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Spontaneous Intrahepatic Hemorrhage: A Case Report
The Journal of Emergency Medicine, Vol. 40, No. 4, pp. 385–387, 2011 Copyright © 2011 Elsevier Inc. Printed in the USA. All rights reserved 0736-4679/$–see front matter
doi:10.1016/j.jemermed.2007.11.079
Clinical Communications: Adults
SPONTANEOUS INTRAHEPATIC HEMORRHAGE: A CASE REPORT Harman Arora,
MD,*
Jennifer Romero,
PA,*
Eugene Rubach,
MD,†
and Robert Silverman,
MD, FACEP*
*Department of Emergency Medicine, Long Island Jewish Medical Center, New Hyde Park, New York and †Department of Surgery, North Shore University Hospital, Manhasset, New York Reprint Address: Harman Arora, MD, Department of Emergency Medicine, Long Island Jewish Medical Center, 270-05 76th Avenue, New Hyde Park, NY 11040
e Abstract—Etiology of the acute abdomen can be difficult to determine in the acute care setting, as both medical and surgical emergencies can present with a similar clinical presentation. Prompt work-up is essential to reveal the diagnosis and allow for successful treatment. We present a rare case of spontaneous intrahepatic hemorrhage in a patient with multiple comorbidities, including multiple myeloma and lung cancer. Although the underlying cause of hemorrhage remained unknown, appropriate recognition of the patient’s presenting signs and symptoms allowed for immediate treatment and satisfactory outcome. © 2011 Elsevier Inc.
agement of hepatic rupture are discussed. A familiarity with the diagnosis of intrahepatic hemorrhage may help to decrease the high mortality rate associated with this disease. CASE REPORT A 61-year-old woman was brought to the Emergency Department (ED) from a nursing home with a chief complaint of ongoing abdominal pain for the last month, which had increased in severity over the last 24 hours. She had been discharged the previous day to the care of the nursing home after a 1-week hospitalization with a diagnosis of spontaneous left rectus sheath hematoma. Her past medical history included hypertension, multiple myeloma, squamous cell carcinoma of the lung, deep venous thrombosis with inferior vena cava filter in place, and spinal cord compression secondary to ventral epidural tumor. She denied any allergies. Medications on ED presentation included pantoprazole, amlodipine, carvedilol, decadron, duragesic patch, stool softeners, and calcium supplementation. Initial triage evaluation revealed a diaphoretic elderlyappearing black woman in severe distress secondary to abdominal pain. Initial vital signs included a core body temperature of 37°C (98.6°F), blood pressure of 123/91 mm Hg, pulse of 89 beats/min, respiratory rate of 24 breaths/min, and oxygen saturation of 99% on room air. Forty-five minutes after ED arrival, her blood pressure
e Keywords—intrahepatic hemorrhage; hepatic rupture; acute abdomen; angiographic embolization
INTRODUCTION Spontaneous hepatic rupture is a rare phenomenon. An extensive literature review revealed that this phenomenon most commonly occurs in the setting of preeclampsia and HELLP (hemolysis, elevated liver function tests, low platelets) syndrome as well as amyloidosis (1,2). Sporadic cases have also been described after perforated gastric ulcer, stem cell transplant, and in the setting of hepatic tumor or peliosis hepatis (3– 6). Survival depends on timely diagnosis and appropriate management, which can be difficult considering the rarity of this phenomenon. We describe herein the case of a 61-year-old woman found to have massive intrahepatic hemorrhage of unknown etiology. The presentation, diagnosis, and man-
RECEIVED: 31 May 2007; FINAL ACCEPTED: 4 September 2007
SUBMISSION RECEIVED:
4 September 2007; 385
386
dropped to 98/78 mm Hg with a pulse of 86 beats/min. Her abdominal examination was significant for a tender, firm, palpable mass to the left of the umbilicus with diffuse abdominal tenderness. Bowel sounds were present and the abdomen was soft but distended. Guaiac-negative brown stool was noted. The remainder of the examination was normal. Initial laboratory tests revealed a white blood cell count of 14,000/mm3, hemoglobin of 10.3 g/dL, hematocrit of 31%, and platelet count of 231,000/mm3. Coagulation studies revealed a protime of 14 s, activated partial thromboplastin time of 34 s, and international normalized ratio of 1.2. Liver function tests showed an aspartate transaminase of 113 units/L and alanine transaminase of 224 units/L. Alkaline phosphatase was elevated at 216 units/L. Serum bilirubin was normal. Lactate was normal. ED course was complicated by worsening hypotension that was initially managed by fluid resuscitation via large-bore intravenous access and stress dose steroids. The patient also became hypoxic to 85% on room air, which was treated by oxygen via non-rebreather mask application. Arterial blood gas analysis was done, which was normal. Bedside ultrasonography was considered, but the ED and surgical consult team decided that computed tomography (CT) would be the preferred imaging modality considering immediate availability and recent history of abdominal CT scan for comparison. CT scan of the abdomen as well as CT angiography of the chest was performed. Compared to previous CT scan done 2 days prior, a massive amount of hemorrhage within the parenchyma of the liver and peritoneal space was noted (Figure 1). Extensive active extravasation was described in the right hepatic lobe, with origin appearing from hepatic arterial or portal venous branches. CT angiography of the chest was unremarkable. Repeat laboratory tests were drawn 3 h after initial blood work, revealing a drop in hemoglobin to 6.1 g/dL and a drop in hematocrit
Figure 1. Delayed venous phase abdominal CT scan showing active extravasation of blood into liver parenchyma (small arrow) as well as hematoma formation within the peritoneum (large arrow).
H. Arora et al.
to 19.5%. Further resuscitative maneuvers, including transfusion of packed red blood cells and bladder catheterization, were performed. Surgery and interventional radiology were consulted, and the decision was made to immediately take the patient to the interventional radiology suite for direct angiographic visualization. Hepatic angiography was then performed, demonstrating at least two distinct sites of intrahepatic contrast extravasation within the right lobe, consistent with active hemorrhage. Diffuse irregularity of the caliber of the visualized hepatic arterial branches suggested an underlying vasculitis. Successful embolization was performed, with completion angiography demonstrating no evidence of contrast extravasation. The patient was transferred to Surgical Intensive Care with no major complications over the next few days. After extensive discussion with family, the decision was then made to transfer the patient to a hospice facility on post-operative day 6 for pain management of her underlying oncologic diagnoses.
DISCUSSION Spontaneous hepatic rupture is a rare but life-threatening complication of a number of disease states, most commonly occurring in cases of preeclampsia and HELLP syndrome. In fact, much of our understanding of this phenomenon and its management has been gathered from obstetric literature. The incidence of spontaneous hepatic rupture in pregnancy has been reported in the range of 1 in 45,000 to 1 in 225,000 deliveries, with maternal mortality ranging from 18% to 86% (1). This complication usually occurs during the third trimester of pregnancy or early postpartum. The pathogenesis is related to extravasation of blood below Glisson’s capsule from areas of periportal hemorrhage associated with coagulopathy of related disease. Subsequent hematoma formation increases pressure within the capsule, ultimately causing rupture with bleeding into the peritoneum (7). This diagnosis must be considered in any pregnant patient who presents with severe right upper quadrant, epigastric, or right shoulder pain, nausea and vomiting, abdominal distension, or hypovolemic shock (8). Intrahepatic hemorrhage has also been documented in the literature as an uncommon complication of hepatic amyloidosis, with the majority of cases occurring after liver biopsy (2). Widespread amyloid deposition within the blood vessels of patients with amyloidosis is thought to result in the vascular fragility that further exacerbates this disease state. Spontaneous micro-hemorrhages within the liver subsequently lead to a final common pathway of capsular distension, hematoma formation, and possible spontaneous rupture (9).
Spontaneous Intrahepatic Hemorrhage
Early diagnosis in cases of hepatic rupture is essential. Patient history and clinical examination supplemented by laboratory findings and hepatic imaging allow for prompt diagnosis. Key laboratory parameters include hematologic, liver function, and coagulation studies. Imaging techniques include ultrasound, CT scan with or without contrast, and magnetic resonance imaging. CT scan is the preferred diagnostic modality in an emergent situation, as it can be readily obtained and offers an unobstructed perspective of the abdomen, allowing for visualization of differential intra-abdominal pathology. Bedside emergency ultrasound should be utilized in patients who are hemodynamically unstable. Once the diagnosis has been made, aggressive early management is crucial. Resuscitation with intravenous fluids and transfusion of blood as well as fresh frozen plasma and platelets may be necessary, especially in patients who present in shock. Historically, surgical intervention has been the standard of treatment in all cases. Operative interventions include evacuation of hematoma, packing, application of gelfoam- or collagen-impregnated materials, over-sewing of lacerations, and drainage to prevent reaccumulation of blood (10). Hepatic artery ligation has been used successfully in cases where hemorrhage originates from hepatic artery circulation rather than portal venous distribution. Hepatic resection may be necessary if the above measures are unsuccessful. In cases of massive necrosis and uncontrollable hemorrhage, liver transplantation has become necessary (5,10). More recently, interventional angiography with selective hepatic artery embolization has been heralded as a safe alternative if an arterial source can be identified (11). This modality is especially useful in patients who are poor candidates for surgery, as adjunctive therapy, or in those who have failed surgical intervention. Some authors recommend conservative management in the case of the hemodynamically stable patient with an intact liver capsule. Algorithms for such conservative management with the aid of serial CT scanning have been developed (12). Recent anecdotal cases of management with recombinant factor VIIa in spontaneous subcapsular liver hematoma as well as in hepatic rupture complicated by abdominal compartment syndrome have been described (13,14). Although the patient had multiple co-morbidities, the underlying cause for spontaneous rupture of the liver in our case is unknown. We presume that her history of multiple myeloma and its association with amyloidosis may have been responsible. The vasculitic nature of her
387
blood vessels noted on angiography may also have resulted in hemorrhage. She presented to our ED with an acute abdomen-like picture. Although her initial laboratory studies were only mildly abnormal, the development of hypotension prompted rapid imaging with CT scan, allowing for prompt diagnosis and management via angiographic embolization. Inclusion of this rare diagnosis in the differential of abdominal pain and acute abdomen is vital to successful management. REFERENCES 1. Araujo AC, Leao MD, Nobrega MH, et al. Characteristics and treatment of hepatic rupture caused by HELLP syndrome. Am J Obstet Gynecol 2006;195:129 –33. 2. Kacem C, Helali K, Puisieux F. Recurrent spontaneous hepatic rupture in primary hepatic amyloidosis. Ann Intern Med 1998;29: 339. 3. Tsokos M, Schulz F. Non-traumatic liver rupture due to perforated gastric ulcer. Int J Legal Med 1999;112:321–3. 4. Barnett SJ, Weisdorf-Schindle S, Baker KS, Saltzman DA. Spontaneous liver rupture in a child with graft-versus-host-disease. J Pediatr Surg 2004;39:e1–3. 5. Erdogan D, Busch OR, van Delden OM, Ten Kate FJ, Gouma DJ, van Gulik DM. Management of spontaneous hemorrhage and rupture of hepatocellular adenomas. A single center experience. Liver Int 2006;26:433– 8. 6. Wang SY, Ruggles S, Vade A, Newman BM, Borge MA. Hepatic rupture caused by peliosis hepatis. J Pediatr Surg 2001;36:1456 –9. 7. Reinus JF, Riely CA. Gastrointestinal and hepatic disorders in the pregnant patient. In: Feldman M, Friedman LS, Brandt LJ, eds. Sleisenger and Fordtran’s gastrointestinal and liver disease: pathophysiology, diagnosis, management, 8th edn. W.B. Saunders; 2006: 803. 8. Wicke C, Pereira PL, Neeser E, Flesch I, Rodegerdts EA, Becker HD. Subcapsular liver hematoma in HELLP syndrome: evaluation of diagnostic and therapeutic options—a unicenter study. Am J Obstet Gynecol 2004;190:106 –12. 9. Hurd WW, Katholi RE. Acquired functional asplenia: association with spontaneous rupture of the spleen and fatal spontaneous rupture of the liver in amyloidosis. Arch Intern Med 1980;140: 844 –5. 10. Sheikh RA, Yasmeen S, Pauly MP, Riegler JL. Spontaneous intrahepatic hemorrhage and hepatic rupture in the HELLP syndrome: four cases and a review. J Clin Gastroenetrol 1999;28: 323– 8. 11. Mukhapadhya A, Raghuram L, Justus A, Joseph AJ, Eapen CE, Chandy GM. Transcatheter hepatic artery embolization for spontaneous rupture of amyloid liver. Indian J Gastroenterol 2004;23: 26 –7. 12. Smith LG, Moise KG, Dildy GA, et al. Spontaneous rupture of the liver during pregnancy: current therapy. Obstet Gynecol 1991;77: 171–5. 13. Dart BW, Cockerham WT, Torres C, Kipikasa JH, Maxwell RA. A novel use of recombinant factor VIIa in HELLP syndrome associated with spontaneous hepatic rupture and abdominal compartment syndrome. J Trauma 2004;57:171– 4. 14. Merchant SH, Mathew P, Vanderjagt TJ, Howdieshell TR, Crookston KP. Recombinant factor VIIa in management of spontaneous subcapsular liver hematoma associated with pregnancy. Obstet Gynecol 2004;103:1055– 8.
doi:10.1016/j.jemermed.2007.11.079
Clinical Communications: Adults
SPONTANEOUS INTRAHEPATIC HEMORRHAGE: A CASE REPORT Harman Arora,
MD,*
Jennifer Romero,
PA,*
Eugene Rubach,
MD,†
and Robert Silverman,
MD, FACEP*
*Department of Emergency Medicine, Long Island Jewish Medical Center, New Hyde Park, New York and †Department of Surgery, North Shore University Hospital, Manhasset, New York Reprint Address: Harman Arora, MD, Department of Emergency Medicine, Long Island Jewish Medical Center, 270-05 76th Avenue, New Hyde Park, NY 11040
e Abstract—Etiology of the acute abdomen can be difficult to determine in the acute care setting, as both medical and surgical emergencies can present with a similar clinical presentation. Prompt work-up is essential to reveal the diagnosis and allow for successful treatment. We present a rare case of spontaneous intrahepatic hemorrhage in a patient with multiple comorbidities, including multiple myeloma and lung cancer. Although the underlying cause of hemorrhage remained unknown, appropriate recognition of the patient’s presenting signs and symptoms allowed for immediate treatment and satisfactory outcome. © 2011 Elsevier Inc.
agement of hepatic rupture are discussed. A familiarity with the diagnosis of intrahepatic hemorrhage may help to decrease the high mortality rate associated with this disease. CASE REPORT A 61-year-old woman was brought to the Emergency Department (ED) from a nursing home with a chief complaint of ongoing abdominal pain for the last month, which had increased in severity over the last 24 hours. She had been discharged the previous day to the care of the nursing home after a 1-week hospitalization with a diagnosis of spontaneous left rectus sheath hematoma. Her past medical history included hypertension, multiple myeloma, squamous cell carcinoma of the lung, deep venous thrombosis with inferior vena cava filter in place, and spinal cord compression secondary to ventral epidural tumor. She denied any allergies. Medications on ED presentation included pantoprazole, amlodipine, carvedilol, decadron, duragesic patch, stool softeners, and calcium supplementation. Initial triage evaluation revealed a diaphoretic elderlyappearing black woman in severe distress secondary to abdominal pain. Initial vital signs included a core body temperature of 37°C (98.6°F), blood pressure of 123/91 mm Hg, pulse of 89 beats/min, respiratory rate of 24 breaths/min, and oxygen saturation of 99% on room air. Forty-five minutes after ED arrival, her blood pressure
e Keywords—intrahepatic hemorrhage; hepatic rupture; acute abdomen; angiographic embolization
INTRODUCTION Spontaneous hepatic rupture is a rare phenomenon. An extensive literature review revealed that this phenomenon most commonly occurs in the setting of preeclampsia and HELLP (hemolysis, elevated liver function tests, low platelets) syndrome as well as amyloidosis (1,2). Sporadic cases have also been described after perforated gastric ulcer, stem cell transplant, and in the setting of hepatic tumor or peliosis hepatis (3– 6). Survival depends on timely diagnosis and appropriate management, which can be difficult considering the rarity of this phenomenon. We describe herein the case of a 61-year-old woman found to have massive intrahepatic hemorrhage of unknown etiology. The presentation, diagnosis, and man-
RECEIVED: 31 May 2007; FINAL ACCEPTED: 4 September 2007
SUBMISSION RECEIVED:
4 September 2007; 385
386
dropped to 98/78 mm Hg with a pulse of 86 beats/min. Her abdominal examination was significant for a tender, firm, palpable mass to the left of the umbilicus with diffuse abdominal tenderness. Bowel sounds were present and the abdomen was soft but distended. Guaiac-negative brown stool was noted. The remainder of the examination was normal. Initial laboratory tests revealed a white blood cell count of 14,000/mm3, hemoglobin of 10.3 g/dL, hematocrit of 31%, and platelet count of 231,000/mm3. Coagulation studies revealed a protime of 14 s, activated partial thromboplastin time of 34 s, and international normalized ratio of 1.2. Liver function tests showed an aspartate transaminase of 113 units/L and alanine transaminase of 224 units/L. Alkaline phosphatase was elevated at 216 units/L. Serum bilirubin was normal. Lactate was normal. ED course was complicated by worsening hypotension that was initially managed by fluid resuscitation via large-bore intravenous access and stress dose steroids. The patient also became hypoxic to 85% on room air, which was treated by oxygen via non-rebreather mask application. Arterial blood gas analysis was done, which was normal. Bedside ultrasonography was considered, but the ED and surgical consult team decided that computed tomography (CT) would be the preferred imaging modality considering immediate availability and recent history of abdominal CT scan for comparison. CT scan of the abdomen as well as CT angiography of the chest was performed. Compared to previous CT scan done 2 days prior, a massive amount of hemorrhage within the parenchyma of the liver and peritoneal space was noted (Figure 1). Extensive active extravasation was described in the right hepatic lobe, with origin appearing from hepatic arterial or portal venous branches. CT angiography of the chest was unremarkable. Repeat laboratory tests were drawn 3 h after initial blood work, revealing a drop in hemoglobin to 6.1 g/dL and a drop in hematocrit
Figure 1. Delayed venous phase abdominal CT scan showing active extravasation of blood into liver parenchyma (small arrow) as well as hematoma formation within the peritoneum (large arrow).
H. Arora et al.
to 19.5%. Further resuscitative maneuvers, including transfusion of packed red blood cells and bladder catheterization, were performed. Surgery and interventional radiology were consulted, and the decision was made to immediately take the patient to the interventional radiology suite for direct angiographic visualization. Hepatic angiography was then performed, demonstrating at least two distinct sites of intrahepatic contrast extravasation within the right lobe, consistent with active hemorrhage. Diffuse irregularity of the caliber of the visualized hepatic arterial branches suggested an underlying vasculitis. Successful embolization was performed, with completion angiography demonstrating no evidence of contrast extravasation. The patient was transferred to Surgical Intensive Care with no major complications over the next few days. After extensive discussion with family, the decision was then made to transfer the patient to a hospice facility on post-operative day 6 for pain management of her underlying oncologic diagnoses.
DISCUSSION Spontaneous hepatic rupture is a rare but life-threatening complication of a number of disease states, most commonly occurring in cases of preeclampsia and HELLP syndrome. In fact, much of our understanding of this phenomenon and its management has been gathered from obstetric literature. The incidence of spontaneous hepatic rupture in pregnancy has been reported in the range of 1 in 45,000 to 1 in 225,000 deliveries, with maternal mortality ranging from 18% to 86% (1). This complication usually occurs during the third trimester of pregnancy or early postpartum. The pathogenesis is related to extravasation of blood below Glisson’s capsule from areas of periportal hemorrhage associated with coagulopathy of related disease. Subsequent hematoma formation increases pressure within the capsule, ultimately causing rupture with bleeding into the peritoneum (7). This diagnosis must be considered in any pregnant patient who presents with severe right upper quadrant, epigastric, or right shoulder pain, nausea and vomiting, abdominal distension, or hypovolemic shock (8). Intrahepatic hemorrhage has also been documented in the literature as an uncommon complication of hepatic amyloidosis, with the majority of cases occurring after liver biopsy (2). Widespread amyloid deposition within the blood vessels of patients with amyloidosis is thought to result in the vascular fragility that further exacerbates this disease state. Spontaneous micro-hemorrhages within the liver subsequently lead to a final common pathway of capsular distension, hematoma formation, and possible spontaneous rupture (9).
Spontaneous Intrahepatic Hemorrhage
Early diagnosis in cases of hepatic rupture is essential. Patient history and clinical examination supplemented by laboratory findings and hepatic imaging allow for prompt diagnosis. Key laboratory parameters include hematologic, liver function, and coagulation studies. Imaging techniques include ultrasound, CT scan with or without contrast, and magnetic resonance imaging. CT scan is the preferred diagnostic modality in an emergent situation, as it can be readily obtained and offers an unobstructed perspective of the abdomen, allowing for visualization of differential intra-abdominal pathology. Bedside emergency ultrasound should be utilized in patients who are hemodynamically unstable. Once the diagnosis has been made, aggressive early management is crucial. Resuscitation with intravenous fluids and transfusion of blood as well as fresh frozen plasma and platelets may be necessary, especially in patients who present in shock. Historically, surgical intervention has been the standard of treatment in all cases. Operative interventions include evacuation of hematoma, packing, application of gelfoam- or collagen-impregnated materials, over-sewing of lacerations, and drainage to prevent reaccumulation of blood (10). Hepatic artery ligation has been used successfully in cases where hemorrhage originates from hepatic artery circulation rather than portal venous distribution. Hepatic resection may be necessary if the above measures are unsuccessful. In cases of massive necrosis and uncontrollable hemorrhage, liver transplantation has become necessary (5,10). More recently, interventional angiography with selective hepatic artery embolization has been heralded as a safe alternative if an arterial source can be identified (11). This modality is especially useful in patients who are poor candidates for surgery, as adjunctive therapy, or in those who have failed surgical intervention. Some authors recommend conservative management in the case of the hemodynamically stable patient with an intact liver capsule. Algorithms for such conservative management with the aid of serial CT scanning have been developed (12). Recent anecdotal cases of management with recombinant factor VIIa in spontaneous subcapsular liver hematoma as well as in hepatic rupture complicated by abdominal compartment syndrome have been described (13,14). Although the patient had multiple co-morbidities, the underlying cause for spontaneous rupture of the liver in our case is unknown. We presume that her history of multiple myeloma and its association with amyloidosis may have been responsible. The vasculitic nature of her
387
blood vessels noted on angiography may also have resulted in hemorrhage. She presented to our ED with an acute abdomen-like picture. Although her initial laboratory studies were only mildly abnormal, the development of hypotension prompted rapid imaging with CT scan, allowing for prompt diagnosis and management via angiographic embolization. Inclusion of this rare diagnosis in the differential of abdominal pain and acute abdomen is vital to successful management. REFERENCES 1. Araujo AC, Leao MD, Nobrega MH, et al. Characteristics and treatment of hepatic rupture caused by HELLP syndrome. Am J Obstet Gynecol 2006;195:129 –33. 2. Kacem C, Helali K, Puisieux F. Recurrent spontaneous hepatic rupture in primary hepatic amyloidosis. Ann Intern Med 1998;29: 339. 3. Tsokos M, Schulz F. Non-traumatic liver rupture due to perforated gastric ulcer. Int J Legal Med 1999;112:321–3. 4. Barnett SJ, Weisdorf-Schindle S, Baker KS, Saltzman DA. Spontaneous liver rupture in a child with graft-versus-host-disease. J Pediatr Surg 2004;39:e1–3. 5. Erdogan D, Busch OR, van Delden OM, Ten Kate FJ, Gouma DJ, van Gulik DM. Management of spontaneous hemorrhage and rupture of hepatocellular adenomas. A single center experience. Liver Int 2006;26:433– 8. 6. Wang SY, Ruggles S, Vade A, Newman BM, Borge MA. Hepatic rupture caused by peliosis hepatis. J Pediatr Surg 2001;36:1456 –9. 7. Reinus JF, Riely CA. Gastrointestinal and hepatic disorders in the pregnant patient. In: Feldman M, Friedman LS, Brandt LJ, eds. Sleisenger and Fordtran’s gastrointestinal and liver disease: pathophysiology, diagnosis, management, 8th edn. W.B. Saunders; 2006: 803. 8. Wicke C, Pereira PL, Neeser E, Flesch I, Rodegerdts EA, Becker HD. Subcapsular liver hematoma in HELLP syndrome: evaluation of diagnostic and therapeutic options—a unicenter study. Am J Obstet Gynecol 2004;190:106 –12. 9. Hurd WW, Katholi RE. Acquired functional asplenia: association with spontaneous rupture of the spleen and fatal spontaneous rupture of the liver in amyloidosis. Arch Intern Med 1980;140: 844 –5. 10. Sheikh RA, Yasmeen S, Pauly MP, Riegler JL. Spontaneous intrahepatic hemorrhage and hepatic rupture in the HELLP syndrome: four cases and a review. J Clin Gastroenetrol 1999;28: 323– 8. 11. Mukhapadhya A, Raghuram L, Justus A, Joseph AJ, Eapen CE, Chandy GM. Transcatheter hepatic artery embolization for spontaneous rupture of amyloid liver. Indian J Gastroenterol 2004;23: 26 –7. 12. Smith LG, Moise KG, Dildy GA, et al. Spontaneous rupture of the liver during pregnancy: current therapy. Obstet Gynecol 1991;77: 171–5. 13. Dart BW, Cockerham WT, Torres C, Kipikasa JH, Maxwell RA. A novel use of recombinant factor VIIa in HELLP syndrome associated with spontaneous hepatic rupture and abdominal compartment syndrome. J Trauma 2004;57:171– 4. 14. Merchant SH, Mathew P, Vanderjagt TJ, Howdieshell TR, Crookston KP. Recombinant factor VIIa in management of spontaneous subcapsular liver hematoma associated with pregnancy. Obstet Gynecol 2004;103:1055– 8.