Chapter 43: Managing Hepatic Disorders

Managing Hepatic Disorders medical-surgical nursing chapter details the etiology, clinical evaluation, and therapeutic strategies for patients experiencing hepatic disorders, emphasizing the liver’s complex roles as a chemical factory responsible for metabolism, storage, alteration, and excretion of vital substances. Key liver functions reviewed include glucose metabolism (glycogen synthesis and gluconeogenesis), protein synthesis (albumin and clotting factors dependent on Vitamin K), fat metabolism, and the detoxification process of converting harmful ammonia into urea. Hepatic dysfunction commonly manifests as jaundice (a yellowish hue indicating high bilirubin levels, categorized as hemolytic, hepatocellular, or obstructive), nutritional deficiencies of fat-soluble vitamins (A, D, E, K), bleeding tendencies due to coagulation factor impairment, and unique physical signs like spider angiomas, palmar erythema, and involuntary hand flapping known as asterixis. A critical consequence of advanced liver damage is portal hypertension, resulting from obstructed blood flow through the liver, which leads directly to the formation of ascites and esophageal varices. Ascites (fluid accumulation in the peritoneal cavity) is often managed with sodium restriction, diuretic therapy (spironolactone preferred), paracentesis, or the placement of a Transjugular Intrahepatic Portosystemic Shunt (TIPS). Varices are fragile, dilated veins prone to massive, life-threatening hemorrhage, managed acutely with vasoactive agents such as octreotide, and prophylactically or definitively with non-surgical procedures like endoscopic variceal ligation (EVL), which has largely replaced sclerotherapy. Pathophysiologic deterioration may lead to hepatic encephalopathy, a severe central nervous system impairment often tied to elevated ammonia, treated primarily with lactulose and antibiotics (e.g., rifaximin) to reduce intestinal bacterial protein conversion, alongside maintenance of adequate protein intake, generally between 1.2 and 1.5 g/kg/day. The chapter extensively compares the different types of viral hepatitis (A, B, C, D, and E), noting that Hepatitis B and C infections pose the highest risk for developing chronic liver disease, cirrhosis, and hepatocellular carcinoma (HCC), with effective antiviral therapies available for chronic B and C. Drug-induced and toxic hepatitis are also discussed, with acetaminophen overdose identified as the leading cause of acute liver failure (ALF), which demands intensive support and may require liver transplantation. Cirrhosis is characterized by fibrotic changes that disrupt the liver structure, differentiated into types (alcoholic, postnecrotic, biliary), and classified by severity using the Child-Pugh system. For end-stage liver disease (ESLD) and unresectable HCC (meeting criteria such as the Milan criteria), orthotopic liver transplantation (OLT) offers the best prognosis, requiring meticulous patient selection, organ allocation based on the MELD scoring system, and long-term immunosuppressive therapy to prevent rejection, with risks including bleeding and life-threatening infection.