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PubMedDate not supplied

Management of acute liver failure.

Acute liver failure represents one of the most challenging conditions in gastroenterology. In most cases, there is no effective therapy making supportive intensive care the most important management tool. These patients frequently develop multi-organ failure, placing them at risk of systemic infections, cerebral edema, hemodynamic instability, coagulopathy and various renal and metabolic complications. Successful management of the patient with acute liver failure requires an understanding of the pathophysiology and management of these complications. An overview of acute liver failure and its most common complications is presented.

Hepatic Encephalopathy↗
PubMed1999

Acute liver failure associated with prolonged use of bromfenac leading to liver transplantation. The Acute Liver Failure Study Group.

Bromfenac, a nonnarcotic analgesic nonsteroidal anti-inflammatory drug, was associated with reversible, minor elevations in serum aminotransferase levels during clinical trials. The aim of this study is to describe the clinical, laboratory, and histological features of 4 patients with severe bromfenac hepatotoxicity identified at 3 tertiary care centers participating in the US Acute Liver Failure Study Group. Bromfenac was administered for chronic musculoskeletal disorders to 4 women in therapeutic doses of 25 to 100 mg/d for a minimum of 90 days. All patients reported a prodrome of malaise and fatigue and presented with severe, symptomatic hepatocellular injury with associated hypoprothrombinemia. None of the subjects had underlying liver or kidney disease, and there was no evidence of a hypersensitivity reaction. Other identifiable causes of acute liver failure were uniformly excluded. Despite supportive measures, all the subjects developed progressive liver failure over 5 to 37 days, leading to emergency liver transplantation in 3 patients and death in 1 patient while awaiting transplantation. Extensive confluent parenchymal necrosis that appeared to begin in the central zones and was accompanied by a predominantly lymphocytic infiltrate was noted in all the livers examined. Nodular regeneration was seen in the 2 patients with a more protracted clinical course. Administration of therapeutic doses of bromfenac for greater than 90 days was associated with the development of acute liver failure leading to liver transplantation or death in 4 adult women. The poor outcomes observed in this series, coupled with the inability to identify individuals at risk for severe, idiosyncratic bromfenac hepatotoxicity, preclude further use of bromfenac in the medical community.

Adult↗
PubMed1994

Cerebral blood flow and metabolism in fulminant liver failure.

Fulminant liver failure is a syndrome that is frequently complicated by cerebral edema and increased intracranial pressure. Cerebral blood flow has been reported as high in some studies but low in others. This study undertook to measure cerebral blood flow and cerebral metabolic rate for oxygen in 30 patients with fulminant liver failure in grade 4 encephalopathy and to assess these parameters after intervention with hyperventilation and infusions of mannitol, epoprostenol and acetylcysteine. Cerebral blood flow varied widely, from 14 to 71 ml/100 gm/min (normal range, widely, from 14 to 71 ml/100 gm/min (normal range, 41 to 66), whereas the cerebral metabolic rate for oxygen was low in all patients, 0.16 to 2.03 ml/100 gm/min (normal range, 3.12 to 3.96). Twenty-one of the 30 patients had evidence of anaerobic metabolism with cerebral lactate production. Hyperventilation resulted in a significant decrease in both cerebral blood flow (median, 36 to 28 ml/100 gm/min) and cerebral metabolic rate for oxygen (median, 0.92 to 0.65 ml/100 gm/min); mannitol and acetylcysteine infusions resulted in significant increases in both of these parameters. Prostaglandin I2 infusion did not significantly after cerebral blood flow, but there was a significant increase in cerebral metabolic rate for oxygen. The depressed cerebral metabolic rate for oxygen in patients with fulminant liver failure is inappropriate to metabolic requirements, as demonstrated by both cerebral lactate production and the increase in cerebral oxygen consumption after improvement in cerebral blood flow. Mannitol infusion should remain the main treatment of the cerebral complications of fulminant liver failure.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetaminophen↗
PubMed2004

Acute liver failure.

Acute liver failure is a rare and life-threatening clinical syndrome following severe hepatic injury. Depending on the rapidity of its development, two distinct complications contribute to a high mortality: in hyperacute liver failure, rapid development of massive hepatic necrosis and apoptosis gives rise to severe hyperammonemia, hepatic encephalopathy and life-threatening cerebral edema. The high risk of cerebral herniation requires early listing for emergency liver transplantation. Patients with hyperacute liver failure surviving the initial episode of cerebral edema have a substantial potential for hepatic recovery. If progressive hepatic failure develops more slowly, astrocytic osmoregulation prevents cerebral herniation in most instances. Unfortunately, these patients have a small potential of hepatic regeneration and transplantation should be performed before renal failure, sepsis or multiorgan failure emerge. Experimental treatment methods including detoxification by artificial or bioartificial liver support or by stimulating hepatic regeneration are currently evaluated. Recognition of ammonia toxicity has stimulated the search for early ammonia-lowering strategies and strongly renewed the interest in dialytic therapies. Anti-apoptotic interventions are among the most promising pharmacological options for the near future.

Brain Edema↗
PubMed2006

[Specific therapy in acute liver failure].

Acute liver failure is defined as hepatic insufficiency (icterus and coagulopathy), hepatorenal syndrome and encephalopathy, associated with a high mortality. A number of conditions can cause this sudden severe liver failure, which finally triggers a multi-organ response. Its etiology shows considerable geographic variation, with viral hepatitis being the most common cause worldwide, whilst drugs, especially acetaminophen-induced hepatotoxicity, form the most common precipitant in many developed countries. The essential feature of a wide variety of agents is apoptosis and/or necrosis of liver cells which is associated with liver injury and insufficiency. Based on new experimental data, the identification of target molecules involved in apoptosis may offer new therapeutic options and improvement of prognosis scores in patients with acute liver failure.

Animals↗
PubMedDate not supplied

No evidence of hematopoietic stem cell mobilization in patients submitted to hepatectomy or in patients with acute on chronic liver failure.

BACKGROUND: Liver regeneration is a heterogeneous phenomenon involving the proliferation of different cell lineages in response to injury. Under a strong positive selection pressure bone marrow derived stem cells may be involved in this process, by making a contribution to both parenchymal restoration and endothelial cell replacement. We investigate bone marrow stem cell migration to the liver in patients undergoing hepatectomy or with acute on chronic liver failure. METHODS: We enrolled 6 patients submitted to hepatectomy, 6 patients to cholecystectomy and 8 patients with acute decompensation of liver cirrhosis. Mobilization of CD34+ cells was evaluated by cytofluorimetry on peripheral blood samples at different time points; baseline, 1, 3, 7, 15 and 30 days after surgery and at admission, 1, 7 and discharge among patients with acute on chronic liver failure. 10 healthy subjects undergoing blood donation were also enrolled to evaluated the basal value of CD34+ cells. RESULTS: White blood cell counts remained in the normal range (4.1-9.8 x 10(9)/L) in all groups throughout the follow-up. In all patients of Groups 1, 2 and 3, circulating CD34+ failed to show statistically significant differences both as the absolute number and as the percentage at any time point compared to healthy controls. CONCLUSIONS: Bone marrow derived cell mobilization can not be detected after hepatectomy or during an acute decompensation on a cirrhotic liver. Under these circumstances liver regeneration can probably call upon mature hepatocytes and endogenous progenitor cells. The involvement of extrahepatic progenitors if any, is a rare and limited phenomenon.

Adult↗
PubMed2003

Acute liver failure.

Acute liver failure in children is associated with a high mortality. Most cases in our setup are due to water borne hepatotropic viruses HAV and HEV. The clinician must be aware of the earliest and the subtle signs of acute liver failure to identify cases early enough and institute supportive therapy. Focus of therapy has to be on prevention, early recognition and appropriate management of complications. Despite good intensive care, about 40-60% children with liver failure die. As and when liver transplantation becomes available in India, it would be an attractive option.

Child↗
PubMed1997

[Perioperative management for patients with chronic liver injury and the strategy for preventing postoperative liver failure].

In liver surgery, postoperative liver failure has been a serious problem of concern. Recently, the advances in the imaging diagnosis and in the operative procedures have contributed to reduce the operative mortality to less than 1%. Between October 1994 and December 1996, a total of 159 patients, including 39 with chronic hepatitis and 66 with cirrhosis, underwent liver resection for hepatocellular carcinomas (n = 103), metastatic tumors (n = 24) and others (n = 32). Although about 20% of patients had some postoperative complications, no patient died of postoperative liver failure. Preoperatively, the liver function was estimated by ICG R15 and CT volume metry, and portal vein embolization and the splenectomy, if necessary, was performed. Blood loss was replaced by plasma as far as possible. Postoperatively, it is most important to maintain the optimal water balance and electrolyte levels using fresh plasma and diuretics. Even in patients with cirrhosis, no operative mortality can be achieved with optimal hepatectomy and careful perioperative management.

Carcinoma, Hepatocellular↗
PubMed1998

Perioperative continuous hepatocyte growth factor supply prevents postoperative liver failure in rats with liver cirrhosis.

Insufficient regeneration and dysfunction of cirrhotic liver following partial hepatectomy often make the resection extremely vulnerable to postoperative liver failure, which frequently leads to multiple organ failure. Hepatocyte growth factor (HGF), first identified as the most potent mitogen for primary hepatocytes, not only stimulates hepatic regeneration but also accelerates liver function, improves fibrosis, and protects liver cells against injury. Therefore, we investigated the ability of a continuous supply of HGF to cirrhotic livers to prevent postoperative liver failure in rats. After liver cirrhosis was induced in 40 rats by the intraperitoneal injection of dimethylnitrosamine (DMN) for 4 weeks, fibroblasts genetically modified to secret rat HGF or control fibroblasts were implanted in the spleens of 20 syngenic rats per group to supply HGF continuously and directly to the cirrhotic livers. Two weeks after the implantation, all rats underwent a 30% hepatectomy. The HGF administration significantly improved liver fibrosis at the time of operation, attenuated the postoperative hepatic damage on histological examination, markedly accelerated the liver regeneration at 24 h after the hepatectomy. The blood chemical analysis indicated that HGF significantly suppressed postoperative liver failure. Most importantly, the HGF treatment significantly improved the survival rate of the rats at 48 h after the hepatectomy. The perioperative continuous supply of HGF from the spleen effectively prevented liver failure following resection of cirrhotic livers in rats.

Animals↗
PubMedDate not supplied

Extended liver resection and hepatic ischemia in pigs: a new, potentially reversible model to induce acute liver failure and study artificial liver support systems.

BACKGROUND: Extended hepatectomy is a valid model for the study of acute liver failure. Since the porcine liver is comparable in size, morphology and anatomy to the human liver, we describe a technique employing hepatic ischemia and extended liver resection to induce acute liver failure in a porcine model as a means of studying bioartificial liver support. METHOD: A subtotal (75-80% resection) extended left hepatectomy was performed in 7 pigs after 60 min warm ischemia of the future remnant liver. After resection, the animals were given the best supportive care and observed until death. RESULTS: All animals died within 18-48 h, none as a result of surgical complications. Gross appearance of the liver showed severe steatosis of the right lateral lobe, and histology revealed severe coagulative necrosis of the whole lobule. CONCLUSION: This technique of extended liver resection after hepatic ischemia in the porcine model may be useful for studies of potentially reversible acute liver failure and experimental bioartificial support.

Animals↗
PubMed2005

Acute liver failure.

Acute liver failure is a complex multisystemic illness that evolves quickly after a catastrophic insult to the liver leading to the development of encephalopathy. The underlying aetiology and the pace of progression strongly influence the clinical course. The commonest causes are paracetamol, idiosyncratic drug reactions, hepatitis B, and seronegative hepatitis. The optimal care is multidisciplinary and up to half of the cases receive liver transplants, with survival rates around 75%-90%. Artificial liver support devices remain unproven in efficacy in acute liver failure.

Humans↗
PubMed2003

Incidence of idiopathic acute liver failure and hospitalized liver injury in patients treated with troglitazone.

OBJECTIVE: Troglitazone, a thiazolidinedione antidiabetic agent, was withdrawn from the U.S. market in March, 2000, after 94 cases of acute liver failure (ALF) were reported with its use. Based on a literature review, the estimated background rate of hospitalization for idiopathic acute liver injury is 22 per million person-years and for idiopathic ALF, less than 1 per million person-years. This study was conducted to estimate the incidence rates of hospitalized idiopathic acute liver injury and ALF among troglitazone-treated patients. METHODS: An observational retrospective inception cohort of patients treated with troglitazone was assembled using claims data from a large multistate health care organization. Patients with at least 90 days of health plan enrollment before their first troglitazone prescription between April, 1997 and December, 1998 were enrolled. Hospitalized cases of potential troglitazone-induced acute liver injury or ALF were identified from claims data based on International Classification of Diseases, 9th Revision, coding. Primary medical records were reviewed for case validation, and incidence rates of acute liver injury were calculated using person-years of troglitazone exposure as the denominator. RESULTS: A total of 7568 patients contributed 4020 person-years of troglitazone exposure. Of these, five were hospitalized with acute liver injury attributed to the drug and not explained by other causes. Incidence rates (95% CI) per million person-years of acute idiopathic liver injury were as follows: hospitalization (n = 5), 1244 (404, 2900); hospitalized jaundice (n = 4), 995 (271, 2546); and ALF (n = 1), 240 (6.3, 1385). CONCLUSIONS: Troglitazone use was associated with a marked increase in risk of hospitalized acute idiopathic liver injury and ALF.

Aged↗
PubMed2003

MARS treatment in posthepatectomy liver failure.

Posthepatectomy liver failure (PHLF) is a dramatic complication following extensive liver resection or liver resection in a compromised liver, leading to death in 80% of cases. Molecular Adsorbent Recirculating System (MARS) is able to extract water and protein bound toxins out of the blood in liver failure patients. This paper describes the initial experience in the Netherlands using the MARS liver assist device in five patients with PHLF. In all patients, improvement of biochemical parameters was observed during MARS treatment along with clinical improvement in three patients. One patient survived. No clear guidelines for MARS treatment and prognostic factors for outcome after MARS treatment with regard to this patient group are available. In this paper, a MARS treatment regimen for PHLF is suggested based on literature and our own experience.

Aged↗
PubMed2002

Acute liver failure.

Acute liver failure (ALF) is a rare condition in the pediatric population. Patients who present with severe failure of liver synthetic function have a high mortality with medical therapy alone. The main causes of death are cerebral edema, hemorrhage, renal failure and sepsis. The etiology of ALF is age specific, with a significant number due to inborn errors of metabolism especially in neonates and infants. Treatment of children with ALF is supportive, aimed at preventing and managing associated complications until the native liver recovers or liver transplantation. Sedation should not be administered unless a decision for artificial ventilation has been made. As all children are potential transplant candidates, transfer to and management in a liver transplant centre is recommended. Prognostic criteria for mortality are less well defined compared to the adult population, although a significantly elevated INR > or = 4 carries a high chance of death, and liver transplantation should be considered at this stage. Auxiliary transplantation is an attractive option in selected individuals and provides the chance to stop immunosuppression should sufficient hepatic regeneration occur. The use of various liver assist devices and hepatocyte transplantation as a bridge to liver transplantation show promise, although when used in isolation, they do not have an impact on overall patient survival.

Child↗
PubMed2003

[Acute liver failure].

Acute liver failure is characterized by a dynamic clinical course associated with high mortality. The main prognostic determinant is the development of extrahepatic complications. Close monitoring is mandatory, and prophylactic measures to avoid complications should be initiated. In case of complications, early and aggressive treatment is indicated. To date, artificial liver support devices are still in the experimental phase. Liver transplantation should be considered in patients with predictors of a poor spontaneous prognosis. Therefore, a transplant center should be contacted in every case of acute liver failure.

Emergencies↗
PubMed2004

Liver transplantation for acute liver failure from drug induced liver injury in the United States.

Studies of acute liver failure from drugs have included cases mostly attributed to acetaminophen (APAP) but have reported limited data on other drugs. We used the United Network for Organ Sharing (UNOS) liver transplant database from 1990 to 2002 to identify recipients and estimate a U.S. population-based rate of liver transplantation due to acute liver failure from drugs. Patients were identified if their diagnosis was acute hepatic necrosis from an implicated drug at the time of transplant. Liver transplantation for drug hepatotoxicity accounted for 15% of liver transplants for acute liver failure over the study period. In our cohort (n = 270), 206 (76%) recipients were female. APAP alone, or in combination with another drug, accounted for 133 (49%) cases. In the non-acetaminophen (non-APAP) group (n = 137), the most frequently implicated drugs were: isoniazid, n = 24 (17.5%); propylthiouracil, n = 13 (9.5%); and phenytoin and valproate in 10 (7.3%) cases each. One-year patient and graft survival for the entire cohort was 77 and 71%, respectively. Among Caucasians (n = 206) and African-Americans (n = 48), APAP only was implicated in 110 (53%) patients and 12 (25%) patients, respectively, and non-APAP drugs were implicated in 96 (47%) patients and 36 (75%) patients, respectively (P =.0004). Among African-Americans in the non-APAP group, 28 (78%) were women. In conclusion four drugs were implicated in 42% of patients undergoing liver transplantation for acute liver failure due to drugs other than APAP. The increased frequency of African-American women undergoing liver transplantation for non-APAP drug induced liver injury warrants further study.

Acetaminophen↗
PubMed2004

Effects of liver failure on branched-chain alpha-keto acid dehydrogenase complex in rat liver and muscle: comparison between acute and chronic liver failure.

BACKGROUND/AIMS: Branched-chain alpha-keto acid dehydrogenase (BCKDH) complex catalyses the committed step in the branched-chain amino acid (BCAA) catabolic pathway. In many cases of liver failure, the serum BCAAs/aromatic amino acids ratio (Fisher's ratio) decreases, and BCAAs have been administered to patients with liver failure to correct this ratio. We conducted an animal study to examine whether the effects on hepatic BCKDH complex differ between acute liver failure (ALF) and chronic liver failure (CLF). METHODS: ALF and CLF was induced in rats by a single high-dose injection and 21 weeks of repeated low-dose injections of carbon tetrachloride, respectively. Plasma BCAA and branched-chain alpha-keto acid (BCKA) levels, and activities and protein amounts of hepatic BCKDH complex and kinase were measured. RESULTS: ALF was characterized by elevated plasma BCAA and BCKA levels and decreased hepatic BCKDH activity. CLF was characterized by decreased plasma BCAA and BCKA levels and increased hepatic BCKDH activity. This increase in BCKDH activity in CLF was associated with the decreased BCKDH kinase, which is responsible for the BCKDH inactivation. CONCLUSIONS: The results obtained in the present study suggest that BCAA catabolism is suppressed in ALF and increased in CLF.

3-Methyl-2-Oxobutanoate Dehydrogenase (Lipoamide)↗