Digestive Diseases and Sciences, Vol. 37, No. 1 (January 1992), pp. 153-154
CASE REPORT
Hemoperitoneum in the Setting of Metastatic Cancer to the Liver A Report of Two Cases with Review of the Literature K A R E N E. S C H O E D E L , MD, and A N D R E W D E K K E R , MD KEY WORDS: hemoperitoneum; metastatic cancer; liver; rupture.
H e p a t i c rupture with resulting h e m o p e r i t o n e u m due to metastatic cancer is u n c o m m o n . Reports in the literature h a v e described a wide variety of neoplasms causing this usually fatal p h e n o m e n o n (1). T w o such cases w e r e evaluated in the past y e a r at the University o f Pittsburgh and are described below including their a u t o p s y findings. CASE REPORTS
Case 1. A 57-year-old white male nursing home resident with a history of extensive alcohol and cigarette use and metastatic right hilar lung adenocarcinoma was transferred to the Oakland Veterans Administration Hospital for evaluation of confusion and hypotension. Physical examination demonstrated a systolic blood pressure of 70 mm Hg and pulse of 120 beats per minute. The patient was afebrile. H e appeared cyanotic and disoriented. Physical findings included right basilar iung rales, tachycardia, and a slightly distended but nontender abdomen. Stool examination was guaiac poSitive, Mild lower extremity edema was noted. Laboratory data were remarkable for hemoglobin and hematocrit of 6.8 g/dl and 21.4%, respectively. The white count was 1i. 1 x 10E§ 3 and platelet count was 59 • 10E+03/mm 3. [x i0E+03/mm 3 is equivalent to ten to the third power cells per millimeter cubed (conventional unit system)]. The electrolyte panel was remarkable for a sodium of 129 Meq/liter. The prothrombin time was prOlonged at i8.3 sec. Chest x-ray showed haziness in the Manuscript received October 12, 1990; revised manuscript received January 25, 199!; accepted January 28, 1991. From the Department of Pathology, University of Pittsburgh, School of Medicine, Pittsburgh, Pennsylvania 15261. Supported in part by the Pathology Education and Research Foundation (P.E.R.F.) Dr. Schoedel is a Resident Physician in Pathology of the University of Pittsburgh Health Center. Dr. Dekker is a Professor of Pathology, University of Pittsburgh School of Medicine. Address for reprint requests: Dr. Andrew Dekker, Presbyterian university Hospital of Pittsburgh, Desoto at O'Hara Streets, Pittsburgh, Pennsylvania 15213.
right middle lobe. The electrocardiogram (ECG) showed sinus tachycardia. A head computed tomographic (CT) scan was negative for intracranial bleeding. The patient was empirically begun on antibiotics. Fluid and pressor support was given. A diffuse intravascular coagulation (DIC) screen was negative. After discussion with the family, only supportive care was given. He died six days after admission. An autopsy revealed hemoperitoneum due to a ruptured hepatic metastasis o f pulmonary adenocarcinoma. Metastases were also discovered in the lUngs, diaphragm, thyroid, omentum, adrenals, right kidney, and bone. Death was attributed to widely metastatic pulmonary adenocarcinoma complicated by hemoperitoneum due to a ruptured tumor nodule. Case 2. A 42-year-old white woman with widespread known malignant melanoma presented on her final admission with complaints of migratory bone pain, abdominal discomfort, and dyspnea. Physical examination on admission demonstrated orthostasis and fever to 39.9 ~ C. A 0.5-cm skin nodule and a palpable left supraclavicular lymph node were present in the neck. The exam was otherwise remarkable for abdominal tenderness in both upper quadrants, Laboratory studies demonstrated hemoglobin 6.8 g/dl, hematocrit 19.7%, white count 8.6 • 10E+03/mm ~ with 73% neutrophils, 13% bands, 9% lymphocytes, 2% monocyteS, 2% eosinophils, and 1% atypical lymphocytes. Electrolytes were remarkable for a potassium of 3.4 Meq/liter. Calcium was 8.2 mg/dl~ total bilirubin 0.7 mg/dl, and direct bilirubin 0.2 mg/dl. Alkaline phosphatase was 227 IU/liter, 7-glutamyl transferase (GGT P) 319 IU/liter, aspartate aminotransferase (AST) 100 IU/liter, and alanine aminotransferase (ALT) 94 IU/liter. Bone scan showed a right femur lesion. Abdominal CT demonstrated multiple liver lesions, During her hospital course, she developed sudden onset of left arm weakness. A head CT showed bilateral parietal lobe lesions. She continued to complain of abdominal pain. Her ALT and AST rose to 341 IU/liter and 471 IU/liter, respectively. The GGTP rose tO 1323 IU/ liter. Her hematocrit and urine output fell, and she subsequently died. At autopsy, widespread tumor nodules were discovered in the lungs, pericardium, left
Digestive Diseases and Sciences, Vol. 37, No. 1 (January 1992) 0163-2116/92/0100-0153506.50/0 9 1992 Plenum Publishing Corporation
153
SCHOEDEL AND DEKKER adrenal, Gerota's fascia of the right kidney, and liver. A large, ruptured subcapular tumor in the liver was associated with hemoperitoneum (est. 1200 cc). DISCUSSION Metastatic disease involving the liver and resulting in hepatic rupture is uncommon. A review of the literature by Urdaneta and Nielson in 1986 (I) reported 18 cases of spontaneous hepatic rupture due to metastatic disease. Primary sites included lung, pancreas, stomach, kidney, gallbladder, breast, prostate, testicle, and colon. In addition to these cases, two choriocarcinomas (2, 3), one ovarian primary (4), one lung primary (5), and three tumors of testicular origin (6, 7) have been described as having caused hepatic rupture and hemoperitoneum due to metastatic cancer. The mechanism of hepatic rupture and bleeding due to tumor metastases is probably related to several factors. The tumor itself may be highly vascular and necrotic. The latter was amply demonstrated in the two cases described above. Erosion or alteration of the hepatic vascular system with shunting of blood flow may occur (6, 8). Extensive hepatic replacement by tumor may reduce clotting factors and chemotherapy may promote tumor necrosis and thrombocytopenia (6), all of which may contribute to rapid exsanguination once rupture has occurred. The hepatic rupture itself may occur as a result of sudden increased abdominal pressure related to coughing or sneezing (8). Important clinical features of these cases include history of malignancy, abdominal pain, hypotension, severe anemia, and elevated liver enzymes. Both our patients died within one week following hepatic rupture, illustrating the lethal nature of this phenomenon. Survival rates documented elsewhere have been poor. Urdaneta and Nielson report that almost all patients live less than six months, most less than six weeks, despite treatment (1). Treatment options are palliative only and include hepatic wedge resection or lobectomy, suture liga-
154
tion of the bleeding source, and ligation of the hepatic artery (1). Although liver rupture due to metastatic disease is uncommon, it is a dramatic, devastating entity. Physicians caring for these patients should be aware of the possibility of hepatic rupture and its invariably poor outcome. SUMMARY
Two cases of hemoperitoneum occurring as a result of hepatic rupture due to metastatic neoplasms are presented. They represent examples of a striking and devastating but fortunately uncommon entity. The variety of primary neoplastic sites is diverse. Several possible mechanisms have been put forward to explain the event of hepatic rupture itself. Finally, it is important to note the uniformly poor survival rates following hepatic rupture despite therapy. REFERENCES 1. Urdaneta LF, Nielson JV: Massive hemoperitoneum secondary to spontaneous rupture of hepatic metastases: Report of two cases and review of the literature. J Surg Oncol 31:104107, 1986 2. Erb RE, Gibler WB: Massive hemoperitoneum following rupture of hepatic metastases from unsuspected choriocarcinoma. Am J Emerg Med 7(2):196-198, 1989 3. Alveyn CG, Loehry CA: Hepatic metastases due to choriocarcinoma. Postgrad Med J 64:941-942, 1988 4. Margolin KA, Pak HY, Esensten ML, Doroshow JH: Hepatic metastases in granulosa cell tumor of the ovary. Cancer 56:691-695, 1985 5. Mittleman RE: Hepatic rupture due to metastatic lung carcinoma. Am J Clin Path 88:506-509, 1987 6. Fidas-Kamini A, Busuttil A: Fatal haemoperitoneum from ruptured hepatic metastases from testicular teratomas. Br J Urol 60(1):80-81, 1987 7. Cunningham LN, Ginsberg P, Manfrey S, Finkelstein LH: Massive hemorrhage secondary to metastatic testicular carcinoma. J Am Osteopath Assoc 89:341-344, 1989 8. Cooperman AM, Weiland LH, Welch JS: Massive bleeding from a ruptured metastatic hepatic melanoma treated by hepatic lobectomy. Mayo Clin Proc 51:167-170, 1976.
Digestive Diseases and Sciences, Vol. 37, No. I (January 1992)
CASE REPORT
Hemoperitoneum in the Setting of Metastatic Cancer to the Liver A Report of Two Cases with Review of the Literature K A R E N E. S C H O E D E L , MD, and A N D R E W D E K K E R , MD KEY WORDS: hemoperitoneum; metastatic cancer; liver; rupture.
H e p a t i c rupture with resulting h e m o p e r i t o n e u m due to metastatic cancer is u n c o m m o n . Reports in the literature h a v e described a wide variety of neoplasms causing this usually fatal p h e n o m e n o n (1). T w o such cases w e r e evaluated in the past y e a r at the University o f Pittsburgh and are described below including their a u t o p s y findings. CASE REPORTS
Case 1. A 57-year-old white male nursing home resident with a history of extensive alcohol and cigarette use and metastatic right hilar lung adenocarcinoma was transferred to the Oakland Veterans Administration Hospital for evaluation of confusion and hypotension. Physical examination demonstrated a systolic blood pressure of 70 mm Hg and pulse of 120 beats per minute. The patient was afebrile. H e appeared cyanotic and disoriented. Physical findings included right basilar iung rales, tachycardia, and a slightly distended but nontender abdomen. Stool examination was guaiac poSitive, Mild lower extremity edema was noted. Laboratory data were remarkable for hemoglobin and hematocrit of 6.8 g/dl and 21.4%, respectively. The white count was 1i. 1 x 10E§ 3 and platelet count was 59 • 10E+03/mm 3. [x i0E+03/mm 3 is equivalent to ten to the third power cells per millimeter cubed (conventional unit system)]. The electrolyte panel was remarkable for a sodium of 129 Meq/liter. The prothrombin time was prOlonged at i8.3 sec. Chest x-ray showed haziness in the Manuscript received October 12, 1990; revised manuscript received January 25, 199!; accepted January 28, 1991. From the Department of Pathology, University of Pittsburgh, School of Medicine, Pittsburgh, Pennsylvania 15261. Supported in part by the Pathology Education and Research Foundation (P.E.R.F.) Dr. Schoedel is a Resident Physician in Pathology of the University of Pittsburgh Health Center. Dr. Dekker is a Professor of Pathology, University of Pittsburgh School of Medicine. Address for reprint requests: Dr. Andrew Dekker, Presbyterian university Hospital of Pittsburgh, Desoto at O'Hara Streets, Pittsburgh, Pennsylvania 15213.
right middle lobe. The electrocardiogram (ECG) showed sinus tachycardia. A head computed tomographic (CT) scan was negative for intracranial bleeding. The patient was empirically begun on antibiotics. Fluid and pressor support was given. A diffuse intravascular coagulation (DIC) screen was negative. After discussion with the family, only supportive care was given. He died six days after admission. An autopsy revealed hemoperitoneum due to a ruptured hepatic metastasis o f pulmonary adenocarcinoma. Metastases were also discovered in the lUngs, diaphragm, thyroid, omentum, adrenals, right kidney, and bone. Death was attributed to widely metastatic pulmonary adenocarcinoma complicated by hemoperitoneum due to a ruptured tumor nodule. Case 2. A 42-year-old white woman with widespread known malignant melanoma presented on her final admission with complaints of migratory bone pain, abdominal discomfort, and dyspnea. Physical examination on admission demonstrated orthostasis and fever to 39.9 ~ C. A 0.5-cm skin nodule and a palpable left supraclavicular lymph node were present in the neck. The exam was otherwise remarkable for abdominal tenderness in both upper quadrants, Laboratory studies demonstrated hemoglobin 6.8 g/dl, hematocrit 19.7%, white count 8.6 • 10E+03/mm ~ with 73% neutrophils, 13% bands, 9% lymphocytes, 2% monocyteS, 2% eosinophils, and 1% atypical lymphocytes. Electrolytes were remarkable for a potassium of 3.4 Meq/liter. Calcium was 8.2 mg/dl~ total bilirubin 0.7 mg/dl, and direct bilirubin 0.2 mg/dl. Alkaline phosphatase was 227 IU/liter, 7-glutamyl transferase (GGT P) 319 IU/liter, aspartate aminotransferase (AST) 100 IU/liter, and alanine aminotransferase (ALT) 94 IU/liter. Bone scan showed a right femur lesion. Abdominal CT demonstrated multiple liver lesions, During her hospital course, she developed sudden onset of left arm weakness. A head CT showed bilateral parietal lobe lesions. She continued to complain of abdominal pain. Her ALT and AST rose to 341 IU/liter and 471 IU/liter, respectively. The GGTP rose tO 1323 IU/ liter. Her hematocrit and urine output fell, and she subsequently died. At autopsy, widespread tumor nodules were discovered in the lungs, pericardium, left
Digestive Diseases and Sciences, Vol. 37, No. 1 (January 1992) 0163-2116/92/0100-0153506.50/0 9 1992 Plenum Publishing Corporation
153
SCHOEDEL AND DEKKER adrenal, Gerota's fascia of the right kidney, and liver. A large, ruptured subcapular tumor in the liver was associated with hemoperitoneum (est. 1200 cc). DISCUSSION Metastatic disease involving the liver and resulting in hepatic rupture is uncommon. A review of the literature by Urdaneta and Nielson in 1986 (I) reported 18 cases of spontaneous hepatic rupture due to metastatic disease. Primary sites included lung, pancreas, stomach, kidney, gallbladder, breast, prostate, testicle, and colon. In addition to these cases, two choriocarcinomas (2, 3), one ovarian primary (4), one lung primary (5), and three tumors of testicular origin (6, 7) have been described as having caused hepatic rupture and hemoperitoneum due to metastatic cancer. The mechanism of hepatic rupture and bleeding due to tumor metastases is probably related to several factors. The tumor itself may be highly vascular and necrotic. The latter was amply demonstrated in the two cases described above. Erosion or alteration of the hepatic vascular system with shunting of blood flow may occur (6, 8). Extensive hepatic replacement by tumor may reduce clotting factors and chemotherapy may promote tumor necrosis and thrombocytopenia (6), all of which may contribute to rapid exsanguination once rupture has occurred. The hepatic rupture itself may occur as a result of sudden increased abdominal pressure related to coughing or sneezing (8). Important clinical features of these cases include history of malignancy, abdominal pain, hypotension, severe anemia, and elevated liver enzymes. Both our patients died within one week following hepatic rupture, illustrating the lethal nature of this phenomenon. Survival rates documented elsewhere have been poor. Urdaneta and Nielson report that almost all patients live less than six months, most less than six weeks, despite treatment (1). Treatment options are palliative only and include hepatic wedge resection or lobectomy, suture liga-
154
tion of the bleeding source, and ligation of the hepatic artery (1). Although liver rupture due to metastatic disease is uncommon, it is a dramatic, devastating entity. Physicians caring for these patients should be aware of the possibility of hepatic rupture and its invariably poor outcome. SUMMARY
Two cases of hemoperitoneum occurring as a result of hepatic rupture due to metastatic neoplasms are presented. They represent examples of a striking and devastating but fortunately uncommon entity. The variety of primary neoplastic sites is diverse. Several possible mechanisms have been put forward to explain the event of hepatic rupture itself. Finally, it is important to note the uniformly poor survival rates following hepatic rupture despite therapy. REFERENCES 1. Urdaneta LF, Nielson JV: Massive hemoperitoneum secondary to spontaneous rupture of hepatic metastases: Report of two cases and review of the literature. J Surg Oncol 31:104107, 1986 2. Erb RE, Gibler WB: Massive hemoperitoneum following rupture of hepatic metastases from unsuspected choriocarcinoma. Am J Emerg Med 7(2):196-198, 1989 3. Alveyn CG, Loehry CA: Hepatic metastases due to choriocarcinoma. Postgrad Med J 64:941-942, 1988 4. Margolin KA, Pak HY, Esensten ML, Doroshow JH: Hepatic metastases in granulosa cell tumor of the ovary. Cancer 56:691-695, 1985 5. Mittleman RE: Hepatic rupture due to metastatic lung carcinoma. Am J Clin Path 88:506-509, 1987 6. Fidas-Kamini A, Busuttil A: Fatal haemoperitoneum from ruptured hepatic metastases from testicular teratomas. Br J Urol 60(1):80-81, 1987 7. Cunningham LN, Ginsberg P, Manfrey S, Finkelstein LH: Massive hemorrhage secondary to metastatic testicular carcinoma. J Am Osteopath Assoc 89:341-344, 1989 8. Cooperman AM, Weiland LH, Welch JS: Massive bleeding from a ruptured metastatic hepatic melanoma treated by hepatic lobectomy. Mayo Clin Proc 51:167-170, 1976.
Digestive Diseases and Sciences, Vol. 37, No. I (January 1992)
