Hypoxic hepatitis – epidemiology, pathophysiology and clinical management

Abstract

Hypoxic hepatitis (HH), also known as ischemic hepatitis or shock liver, is characterized by centrilobular liver cell necrosis and sharply increasing serum aminotransferase levels in a clinical setting of cardiac, circulatory or respiratory failure. Nowadays it is recognized as the most frequent cause of acute liver injury with a reported prevalence of up to 10% in the intensive care unit. Patients with HH and vasopressor therapy have a significantly increased mortality risk in the medical intensive care unit population. The main underlying conditions contributing to HH are low cardiac output and septic shock, although a multifactorial etiology is found in the majority of patients. HH causes several complications such as spontaneous hypoglycemia, respiratory insufficiency due to the hepatopulmonary syndrome, and hyperammonemia. HH reverses after successful treatment of the basic HH-causing disease. No specific therapies improving the hepatic function in patients with HH are currently established. Early recognition of HH and its underlying diseases and subsequent initiation of therapy is of central prognostic importance. The purpose of this review is to provide an update on the epidemiology, pathophysiology, and diagnostic and therapeutic options of HH.

Ischemic Hepatitis – Intercorrelated Pathology

“…In heart failure patients, a supplementary decrease, even transient (minimum 20 minutes), in cardiac output and hepatic blood flow, often clinically undiagnosed, leads to hepatic necrosis, considering the liver has already been exposed to hypoxia due to passive hepatic congestion (6,12).…”

“…Septic shock prevalence varies from 11% to 16% and 23% (12,13). The pathophysiologic mechanisms of IH/HH in patients with septic shock are different from cardiogenic shock.…”

Acute Liver Failure in Adults: Etiology, Clinical Manifestations, Methods of Correction

“…Ишемическое повреждение печени и ОПН могут быть обусловлены кардиогенным шоком при остром ин-фаркте миокарда, длительным периодом сердечно-легочной реанимации при остановке сердца, пери-одом значительной гиповолемии/гипотензии или декомпенсацией хронической сердечной недоста-точности [18]. В отдельных случаях гипотензия или гипоперфузия могут быть лекарственно обусловле-ны воздействием ниацина [9], кокаина, метамфета-мина [26].…”

A Case of Acute Hepatitis Following Mad Honey Ingestion

“…8,9 Serum transaminase and lactate dehydrogenase (LDH) levels frequently rise to at least twenty times the normal values, and return to normal in a short span of time. Generally, three basic criteria are used in diagnosis: 1 e acute cardiac, circulatory or respiratory failure; 2 e a temporary elevation in aminotransferases, which corresponds to at least twenty times the normal level; 3 e exclusion of a potential viral or medicationrelated hepatitis that may cause liver cell necrosis.…”

“…Generally, three basic criteria are used in diagnosis: 1 e acute cardiac, circulatory or respiratory failure; 2 e a temporary elevation in aminotransferases, which corresponds to at least twenty times the normal level; 3 e exclusion of a potential viral or medicationrelated hepatitis that may cause liver cell necrosis. 8 The ratio of ALT/LDH in ischemic hepatitis is usually <1.5. On the other hand, this ratio is much higher in acute viral hepatitis.…”