Keith K. Terasaki, MD • Michael F. Quinn, MD • Caroline J. Lundell, MD • Ethel J. Finck, MD • Michael J. Pentecost, MD
Spontaneous Hepatic Hemorrhage in Preeclampsia: Treatment with Hepatic Arterial Embolization 1 Four patients with spontaneous rupture of the liver due to preeclampsia of pregnancy underwent diagnostic angiography followed by successful transcatheter embolization of the hepatic artery with gelatin particles. All patients stopped bleeding and were discharged in good condition. Transcatheter embolization of the hepatic artery may be an attractive alternative to surgery for control of spontaneous rupture of the liver in preeclampsia. Index terms: Arteries, therapeutic blockade, 761.411, 952.1299 • Hepatic arteries, therapeutic blockade, 952.1299 • Liver, hemorrhage, 761.412 • Pregnancy, complications, 761.411 Radiology 1990; 174:1039-1041
a. b. Figure 1. Case 1. (a) Hepatic angiogram shows displacement of hepatic vessels from large subcapsular hematoma. Multiple small pseudoaneurysms are present in the right lobe (arrows). (b) Enlarged, later phase of hepatic angiogram shows multiple small pseudoaneurysms (arrows).
rupture of the liver is a rare complication of preeclampsia during pregnancy. Approximately 120 cases have been reported in the literature. Maternal mortality has been reported to be as high as 59%-86% (1,2). We report four such cases that were successfully managed by means of percutaneous angiographic embolization.
S
PONTANEOUS
CASE REPORTS Case 1.—A 20-year-old gravida 2, para 1
From the Department of Radiology, Los Angeles County-University of Southern California Medical Center, 1200 N State St, Los Angeles, CA 90033. Received April 3, 1989; accepted May 22. Address reprint requests to M.P. RSNA, 1990
woman in her 28th week of pregnancy was admitted because of a blood pressure of 175/110 mm Hg and peripheral edema. She had no history of hypertension, diabetes, or drug or birth-control use. Her hematocrit was 42% (0.42) and urine protein level was 2+. Her liver function test results were slightly elevated. Two days after admission, fetal distress was detected, and the patient underwent emergency cesarean section. Placental abruption was found. The intraoperative course was uneventful, with blood loss of 500 mL. The fetus did not survive. Twenty-four hours after operation, the patierit's blood pressure dropped to 80/50
mm Hg, and her hematocrit fell to 22%
(0.22). An ultrasound scan showed an extensive subcapsular hematoma of the right lobe of her liver and free intraperitoneal fluid. She required intubation for respiratory failure and was placed in a medical anti-shock trouser suit. Laboratory analysis showed the following levels: serum glutamic oxaloacetic transaminase, 1,560 mU/mL (1,560 U/L); serum glutamic pyruvic transaminase, 2,040 mU/mL (2,040 U/L); plasma fibrinogen, 106 mg/ dL (1.06 g/L); platelets, 40,000 cells/mm 3 (40 G/L); and serum creatinine, 3.5 mg/ dL (309.4 Amol/L). An emergency angiogram demonstrated multiple small punctate areas of extravasation in the right and left liver lobes (Fig 1). Angiographic embolization of the hepatic artery was then performed. Gelfoam (gelatin; Upjohn, Kalamazoo, Mich) particles 1 mm large were infused into the proper hepatic artery until arterial blood flow to the liver was completely blocked. After embolization, the patient's vital signs stabilized, and the medical antishock trouser suit was removed after 24 hours. Her hematocrit stabilized, and coagulopathy gradually resolved. Her renal function also improved. A computed
1039
a b. c Figure 2. Case 2. (a) CT scan with intravenous contrast agent shows large hematoma within right lobe of liver. Lower sections showed free intraperitoneal blood. (b) Angiogram with catheter in replaced right hepatic artery shows displacement of vessels and multiple small pseu.
.
doaneurysms (arrows). (c) Postembolization view of right hepatic artery. The left hepatic artery was embolized separately.
tomographic (CT) scan 7 days after embolization showed large areas of low attenuation in the liver. Nine days after embolization, she had a low-grade fever, so laparotomy was performed and an extensive liver hematoma was evacuated. Her gallbladder showed signs of necrosis and so was removed. Recovery from this operation was uneventful, and she was discharged 2 weeks later in good condition. Case 2.—A 17-year-old primigravida with a 38-week gestation was referred for preeclampsia, with blood pressure of 170/ 120 mm Hg, 4+ proteinuria, and pitting edema. Results of other laboratory tests, including liver function tests, were normal. She underwent cesarean section, although the fetus did not survive. Two days after delivery, she developed sudden pain in her right upper quadrant and right shoulder. Her hematocrit fell from 40% (0.40) to 25% (.25). Her systolic blood pressure fell from 150 to 80 mm Hg. An emergency CT scan showed-a large right-lobe hepatic hematoma (Fig 2a) and free intraperitoneal blood. Coagulation studies showed a platelet count of 50,000 cells/ mm 3 (50 G/L) with a plasma fibrinogen level of 55 mg /dL (.55 g /L). Transfusions were begun, and an emergency hepatic angiogram was obtained. Multiple small areas of active extravasation were present in both lobes (Fig 2b). Embolization of a right hepatic artery arising from the superior mesenteric artery and a left hepatic artery arising from the celiac axis with 1-mm Gelfoam particles was performed (Fig 2c). After embolization, the patient's vital signs immediately stabilized. She had persistent fevers for 1 week but gradually recovered and was discharged after 4 weeks in good condition. Case 3.—A 32-year-old gravida 5, para 4 woman who was 27 weeks pregnant was admitted with a blood pressure of 140/80 mm Hg, 4+ proteinuria, and edema. She underwent cesarean section for fetal distress, but the fetus did not survive. The patient developed intraperitoneal bleeding postoperatively, with coagula-
1040 • Radiology
tion studies showing a moderate coagulopathy. She underwent laparotomy 48 hours after delivery. Hepatic rupture was found. Partial hemostasis was obtained, and she was immediately referred for angiography and embolization of the hepatic artery. Angiography showed multiple small pseudoaneurysms in both lobes of the liver with active bleeding (Fig 3). As in the other patients, embolization of the proper hepatic artery was performed with 1-mm Gelfoam particles. The patient rapidly recovered and was discharged 2 weeks later in good condition. Case 4.—A 38-year-old gravida 10, para 9 woman in her 34th week of pregnancy was admitted with severe preeclampsia. She had a successful vaginal delivery but developed severe right upper-quadrant pain 2 days after delivery. Her hematocrit fell from 32% (0.32) to 18% (0.18), and CT showed a large right subcapsular hematoma with no free intraperitoneal fluid (Fig 4). A hepatic angiogram showed no active extravasation. To prevent possible enlargement of the liver hematoma or free intraperitoneal rupture, the right hepatic artery was embolized. After embolization, her hematocrit remained stable, and follow-up CT scans showed no further enlargement of the liver hematoma. She was discharged in good condition 8 days after embolization.
DISCUSSION
Preeclampsia occurs in approximately 5% of pregnancies, usually during the latter stages of pregnancy and more often in primagravidas. It is characterized by hypertension, proteinuria, and edema. Patients with severe cases may develop coagulation abnormalities and deterioration of liver function. Early hepatic involvement is characterized by elevation of liver function test results, elevated bilirubin level, and right
upper-quadrant abdominal pain (3). Progressive hepatic disease results in hepatic infarction, hepatic hematoma, and free peritoneal hemorrhage, and is responsible for about 10%-15% of deaths from preeclampsia. Most severe cases of hepatic involvement are complicated by pulmonary edema, renal failure, hematologic abnormalities, and central nervous system alterations. Interestingly, hepatic rupture occurs more often in multiparous women (1). Pathologic examination of the liver in severely preeclamptic patients has shown fibrin deposits within periportal sinusoids with periportal hemorrhagic necrosis (4). This condition may result from disseminated intravascular coagulation, because many women have a consumptive coagulopathy (5). One-third of women who die of preeclampsia have hepatocyte necrosis, hepatic infarcts, and hepatic hemorrhages (4). The cause of hepatic necrosis is not known. Necrosis may result from hypoperfusion due to shock, arterial spasm, or obstruction of blood flow from fibrin deposits. The role of minor trauma causing hemorrhage or rupture of the diseased liver is uncertain. The hepatic hematomas may be either subcapsular or completely intraparenchymal, or they may progress to free rupture into the peritoneal cavity. Angiography in such cases has shown multiple small areas of extravasation within the liver (6). Spontaneous rupture of the spleen and retroperitoneal hemorrhage have also been reported in preeclampsia (7), as has an increased incidence of placenta abruption and cerebral hemorrhage. Free rupture of the liver into the peritoneal cavity is often a cataMarch 1990 • Part 2
of liver involvement, we believe hepatic arterial embolization should play a major role in the control of hepatic rupture associated with preeclampsia. n References 1.
Figure 4. Case 4. CT scan after intravenous
Figure 3. Case 3. Hepatic angiogram shows stretching of vessels within the liver and multiple small pseudoaneurysms (arrows).
strophic event. Without surgery, mortality is nearly 100%. Even with surgery, mortality rates are reportedly 35%-80% (1,2). Uncontrollable intraoperative liver hemorrhage, exacerbated by a frequently associated coagulopathy, is the most common cause of death. Even with surgical achievement of hemostasis, the patient may die in the postoperative period due to multiorgan failure (8). Conservative treatment of contained intraparenchymal or subcapsular liver hemorrhage without free intraperitoneal rupture has been performed without subsequent death (9). Supportive treatment consisted of blood-pressure control, transfusions, and correction of coagulopathy. In these cases the fetus was delivered because severe preeclampsia rarely improves iri expectant patients (5). The incidence of liver rupture in patients with contained hepatic hematoma is unknown. Most case reports of spontaneous rupture of the liver describe the patient as having severe right upper-quadrant abdominal pain for several hours to days prior to the deirelopment of hypotension. These cases may represent a slowly enlarging hematoma within the liver, which then undergoes sudden intraperitoneal rupture. More frequent CT scanning may allow detection of many more cases of confined liver hematomas in preeclamptic women. Many of these women may not require interventional treatment; however, in the presence of hypotension or rapidly enlarging hematoma, surgical or radiologic intervention may be prudent. Because of the difficulty of achieving liver hemostasis surgically in the presence of multiple areas of infarction and hematoma, especially in the presence of a coagulopathy, we have attempted therapeutic blockade of Volume 174 • Number 3 • Part 2
injection of contrast agent shows large subcapsular hematoma in anterior right lobe of liver, with smaller hematoma posteriorly in right lobe.
2.
3.
4.
the hepatic artery as a means of obtaining hemostasis. All four of our patients had life-threatening hemorrhages, with free peritoneal rupture in three. All four presented within 48 hours after delivery. Three of the four fetuses did not survive, due to prematurity and prolonged fetal anoxia. Successful embolization of the hepatic artery for spontaneous rupture of the liver in preeclampsia has been reported once before, to our knowledge (10). As with our patients, embolization was chosen in this instance because of the presence of a consumptive coagulopathy. Embolization of the hepatic artery for control of hemorrhage and treatment of hepatic neoplasms has been well described (11,12). We used 1mm cubes of Gelfoam sponge for our patients because we hoped that after several weeks the blocked hepatic vessels would become reperfused. Our embolizations were performed with the catheter tip in the proper hepatic artery. More selective catheterization was not attempted because there was diffuse bleeding in both lobes, and our patients were hemodynamically unstable with spasm of vessels. Several complications have been reported after embolization of the hepatic artery. Right upper-quadrant pain, nausea, and fever are not unusual following embolization (13). There is often transient elevation of liver enzyme levels. Other, more serious complications include acute hepatic necrosis, acute cholecystitis, sepsis, and death (14,15). In summary, we report four patients whose spontaneous liver rupture in preeclampsia we successfully managed by means of transcatheter embolization. Prior attempts at surgical control were unsuccessful in one patient. Because of frequent severe coagulopathy and the diffuse nature
5.
6.
7. 8.
9.
10.
11.
12.
13.
14.
15.
Bis KA, Waxman B. Rupture of the liver associated with pregnancy: a review of the literature and report of 2 cases. Obstet Gynecol Sury 1976; 31:763-773. Hibbard LT. Spontaneous rupture of the liver in pregnancy: report of eight cases. Am J Obstet Gynecol 1976; 126:334-338. Alexander J, Cuellar RE, Van Thiel DH. Toxemia of pregnancy and the liver. Semin Liver Dis 1987; 7:55-58. Rolfes DB, Ishak KG. Liver disease in toxemia of pregnancy. Am J Gastroenterol 1986; 81:1138-1144. Killam AP, Dillard SH, Patton RC, Pederson PR. Pregnancy-induced hypertension complicated by acute liver disease and disseminated intravascular coagulation. Am J Obstet Gynecol 1975; 123:823828. Sommer DG, Greenway GD, Bookstein JJ, Orloff MJ. Hepatic rupture with toxemia of pregnancy: angiographic diagnosis. AJR 1978; 132:455-456. Ogden JK. Retroperitoneal haemorrhage in pregnancy. Br Med J 1948; 1:389-391. Aziz S, Merrell RC, Collins JA. Spontaneous hepatic hemorrhage during pregnancy. Am J Surg 1983; 146:680-682. Manas KJ, Welsh JD, Rankin RA, Miller DD. Hepatic hemorrhage without rupture in preeclampsia. N Engl J Med 1985; 312:424-426. Loevinger EH, Vujic I, Lee WM, Anderson M. Hepatic rupture associated with pregnancy: treatment with transcatheter embolotherapy. Obstet Gynecol 1985; 65:281284. Hirai K, Kawazoe Y, Yamashita K, et al. Transcatheter arterial embolization for spontaneous rupture of hepatocellular carcinoma. Am J Gastroenterol 1986; 81: 275-279. Chuang VP, Wallace S. Hepatic artery embolization in the treatment of hepatic neoplasms. Radiology 1981; 140:51-58. Allison DJ, Jordan H, Hennessy 0. Therapeutic embolisation of the hepatic artery: a review of 75 procedures. Lancet 1985; 8429:595-599. Kuroda C, Iwasaki M, Tanaka T, et al. Gallbladder infarction following hepatic transcatheter arterial embolization. Radiology 1983; 149:85-89. Hemingway AP, Allison DJ. Complications of embolization: analysis of 410 procedures. Radiology 1988; 166:669-672.
Radiology • 1041
Spontaneous Hepatic Hemorrhage in Preeclampsia: Treatment with Hepatic Arterial Embolization 1 Four patients with spontaneous rupture of the liver due to preeclampsia of pregnancy underwent diagnostic angiography followed by successful transcatheter embolization of the hepatic artery with gelatin particles. All patients stopped bleeding and were discharged in good condition. Transcatheter embolization of the hepatic artery may be an attractive alternative to surgery for control of spontaneous rupture of the liver in preeclampsia. Index terms: Arteries, therapeutic blockade, 761.411, 952.1299 • Hepatic arteries, therapeutic blockade, 952.1299 • Liver, hemorrhage, 761.412 • Pregnancy, complications, 761.411 Radiology 1990; 174:1039-1041
a. b. Figure 1. Case 1. (a) Hepatic angiogram shows displacement of hepatic vessels from large subcapsular hematoma. Multiple small pseudoaneurysms are present in the right lobe (arrows). (b) Enlarged, later phase of hepatic angiogram shows multiple small pseudoaneurysms (arrows).
rupture of the liver is a rare complication of preeclampsia during pregnancy. Approximately 120 cases have been reported in the literature. Maternal mortality has been reported to be as high as 59%-86% (1,2). We report four such cases that were successfully managed by means of percutaneous angiographic embolization.
S
PONTANEOUS
CASE REPORTS Case 1.—A 20-year-old gravida 2, para 1
From the Department of Radiology, Los Angeles County-University of Southern California Medical Center, 1200 N State St, Los Angeles, CA 90033. Received April 3, 1989; accepted May 22. Address reprint requests to M.P. RSNA, 1990
woman in her 28th week of pregnancy was admitted because of a blood pressure of 175/110 mm Hg and peripheral edema. She had no history of hypertension, diabetes, or drug or birth-control use. Her hematocrit was 42% (0.42) and urine protein level was 2+. Her liver function test results were slightly elevated. Two days after admission, fetal distress was detected, and the patient underwent emergency cesarean section. Placental abruption was found. The intraoperative course was uneventful, with blood loss of 500 mL. The fetus did not survive. Twenty-four hours after operation, the patierit's blood pressure dropped to 80/50
mm Hg, and her hematocrit fell to 22%
(0.22). An ultrasound scan showed an extensive subcapsular hematoma of the right lobe of her liver and free intraperitoneal fluid. She required intubation for respiratory failure and was placed in a medical anti-shock trouser suit. Laboratory analysis showed the following levels: serum glutamic oxaloacetic transaminase, 1,560 mU/mL (1,560 U/L); serum glutamic pyruvic transaminase, 2,040 mU/mL (2,040 U/L); plasma fibrinogen, 106 mg/ dL (1.06 g/L); platelets, 40,000 cells/mm 3 (40 G/L); and serum creatinine, 3.5 mg/ dL (309.4 Amol/L). An emergency angiogram demonstrated multiple small punctate areas of extravasation in the right and left liver lobes (Fig 1). Angiographic embolization of the hepatic artery was then performed. Gelfoam (gelatin; Upjohn, Kalamazoo, Mich) particles 1 mm large were infused into the proper hepatic artery until arterial blood flow to the liver was completely blocked. After embolization, the patient's vital signs stabilized, and the medical antishock trouser suit was removed after 24 hours. Her hematocrit stabilized, and coagulopathy gradually resolved. Her renal function also improved. A computed
1039
a b. c Figure 2. Case 2. (a) CT scan with intravenous contrast agent shows large hematoma within right lobe of liver. Lower sections showed free intraperitoneal blood. (b) Angiogram with catheter in replaced right hepatic artery shows displacement of vessels and multiple small pseu.
.
doaneurysms (arrows). (c) Postembolization view of right hepatic artery. The left hepatic artery was embolized separately.
tomographic (CT) scan 7 days after embolization showed large areas of low attenuation in the liver. Nine days after embolization, she had a low-grade fever, so laparotomy was performed and an extensive liver hematoma was evacuated. Her gallbladder showed signs of necrosis and so was removed. Recovery from this operation was uneventful, and she was discharged 2 weeks later in good condition. Case 2.—A 17-year-old primigravida with a 38-week gestation was referred for preeclampsia, with blood pressure of 170/ 120 mm Hg, 4+ proteinuria, and pitting edema. Results of other laboratory tests, including liver function tests, were normal. She underwent cesarean section, although the fetus did not survive. Two days after delivery, she developed sudden pain in her right upper quadrant and right shoulder. Her hematocrit fell from 40% (0.40) to 25% (.25). Her systolic blood pressure fell from 150 to 80 mm Hg. An emergency CT scan showed-a large right-lobe hepatic hematoma (Fig 2a) and free intraperitoneal blood. Coagulation studies showed a platelet count of 50,000 cells/ mm 3 (50 G/L) with a plasma fibrinogen level of 55 mg /dL (.55 g /L). Transfusions were begun, and an emergency hepatic angiogram was obtained. Multiple small areas of active extravasation were present in both lobes (Fig 2b). Embolization of a right hepatic artery arising from the superior mesenteric artery and a left hepatic artery arising from the celiac axis with 1-mm Gelfoam particles was performed (Fig 2c). After embolization, the patient's vital signs immediately stabilized. She had persistent fevers for 1 week but gradually recovered and was discharged after 4 weeks in good condition. Case 3.—A 32-year-old gravida 5, para 4 woman who was 27 weeks pregnant was admitted with a blood pressure of 140/80 mm Hg, 4+ proteinuria, and edema. She underwent cesarean section for fetal distress, but the fetus did not survive. The patient developed intraperitoneal bleeding postoperatively, with coagula-
1040 • Radiology
tion studies showing a moderate coagulopathy. She underwent laparotomy 48 hours after delivery. Hepatic rupture was found. Partial hemostasis was obtained, and she was immediately referred for angiography and embolization of the hepatic artery. Angiography showed multiple small pseudoaneurysms in both lobes of the liver with active bleeding (Fig 3). As in the other patients, embolization of the proper hepatic artery was performed with 1-mm Gelfoam particles. The patient rapidly recovered and was discharged 2 weeks later in good condition. Case 4.—A 38-year-old gravida 10, para 9 woman in her 34th week of pregnancy was admitted with severe preeclampsia. She had a successful vaginal delivery but developed severe right upper-quadrant pain 2 days after delivery. Her hematocrit fell from 32% (0.32) to 18% (0.18), and CT showed a large right subcapsular hematoma with no free intraperitoneal fluid (Fig 4). A hepatic angiogram showed no active extravasation. To prevent possible enlargement of the liver hematoma or free intraperitoneal rupture, the right hepatic artery was embolized. After embolization, her hematocrit remained stable, and follow-up CT scans showed no further enlargement of the liver hematoma. She was discharged in good condition 8 days after embolization.
DISCUSSION
Preeclampsia occurs in approximately 5% of pregnancies, usually during the latter stages of pregnancy and more often in primagravidas. It is characterized by hypertension, proteinuria, and edema. Patients with severe cases may develop coagulation abnormalities and deterioration of liver function. Early hepatic involvement is characterized by elevation of liver function test results, elevated bilirubin level, and right
upper-quadrant abdominal pain (3). Progressive hepatic disease results in hepatic infarction, hepatic hematoma, and free peritoneal hemorrhage, and is responsible for about 10%-15% of deaths from preeclampsia. Most severe cases of hepatic involvement are complicated by pulmonary edema, renal failure, hematologic abnormalities, and central nervous system alterations. Interestingly, hepatic rupture occurs more often in multiparous women (1). Pathologic examination of the liver in severely preeclamptic patients has shown fibrin deposits within periportal sinusoids with periportal hemorrhagic necrosis (4). This condition may result from disseminated intravascular coagulation, because many women have a consumptive coagulopathy (5). One-third of women who die of preeclampsia have hepatocyte necrosis, hepatic infarcts, and hepatic hemorrhages (4). The cause of hepatic necrosis is not known. Necrosis may result from hypoperfusion due to shock, arterial spasm, or obstruction of blood flow from fibrin deposits. The role of minor trauma causing hemorrhage or rupture of the diseased liver is uncertain. The hepatic hematomas may be either subcapsular or completely intraparenchymal, or they may progress to free rupture into the peritoneal cavity. Angiography in such cases has shown multiple small areas of extravasation within the liver (6). Spontaneous rupture of the spleen and retroperitoneal hemorrhage have also been reported in preeclampsia (7), as has an increased incidence of placenta abruption and cerebral hemorrhage. Free rupture of the liver into the peritoneal cavity is often a cataMarch 1990 • Part 2
of liver involvement, we believe hepatic arterial embolization should play a major role in the control of hepatic rupture associated with preeclampsia. n References 1.
Figure 4. Case 4. CT scan after intravenous
Figure 3. Case 3. Hepatic angiogram shows stretching of vessels within the liver and multiple small pseudoaneurysms (arrows).
strophic event. Without surgery, mortality is nearly 100%. Even with surgery, mortality rates are reportedly 35%-80% (1,2). Uncontrollable intraoperative liver hemorrhage, exacerbated by a frequently associated coagulopathy, is the most common cause of death. Even with surgical achievement of hemostasis, the patient may die in the postoperative period due to multiorgan failure (8). Conservative treatment of contained intraparenchymal or subcapsular liver hemorrhage without free intraperitoneal rupture has been performed without subsequent death (9). Supportive treatment consisted of blood-pressure control, transfusions, and correction of coagulopathy. In these cases the fetus was delivered because severe preeclampsia rarely improves iri expectant patients (5). The incidence of liver rupture in patients with contained hepatic hematoma is unknown. Most case reports of spontaneous rupture of the liver describe the patient as having severe right upper-quadrant abdominal pain for several hours to days prior to the deirelopment of hypotension. These cases may represent a slowly enlarging hematoma within the liver, which then undergoes sudden intraperitoneal rupture. More frequent CT scanning may allow detection of many more cases of confined liver hematomas in preeclamptic women. Many of these women may not require interventional treatment; however, in the presence of hypotension or rapidly enlarging hematoma, surgical or radiologic intervention may be prudent. Because of the difficulty of achieving liver hemostasis surgically in the presence of multiple areas of infarction and hematoma, especially in the presence of a coagulopathy, we have attempted therapeutic blockade of Volume 174 • Number 3 • Part 2
injection of contrast agent shows large subcapsular hematoma in anterior right lobe of liver, with smaller hematoma posteriorly in right lobe.
2.
3.
4.
the hepatic artery as a means of obtaining hemostasis. All four of our patients had life-threatening hemorrhages, with free peritoneal rupture in three. All four presented within 48 hours after delivery. Three of the four fetuses did not survive, due to prematurity and prolonged fetal anoxia. Successful embolization of the hepatic artery for spontaneous rupture of the liver in preeclampsia has been reported once before, to our knowledge (10). As with our patients, embolization was chosen in this instance because of the presence of a consumptive coagulopathy. Embolization of the hepatic artery for control of hemorrhage and treatment of hepatic neoplasms has been well described (11,12). We used 1mm cubes of Gelfoam sponge for our patients because we hoped that after several weeks the blocked hepatic vessels would become reperfused. Our embolizations were performed with the catheter tip in the proper hepatic artery. More selective catheterization was not attempted because there was diffuse bleeding in both lobes, and our patients were hemodynamically unstable with spasm of vessels. Several complications have been reported after embolization of the hepatic artery. Right upper-quadrant pain, nausea, and fever are not unusual following embolization (13). There is often transient elevation of liver enzyme levels. Other, more serious complications include acute hepatic necrosis, acute cholecystitis, sepsis, and death (14,15). In summary, we report four patients whose spontaneous liver rupture in preeclampsia we successfully managed by means of transcatheter embolization. Prior attempts at surgical control were unsuccessful in one patient. Because of frequent severe coagulopathy and the diffuse nature
5.
6.
7. 8.
9.
10.
11.
12.
13.
14.
15.
Bis KA, Waxman B. Rupture of the liver associated with pregnancy: a review of the literature and report of 2 cases. Obstet Gynecol Sury 1976; 31:763-773. Hibbard LT. Spontaneous rupture of the liver in pregnancy: report of eight cases. Am J Obstet Gynecol 1976; 126:334-338. Alexander J, Cuellar RE, Van Thiel DH. Toxemia of pregnancy and the liver. Semin Liver Dis 1987; 7:55-58. Rolfes DB, Ishak KG. Liver disease in toxemia of pregnancy. Am J Gastroenterol 1986; 81:1138-1144. Killam AP, Dillard SH, Patton RC, Pederson PR. Pregnancy-induced hypertension complicated by acute liver disease and disseminated intravascular coagulation. Am J Obstet Gynecol 1975; 123:823828. Sommer DG, Greenway GD, Bookstein JJ, Orloff MJ. Hepatic rupture with toxemia of pregnancy: angiographic diagnosis. AJR 1978; 132:455-456. Ogden JK. Retroperitoneal haemorrhage in pregnancy. Br Med J 1948; 1:389-391. Aziz S, Merrell RC, Collins JA. Spontaneous hepatic hemorrhage during pregnancy. Am J Surg 1983; 146:680-682. Manas KJ, Welsh JD, Rankin RA, Miller DD. Hepatic hemorrhage without rupture in preeclampsia. N Engl J Med 1985; 312:424-426. Loevinger EH, Vujic I, Lee WM, Anderson M. Hepatic rupture associated with pregnancy: treatment with transcatheter embolotherapy. Obstet Gynecol 1985; 65:281284. Hirai K, Kawazoe Y, Yamashita K, et al. Transcatheter arterial embolization for spontaneous rupture of hepatocellular carcinoma. Am J Gastroenterol 1986; 81: 275-279. Chuang VP, Wallace S. Hepatic artery embolization in the treatment of hepatic neoplasms. Radiology 1981; 140:51-58. Allison DJ, Jordan H, Hennessy 0. Therapeutic embolisation of the hepatic artery: a review of 75 procedures. Lancet 1985; 8429:595-599. Kuroda C, Iwasaki M, Tanaka T, et al. Gallbladder infarction following hepatic transcatheter arterial embolization. Radiology 1983; 149:85-89. Hemingway AP, Allison DJ. Complications of embolization: analysis of 410 procedures. Radiology 1988; 166:669-672.
Radiology • 1041
