Late onset hepatic failure: Clinical, serological and histological features

Abstract

The clinical, laboratory and histological features of 47 patients with what is defined as late onset hepatic failure are reviewed. Twenty-five of the patients were female and 22 male with a median age of 45 years. Hepatic dysfunction was severe as evidenced by the prolongation of prothrombin time (median = 32 sec, range = 17 to 120 sec). In only four cases was a viral etiology proven (2 hepatitis B, 2 hepatitis A) although the similarity of the clinical features to patients with fulminant viral hepatitis--apart from the longer period of illness prior to the onset of encephalopathy (median = 9 weeks, range = 8 to 24 weeks)--made non-A, non-B infection a possibility in the remainder. There were also similarities to chronic active hepatitis with low titer antibodies to smooth muscle or antinuclear factor in 17% and elevation of the serum IgG in 49%. Liver biopsy in 5 of 8 survivors more than 1 year after initial presentation showed chronic active hepatitis in three. Lobular inflammatory infiltrate, bridging necrosis and multilobular collapse were the features of the acute stage of illness in both the survivors and fatal cases. The patients given corticosteroids did not have a statistically significant improvement in survival, and overall mortality for the series was 81%. Hepatic transplantation, successfully performed in one patient, would appear to offer the best chance of survival for the majority of these patients.

Characteristics of patients dying from acute viral hepatitis in Serbia

“…However, in a large series from the United States, survival of ALF patients with encephalopathy grade 1-2 without transplantation was 52% over three weeks (10). In our study, the majority of patients suffered from FVH rather than SFVH (83% vs. 17%), although an early study reported high mortality in both acute and subacute ("late onset") hepatic failure (2). Later investigations demonstrated that the patients with shorter time intervals between onset of jaundice and HE showed a better prognosis (3,(11)(12)(13).…”

“…Otherwise, HRS and bleeding (from the gastrointestinal or genital tract) were observed in a minority of patients (<30% in both clinical forms). However, it is reported that functional renal failure develops in approximately 55% of ALF patients and is more common in SFVH (2,14). The finding of bleeding in a minority of patients is believed to be a consequence of extensive treatment with high doses of fresh frozen plasma in those not listed for liver transplantation.…”

“…encephalopathy and hemorrhage, which is clinically designated as fulminant hepatitis failure (FHF) (2,3). Systemic inflammatory response syndrome (SIRS), expressed by increased pro-and anti-inflammatory cytokines, has recently been identified as the essential event in the progression and determination of the outcome in ALF patients (4).…”

Acute on Chronic Liver Failure—What is in a ‘Definition’?

“…Earlier, East and West could never agree on a common definition for acute and subacute hepatic failure. [1][2][3][4][5] The new kid on the block, acute on chronic liver failure (ACLF) seems to have inherited all of that and more. 6 The term ACLF was possibly first used way back in early 1990s and denoted two components of same disease-a preexisting chronic liver disease with superadded acute deterioration brought on by a precipitating event.…”

Cause and prognosis in acute liver failure

“…The first attempt at a formal definition by Trey and Davidson 31 used the term fulminant hepatic failure to describe ''a potentially reversible condition, the consequence of severe liver injury, in which the onset of hepatic encephalopathy was within 8 weeks of the first symptoms of illness and in the absence of preexisting liver disease.'' 31 Inherent in this definition, along with the term late-onset hepatic failure subsequently coined by Gimson et al 32 to refer to the development of encephalopathy between 8 and 24 weeks after the first symptoms, is the recognition that many patients develop constitutional symptoms before the onset of liver damage. However, the nonspecific nature of many of these symptoms often renders the precise timing of the onset of the illness difficult.…”