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Implication of Hypotension in the Pathogenesis of Cognitive Impairment and Brain Injury in Chronic Liver Disease

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Abstract

The incidence of chronic liver disease is on the rise. One of the primary causes of hospital admissions for patients with cirrhosis is hepatic encephalopathy (HE), a debilitating neurological complication. HE is defined as a reversible syndrome, yet there is growing evidence stating that, under certain conditions, HE is associated with permanent neuronal injury and irreversibility. The pathophysiology of HE primarily implicates a strong role for hyperammonemia, but it is believed other pathogenic factors are involved. The fibrotic scarring of the liver during the progression of chronic liver disease (cirrhosis) consequently leads to increased hepatic resistance and circulatory anomalies characterized by portal hypertension, hyperdynamic circulatory state and systemic hypotension. The possible repercussions of these circulatory anomalies on brain perfusion, including impaired cerebral blood flow (CBF) autoregulation, could be implicated in the development of HE and/or permanent brain injury. Furthermore, hypotensive insults incurring during gastrointestinal bleed, infection, or liver transplantation may also trigger or exacerbate brain dysfunction and cell damage. This review will focus on the role of hypotension in the onset of HE as well as in the occurrence of neuronal cell loss in cirrhosis.

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Abbreviations

BBB:

Blood-brain barrier

CBF:

Cerebral blood flow

CLD:

Chronic liver disease

EC:

Endothelial cells

GI:

Gastrointestinal

HE:

Hepatic encephalopathy

LT:

Liver transplant

MAP:

Mean arterial pressure

NO:

Nitric oxide

RI:

Reperfusion injury

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SLE is a recipient of a Doctoral Training Scholarship from Fonds de Recherche du Québec-Santé. CFR is supported through CIHR grant..

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L’Écuyer, S., Charbonney, E., Carrier, F.M. et al. Implication of Hypotension in the Pathogenesis of Cognitive Impairment and Brain Injury in Chronic Liver Disease. Neurochem Res (2023). https://doi.org/10.1007/s11064-022-03854-z

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