Etiology and outcome of acute liver failure: experience from a liver transplantation centre in Montreal.

BACKGROUND: Acute liver failure is a rare condition in which massive liver injury is associated with the rapid development of hepatic encephalopathy. Although viral hepatitis and drug-induced liver injury are the most common causes, no specific etiology is found in a substantial proportion of cases reported from Europe and the United States. AIM: To determine the etiology and outcome of patients with acute liver failure in the authors' institution. PATIENTS AND METHODS: The charts of 81 consecutive patients admitted to Saint-Luc between 1991 and 1999 were reviewed. RESULTS: The etiology was viral in 27 cases (33.2%), toxic or drug-induced in 22 (27.2%), of unknown origin in 22 (27.2%) and due to various causes in 10 (12.3%) (autoimmune, vascular, cancer). Of the 81 patients, 16% survived without liver transplantation, and 84% died or underwent liver transplantation. Survival without liver transplantation differed according to the mode of presentation: the survival rate was 27% in patients with hyperacute liver failure, 7% in those with acute liver failure and 0% in those with subacute liver failure. Among the 38 patients who underwent liver transplantation, survival one year after transplantation was 71%. In the 30 patients who died without liver transplantation, the main causes of death were cerebral edema and sepsis. CONCLUSIONS: Acute liver failure is associated with a high mortality, and liver transplantation is the treatment of choice. In a significant proportion of cases, the etiology remains undetermined and is probably related to yet unidentified hepatotropic viruses.     

Fulminant hepatitis and late onset hepatic failure in Japan.

Aim: A nationwide survey was performed to clarify the present state of fulminant hepatitis and late onset hepatic failure (LOHF) between 1998 and 2003 in Japan. Methods: Three hundred and sixteen, 318 and 64 patients, respectively, with acute and subacute types of fulminant hepatitis and LOHF, in which grade II or more severe hepatic encephalopathy occurred within 10 days, between 11 days and 8 weeks and between 8 and 24 weeks, respectively, after the onset of disease symptoms, were analyzed. Results: Complications such as metabolic syndrome were underlying in 41.5% of patients with subacute fulminant hepatitis and 51.6% of patients with LOHF, and most of such patients had received daily medications. The etiology of fulminant hepatitis was viral infection in 71.2% of the acute type and 31.8% in the subacute type. Hepatitis B virus (HBV) infection was found in most of these patients; transient infection prevailed in the acute type; and HBV carrier prevailed in the subacute type. The etiology was unknown in 42.8% and 53.1% of the subacute type and LOHF, respectively. Autoimmune hepatitis and drug allergy-induced liver injury were found in 10.7% and 11.3%, respectively, of the subacute type. Artificial liver support with plasma exchange and/or hemodiafiltration took place in more than 90% of all patients. The survival rates of the patients without liver transplantation were 53.7% in the acute and 24.4% in the subacute type, and 11.5% in LOHF. The prognosis was especially poor in HBV carriers and patients with autoimmune hepatitis. The survival rates of those who underwent liver transplantation were 56.3%, 39.3% and 23.4% in the acute type, subacute type and LOHF, respectively. Conclusion: The etiology and prognosis differed in patients with fulminant hepatitis and LOHF depending on the disease types in Japan, and liver transplantation improved the prognosis of the patients irrespective of the disease type and etiology.     

Diagnostic criteria of acute liver failure: A report by the Intractable Hepato-Biliary Diseases Study Group of Japan

The diagnostic criteria of fulminant hepatitis in Japan are different from those of acute liver failure in Europe and the United States, both in regard to the histological features in the liver and the cutoff values of the prothrombin time. Thus, the Intractable Hepato‐Biliary Disease Study Group established novel diagnostic criteria for “acute liver failure” in Japan based on the demographic and clinical features of the patients. Patients showing prothrombin time values of 40% or less of the standardized values or international normalized ratios of 1.5 or more caused by severe liver damage within 8 weeks of onset of the symptoms are diagnosed as having “acute liver failure”, where the liver function prior to the current onset of liver damage is estimated to be normal. Acute liver failure is classified into “acute liver failure without hepatic coma” and “acute liver failure with hepatic coma,” depending on the severity of the hepatic encephalopathy; the latter is further classified into two types, the “acute type” and the “subacute type”, in which grade II or more severe hepatic coma develops within 10 days and between 11 and 56 days, respectively, after the onset of disease symptoms. Patients without histological findings of hepatitis, such as those with liver damage caused by drug toxicity, circulatory disturbance or metabolic disease, are also included in the disease entity of “acute liver failure”, while acute‐on‐chronic liver injuries, such as liver injury caused by alcohol, are excluded. A nationwide survey of “acute liver failure” in Japan based on the novel criteria is proposed.     

79例亚急性肝衰竭患者的临床分析

目的分析79例亚急性肝衰竭患者的临床特征、预后及特殊治疗对预后的影响。方法收集2004年1月～2010年1月北京地坛医院收治的亚急性肝衰竭病例共79例,对其性别、年龄、病因、并发症、预后及特殊治疗方法进行归纳总结。结果 79例患者中,男性60例,女性19例,平均年龄(47.59±19.01)岁,最常见的病因为戊型肝炎病毒(HEV)感染(43.04%),其次为HBV感染(27.85%)。发生率最高的3类并发症依次为腹水、腹腔感染、肝性脑病,与死亡明显相关的并发症为肝肾综合征及肝性脑病。本组资料的病死率约为18.99%。结论亚急性肝衰竭好发于男性及40岁以上人群,病死率较高。HEV感染是本组资料中最常见的致病因素,腹水、腹腔感染为最常见的并发症,肝肾综合征是最常见的致死因素。     

Akutes Leberversagen

Acute liver failure is a rare dynamic disease with a high spontaneous mortality. It is defined as acute (<26 weeks) severe liver insufficiency (INR?>1.5) with hepatic encephalopathy in the absence of chronic liver disease. The most important prognostic parameters in acute liver failure are the etiology as well as the stage of hepatic encephalopathy. Multiorgan failure, infections as well as advanced cerebral edema are the most frequent causes of death in patients with acute liver failure. Management of acute liver failure always requires intensive care surveillance with close monitoring. In case of complications an early and aggressive therapy is recommended. This includes a fluid and blood glucose monitoring, tracheal intubation and mannitol in cases of cerebral edema, a substitution of coagulation factors only in case of hemorrhage, early antibiotics for infections, early renal replacement therapy, N-acetyl cysteine for stage I/II hepatic encephalopathy as well as etiology-specific therapeutic measures. Liver transplantation is the last step therapy.     

Intensive liver care and management of acute hepatic failure

In describing acute liver failure, the term fulminant hepatic failure (FHF) is used to denote patients with the most rapid progression, normally defined as the onset of encephalopathy within eight weeks of the onset of symptoms. For patients with a slower onset of encephalopathy, ranging from eight weeks to six months after the onset of symptoms, late-onset hepatic failure is the term used to reflect the overlap in clinical features with some patients with FHF. The importance of accurately determining the type of acute liver failure results from increasing evidence of an inverse relationship between the tempo of disease progression and the chances of recovery. Prognosis is also dependent on the underlying etiology. Principles of management are as follows: (1) an accurate recognition of the tempo of the hepatic failure—fulminant, late onset, acute on chronic—and the establishment of a likely etiology; (2) early detection and treatment of complications, particularly metabolic acidosis (early), renal failure, cerebral edema, and infection (late); (3) optimization of conditions for regeneration by maintenance of a near normal metabolic milieu (with removal of toxins by various methods of artificial liver support if necessary); and (4) early consideration of an orthotopic liver transplant for those patients in the poor prognosis group. Variations in the natural history and clinical features of acute liver failure (ALF) have led to a number of different classifications and subgroupings. Knowledge of these is important in relation to the assessment of prognosis and is even more important now that transplantation is a therapeutic option. Fulminant hepatic failure (FHF) is the term used to denote the subgroup where the tempo is greatest and is variously defined as the onset of encephalopathy within four weeks (1), six weeks (EASL, 1979) and eight weeks [as described by Trey and Davidson (2)] of the onset of symptoms, or within two weeks of the onset of jaundice (3). The patients with a more protracted course are designated by the terms subacute or late-onset hepatic failure (LOHF) (4) or subfulminant hepatic failure (3). The etiology of the hepatic failure also has a major influence on the likely prognosis.Presented at the Proceedings of International Meeting on Normal and Neoplastic Growth in Hepatology, Bari, Italy, June 1989.     

Fulminant liver disease

Fulminant liver disease, acute liver failure (ALF), is one of the most intriguing and challenging conditions in the entire field of internal medicine. ALF is defined as the onset of hepatic encephalopathy and coagulopathy in patients with no known underlying liver disease within 8 to 26 weeks of onset of illness. Many cases develop within a few days, dramatically transforming an otherwise healthy individual to a patient with a high risk for developing multi-organ failure and death.     

Diagnostic Approach to Acute Liver Failure in Children: A Position Paper by the SIGENP Liver Disease Working Group

Acute liver failure (ALF) is a clinical condition characterized by the abrupt onset of coagulopathy and biochemical evidence of hepatocellular injury, leading to rapid deterioration of liver cell function.In children, ALF has been characterized by raised transaminases, coagulopathy, and no known evidence of pre-existing chronic liver disease; unlike in adults, the presence of hepatic encephalopathy is not required to establish the diagnosis. Although rare, ALF has a high mortality rate without liver transplantation (LT).Etiology of ALF varies with age and geographical location, although it may remain indeterminate in a significant proportion of cases. However, identifying its etiology is crucial to undertake disease-specific management and evaluate indication to LT.In this position statement, the Liver Disease Working Group of the Italian Society of Gastroenterology, Hepatology and Nutrition (SIGENP) reviewed the most relevant studies on pediatric ALF to provide recommendations on etiology, clinical features and diagnostic work-up of neonates, infants and children presenting with ALF. Recommendations on medical management and transplant candidacy will be discussed in a following consensus conference.     

Prognostic Evaluation of Early Indicators in Fulminant Hepatic Failure by Multivariate Analysis

Viral hepatitis is the commonest cause offulminant hepatic failure (FHF) in developing countries.We evaluated the early indicators of prognosis in thesepatients by multivariate analysis. The records of 204 consecutive patients with acute liverfailure admitted with hepatic encephalopathy over fiveyears were studied. The etiology of these patientsincluded virus related in 186 (91.1%), drug induced in 15 (7.4%), Wilson's disease in one (0.5%),acute Budd-Chiari syndrome in one (0.5%), and malignantinfiltration in one (0.5%). Patients with FHFcomplicating viral hepatitis were analyzed by univariate and multivariate analysis. These patients werefurther subclassified depending upon the intervalbetween the onset of jaundice and the onset ofencephalopathy into hyperacute (HALF; interval 0-7days), acute (ALF; interval 8-28 days) and subacuteliver failure (SALF; interval 4-12 weeks). Sixty (32.3%)patients with viral hepatitis survived. Univariateanalysis showed that the interval between onset of encephalopathy and onset of jaundice, grade ofencephalopathy, raised intracranial pressure,prothrombin time, and serum bilirubin levels onadmission were related to outcome in these patients.Multivariate logistic regression analysis showed that thepresence of raised intracranial pressure at the time ofadmission, prothrombin time >100 sec on admission,age (>50 yr), and onset of encephalopathy seven days after onset of jaundice were associated withpoor prognosis. Forty seven (37.0%) of 129 patients withHALF survived compared with 9 (22.5%) of 40 with ALF and4 (21.1%) of 19 with SALF (P = NS). Raised intracranial pressure was more frequent in patients withHALF (48.8%) than in patients with ALF (32.5%) and SALF(15.8%; P = 0.01), while clinically detectable asciteswas more frequent in patients with SALF (78.9%) compared with HALF (19.7%) and ALF (37.5%; P< 0.0001). The factors adversely affecting theoutcome in our patients with FHF complicating viralhepatitis include presence of overt clinical features of raised ICP at the time of hospitalization,prothrombin time (>100 sec) on admission, age (>50yr), and onset of encephalopathy seven days after onsetof jaundice.     

Acute Liver Failure

Acute liver failure is a rare but often catastrophic illness affecting the liver and multiple organ systems. Patients with acute liver failure require a multidisciplinary approach for adequate management. With improved critical care and the availability of liver transplantation, survival has significantly improved. Hepatic encephalopathy, cerebral edema and infections are the most common complications of acute liver failure. The evaluation requires a diligent search for a specific etiology of the liver failure, since certain causes may respond well to specific pharmacological therapies. Acetaminophen and non-acetaminophen drug-induced hepatotoxicity account for more than 50% of cases of acute liver failure. Assessment of prognosis frequently (at least on a daily basis) by using various prognostic tools, allows the treating team to decide whether or not to proceed with urgent liver transplantation. Artificial liver support devices are still in evaluation and not ready for use in clinical practice. While it is determined whether or not there is sufficient hepatic regeneration, the care of the patient with acute liver failure revolves around managing the dysfunction of multiple extra hepatic systems.     

Liver transplantation in acute liver failure:A challenging scenario

Acute liver failure is a critical medical condition defined as rapid development of hepatic dysfunction associated with encephalopathy. The prognosis in these patients is highly variable and depends on the etiology, intervalbetween jaundice and encephalopathy, age, and the degree of coagulopathy. Determining the prognosis for this population is vital. Unfortunately, prognostic models with both high sensitivity and specificity for prediction of death have not been developed. Liver transplantation has dramatically improved survival in patients with acute liver failure. Still, 25% to 45% of patients will survive with medical treatment. The identification of patients who will eventually require liver transplantation should be carefully addressed through the combination of current prognostic models and continuous medical assessment. The concerns of inaccurate selection for transplantation are significant, exposing the recipient to a complex surgery and lifelong immunosuppression. In this challenging scenario, where organ shortage remains one of the main problems, alternatives to conventional orthotopic liver transplantation, such as living-donor liver transplantation, auxiliary liver transplant, and ABO-incompatible grafts, should be explored. Although overall outcomes after liver transplantation for acute liver failure are improving, they are not yet comparable to elective transplantation.     

Fulminant hepatic failure secondary to congestive heart failure

Summary An elderly female with an acute episode of congestive heart failure, unaccompanied by any periods of hypotension, developed fulminant hepatic failure with an accompanying coagulopathy. Attempts to establish an etiology for her acute hepatic insufficiency, other than cardiac failure, proved negative. Fulminant hepatic failure as a consequence of congestive heart failure, without prolonged periods of hypotension preceding alteration in hepatic function, has not heretofore been described. Liver function is adversely effected in congestive heart failure. Hepatic ammonia clearance is impaired in cardiac failure and may be diminished to the point of resulting in hepatic encephalopathy. Coagulopathy is a frequent concomitant of fulminant hepatic failure. Establishing a clear etiology for a coagulopathy in the face of concomitant liver disease is difficult, thus making any therapeutic intervention fraught with peril.Dr. Kisloff is supported by a training grant in gastroenterology AM 0567-08 from the National Institutes of Health. The authors wish to express their gratitude to Dr. Harold J. Fallon for his suggestions.     

Re‐evaluation of the Guideline published by the Acute Liver Failure Study Group of Japan in 1996 to determine the indications of liver transplantation in patients with fulminant hepatitis

Aim: The indications for liver transplantation in cases of fulminant hepatitis are currently determined according to the Guideline of the Acute Liver Failure Study Group of Japan in 1996, which is based on assessment of the prognosis of the patients at the onset of hepatic encephalopathy and reassessed 5 days later. This Guideline was prepared based on the clinical findings in patients seen between 1988 and 1992, and showed a predictive accuracy of 82% in the patients seen between 1993 and 1995. In this study, the usefulness of the Guideline was re‐evaluated, since the therapeutic strategies for fulminant hepatitis have advanced remarkably over the last 10 years. Methods: The predictive accuracy of the Guideline was assessed in 698 patients with fulminant hepatitis and late onset hepatic failure (LOHF) between 1998 and 2003. The time‐point in the course of the disease at which physicians considered liver transplantation was examined. Results: The accuracy in patients not receiving liver transplantation was 68% and 78% in acute and subacute types, respectively, of fulminant hepatitis, and 84% among LOHF cases. The values did not improve following the reassessment. The sensitivity and specificity of the assessment in patients with acute and subacute types, respectively, were extremely low. Liver transplantation was considered in 42% of LOHF patients at 8 or more days before encephalopathy development. Conclusion: The Guideline should be modified to improve its accuracy. The Guideline should also be made adoptable for the assessment of LOHF patients before hepatic encephalopathy onset.     

Early indicators of prognosis in fulminant hepatic failure

The successful use of orthotopic liver transplantation in fulminant hepatic failure has created a need for early prognostic indicators to select the patients most likely to benefit at a time when liver transplantation is still feasible. Univariate and multivariate analysis was performed on 588 patients with acute liver failure managed medically during 1973-1985, to identify the factors most likely to indicate a poor prognosis. In acetaminophen-induced fulminant hepatic failure, survival correlated with arterial blood pH, peak prothrombin time, and serum creatinine--a pH less than 7.30, prothrombin time greater than 100 s, and creatinine greater than 300 mumol/L indicating a poor prognosis. In patients with viral hepatitis and drug reactions three static variables [etiology (non A, non B hepatitis or drug reactions), age less than 11 and greater than 40 yr, duration of jaundice before the onset of encephalopathy greater than 7 days] and two dynamic variables (serum bilirubin greater than 300 mumol/L and prothrombin time greater than 50 s) indicated a poor prognosis. The value of these indicators in determining outcome was tested retrospectively in a further 175 patients admitted during 1986-1987, leading to the construction of models for the selection of patients for liver transplantation.     

Albumin dialysis: effective removal of copper in a patient with fulminant Wilson disease and successful bridging to liver transplantation: a new possibility for the elimination of protein-bound toxins

BACKGROUND: Acute liver failure may be the first manifestation of Wilson disease. If copper elimination fails, liver transplantation is the only remaining therapeutic option. Albumin dialysis, a new method for the removal of protein-bound toxins, was performed in a patient with fulminant Wilson disease. METHODS: An 18-year-old man with Wilson disease presented with hyperacute liver failure, hepatic encephalopathy III, oligo-anuric renal failure, haemolytic anaemia, rhabdomyolysis, pancreatitis and thrombocytopenia. He was treated with albumin dialysis using a 44 g/l albumin-containing dialysate and a slow dialysate flow rate (1-2 l/h). The other details of the technique used are similar to routine continuous veno-venous haemodiafiltration. RESULTS: One hundred and five milligrams of copper were removed by albumin dialysis within the first six treatments, resulting in normalisation of blood-copper levels. Successful treatment of the multiorgan failure was achieved. Hepatic encephalopathy improved within 2 days. The patient initially refused liver transplantation. Therefore 35 additional albumin dialysis treatments were performed. Forty-three grams of bilirubin (an indicator of detoxified substances in the liver) and 196 mg of copper were removed. Multiorgan failure, in particular hepatic encephalopathy, did not recur during 59 days of treatment. Eventually, the patient agreed to liver transplantation and that was successful. CONCLUSION: Albumin dialysis is a new method for the effective treatment of fulminant Wilson disease, resulting in the removal of protein-bound toxins copper and bilirubin. It may serve as a new treatment option in hyperacute liver failure of other origin, acting as an extracorporeal detoxifier.     

重型病毒性肝炎临床诊断标准探讨(附565例重型病毒性肝炎的临床主要特点分析)

目的分析重型肝炎的临床特点,重新探讨重型肝炎的临床诊断标准。方法使用SPASS软件和SDAS软件将我院近3年收治的565例重型肝炎患者的临床特点进行分析。结果①发生于急性肝炎的45例,发生于慢性的有明确的肝病史及无明确的肝病史分别为400例及120例。②9例急性重型肝炎,出现肝性脑病7例,均在7天内出现。36例亚急性及520例慢性重型肝炎患者,在12周内达到重型肝炎诊断标准分别为100. 0％及82. 2％。③急性重型肝炎发生的肝性脑病均为首先出现,无1例发生腹水。亚急性重型肝炎及慢性重型肝炎首先出现肝性脑病仅为11. 1％及1. 7％,仅发生腹水分别为5. 6％及3. 5％。④无明确肝病史的120例患者,最后诊断为慢性重型肝炎早、中及晚期分别为17例、31例及72例。结论①重型肝炎依发病基础分为急性重型肝炎(暴发性肝衰竭)、亚急性重型肝炎(亚暴发性肝衰竭)及慢性重型肝炎;②暴发性肝衰竭、亚暴发性肝衰竭的时限分别为14天内、15天至24周(半年);③亚急性重型肝炎分腹水型及脑病型;④亚急性重型肝炎及慢性重型肝炎仍应区分为早期、中期及晚期。     

Population-based surveillance for acute liver failure

OBJECTIVES: Most U.S. studies of acute liver failure (ALF) patients have been conducted at tertiary care liver transplantation centers. The aim of this study was to conduct population-based surveillance for ALF. METHODS: We conducted population-based surveillance for ALF within the 8 counties comprising Metropolitan Atlanta between November 2000 and October 2004. ALF cases were defined as the presence of coagulopathy, any grade of hepatic encephalopathy within 26 wk of illness onset, and no history of underlying liver disease. A questionnaire was administered and medical records were reviewed to determine clinical features, etiologies, and outcomes. RESULTS: A total of 65 cases were enrolled, yielding an annualized incidence for all causes of ALF of 5.5 (95% CI 4.3-7.0) per million. Acetaminophen (APAP)-related ALF was the most common (41%) etiology in adults while ALF of undetermined etiology was most common (38%) in children, followed by APAP-related ALF (25%). Unintentional APAP overdose was the most common type (61%) of APAP-related cause. Blacks were more likely than other races to have ALF of undetermined etiology (32%vs 11%). Overall mortality was 40%, with 27 (42%) surviving with supportive care alone and 8 (12%) requiring orthotopic liver transplantation. CONCLUSIONS: Our population-based study suggests approximately 1,600 ALF cases occur in the United States each year. Consistent with findings from studies conducted exclusively at liver transplantation centers, APAP-related ALF was the most common etiology. Increased awareness of APAP-related ALF in the medical community may limit future cases. More research is warranted into ALF of undetermined etiology, especially in children.     

Advances in the management of acute liver failure

Acute liver failure(ALF)is an uncommon but dramatic clinical syndrome characterized by hepatic encephalopathy and a bleeding tendency due to abrupt loss of liver function caused by massive or submassive liver necrosis in a patient with a previously healthy liver.The causes of ALF encompass a wide variety of toxic,viral,metabolic,vascular and autoimmune insults to the liver,and identifying the correct cause can be difficult or even impossible.Many patients with ALF develop a cascade of serious complications involving almost every organ system,and death is mostly due to multi-organ failure,hemorrhage,infection,and intracranial hypertension.Fortunately,the outcome of ALF has been improved in the last 3 decades through the specific treatment for the disease of certain etiology,and the advanced intensive care management.For most severely affected patients who fail to recover after treatment,rapid evaluation for transfer to a transplantation center and consideration for liver transplantation is mandatory so that transplantation can be applied before contraindications develop.This review focuses on the recent advances in the understanding of various contributing etiologies,the administration of etiology-specific treatment to alleviate the liver injury,and the management of complications(e.g.,encephalopathy,coagulopathy,cardiovascular instability,respiratory failure,renal failure,sepsis and metabolic disturbance)in patients with ALF.Assessment of the need for liver transplantation is also presented.     

Acute hepatic failure in India: a perspective from the East

Acute hepatic failure (AHF) in India almost always presents with encephalopathy within 4 weeks of the onset of acute hepatitis. Further subclassification of AHF into hyperacute, acute and subacute forms may not be necessary in this geographical area, where the rapidity of onset of encephalopathy does not seem to influence survival. Viral hepatitis is the cause in approximately 95-100% of patients, who therefore constitute a more homogeneous population than AHF patients in the West. In India, hepatitis E (HEV) and hepatitis B (HBV) viruses are the most important causes of AHF; approximately 60% of cases are caused by to these viruses. Hepatitis B virus core mutants are very important agents in cases where hepatitis B results in AHF in this country. Half of the patients with AHF admitted to our centre are female, one-quarter of whom are pregnant. Therefore, pregnant females who contract viral hepatitis constitute a high-risk group for the development of AHF. However, the outcome of AHF in this group is similar to that in non-pregnant women and men. No association with any particular virus has been identified among sporadic cases of AHF. In our centre, approximately one-third of AHF patients survive with aggressive conservative therapy, whereas two-thirds of deaths occur within 72 h of hospitalization. Cerebral oedema and sepsis are the major fatal complications. Both fungal and gram-negative bacteria are major causes of sepsis. Among patients with AHF, despite the presence of sepsis, its overt clinical features (i.e. fever, leucocytosis) may be absent and objective documentation of the presence of sepsis in such patients is achieved by repeated culture of various body fluids. It should be possible to develop simple, clinical prognostic markers for AHF in this geographical region, in order to identify patients suitable for liver transplantation.     

Clinical Considerations of Coagulopathy in Acute Liver Failure

Acute liver failure (ALF) is the rapid onset of severe liver dysfunction, defined by the presence of hepatic encephalopathy and impaired synthetic function (international normalized ratio of ≥1.5) in the absence of underlying liver disease. The elevated international normalized ratio value in ALF is often misinterpreted as an increased hemorrhagic tendency, which can lead to inappropriate, prophylactic transfusions of blood products. However, global assessments of coagulopathy via viscoelastic tests or thrombin generation assay suggest a reestablished hemostatic, or even hypercoagulable, status in patients with ALF. Although the current versions of global assays are not perfect, they can provide more nuanced insights into the hemostatic system in ALF than the conventional measures of coagulopathy.