Abstract
Portal hypertension develops as a consequence of increased resistance to portal blood flow as well as increased portal blood flow due to splanchnic vasodilation. Increased resistance due to cirrhosis is due to both structural changes from increased vascular resistance as well as dynamic variables due to release of endothelial vasodilators (such as nitrous oxide) and increased production of vasoconstrictors (such as endothelin 1). While portal hypertension is initially asymptomatic, its development is a necessary precursor for many of the potentially lethal complications related to liver disease. Portosystemic collateral vessels, or varices, develop as an inefficient means to decompress the portal system and can result in esophageal or gastric hemorrhage associated with high morbidity and mortality. A compensatory activation of neurohormonal mechanism to reduced effective circulating volume leads to sodium and water retention results in ascites and eventually to hepatorenal syndrome. Acute liver failure is characterized as the acute development of liver injury, hepatic encephalopathy, and impaired synthetic dysfunction and leads to hemodynamic instability and multi-organ system failure. Acute on chronic liver failure is a recently defined syndrome characterized by hemodynamic abnormalities with complications resulting from portal hypertension.
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Further Reading
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Norvell, J.P., Pillai, A.A., Flynn, M.M. (2018). Gastrointestinal and Hepatic Physiology in Liver Disease. In: Nanchal, R., Subramanian, R. (eds) Hepatic Critical Care . Springer, Cham. https://doi.org/10.1007/978-3-319-66432-3_4
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