent exploratory thoracotomy. Findings confirmed fat necrosis with inflammation and hemorrhage of the mediastinal and pericardial fat pad. The pathology report showed numerous segments of yellowbrown tissue, the largest measuring 4 by 1.5 by I em. Sections revealed fat lobulations and areas of hemorrhage. A diagnosis of organizing fat necrosis was made. Postoperatively her hospital stay was uneventful, and 7 years later she continues to do well.
Discussion. Pericardial fat necrosis characteristically occurs between 23 and 64 years of age. With some
exceptions, the patient is a moderately obese man or woman who complains of the sudden onset of low anterior chest pain that is pleuritic in nature. No history of antecedent infectious process or trauma is noted. In two patients heavy activity was temporally related to the onset of the pain." The chest pain may radiate to the axilla or the shoulder and is characteristically selflimited. Pain may be intermittent, lasting initially for 3 days to a week, only to recur after a few to several days, usually with less intensity. If untreated, the duration of the pain may exceed a year." Some patients receive partial relief from pain by resting. Associated dyspnea is frequent. Occasionally, the patient may be pale, diaphoretic, and in shock on admission.' ) The cause of pericardial fat necrosis is unknown. It has been reported in cases of severe pancreatitis" in association with fat necrosis elsewhere. None of the 13 patients had a causally related medical condition. In two patients a pedicle was found," and torsion with ischemic necrosis has been implicated as causative. Two patients had episodes of straining and lifting, and a Valsalva maneuver with increased intrathoracic pressure has been postulated." Six of the patients were mildly to moderately obese. Point tenderness over the fifth or sixth rib anteriorly was noted in three patients, and three patients had a low-grade fever." A friction rub was present in two individuals. Laboratory examinations were noncontributory. Mild
Volume 95 Number 4
Brief communications
April 1988
729
REFERENCES
leukocytosis or an elevated erythrocyte sedimentation rate was present occasionally. Results of other investigations, including amylase and the SMAC-18, were normal. Electrocardiographic abnormalities were seen in only two patients; one had a pattern of resolving pericarditis" and the other had a right bundle branch block. 10 In all patients plain roentgenogram showed a juxtacardiac mass in the anterior costophrenic angle on the side of the pain, more commonly on the left side. The computed tomographic scan showed a well-defined soft tissue density, compatible with fat, in the anterior cardiophrenic angle. Immediately after the onset of pain, the initial appearance has mimicked symptoms of angina or frank myocardial infarction, pulmonary embolus, pericarditis, or pleurisy. The patients have undergone confirmatory enzyme evaluations, serial electrocardiograms, ventilation/perfusion scans, and even pulmonary angiograms. After the appearance of the mass, usually within 2 to 3 days after the onset of pain, diagnoses have included pericardial cyst or pericardial or pulmonary neoplasm. Further investigation at this point has been to undertake plain chest or computed tomograms, bronchoscopic examinations, thoracentesis, and cytologic washings. After a nondiagnostic workup, the patient has undergone exploratory thoracotomy, which has revealed pericardial fat pad necrosis in varying stages of evolution, depending on the timing of the operation. The mass has varied in size from 2 to more than 8 em. The necrotic tissue is generally easily removed during the operation. The pathologic features are typical of fat necrosis elsewhere in the body, including that seen in the epiploic appendices and breast.': 8 Gross and microscopic findings are dependent on the age of the lesion. 12 Early lesions are characterized by hemorrhagic necrosis, which progresses to central liquefactive necrosis. A dense fibrous scar eventually forms or the lesion becomes encapsulated as a pigmented, calcified nodule. Histologically, early lesions form a central focus of necrotic fat cells encompassed by macrophages with intense neutrophilic infiltration. Within days, fibroblastic proliferation occurs, vascularity increases, and a chronic inflammatory infiltrate appears. The necrotic fat cells gradually give way to a central focus filled with lipid-laden macrophages. Foreign body giant cells appear, along with calcium salts and hemosiderin pigment. Finally the lesion resolves into scar tissue or is walled off by a dense collagenous capsule. Postoperatively, the patients do well.
Damage to the posterolateral wall of the left ventricle was found in eight of approximately 700 sheep undergoing mitral valvular replacement as part of animal model studies of bioprosthetic valves. The damage consisted of left ventricular aneurysms in five animals, subacute rupture of the left ventricle in one, acute left ventricular laceration in one, and endocardial scarring in one. Six of the eight bioprostheses were bovine pericardial valves, including five low-profile valves and one standard valve;
We would like to thank Carole F. Klingler for her secretarial and editorial assistance.
Address for reprints: Michael Jones, MD, Building 10, Room 2N244, National Institutes of Health, Bethesda, MD 20892.
I. Jackson RC, Clagett OT, McDonald JR. Pericardial fat necrosis: report of three cases. J THORAC SURG 1957; 33:723-9.
2. Kasserman WHo Pericardial fat necrosis: an unusual entity. J THORAC SURG 1958;35:689-91. 3. Chester MH, Tully JB. Acute pericardiaI fat necrosis. J THoRAe CARDIOVASC SURG 1959;38:62-6. 4. Perrin MB. PericardiaI fat necrosis. Can J Surg 1960; 4:76-8.
5. Kyllonen KEJ, PerasaloO. Acute pericardialfat necrosis. Acta Chir Scand 1961;122:275-7. 6. Chipman CD, Aikens RL, Nonamaker EP. Pericardia! fat necrosis. Can Med Assoc J 1962;86:237-9. 7. Kyllonen KEJ. A case of pericardiaI fat necrosis simulating tumor of the lung. Acta Chir Scand 1964;128:77880.
8. Behrendt DM, Scannell JG. Pericardial fat necrosis: an
unusualcase of severe chest pain and thoracic "tumor." N Engl J Med 1968;279:473-5. 9. Wychulis AR, Connolly DC, McGoon DC. Pericardial cysts, tumors, and fat necrosis. J THORAC CARDIOVASC SURG 1971 ;62:294-300. 10. Webster MW, Bahnson HT. Pericardial fat necrosis: case report and review. J THORAC CARDIOVASC SURG 1974;67: 430-3. II. Cannon JR, Pitha JV, Everett MA. Subcutaneous fat necrosis in pancreatitis. J Cutan Pathol 1979;6:501-6. 12. Robbins SL, Cotran RS, Kumar V. Pathological basis of disease. Philadelphia: WB Saunders, 1984:1168.
Ventricular aneurysms and other lesions produced by the struts of bioprosthetic valves implanted in sheep Michael Jones, MD, Elling E. Eidbo, BA, E. Rene Rodriguez, MD, Victor J. Ferrans, MD, PhD, and Richard E. Clark, MD, Bethesda. Md. From the Surgery and Pathology Branches, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Md.