11 May 2009
17 January 2008
7 January 2008
Hepatitis E and pregnancy
Outcome of acute liver failure due to acute hepatitis E in pregnant women
Banait Vaibhav S1, Sandur Virendra1, Parikh Falguni2, Murugesh M1, Ranka Purnima3, Ramesh VS1, Sasidharan Madhu1, Sattar Abid1, Kamat Sandhya2, Dalal Asha3, Bhatia Shobna J11
Department of Gastroenterology, T N Medical College and BYL Nair Ch. Hospital, Mumbai 400 008, India2 Department of Medicine, T N Medical College and BYL Nair Ch. Hospital, Mumbai 400 008, India3 Department of Obstetrics and Gynecology, T N Medical College and BYL Nair Ch. Hospital, Mumbai 400 008, India
Correspondence Address:Bhatia Shobna JDepartment of Gastroenterology, Seth GS Medical College and KEM Hospital, Mumbai 400 012 IndiaSource of Support: None, Conflict of Interest: None»
Abstract
Introduction: Acute liver failure due to acute hepatitis E carries a high mortality. Methods: Clinical and laboratory parameters of 42 pregnant women (median age 25.5 years) with acute liver failure due to acute hepatitis E were retrospectively analyzed. Results: 22 women delivered, whereas pregnancy continued in 20 women. The maternal mortality in these two groups was similar (9/22 [41%] versus 14/20 [70%], p=0.056). However, in patients with grade I, II or III hepatic encephalopathy, delivery of fetus was associated with reduced mortality in those who delivered as against those who continued pregnancy (5/16 (31%) vs. 13/20 (65%), p=0.046). On multivariate analysis, higher grade of encephalopathy at admission was associated with risk of death (p=0.005). Conclusion : Mortality in pregnant women with acute liver failure with acute hepatitis E is high, especially in patients who present with higher grades of encephalopathy.
Details
Hepatitis E is the most common cause of acute viral hepatitis in the adult population in India.[1] Acute hepatitis E is generally mild and self-limited, resolving within 6 weeks, with no chronic sequelae.[2] Fulminant hepatitis due to acute hepatitis E occurs rarely in adult men and non-pregnant women.[2] Pregnant women are at increased risk, with the risk increasing as the pregnancy progresses. In an epidemic of hepatitis E in southern Xinjiang, China, the maternal mortality rates were 1.5%, 8.5% and 21% for infections in the first, second and third trimesters, respectively.[3] The reasons for this increased maternal morbidity and mortality during pregnancy are not clear. It is possible that in-utero fetal transmission of HEV[4],[5] results in fetal hepatitis. As occurs in patients with acute fatty liver of pregnancy with LCHAD deficiency, which also affects the fetus,[6] the added load of toxins from the fetal circulation may result in hepatic encephalopathy in the mother. Little data are available on the outcome of acute liver failure (ALF) following hepatitis E in pregnant women. We retrospectively analyzed the medical records of our pregnant patients with hepatitis E and ALF.» MethodsThe study included pregnant women with acute liver failure due to infection with HEV who had been admitted in the medical intensive care unit, between July 2003 and December 2004. All patients with acute hepatitis E were admitted to the gastroenterology wards and transferred to the intensive care if they developed change in sensorium; women who had encephalopathy at admission were directly admitted to the intensive care. Patients with drug-induced hepatitis, other severe infection, idiopathic cholestasis of pregnancy, pregnancy-induced hypertension, HELLP syndrome, acute fatty liver of pregnancy, chronic liver disease, or with evidence of portal hypertension were excluded. Detailed history was obtained with special emphasis on alcohol abuse, family history of recent jaundice, contact with jaundiced patient, outstation travel, blood transfusions and sexual behavior in the preceding 2 months. Complete blood count, serum bilirubin, AST, ALT, serum alkaline phosphatase, total proteins, serum albumin, prothrombin time, blood urea, serum creatinine, electrolytes, examination of the ascitic fluid (when present) were done in all patients at admission and periodically as clinically indicated. For each test, the worst value over the entire hospital stay was used for analysis. Upper gastrointestinal endoscopy was done in patients who had overt upper gastrointestinal bleed.Duration of gestation was estimated from duration of amenorrhea and pelvic ultrasound findings. DefinitionsAcute hepatitis was diagnosed when a patient presented with a combination of (a) recent-onset jaundice; (b) absence of evidence of chronic liver disease on clinical and biochemical features, or ultrasonography showing evidence of portal hypertension; (C) elevation of serum alanine transferase above five times upper limit of normal range.ALF was defined as presence of encephalopathy within 8 weeks of development of clinical illness in the absence of clinical evidence of chronic liver disease.[7] Encephalopathy was graded using the West Haven criteria.[8]Acute renal failure was diagnosed when urine output fell below 400 mL/24 hour and/or serum creatinine rose above 2 mg/dL. Clinical coagulopathy was diagnosed when there was bleeding from multiple sites (skin, mucosa, venesection sites, etc); abnormal prothrombin time was defined if the patient's value was 4 seconds more than control value. Thrombocytopenia was defined as platelet count less than 100 x 10 9/L. Disseminated intravascular coagulation (DIC) was diagnosed when bleeding occurred from multiple anatomical sites (skin, mucosa, venipuncture sites) along with low levels of fibrinogen
Results
One hundred and fifty-six pregnant women with liver disease attended the gastroenterology services at our hospital during the study period. Of these, 69 had non-HEV-related disease (13 malaria, 6 dengue fever, 12 sepsis-related, 8 chronic liver disease, 2 acute hepatitis B, 20 pregnancy-induced hypertension, 5 HELLP, 1 acute fatty liver of pregnancy, 2 intrahepatic cholestasis of pregnancy) and 87 had acute hepatitis due to HEV. Forty-eight patients (30.7%) developed ALF. Six patients with non-HEV-related liver disease (4 eclampsia, 1 HELLP, 1 acute fatty liver of pregnancy) developed ALF. Forty-two pregnant women who had ALF due to acute hepatitis E constituted the study group.The median age of patients was 25.5 years (range 18-38). Two patients (4.8%) were in the first trimester of pregnancy, 14 (33.3%) in the second trimester, and 26 (61.9%) in the third trimester. Twelve (28.6%) women were primigravida. None of the patients had history of alcohol abuse, family history of recent jaundice, or contact with jaundiced patient, recent travel, blood transfusions and promiscuous sexual behavior in the preceding two months. At the time of admission to the intensive care unit, 3 (7.1%), 17 (40.5%), 16 (38.1%) and 6 (14.3%) patients had with grade I, II, III, and IV hepatic encephalopathy, respectively. Thirty-nine patients had history of altered behavior for median 2 days (range 8 hours to 3 days) before admission to the ICU; three patients developed hepatic encephalopathy after 2, 5 and 6 days of hospital admission, and were shifted to the ICU. Four (9.5%) patients developed generalized tonic-clonic seizures. Two patients had ascites detectable by ultrasound examination alone. Twenty-three (54.8%) had clinical coagulopathy. Four patients developed disseminated intravascular coagulopathy (DIC). Six patients developed bleeding due to gastric erosions. Hypoglycemia was detected in 14 patients during hourly monitoring of blood glucose, in spite of continuous infusion of 50% dextrose at 10 mL per hour. One patient developed acute renal failure during the course of disease.Twenty-three (54.8%) women died; these included 7 of 17 (41%), 11 of 16 (68.8%) and 5 (83.3%) pregnant women with grade II, III and IV hepatic encephalopathy at admission, respectively. The median duration between development of hepatic encephalopathy and death was 4 (range 2-9) days.Twenty-two (52.4%) patients delivered, including 4 in the second trimester and 18 in the third trimester of pregnancy. Labor started spontaneously in 13 women. In the remaining 9 women, it was induced because of intra-uterine fetal death (IUFD). All deliveries were by vaginal route. Fourteen of these 22 women delivered a dead fetus (fetal mortality 63.6%).Pregnancy continued in 20 women; 14 of them died. Of the 6 women who continued pregnancy and survived, 5 delivered a normal baby at term and one delivered a premature baby seven days after recovery from hepatic encephalopathy. The baby died on the third postnatal day. Overall, there were 29 (69%) fetal deaths and 23 (54%) maternal deaths. The Table compares clinical and biochemical parameters at admission among mothers who survived and those who did not. Maternal mortality was similar in women who had delivered and in those who had not. However, when women who presented with grade IV hepatic encephalopathy were excluded, maternal mortality was less in those who delivered (7/20, 35%) as against those who continued pregnancy (11/16, 68.75%; p=0.046). Recovery from hepatic encephalopathy took 2-8 days (median 3) in those who had delivered, and 2-5 days (median 3) in those who had not (p=0.70). On multivariate analysis, grade of encephalopathy at admission was the only parameter that was associated with mortality (p=0.017)The pregnant women who died due to ALF had worse prothrombin time, higher still-birth rate and worse hepatic encephalopathy at time of admission
Discussion
We analyzed the outcome of acute liver failure due to acute viral hepatitis E in pregnant women. Of 48 pregnant women with ALF, 42 had acute hepatitis E. This distribution is different from that in other studies, probably due to referral bias as our hospital caters to the socioeconomically poor section and is also a major referral center from a hospital that caters to infectious diseases.Recent studies have shown that hepatitis E affects pregnant women more frequently and is associated with high mortality.[9],[10] The frequency of infection and mortality rate increase with the gestational age.[6]As noticed in other studies,[3],[11] patients were young and were in either second or third trimester of pregnancy, with median gestational age of 28 weeks. ALF was associated with maternal mortality of 54% and fetal mortality of 69%. Similar high mortality was evident in other studies.[12],[13]Clinical coagulopathy was observed in 23 patients, 4 of whom had DIC. All these 4 patients had intrauterine fetal loss and were observed for spontaneous onset of labor for 8-12 hours. In otherwise normal pregnant women with IUFD, fibrinolysis develops only over several weeks.[14] In four of our patients with ALF and IUFD, DIC was noted as early as 12 hours after fetal death. Though ALF is known to induce fibrinolysis, it is not clear whether IUFD hastened development of DIC in our cases. Singh et al [15] from Agra studied coagulation factors in 30 patients with acute viral hepatitis with or without hepatic encephalopathy. DIC with significant clinical bleeding was seen in 10 of 15 patients with fulminant hepatic failure. The pathogenesis of early DIC in hepatitis E in pregnancy is not known; Khuroo et al [16] suggested Schwartzman-like reaction to viral proteins.Mortality in our series was associated with higher grade of encephalopathy at admission. In ALF, it is recommended that patients with altered mentation be admitted to an ICU,[17] since the condition may progress rapidly, with changes in consciousness occurring hour-by-hour. In case liver transplantation is available, we suggest that pla for transfer to a transplant center should begin in patients with grade I or II encephalopathy. There was no difference in maternal mortality in pregnant women who delivered and in those who continued the pregnancy. But when patients with grade 4 encephalopathy at admission were excluded from the analysis, delivery of the fetus appeared to improve survival. HEV RNA has been demonstrated in fetal umbilical blood sample.[4] Babies born to mothers have also been to shown to develop hepatitis.[4],[18] The increased fetal loss and improved survival in patients who delivered support the possibility that intrauterine transmission of hepatitis E and intrauterine fetal hepatitis contribute to worsening of maternal condition.Patients who underwent spontaneous or induced labor were similar in their clinical and biochemical profile to women who continued pregnancy. Therefore it is likely that only fetal status, and not clinical profile, influenced the decision to induce.Our study has certain drawbacks. It is a retrospective study. We did not induce labor if the fetus was viable; it is possible that spontaneous deliveries resulted from progressive worsening of liver condition. However, there was no difference in clinical and biochemical parameters amongst those who delivered and those who continued the pregnancy. Third, we did not examine fetuses for presence of HEV. The number of patients in each subgroup was small, with a possibility of type I error.In conclusion, acute liver failure due to acute hepatitis E in pregnant women has high mortality, especially in those who present with higher grades of encephalopathy. Whether termination of pregnancy is to be considered in this situation has not been resolved.
References
1.Khuroo MS, Rustgi VK, Dawson GJ, Mushahwar IK, Yattoo GN, Kamili S, et al . Spectrum of hepatitis E virus infection in India. J Med Virol 1994;43:281-6. [PUBMED] 2.Aggarwal R, Krawczynski K. Hepatitis E: an overview and recent advances in clinical and laboratory research. J Gastroenterol Hepatol 2000;5:9-20 3.Cao XY, Ma XZ, Liu YZ, Jin XM, Gao Q, Dong HJ, et al . Epidemiological and etiological studies on enterically transmitted non-A non-B hepatitis in the south part of Xinijiang. In : Shikata T, Purcell R, Uchida T, Eds. Viral Hepatitis C, D, and E. Amsterdam: Excerpta Medica. 1991: p. 297-312. 4.Singh S, Mohanty A, Joshi YK, Deka D, Mohanty S, Panda SK. Mother-to-child transmission of hepatitis E virus infection. Indian J Pediatr 2003;70:37-9. [PUBMED] 5.Kumar RM, Uduman S, Rana S, Kochiyil JK, Usmani A, Thomas L. Sero-prevalence and mother-to-infant transmission of hepatitis E virus among pregnant women in the United Arab Emirates. Eur J Obstet Gynecol Reprod Biol 2001;100:9-15. [PUBMED] [FULLTEXT]6.Ibdah JA, Bennett MJ, Rinaldo P, Zhao Y, Gibson B, Sims HF, et al . A fetal fatty-acid oxidation disorder as a cause of liver disease in pregnant women. N Engl J Med 1999;340:1723-31. [PUBMED] [FULLTEXT]7.Trey C, Davidson C. The management of fulminant hepatic failure . Prog Liver Dis 1970;3:292. 8.Conn HO. The hepatic encephalopathies. In: Conn HO, Bircher J, Eds. Hepatic Encephalopathy: Syndrome and Therapies. Bloomington, IL: Medi-Ed Press. 1994: p. 1-12. 9.Tsega E, Hansson BG, Krawczynski K, Nordenfelt E. Acute sporadic viral hepatitis in Etiopia. Causes, risk factors and effect on pregnancy. Clin Infect Dis 1992;14:961-5. 10.Kane MA, Bradley DW, Shrestha SM, Maynard JE, Cook EH, Mishra RP, et al . Epidemic non-A non-B hepatitis in Nepal: recovery of possible etiologic agent and transmission studies in marmosets. JAMA 1984;252:3140-5. [PUBMED] 11.Khuroo MS, Teli MR, Skidmore S, Sofi MA, Khuroo MI. Incidence and severity of viral hepatitis in pregnancy. Am J Med 1981;70:252-5. [PUBMED] 12.Vishwanathan R. Infectious hepatitis in Delhi (1955-1956): A critical study. Epidemiology. Indian J Med Res 1957;45(Suppl 1):1-29. 13.Khuroo MS, Kamli S. Aetiology, clinical course, and outcome of sporadic acute viral hepatitis in pregnancy. J Viral Hepatitis 2003;10:61-9. 14.Trevor B. Disseminated intravascular coagulation: diagnosis and treatment. Br Med J 1996;312:683-6. 15.Singh R, Singh MM, Hazra DK, Agarwal N, Patney NL, Goyal SP, et al . A study of disseminated intravascular coagulopathy in hepatic coma complicating acute viral hepatitis. Angiology 1983;34:470-9. [PUBMED] 16.Khuroo MS. Study of epidemic of non-A non-B hepatitis: possibility of another human hepatitis virus distinct from post transfusion non-A non-B type. Am J Med 1980;68:818-23. [PUBMED] 17.Williams R, Gimson AES. Intensive liver care and management of acute hepatic failure. Dig Dis Sci 1991;36:820-6. 18.Khuroo MS, Kamili S, Jameel S. Vertical transmission of hepatitis E virus. Lancet 1995;345:1025-6. [PUBMED]
Banait Vaibhav S1, Sandur Virendra1, Parikh Falguni2, Murugesh M1, Ranka Purnima3, Ramesh VS1, Sasidharan Madhu1, Sattar Abid1, Kamat Sandhya2, Dalal Asha3, Bhatia Shobna J11
Department of Gastroenterology, T N Medical College and BYL Nair Ch. Hospital, Mumbai 400 008, India2 Department of Medicine, T N Medical College and BYL Nair Ch. Hospital, Mumbai 400 008, India3 Department of Obstetrics and Gynecology, T N Medical College and BYL Nair Ch. Hospital, Mumbai 400 008, India
Correspondence Address:Bhatia Shobna JDepartment of Gastroenterology, Seth GS Medical College and KEM Hospital, Mumbai 400 012 IndiaSource of Support: None, Conflict of Interest: None»
Abstract
Introduction: Acute liver failure due to acute hepatitis E carries a high mortality. Methods: Clinical and laboratory parameters of 42 pregnant women (median age 25.5 years) with acute liver failure due to acute hepatitis E were retrospectively analyzed. Results: 22 women delivered, whereas pregnancy continued in 20 women. The maternal mortality in these two groups was similar (9/22 [41%] versus 14/20 [70%], p=0.056). However, in patients with grade I, II or III hepatic encephalopathy, delivery of fetus was associated with reduced mortality in those who delivered as against those who continued pregnancy (5/16 (31%) vs. 13/20 (65%), p=0.046). On multivariate analysis, higher grade of encephalopathy at admission was associated with risk of death (p=0.005). Conclusion : Mortality in pregnant women with acute liver failure with acute hepatitis E is high, especially in patients who present with higher grades of encephalopathy.
Details
Hepatitis E is the most common cause of acute viral hepatitis in the adult population in India.[1] Acute hepatitis E is generally mild and self-limited, resolving within 6 weeks, with no chronic sequelae.[2] Fulminant hepatitis due to acute hepatitis E occurs rarely in adult men and non-pregnant women.[2] Pregnant women are at increased risk, with the risk increasing as the pregnancy progresses. In an epidemic of hepatitis E in southern Xinjiang, China, the maternal mortality rates were 1.5%, 8.5% and 21% for infections in the first, second and third trimesters, respectively.[3] The reasons for this increased maternal morbidity and mortality during pregnancy are not clear. It is possible that in-utero fetal transmission of HEV[4],[5] results in fetal hepatitis. As occurs in patients with acute fatty liver of pregnancy with LCHAD deficiency, which also affects the fetus,[6] the added load of toxins from the fetal circulation may result in hepatic encephalopathy in the mother. Little data are available on the outcome of acute liver failure (ALF) following hepatitis E in pregnant women. We retrospectively analyzed the medical records of our pregnant patients with hepatitis E and ALF.» MethodsThe study included pregnant women with acute liver failure due to infection with HEV who had been admitted in the medical intensive care unit, between July 2003 and December 2004. All patients with acute hepatitis E were admitted to the gastroenterology wards and transferred to the intensive care if they developed change in sensorium; women who had encephalopathy at admission were directly admitted to the intensive care. Patients with drug-induced hepatitis, other severe infection, idiopathic cholestasis of pregnancy, pregnancy-induced hypertension, HELLP syndrome, acute fatty liver of pregnancy, chronic liver disease, or with evidence of portal hypertension were excluded. Detailed history was obtained with special emphasis on alcohol abuse, family history of recent jaundice, contact with jaundiced patient, outstation travel, blood transfusions and sexual behavior in the preceding 2 months. Complete blood count, serum bilirubin, AST, ALT, serum alkaline phosphatase, total proteins, serum albumin, prothrombin time, blood urea, serum creatinine, electrolytes, examination of the ascitic fluid (when present) were done in all patients at admission and periodically as clinically indicated. For each test, the worst value over the entire hospital stay was used for analysis. Upper gastrointestinal endoscopy was done in patients who had overt upper gastrointestinal bleed.Duration of gestation was estimated from duration of amenorrhea and pelvic ultrasound findings. DefinitionsAcute hepatitis was diagnosed when a patient presented with a combination of (a) recent-onset jaundice; (b) absence of evidence of chronic liver disease on clinical and biochemical features, or ultrasonography showing evidence of portal hypertension; (C) elevation of serum alanine transferase above five times upper limit of normal range.ALF was defined as presence of encephalopathy within 8 weeks of development of clinical illness in the absence of clinical evidence of chronic liver disease.[7] Encephalopathy was graded using the West Haven criteria.[8]Acute renal failure was diagnosed when urine output fell below 400 mL/24 hour and/or serum creatinine rose above 2 mg/dL. Clinical coagulopathy was diagnosed when there was bleeding from multiple sites (skin, mucosa, venesection sites, etc); abnormal prothrombin time was defined if the patient's value was 4 seconds more than control value. Thrombocytopenia was defined as platelet count less than 100 x 10 9/L. Disseminated intravascular coagulation (DIC) was diagnosed when bleeding occurred from multiple anatomical sites (skin, mucosa, venipuncture sites) along with low levels of fibrinogen
Results
One hundred and fifty-six pregnant women with liver disease attended the gastroenterology services at our hospital during the study period. Of these, 69 had non-HEV-related disease (13 malaria, 6 dengue fever, 12 sepsis-related, 8 chronic liver disease, 2 acute hepatitis B, 20 pregnancy-induced hypertension, 5 HELLP, 1 acute fatty liver of pregnancy, 2 intrahepatic cholestasis of pregnancy) and 87 had acute hepatitis due to HEV. Forty-eight patients (30.7%) developed ALF. Six patients with non-HEV-related liver disease (4 eclampsia, 1 HELLP, 1 acute fatty liver of pregnancy) developed ALF. Forty-two pregnant women who had ALF due to acute hepatitis E constituted the study group.The median age of patients was 25.5 years (range 18-38). Two patients (4.8%) were in the first trimester of pregnancy, 14 (33.3%) in the second trimester, and 26 (61.9%) in the third trimester. Twelve (28.6%) women were primigravida. None of the patients had history of alcohol abuse, family history of recent jaundice, or contact with jaundiced patient, recent travel, blood transfusions and promiscuous sexual behavior in the preceding two months. At the time of admission to the intensive care unit, 3 (7.1%), 17 (40.5%), 16 (38.1%) and 6 (14.3%) patients had with grade I, II, III, and IV hepatic encephalopathy, respectively. Thirty-nine patients had history of altered behavior for median 2 days (range 8 hours to 3 days) before admission to the ICU; three patients developed hepatic encephalopathy after 2, 5 and 6 days of hospital admission, and were shifted to the ICU. Four (9.5%) patients developed generalized tonic-clonic seizures. Two patients had ascites detectable by ultrasound examination alone. Twenty-three (54.8%) had clinical coagulopathy. Four patients developed disseminated intravascular coagulopathy (DIC). Six patients developed bleeding due to gastric erosions. Hypoglycemia was detected in 14 patients during hourly monitoring of blood glucose, in spite of continuous infusion of 50% dextrose at 10 mL per hour. One patient developed acute renal failure during the course of disease.Twenty-three (54.8%) women died; these included 7 of 17 (41%), 11 of 16 (68.8%) and 5 (83.3%) pregnant women with grade II, III and IV hepatic encephalopathy at admission, respectively. The median duration between development of hepatic encephalopathy and death was 4 (range 2-9) days.Twenty-two (52.4%) patients delivered, including 4 in the second trimester and 18 in the third trimester of pregnancy. Labor started spontaneously in 13 women. In the remaining 9 women, it was induced because of intra-uterine fetal death (IUFD). All deliveries were by vaginal route. Fourteen of these 22 women delivered a dead fetus (fetal mortality 63.6%).Pregnancy continued in 20 women; 14 of them died. Of the 6 women who continued pregnancy and survived, 5 delivered a normal baby at term and one delivered a premature baby seven days after recovery from hepatic encephalopathy. The baby died on the third postnatal day. Overall, there were 29 (69%) fetal deaths and 23 (54%) maternal deaths. The Table compares clinical and biochemical parameters at admission among mothers who survived and those who did not. Maternal mortality was similar in women who had delivered and in those who had not. However, when women who presented with grade IV hepatic encephalopathy were excluded, maternal mortality was less in those who delivered (7/20, 35%) as against those who continued pregnancy (11/16, 68.75%; p=0.046). Recovery from hepatic encephalopathy took 2-8 days (median 3) in those who had delivered, and 2-5 days (median 3) in those who had not (p=0.70). On multivariate analysis, grade of encephalopathy at admission was the only parameter that was associated with mortality (p=0.017)The pregnant women who died due to ALF had worse prothrombin time, higher still-birth rate and worse hepatic encephalopathy at time of admission
Discussion
We analyzed the outcome of acute liver failure due to acute viral hepatitis E in pregnant women. Of 48 pregnant women with ALF, 42 had acute hepatitis E. This distribution is different from that in other studies, probably due to referral bias as our hospital caters to the socioeconomically poor section and is also a major referral center from a hospital that caters to infectious diseases.Recent studies have shown that hepatitis E affects pregnant women more frequently and is associated with high mortality.[9],[10] The frequency of infection and mortality rate increase with the gestational age.[6]As noticed in other studies,[3],[11] patients were young and were in either second or third trimester of pregnancy, with median gestational age of 28 weeks. ALF was associated with maternal mortality of 54% and fetal mortality of 69%. Similar high mortality was evident in other studies.[12],[13]Clinical coagulopathy was observed in 23 patients, 4 of whom had DIC. All these 4 patients had intrauterine fetal loss and were observed for spontaneous onset of labor for 8-12 hours. In otherwise normal pregnant women with IUFD, fibrinolysis develops only over several weeks.[14] In four of our patients with ALF and IUFD, DIC was noted as early as 12 hours after fetal death. Though ALF is known to induce fibrinolysis, it is not clear whether IUFD hastened development of DIC in our cases. Singh et al [15] from Agra studied coagulation factors in 30 patients with acute viral hepatitis with or without hepatic encephalopathy. DIC with significant clinical bleeding was seen in 10 of 15 patients with fulminant hepatic failure. The pathogenesis of early DIC in hepatitis E in pregnancy is not known; Khuroo et al [16] suggested Schwartzman-like reaction to viral proteins.Mortality in our series was associated with higher grade of encephalopathy at admission. In ALF, it is recommended that patients with altered mentation be admitted to an ICU,[17] since the condition may progress rapidly, with changes in consciousness occurring hour-by-hour. In case liver transplantation is available, we suggest that pla for transfer to a transplant center should begin in patients with grade I or II encephalopathy. There was no difference in maternal mortality in pregnant women who delivered and in those who continued the pregnancy. But when patients with grade 4 encephalopathy at admission were excluded from the analysis, delivery of the fetus appeared to improve survival. HEV RNA has been demonstrated in fetal umbilical blood sample.[4] Babies born to mothers have also been to shown to develop hepatitis.[4],[18] The increased fetal loss and improved survival in patients who delivered support the possibility that intrauterine transmission of hepatitis E and intrauterine fetal hepatitis contribute to worsening of maternal condition.Patients who underwent spontaneous or induced labor were similar in their clinical and biochemical profile to women who continued pregnancy. Therefore it is likely that only fetal status, and not clinical profile, influenced the decision to induce.Our study has certain drawbacks. It is a retrospective study. We did not induce labor if the fetus was viable; it is possible that spontaneous deliveries resulted from progressive worsening of liver condition. However, there was no difference in clinical and biochemical parameters amongst those who delivered and those who continued the pregnancy. Third, we did not examine fetuses for presence of HEV. The number of patients in each subgroup was small, with a possibility of type I error.In conclusion, acute liver failure due to acute hepatitis E in pregnant women has high mortality, especially in those who present with higher grades of encephalopathy. Whether termination of pregnancy is to be considered in this situation has not been resolved.
References
1.Khuroo MS, Rustgi VK, Dawson GJ, Mushahwar IK, Yattoo GN, Kamili S, et al . Spectrum of hepatitis E virus infection in India. J Med Virol 1994;43:281-6. [PUBMED] 2.Aggarwal R, Krawczynski K. Hepatitis E: an overview and recent advances in clinical and laboratory research. J Gastroenterol Hepatol 2000;5:9-20 3.Cao XY, Ma XZ, Liu YZ, Jin XM, Gao Q, Dong HJ, et al . Epidemiological and etiological studies on enterically transmitted non-A non-B hepatitis in the south part of Xinijiang. In : Shikata T, Purcell R, Uchida T, Eds. Viral Hepatitis C, D, and E. Amsterdam: Excerpta Medica. 1991: p. 297-312. 4.Singh S, Mohanty A, Joshi YK, Deka D, Mohanty S, Panda SK. Mother-to-child transmission of hepatitis E virus infection. Indian J Pediatr 2003;70:37-9. [PUBMED] 5.Kumar RM, Uduman S, Rana S, Kochiyil JK, Usmani A, Thomas L. Sero-prevalence and mother-to-infant transmission of hepatitis E virus among pregnant women in the United Arab Emirates. Eur J Obstet Gynecol Reprod Biol 2001;100:9-15. [PUBMED] [FULLTEXT]6.Ibdah JA, Bennett MJ, Rinaldo P, Zhao Y, Gibson B, Sims HF, et al . A fetal fatty-acid oxidation disorder as a cause of liver disease in pregnant women. N Engl J Med 1999;340:1723-31. [PUBMED] [FULLTEXT]7.Trey C, Davidson C. The management of fulminant hepatic failure . Prog Liver Dis 1970;3:292. 8.Conn HO. The hepatic encephalopathies. In: Conn HO, Bircher J, Eds. Hepatic Encephalopathy: Syndrome and Therapies. Bloomington, IL: Medi-Ed Press. 1994: p. 1-12. 9.Tsega E, Hansson BG, Krawczynski K, Nordenfelt E. Acute sporadic viral hepatitis in Etiopia. Causes, risk factors and effect on pregnancy. Clin Infect Dis 1992;14:961-5. 10.Kane MA, Bradley DW, Shrestha SM, Maynard JE, Cook EH, Mishra RP, et al . Epidemic non-A non-B hepatitis in Nepal: recovery of possible etiologic agent and transmission studies in marmosets. JAMA 1984;252:3140-5. [PUBMED] 11.Khuroo MS, Teli MR, Skidmore S, Sofi MA, Khuroo MI. Incidence and severity of viral hepatitis in pregnancy. Am J Med 1981;70:252-5. [PUBMED] 12.Vishwanathan R. Infectious hepatitis in Delhi (1955-1956): A critical study. Epidemiology. Indian J Med Res 1957;45(Suppl 1):1-29. 13.Khuroo MS, Kamli S. Aetiology, clinical course, and outcome of sporadic acute viral hepatitis in pregnancy. J Viral Hepatitis 2003;10:61-9. 14.Trevor B. Disseminated intravascular coagulation: diagnosis and treatment. Br Med J 1996;312:683-6. 15.Singh R, Singh MM, Hazra DK, Agarwal N, Patney NL, Goyal SP, et al . A study of disseminated intravascular coagulopathy in hepatic coma complicating acute viral hepatitis. Angiology 1983;34:470-9. [PUBMED] 16.Khuroo MS. Study of epidemic of non-A non-B hepatitis: possibility of another human hepatitis virus distinct from post transfusion non-A non-B type. Am J Med 1980;68:818-23. [PUBMED] 17.Williams R, Gimson AES. Intensive liver care and management of acute hepatic failure. Dig Dis Sci 1991;36:820-6. 18.Khuroo MS, Kamili S, Jameel S. Vertical transmission of hepatitis E virus. Lancet 1995;345:1025-6. [PUBMED]
Amoebic Liver Abscess: role of Endoscopic retrograde cholangio-pancreatography
Endoscopic biliary drainage in patients with amebic liver abscess and biliary communication
S Sandeep M, Banait Vaibhav S, Thakur Sanjeev K, Bapat Mukta R, Rathi Pravin M, Abraham Philip
Department of Gastroenterology, Seth G S Medical College and K E M Hospital, Mumbai 400 012, India
Correspondence Address:S Sandeep MDepartment of Gastroenterology, Seth G S Medical College and K E M Hospital, Mumbai 400 012 India
Source of Support: None, Conflict of Interest: None
» Abstract
Background: Percutaneous drainage or surgery is required when amebic liver abscess (ALA) fails to respond to medical management. In some of these patients, non-response may be due to communication of ALA with the biliary tree. This report describes our experience with the use of endoscopic biliary draining in such patients. Methods: Medical records of patients with ALA undergoing either needle aspiration or percutaneous pigtail drainage were retrieved; the indications for drainage were: abscess volume exceeding 250 mL, a thin rim of tissue (<1>25 mL/day persisting for 2 weeks or presence of bile in the drain fluid underwent endoscopic biliary drainage. Results: A total of 115 patients with ALA underwent percutaneous treatment. None of the 25 patients with needle aspiration needed any further treatment. Of the 90 who underwent catheter drainage, the catheter could be removed within one week in 77 patients; the remaining 13 patients (median age 42 years, range 24-65; all men) had an abscess-biliary communication. In them, the median catheter output was 88 mL/day (range 45-347) and 54 mL/day (28-177) at 2 days and 2 weeks after catheter placement. The drain fluid contained bile in all 13 patients, and in addition contained pus in 10 patients. Eleven patients had a solitary abscess and two had multiple abscesses. Cholangiogram showed biliary communication in all 13 patients. All patients were treated with placement of 10F biliary endoprosthesis or 10F nasobiliary drain. Pigtail catheter was removed within 1 week in 11 of 13 patients. Conclusion: In patients with amebic liver abscess communicating with the biliary tree, biliary stenting may hasten clinical recovery and allow early removal of liver abscess catheter drain.
Liver is the most common extraintestinal site of involvement in amebiasis, with amebic liver abscess (ALA) occurring in 3%-9% of patients with Entamoeba histolytica infection.[1] ALA usually improves within 5-7 days on treatment with metronidazole. Some patients need percutaneous drainage or surgery, particularly for complications like rupture into the pericardium, pleura or peritoneum, thoracobiliary fistula and secondary bacterial infection.[2] Biliary communication of ALA has been reported in up to 27% of cases; however, this may not affect the cure rate or alter the treatment.[3],[4] Data on endoscopic intervention in the management of biliary communication in ALA are limited. We report our experience with the use of therapeutic endoscopic retrograde cholangiopancreatography (ERCP) in the management of patients with ALA with biliary communication.
» Methods
Between June 2002 and December 2003, all patients with ALA who required percutaneous drainage as an adjunct to medical therapy were studied. Data on symptoms, signs, laboratory investigation results, amebic serology and ultrasound characteristics were retrieved from medical records. The diagnosis of ALA was made based on ultrasonographic findings and positive amebic serology using indirect hemagglutination test (cut-off titer >1:256). All patients had received metronidazole in adequate doses (800 mg PO tid for 10-14 days). Patients with abscess volume >250 mL, thin rim of liver tissue (<1>25 mL/day) after 2 weeks were referred for ERCP. After obtaining a cholangiogram, therapeutic ERCP was done ( TGF V-70 ; Olympus, Japan) in the event of biliary communication (leak). This included sphincterotomy followed by placement of either a pigtail biliary stent or a nasobiliary drain. Technical and clinical success was assessed and complications were looked for. The pigtail catheter was removed when the drain output was <10 name="Results">» Results
During the study period, 115 patients with ALA underwent percutaneous drainage (pigtail catheter drainage 90, single needle aspiration 25) as adjunct to medical treatment. None of the patients with needle aspiration needed repeat aspiration or drainage. Among those who underwent pigtail catheter drainage of the abscess, the catheter could be removed within one week in 77 patients; in the remaining 13 patients (median age 42 years [range 24-65]; all men), bile was noticed in the drainage fluid. They were diagnosed to have abscess-biliary communication, and underwent ERCP and biliary drainage. All the 13 patients needing ERCP had a long duration of symptoms (median 45 [25-60] days); in addition, nine had fever exceeding >38°C, six had anemia (median hemoglobin 9.1 [6.8-11.2] g/dL) and four had jaundice. Investigations showed leukocytosis (>12,000 cells/dL) in 10 patients, hyperbilirubinemia (median serum bilirubin 3.6 [2.5-8.0] mg/dL) and hypoalbuminemia (median 2.3 [1.8-3.2] g/dL) in eight patients each; six patients had both hyperbilirubinemia and hypoalbuminemia. Eleven patients had a solitary liver abscess (right lobe 7, left lobe 4) and two had abscesses in both the lobes. The median abscess drain output was 88 mL/day (range 45- 347) 48 hours after the abscess drainage and 54 mL/day (range 28-177) two weeks after drainage. The drain fluid contained bile in three patients and bile with pus in 10 patients. Culture of the fluid showed Escherichia coli in two patients and Pseudomonas aeruginosa in one patient; all were sensitive to ceftazidime. ERCP was done median 21 days (range 16-30) after placement of the pigtail catheter. Cholangiogram showed a communication of the biliary tree with the abscess cavity in all patients. A 10F plastic biliary endoprosthesis (19 cm length: 2, 15 cm: 2, 12 cm: 6) or 10F nasobiliary drain (n=3) was placed; the latter were replaced with 10F stent after one week. At 48 hours after the biliary drainage, the output from the drain showed significant decrease.By the end of one week, the drain catheter could be removed in 11 of 13 patients; in the remaining two patients patients #1 and #11) the drain output decreased progressively and the catheter was removed on day 10. One week after biliary drainage, the patients showed clinical improvement and significant decrease (p=0.001) in the volume of the cavity (median 78 [55-165] mL). Cholangiogram obtained at the time of stent removal did not show any biliary leak. On follow up for 9-25 months, there has been no recurrence of abscess in any patient.
» Discussion
A majority of patients with ALA respond rapidly to treatment with metronidazole, though a cavity may persist on ultrasonography for a long time.[2],[5],[6] Poor prognostic factors include serum bilirubin >3.5 mg/dL, hypoalbuminemia (<2>500 mL), multiple abscesses, encephalopathy, pleural effusion and diabetes mellitus.[6],[7] All our patients had long duration of illness and large abscess, and several had jaundice, anemia and/or hypoalbuminemia; none had encephalopathy, pleural effusion or diabetes.The conventional indications for percutaneous drainage include deterioration in clinical condition on adequate treatment, bacterial superinfection and a high risk of abscess rupture, whereas surgery is reserved for patients with ruptured abscess, impending rupture or inadequate drainage through a catheter.[8],[9] Studies have shown that percutaneous needle aspiration is a safe approach, and accelerates resolution and prevents complications.[10],[11],[12],[13] Rajak et al showed that catheter drainage is more effective than needle aspiration (100% vs 60%) in the treatment of ALA.[14] In our study, 13 patients had no reduction in drain output even 2 weeks after percutaneous drainage, and the drain fluid contained bile, even though fluid culture grew organisms in only two of them. Saraswat et al[15] found that the percutaneous catheter could be removed after a mean period of 7 days (range 3-20), when the patient was afebrile, catheter drainage had come down to <10 class="ref" href="http://www.indianjgastro.com/article.asp?issn=0254-8860;year=2006;volume=25;issue=3;spage=125;epage=127;aulast=S#ref3" name="ft3">[3] showed presence of abscess-biliary communication in 27% of cases requiring percutaneous catheter drainage; this subgroup had more frequent jaundice, longer duration of illness, and larger lesions, and required catheter drainage for longer periods (median 17 vs 6.5 days). Standard therapy of ALA does not differ in patients with associated biliary fistula, except for need for prolonged drainage and, in a few cases, surgery.[3],[4],[16] In our study, all patients with ALA and biliary fistula had persistently large and bile-stained drain output even after 2 weeks of drainage. After placement of biliary stents, the drain output decreased rapidly within 48 hours and the catheter could be removed. Thus, ERCP and stent placement seemed to hasten resolution of the abscess and clinical improvement. This may have prevented complications of prolonged percutaneous drainage like secondary infection, fistula formation and loss of bile. Further, it may have shortened the hospital stay, reduced the need for antibiotics and hence treatment costs. Our study is limited by the fact that it was an observational study and lacked control subjects with ALA and biliary communication who had not undergone ERCP.In conclusion, biliary stent placement may be a useful adjunct in patients with ALA with biliary communication. It appears to hasten resolution of the abscess and may obviate the need for prolonged catheter drainage. Future studies should focus on determining parameters that may appear early in the course of the disease and predict the need for ERCP and biliary drainage.
» References
1.
Gall JK, Vincent AL, Greene JN, Sandin RL, Sniffen JC Amebic liver abscess. Infect Med 2001;18:548-53.
2.
Ralls PW, Barnes PF, Johnson MB, De Cock KM, Radin DR, Halls J. Medical treatment of hepatic amebic abscess: rare need for percutaneous drainage. Radiology 1987;165:805-7.
3.
Agarwal DK, Baijal SS, Roy S, Mittal BR, Gupta R, Choudhuri G. Percutaneous catheter drainage of amebic liver abscesses, with and without intrahepatic biliary communication: a comparative study. Eur J Radiol 1995;20:61-4. [PUBMED] [FULLTEXT]
4.
Bayraktar Y, Arslan S, Sivri B, Eryilmaz M, Akova M, Van Thiel DH, et al . Percutaneous drainage of hepatic abscess: therapy does not differ for those with identifiable biliary fistula. Hepatogastroenterology 1996;43:620-6.
5.
Badalamenti S, Jameson JE, Reddy KR. Amebiasis. Curr Treat Options Gastroenterol 1999;2:97-103. [PUBMED] [FULLTEXT]
6.
Sharma MP, Dasarathy S, Sushma S, Verma N. Long term follow-up of amebic liver abscess: clinical and ultrasound patterns of resolution. Trop Gastroenterol 1995;16:24-8. [PUBMED]
7.
Chuah SK, Chang-Chien CS, Sheen IS, Lin HH, Chiou SS, Chiu CT, et al . The prognostic factors of severe amebic liver abscess: a retrospective study of 125 cases. Am J Trop Med Hyg 1992;46:398-402.
8.
van Sonnenberg E, Mueller PR, Schiffman HR, Ferrucci JT Jr, Casola G, Simeone JF, et al . Intrahepatic amebic abscess: indications for and results of percutaneous catheter drainage. Radiology 1985;156:631-5.
9.
Eggleston FC, Verghese M, Handa AK, Gill SS. The results of surgery in amebic liver abscess: experiences in eighty-three patients. Surgery 1978;83:536-9. [PUBMED]
10.
Ramani A, Ramani R, Kumar MS, Lakhkar BN, Kundaje GN. Ultrasound-guided needle aspiration of amoebic liver abscess. Postgrad Med J 1993;69:381-3. [PUBMED]
11.
Tandon A, Jain AK, Dixit VK, Agarwal AK, Gupta JP. Needle aspiration in large amebic liver abscess. Trop Gastroenterol 1997;18:19-21. [PUBMED]
12.
Zafar A, Ahmed S. Amebic liver abscess: a comparative study of needle aspiration versus conservative treatment. J Ayub Med Coll Abbotabad 2002;14:10-2. [PUBMED]
13.
Mogollon PA, Molina SG, Martinez MF, Sanchez VP, Sanchez TS, Devila FBC, et al . Percutaneous drainage of amebic hepatic abscess by guided ultrasound. Preliminary results. Rev Gastroenterol Mex 1999;64:134-8.
14.
Rajak CL, Gupta S, Jain S, Chawla Y, Gulati M, Suri S. Percutaneous treatment of liver abscess: needle aspiration versus catheter drainage. Am J Roentgenol 1998;170:1035-9. [PUBMED]
15.
Saraswat VA, Agarwal DK, Baijal SS, Roy S, Choudhuri G, Dhiman RK, et al . Percutaneous catheter drainage of amebic liver abscess. Clin Radiol 1992;45:187-9.
16.
Ibrarullah M, Agarwal DK, Baijal SS, Mittal BR, Kapoor VK. Amebic liver abscess with intrabiliary rupture. HPB Surg 1994;7:305-10. [PUBMED]
S Sandeep M, Banait Vaibhav S, Thakur Sanjeev K, Bapat Mukta R, Rathi Pravin M, Abraham Philip
Department of Gastroenterology, Seth G S Medical College and K E M Hospital, Mumbai 400 012, India
Correspondence Address:S Sandeep MDepartment of Gastroenterology, Seth G S Medical College and K E M Hospital, Mumbai 400 012 India
Source of Support: None, Conflict of Interest: None
» Abstract
Background: Percutaneous drainage or surgery is required when amebic liver abscess (ALA) fails to respond to medical management. In some of these patients, non-response may be due to communication of ALA with the biliary tree. This report describes our experience with the use of endoscopic biliary draining in such patients. Methods: Medical records of patients with ALA undergoing either needle aspiration or percutaneous pigtail drainage were retrieved; the indications for drainage were: abscess volume exceeding 250 mL, a thin rim of tissue (<1>25 mL/day persisting for 2 weeks or presence of bile in the drain fluid underwent endoscopic biliary drainage. Results: A total of 115 patients with ALA underwent percutaneous treatment. None of the 25 patients with needle aspiration needed any further treatment. Of the 90 who underwent catheter drainage, the catheter could be removed within one week in 77 patients; the remaining 13 patients (median age 42 years, range 24-65; all men) had an abscess-biliary communication. In them, the median catheter output was 88 mL/day (range 45-347) and 54 mL/day (28-177) at 2 days and 2 weeks after catheter placement. The drain fluid contained bile in all 13 patients, and in addition contained pus in 10 patients. Eleven patients had a solitary abscess and two had multiple abscesses. Cholangiogram showed biliary communication in all 13 patients. All patients were treated with placement of 10F biliary endoprosthesis or 10F nasobiliary drain. Pigtail catheter was removed within 1 week in 11 of 13 patients. Conclusion: In patients with amebic liver abscess communicating with the biliary tree, biliary stenting may hasten clinical recovery and allow early removal of liver abscess catheter drain.
Liver is the most common extraintestinal site of involvement in amebiasis, with amebic liver abscess (ALA) occurring in 3%-9% of patients with Entamoeba histolytica infection.[1] ALA usually improves within 5-7 days on treatment with metronidazole. Some patients need percutaneous drainage or surgery, particularly for complications like rupture into the pericardium, pleura or peritoneum, thoracobiliary fistula and secondary bacterial infection.[2] Biliary communication of ALA has been reported in up to 27% of cases; however, this may not affect the cure rate or alter the treatment.[3],[4] Data on endoscopic intervention in the management of biliary communication in ALA are limited. We report our experience with the use of therapeutic endoscopic retrograde cholangiopancreatography (ERCP) in the management of patients with ALA with biliary communication.
» Methods
Between June 2002 and December 2003, all patients with ALA who required percutaneous drainage as an adjunct to medical therapy were studied. Data on symptoms, signs, laboratory investigation results, amebic serology and ultrasound characteristics were retrieved from medical records. The diagnosis of ALA was made based on ultrasonographic findings and positive amebic serology using indirect hemagglutination test (cut-off titer >1:256). All patients had received metronidazole in adequate doses (800 mg PO tid for 10-14 days). Patients with abscess volume >250 mL, thin rim of liver tissue (<1>25 mL/day) after 2 weeks were referred for ERCP. After obtaining a cholangiogram, therapeutic ERCP was done ( TGF V-70 ; Olympus, Japan) in the event of biliary communication (leak). This included sphincterotomy followed by placement of either a pigtail biliary stent or a nasobiliary drain. Technical and clinical success was assessed and complications were looked for. The pigtail catheter was removed when the drain output was <10 name="Results">» Results
During the study period, 115 patients with ALA underwent percutaneous drainage (pigtail catheter drainage 90, single needle aspiration 25) as adjunct to medical treatment. None of the patients with needle aspiration needed repeat aspiration or drainage. Among those who underwent pigtail catheter drainage of the abscess, the catheter could be removed within one week in 77 patients; in the remaining 13 patients (median age 42 years [range 24-65]; all men), bile was noticed in the drainage fluid. They were diagnosed to have abscess-biliary communication, and underwent ERCP and biliary drainage. All the 13 patients needing ERCP had a long duration of symptoms (median 45 [25-60] days); in addition, nine had fever exceeding >38°C, six had anemia (median hemoglobin 9.1 [6.8-11.2] g/dL) and four had jaundice. Investigations showed leukocytosis (>12,000 cells/dL) in 10 patients, hyperbilirubinemia (median serum bilirubin 3.6 [2.5-8.0] mg/dL) and hypoalbuminemia (median 2.3 [1.8-3.2] g/dL) in eight patients each; six patients had both hyperbilirubinemia and hypoalbuminemia. Eleven patients had a solitary liver abscess (right lobe 7, left lobe 4) and two had abscesses in both the lobes. The median abscess drain output was 88 mL/day (range 45- 347) 48 hours after the abscess drainage and 54 mL/day (range 28-177) two weeks after drainage. The drain fluid contained bile in three patients and bile with pus in 10 patients. Culture of the fluid showed Escherichia coli in two patients and Pseudomonas aeruginosa in one patient; all were sensitive to ceftazidime. ERCP was done median 21 days (range 16-30) after placement of the pigtail catheter. Cholangiogram showed a communication of the biliary tree with the abscess cavity in all patients. A 10F plastic biliary endoprosthesis (19 cm length: 2, 15 cm: 2, 12 cm: 6) or 10F nasobiliary drain (n=3) was placed; the latter were replaced with 10F stent after one week. At 48 hours after the biliary drainage, the output from the drain showed significant decrease.By the end of one week, the drain catheter could be removed in 11 of 13 patients; in the remaining two patients patients #1 and #11) the drain output decreased progressively and the catheter was removed on day 10. One week after biliary drainage, the patients showed clinical improvement and significant decrease (p=0.001) in the volume of the cavity (median 78 [55-165] mL). Cholangiogram obtained at the time of stent removal did not show any biliary leak. On follow up for 9-25 months, there has been no recurrence of abscess in any patient.
» Discussion
A majority of patients with ALA respond rapidly to treatment with metronidazole, though a cavity may persist on ultrasonography for a long time.[2],[5],[6] Poor prognostic factors include serum bilirubin >3.5 mg/dL, hypoalbuminemia (<2>500 mL), multiple abscesses, encephalopathy, pleural effusion and diabetes mellitus.[6],[7] All our patients had long duration of illness and large abscess, and several had jaundice, anemia and/or hypoalbuminemia; none had encephalopathy, pleural effusion or diabetes.The conventional indications for percutaneous drainage include deterioration in clinical condition on adequate treatment, bacterial superinfection and a high risk of abscess rupture, whereas surgery is reserved for patients with ruptured abscess, impending rupture or inadequate drainage through a catheter.[8],[9] Studies have shown that percutaneous needle aspiration is a safe approach, and accelerates resolution and prevents complications.[10],[11],[12],[13] Rajak et al showed that catheter drainage is more effective than needle aspiration (100% vs 60%) in the treatment of ALA.[14] In our study, 13 patients had no reduction in drain output even 2 weeks after percutaneous drainage, and the drain fluid contained bile, even though fluid culture grew organisms in only two of them. Saraswat et al[15] found that the percutaneous catheter could be removed after a mean period of 7 days (range 3-20), when the patient was afebrile, catheter drainage had come down to <10 class="ref" href="http://www.indianjgastro.com/article.asp?issn=0254-8860;year=2006;volume=25;issue=3;spage=125;epage=127;aulast=S#ref3" name="ft3">[3] showed presence of abscess-biliary communication in 27% of cases requiring percutaneous catheter drainage; this subgroup had more frequent jaundice, longer duration of illness, and larger lesions, and required catheter drainage for longer periods (median 17 vs 6.5 days). Standard therapy of ALA does not differ in patients with associated biliary fistula, except for need for prolonged drainage and, in a few cases, surgery.[3],[4],[16] In our study, all patients with ALA and biliary fistula had persistently large and bile-stained drain output even after 2 weeks of drainage. After placement of biliary stents, the drain output decreased rapidly within 48 hours and the catheter could be removed. Thus, ERCP and stent placement seemed to hasten resolution of the abscess and clinical improvement. This may have prevented complications of prolonged percutaneous drainage like secondary infection, fistula formation and loss of bile. Further, it may have shortened the hospital stay, reduced the need for antibiotics and hence treatment costs. Our study is limited by the fact that it was an observational study and lacked control subjects with ALA and biliary communication who had not undergone ERCP.In conclusion, biliary stent placement may be a useful adjunct in patients with ALA with biliary communication. It appears to hasten resolution of the abscess and may obviate the need for prolonged catheter drainage. Future studies should focus on determining parameters that may appear early in the course of the disease and predict the need for ERCP and biliary drainage.
» References
1.
Gall JK, Vincent AL, Greene JN, Sandin RL, Sniffen JC Amebic liver abscess. Infect Med 2001;18:548-53.
2.
Ralls PW, Barnes PF, Johnson MB, De Cock KM, Radin DR, Halls J. Medical treatment of hepatic amebic abscess: rare need for percutaneous drainage. Radiology 1987;165:805-7.
3.
Agarwal DK, Baijal SS, Roy S, Mittal BR, Gupta R, Choudhuri G. Percutaneous catheter drainage of amebic liver abscesses, with and without intrahepatic biliary communication: a comparative study. Eur J Radiol 1995;20:61-4. [PUBMED] [FULLTEXT]
4.
Bayraktar Y, Arslan S, Sivri B, Eryilmaz M, Akova M, Van Thiel DH, et al . Percutaneous drainage of hepatic abscess: therapy does not differ for those with identifiable biliary fistula. Hepatogastroenterology 1996;43:620-6.
5.
Badalamenti S, Jameson JE, Reddy KR. Amebiasis. Curr Treat Options Gastroenterol 1999;2:97-103. [PUBMED] [FULLTEXT]
6.
Sharma MP, Dasarathy S, Sushma S, Verma N. Long term follow-up of amebic liver abscess: clinical and ultrasound patterns of resolution. Trop Gastroenterol 1995;16:24-8. [PUBMED]
7.
Chuah SK, Chang-Chien CS, Sheen IS, Lin HH, Chiou SS, Chiu CT, et al . The prognostic factors of severe amebic liver abscess: a retrospective study of 125 cases. Am J Trop Med Hyg 1992;46:398-402.
8.
van Sonnenberg E, Mueller PR, Schiffman HR, Ferrucci JT Jr, Casola G, Simeone JF, et al . Intrahepatic amebic abscess: indications for and results of percutaneous catheter drainage. Radiology 1985;156:631-5.
9.
Eggleston FC, Verghese M, Handa AK, Gill SS. The results of surgery in amebic liver abscess: experiences in eighty-three patients. Surgery 1978;83:536-9. [PUBMED]
10.
Ramani A, Ramani R, Kumar MS, Lakhkar BN, Kundaje GN. Ultrasound-guided needle aspiration of amoebic liver abscess. Postgrad Med J 1993;69:381-3. [PUBMED]
11.
Tandon A, Jain AK, Dixit VK, Agarwal AK, Gupta JP. Needle aspiration in large amebic liver abscess. Trop Gastroenterol 1997;18:19-21. [PUBMED]
12.
Zafar A, Ahmed S. Amebic liver abscess: a comparative study of needle aspiration versus conservative treatment. J Ayub Med Coll Abbotabad 2002;14:10-2. [PUBMED]
13.
Mogollon PA, Molina SG, Martinez MF, Sanchez VP, Sanchez TS, Devila FBC, et al . Percutaneous drainage of amebic hepatic abscess by guided ultrasound. Preliminary results. Rev Gastroenterol Mex 1999;64:134-8.
14.
Rajak CL, Gupta S, Jain S, Chawla Y, Gulati M, Suri S. Percutaneous treatment of liver abscess: needle aspiration versus catheter drainage. Am J Roentgenol 1998;170:1035-9. [PUBMED]
15.
Saraswat VA, Agarwal DK, Baijal SS, Roy S, Choudhuri G, Dhiman RK, et al . Percutaneous catheter drainage of amebic liver abscess. Clin Radiol 1992;45:187-9.
16.
Ibrarullah M, Agarwal DK, Baijal SS, Mittal BR, Kapoor VK. Amebic liver abscess with intrabiliary rupture. HPB Surg 1994;7:305-10. [PUBMED]
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