Hepatic Encephalopathy

Abstract

This article reviews hepatic encephalopathy (HE) in companion animals. Clinical signs and categories of hepatic disease likely to cause HE are discussed. Ammonia has a key role in pathogenesis and current concepts in body ammonia metabolism are reviewed. Inflammation and manganese accumulation are also thought to be important in pathogenesis. Treatment of HE in acute and chronic cases is discussed along with the rationale for current treatment recommendations. Potential avenues for new treatments and human treatments, which may be transferable to companion animals, are reviewed.

ACVIM consensus statement on the diagnosis and treatment of chronic hepatitis in dogs

“…The complications associated with CH in dogs are listed in Supporting Information Table S5 and include PH, ascites, HE, coagulation disorders, infection, and gastroduodenal ulceration . Additional complications reported in humans with CH include hepatopulmonary syndrome, hepatorenal syndrome, spontaneous bacterial peritonitis, and hypersplenism.…”

“…Hyperammonemia aids in the diagnosis of HE, but normal blood ammonia concentration does not eliminate the presence of HE. Evidence supports that HE is a pro‐inflammatory, pro‐oxidant, and hypercoagulable state . Treatment of HE consists of dietary protein modulation, lactulose, and antibiotics, and is summarized in Supporting Information Table S5.…”

“…Treatment of HE consists of dietary protein modulation, lactulose, and antibiotics, and is summarized in Supporting Information Table S5. Recent reviews can be consulted . Investigation, recognition, and elimination of factors that precipitate HE, such as metabolic alkalosis, infection, increased protein load (eg, gastrointestinal bleeding, high protein meals), and synergistic neuroinhibition with sedative and analgesics is essential.…”

“…The diagnosis of HE is based on the presence of neurologic signs such as lethargy, ataxia, behavioral changes, changes in mentation (eg, stupor, obtundation, and coma), head pressing, blindness, circling, shaking, twitching, and ptyalism. 205,343,344 Clinical signs of mild HE can be nonspecific (lethargy) and can easily be attributed to many other conditions. Hyperammonemia aids in the diagnosis of HE, but normal blood ammonia concentration does not eliminate the presence of HE.…”

“…Evidence supports that HE is a pro-inflammatory, pro-oxidant, and hypercoagulable state. 190,251,343,344 Treatment of HE consists of dietary protein modulation, lactulose, and antibiotics, and is summarized in Supporting Information Table S5. Recent reviews can be consulted.…”