Outcome Of Fulminant Hepatic Failure Research Articles

Fulminant hepatic failure during pregnancy.

Objective: To observe clinical characteristics, etiology and maternal outcome in fulminant hepatic failure during pregnancy. Study Design: Descriptive Case Series. Setting: Department of Medicine, Nishtar Hospital Multan. Period: January 2013 to December 2017. Material & Methods: Twenty nine consecutive patients with fulminant hepatic failure during pregnancy were included in the study. Results: Mean age of patients was 27.06±6.92 years. 65.51% patients were from urban areas. Mean duration of gestation was 24.80±6.03 weeks. Jaundice and altered consciousness were observed in 100% cases, pallor in 79.31%, hepatomegaly in 20.68%, flapping tremors in 10.34%, ascites in 10.34% and splenomegaly in 6.89% cases. Complications observed were cerebral edema in 44.82%, renal failure in 24.13%, bleeding in 20.68% and hypoglycemia in 3.44%. Most common cause was acute hepatitis E (75.86%) followed by hepatitis B (13.79%) and hepatitis A (3.44%). No cause was found in 6.89% cases. Overall maternal mortality was 37.93% and fetal mortality was 72.41%. In 17.24% cases pregnancy was terminated therapeutically, 44.82% cases had spontaneous expulsion and in 37.93 % cases pregnancy continued. Maternal mortality was highest (45.45%) in patients who remained pregnant as compared to 20% when pregnancy was terminated therapeutically. Conclusion: Jaundice and altered conscious level is the most common clinical presentation. Hepatitis E is the most common cause of FHF in pregnancy. Maternal mortality in FHF during pregnancy is very high.

Natural course of fulminant hepatic failure: the scenario in Bangladesh and the differences from the west.

Background/Aim:Fulminant hepatic failure (FHF) is a devastating complication of acute viral hepatitis, leading to death in most cases. The etiology and predictors of outcome differ according to the geographical region. This study was conducted with the aim of evaluating the etiology, complications, and outcome of FHF in Bangladesh.Patients and Methods:In this prospective study, we included 67 consecutive cases of FHF presenting to the Department of Hepatology, Bangabandhu Sheikh Mujib Medical University, Dhaka, between November 2003 and May 2008. Thirty-nine of the patients were male and 28 were female. Data was analyzed using SPSS, version 13.0.Results:The mean age of the subjects was 31.9 ± 11.7 years. Hepatitis E virus (HEV) was the commonest etiological factor for FHF (50 cases, 74.6%); of the 50 cases with HEV infection, 43 (64.2%) were not coinfected with any other virus, four cases were Hepatitis B virus (HBV) carriers, and three had coinfection with hepatitis A virus (HAV). HBV was the cause of FHF in nine (13.4%) patients. HCV, paracetamol, and alcohol were not responsible for any of the cases. Most of the patients (57 patients, 85%) developed FHF within 2 weeks of the onset of jaundice. Of the 67 patients, 49 (73.1%) died. Cerebral edema was the single most common cause of death (48 patients, 71.6%). Other complications were renal failure (23 patients, 34.3%), sepsis (15 patients, 22.4%), electrolyte imbalance (12 patients 17.9%), and bleeding tendency (7 patients, 10.4%). Occurrence of cerebral edema, longer prothrombin time, higher grade of encephalopathy, and longer jaundice-to-encephalopathy interval had significant negative influence on outcome.Conclusions:The etiology of FHF in Bangladesh is different from that in the West. Prolongation of prothrombin time and occurrence of cerebral edema are predictors of the worst prognosis.

Are Hepatic Growth Factors Predictors of Clinical Outcome in Fulminant Hepatic Failure?

Are Hepatic Growth Factors Predictors of Clinical Outcome in Fulminant Hepatic Failure?

Factors affecting the mortality of pediatric fulminant hepatic failure in relation to hepatitis B virus infection

To investigate the factors affecting the outcome of fulminant hepatic failure (FHF) in children in relation to hepatitis B virus (HBV) infection. Retrospective review of a total of 94 cases (61 males and 33 females, aged from 1 month to 15 years) recruited from nine tertiary referral centers in Taiwan from 1985 to 1999. The overall mortality rate was 75%. Patients in the mortality group were of an older age, had higher peak total bilirubin levels, a longer prothrombin time, and a lower percentage of HBV positivity (P < 0.001, P = 0.003, P = 0.0027 and P = 0.042, respectively). Mortality was 65% in the HBV positive (n = 42) and 83% in the HBV negative (n = 52) group (P = 0.05). In the HBV positive group, the prothrombin time was noted to be the single factor affecting outcome (P = 0.036). In the HBV negative group, older age and higher peak value of total serum bilirubin were suggestive of poor survival rate (P < 0.001 and P = 0.006, respectively). Multivariate analysis revealed that total bilirubin was the single factor affecting outcome in the HBV-negative group. The mortality rate of HBV positive children in three consecutive time periods without liver transplantation (1985-1989, 1990-1994, 1995-1999) decreased gradually (91, 67 and 38%, respectively, with P = 0.027). This change was not observed in HBV-negative cases. Hepatitis B virus positive FHF had a lower mortality rate than HBV negative FHF, with each group having different factors affecting mortality.

Fulminant hepatic failure

Abstract Analysis of the first 150 cases collected from 73 centers reporting to the Fulminant Hepatic Failure Surveillance Study showed that 80 patients had presumable viral hepatitis, of whom 62 died. Of 41 patients who had recent surgery, 36 died. In 35 patients massive liver necrosis developed less than three weeks after halothane anesthesia, and 27 (77 per cent) of these had multiple exposures to halothane. The risk from halothane is small, but this complication was present in nearly one quarter of the cases reported in our study. When the use of halothane is desired, multiple exposure should be avoided, if possible. Moreover, postoperative fever after exposure to halothane, otherwise "unexplained," is an important warning sign, and should be thoroughly investigated and taken into consideration when further exposure to this anesthetic is contemplated. The physician prescribing halothane must balance need against risk.

Blood lactate but not serum phosphate levels can predict patient outcome in fulminant hepatic failure

Early identification of those patients with fulminant hepatic liver failure (FHF) who need a transplant greatly helps in their management. A number of prognostic criteria have recently been proposed, including arterial blood lactate and serum phosphate concentrations. To validate their use, we retrospectively studied 83 consecutive patients with FHF admitted to our intensive treatment unit between August 2000 and March 2003. A total of 48 patients (58%) survived with medical management only (group I) and 35 patients (42%) failed to survive spontaneously (group II). This group included 19 patients (23%) who underwent orthotopic liver transplantation (LT), and 16 patients (19%) who died without undergoing LT (group IIa). A total of 5 patients (6%) who underwent liver transplantation died. Within paracetamol overdose (POD) and non-POD subgroups, phosphate concentrations were not significantly higher in group II patients (P = 0.08 and P = 0.27, respectively), when compared to group I patients. In multivariate analysis, post admission 12-hour lactate level was the only predictor of survival for the POD subgroup, whereas in non-POD patients, 12-hour lactate and admission bilirubin levels were significant in predicting patients' outcome. In conclusion, we found that while serum phosphate concentrations have limited clinical utility as prognostic markers, persistently elevated arterial blood lactate levels despite adequate fluid resuscitation are indicators of a poor prognosis in FHF.

Predicting the outcome of fulminant hepatic failure

Predicting the outcome of fulminant hepatic failure

P0091 PP OUTCOME OF FULMINANT HEPATIC FAILURE IN CHILDREN IN RELATION TO HBV INFECTION AFTER UNIVERSAL VACCINATION PROGRAM

Introduction: Fulminant hepatic failure (FHF) is a rare disorder with high mortality. The correlation of HBV infection and outcome is not clear.This study aimed to investigate the factors affecting the outcome of fulminant hepatic failure in children within 15 years of universal hepatitis B vaccination program. Methods: Retrospective review of a total of 94 cases (62 males and 33 females, ages 0 month to 15 years) recruited from nine tertiary referral centers in Taiwan during 1985~ 1999 respectively. Results: The overall mortality rate was 75%. Patients in the mortality group had older age, higher peak total bilirubin levels, longer prothrombin time, and lower percentage of HBV positivity (p<0.001, p=0.003, p=0.0027, and 0.042 respectively). Multivariate logistic regression showed that age greater than 2-year-old, PT > 50 seconds, bilirubin > 25 mg/dL were significantly correlated with mortality. Mortality was 65% in the HBV positive and 83% in the HBV negative group (p=0.05). In the HBV positive group, prothrombin time is noted to be the main factor affecting the outcome (p = 0.036). In HBV negative group, older age and higher peak value of total serum bilirubin suggested poor survival rate (p = 0.000, p = 0.006). The mortality rate of the HBV positive children in the consecutive three time periods without liver transplantation (1985~89, 1990~94, 1995~99) decreased (91%, 67%, 38%, p = 0.027). This change was not observed in the HBV-negative cases. Conclusion: HBV positive FHF had a lower mortality rate than HBV negative FHF. The two groups differed in risk factors affecting mortality.

Etiology and outcome of fulminant hepatic failure managed at an Australian liver transplant unit.

The primary aims were to identify the incidence, etiology and outcome of all adult cases of fulminant hepatic failure (FHF) presenting to the Victorian Liver Transplant Unit over the 14 year period since the Unit was established in 1988. The database of the Unit was used to identify all adult patients (>16 years) who were referred to the Austin and Repatriation Medical Center in Melbourne with FHF between 1988 and 2001. The Austin and Repatriation Medical Center is the sole provider of adult liver transplantation services for the states of Victoria and Tasmania. 80 patients (64 female, 14 male) with FHF were referred, at a rate of approximately one case per million population per year. The mean age was 37.6 +/- 13.7 years. Most cases were due to either paracetamol poisoning n = 29 (36%) or non-A non-B (idiopathic) hepatitis n = 27 (34%). Thirty-five patients were listed for transplantation, of which 26 underwent the procedure (77% of transplantation patients currently alive). Nine patients were listed for transplantation but did not undergo the procedure, eight died before a donor became available and one recovered. Of the 30 patients who survived without transplantation, 20 cases were due to paracetamol poisoning. Liver transplantation has had a major impact on survival of patients with FHF, most significantly in patients with FHF due to causes other than paracetamol poisoning, in whom survival without transplantation is uncommon. Survival in those who undergo transplantation for FHF is excellent, but a significant percentage of patients listed for transplantation die before a donor organ becomes available.

Our experience with fulminant hepatic failure in Turkish children: etiology and outcome.

Fulminant hepatic failure is a rare and devastating event during childhood. The etiology of liver failure is reported to change according to age and geographical location. We aimed to investigate, retrospectively, causes and outcome of fulminant hepatic failure in Turkish children. Thirty-four children with fulminant hepatic failure were analysed by means of etiology and outcome. Etiological factor, clinical presentation, encephalopathy stage and biochemical parameters were correlated with outcome. Acute viral hepatitis was detected in 12 cases (35.2 per cent) and hepatitis A was the most commonly detected cause among cases with fulminant hepatic failure (n = 9, 26.4 per cent). Hepatitis B and non A-E infection were diagnosed in two (5.8 per cent) and one (2.9 per cent) cases, respectively. Wilson's disease was defined in four patients (12.5 per cent). Budd-Chiari syndrome (2.9 per cent), autoimmune hepatitis (2.9 per cent) and mushroom poisoning (2.9 per cent) were other detected causes of fulminant hepatic failure in this group. No viral, metabolic, toxic or anatomic reason could be detected in the remaining 15 (44.1 per cent) patients and they were evaluated as cryptogenic. Mortality was 67.6 per cent (23 cases). Encephalopathy grade, total and indirect bilirubin levels were found to be significantly higher in patients who died (p = 0.004, p = 0.03, p = 0.04). Seven patients could have been transplanted (two cadavaric, five living related) and the mortality of this group was 28.5 per cent (n = 2). It was concluded that fulminant hepatitis A virus (HAV) infection is the most common detectable cause of fulminant hepatic failure in Turkish children.

Serum phosphorus levels predict clinical outcome in fulminant hepatic failure

The aim of this pilot study was to evaluate the incidence of hypophosphatemia and its association with clinical outcome in fulminant hepatic failure (FHF). Patients with FHF referred for orthotopic liver transplantation (OLT) between January, 1991 and May, 2002 were identified. FHF was defined as the development of coagulopathy and encephalopathy within 8 weeks of onset of jaundice. Demographic and laboratory data, including serum phosphate, calcium, magnesium, creatinine, and PT/INR were obtained from medical records. Clinical outcomes (death, OLT, or hepatic recovery) and associated morbidities (renal failure, bleeding, and sepsis) also were noted. Thirty-eight patients, 8 men and 30 women, aged 34 ± 4 years, were included in the study. Hypophosphatemia (< 2.5 mg/dL) developed in 33 of 38 (87%) patients within 10 days of referral. Twelve patients (32%) died, 14 patients (37%) underwent OLT, and 12 patients (32%) recovered. The mean nadir serum phosphorus level was significantly lower in those who recovered compared with those who either died or required OLT (1.18 ± 0.54 versus 1.79 ± 1.00 mg/dL; P = .02). A trend toward lower mean serum phosphorus level also was noted in those who recovered compared with those who died (1.18 ± 0.54 versus 1.96 ± 1.35 mg/dL; P = .09). Serum phosphorus levels > 2.5 mg/dL was a predictor of mortality, and when used alone, was equivalent to the King's College Criteria. In conclusion, hypophosphatemia occurred frequently in patients with FHF. Lower serum phosphorus levels were observed in patients who recovered as compared with those who died or required OLT, and may be associated with recovery of hepatic function. The greater decline in serum phosphorus level in those who recover hepatic function may represent cellular use of phosphorus during hepatocyte regeneration. (Liver Transpl 2003;9:248-253.)

800 Do serum phosphate and lactate levels predict patient outcome in fulminant hepatic failure

800 Do serum phosphate and lactate levels predict patient outcome in fulminant hepatic failure

Utility of Hepatic Phosphorus-31 Magnetic Resonance Spectroscopy in a Rat Model of Acute Liver Failure

The ability to document the extent of hepatic injury and predict the outcome of fulminant hepatic failure would be helpful in identifying those patients who might benefit from liver transplantation....

Fulminant hepatic failure: the issue of patient selection for hazardous liver assistance

FULMINANT HEPATIC FAILURE (FHF) overall survival rate is usually ,20%. At least in certain etiologic categories, however, up to 60% of patients survive without transplantation. Similar figures (1-year survival between 56 and 80%) are currently reported in several series after hepatic grafting. The possibility of an early prediction on which patients have little hope of recovery would be of great help in the correct therapeutic management of the disease by identifying early those patients who need transplantation. When the graft is not available, these patients could be selected for “hazardous” liver assistance procedures, and if the procedure has certain benefits, this is more likely to be recognized if it is applied only to patients with a high probability of dying with conventional treatment alone. On the contrary, in the group of patients with concrete possibilities of spontaneous recovery, liver transplantation may represent a significant overtreatment. At present, however, there is no consensus on the prediction of outcome in FHF. Clinical indicators still remain the most important parameters for assessment of prognosis in patients with FHF. The purpose of the present study was to define a score capable of distinguishing early between patients who will recover with a conservative medical support and those who will not.

Plasma hepatocyte growth factor and biliprotein levels and outcome in fulminant hepatic failure

Plasma levels of growth factors may be important in determining the extent of liver regeneration in patients with fulminant hepatic failure and in this study human hepatocyte growth factor and biliprotein (bilirubin covalently bound to albumin) were determined in patients with fulminant hepatic failure, mainly as a result of acetaminophen overdose. Admission values for plasma human hepatocyte growth factor were significantly raised, although with a wide range in acetaminophen-induced fulminant hepatic failure (median 7.4 ng/ml, range 0.45-48.4 ng/ml, n = 34) and in fulminant hepatic failure from other causes (3.8 ng/ml, 1.72-25.1 ng/ml, n = 9) as compared to normal subjects (0.24 ng/ml, 0-0.5 ng/ml, n = 30). Higher plasma human hepatocyte growth factor was observed in patients who died (10.1 ng/ml, 3.8-48.4 ng/ml, n = 19) than in those who survived (4.3 ng/ml, 0.45-25.1 ng/ml, n = 22, p < 0.02), which may reflect lack of hepatic clearance in the former group. The median plasma biliprotein on admission (13.2 mg/l, range 6.3-100.7 mg/l, n = 43) was significantly increased compared to normal subjects (1.3 mg/l, 0-4.1 mg/l, n = 7, p < 0.001) with no difference between patients who survived or died, although when plasma biliprotein results were expressed as a percentage of the total bilirubin, the values were slightly higher in survivors (median 14.4%, range 10.8-40.5%, n = 23) compared to those who died (12.1%, 7.7-20.9%, n = 20, p = 0.004).(ABSTRACT TRUNCATED AT 250 WORDS)

Relation of tumor necrosis factor, complement levels and interleukin-2 receptor to disease severity and outcome of fulminant hepatic failure

Relation of tumor necrosis factor, complement levels and interleukin-2 receptor to disease severity and outcome of fulminant hepatic failure