ch44 part 2: Cirrhosis

• Chronic progressive liver disease characterized by replacement of liver tissue with fibrosis, scar tissue, and regenerative nodules, resulting in progressive liver deformation and decreased function
• Signs & symptoms - ascites (most common), spider hemangiomata, palmar erythema, gynecomastia, hypogonadism, splenomegaly, hepatic encephalopathy

• Group of disorders characterized by hepatic steatosis (fat buildup in liver), not associated with other diseases, disorders, or hepatotoxins
• Accumulation of fat can lead to inflammation and scarring called nonalcoholic steatohepatitis (NASH)
• Risk factors - obesity, diabetes, hypertriglyceridemia, severe weight loss; poor diet, tuberculosis, intestinal bypass, and corticosteroids can lead to NAFDL
• Labs - persistently elevated ALT levels with no other cause

• Chronic inflammatory condition of liver
• T-cell mediated attack of small bile duct epithelial cells resulting in loss of bile ducts and cholestasis, leading to liver necrosis and cirrhosis
• Increased risk for hepatocellular cancer
• 95% of patients are female
• Associated with autoimmune disorders including rheumatoid arthritis, Sjogren's, and scleroderma
• Early symptoms - fatigue and pruritis; hypoprothrombinemia related bleeding may occur
• Late sign - jaundice
• Other signs - fat malabsorption and low levels of fat-soluble vitamins r/t decreased bile secretion; xanthomas, hyperlipidemia, anemia
• Treatment goals - suppress ongoing liver damage, prevent complications, symptom management; med = ursodiol (Actigall)

• Autosomal recessive - progressive, familial, terminal neurologic disease accompanied by chronic liver disease leading to cirrhosis
• Copper storage - decreased hepatocellular excretion of copper into bile, increased hepatic copper accumulation and cell injury
• Hallmark sign - Kayser-Fleischer rings, brownish red colored rings seen in the cornea near limbus on eye exam
• Other neurologic dysfunctions include tremor, involuntary movements, drooling, dysarthria, rigid dystonia, seizures, migraine headaches, and insomnia
• Labs - elevated serum ALT & AST, low serum ceruloplasmin, low serum uric acid, elevated urinary copper
• Treatment - chelating agents such as D-penicillamine or trientine (Syprine), promote excretion of urinary copper

• Iron disorder - increased and inappropriate storage of dietary iron
• Systemic disease, affects liver, heart, pancreas, endocrine system
• Progressive, slow disease
• Major causes of death - decompensated cirrhosis, hepatocellular carcinoma, diabetes mellitus, cardiomyopathy

• Alcoholic (a.k.a. portal or nutritional) cirrhosis: Fatty deposits in liver due to excess alcohol intake; with continued alcohol abuse, widespread scar formation
• Postnecrotic cirrhosis: Complications of viral, toxic, or idiopathic (autoimmune) hepatitis; broad bands of scar tissue formation
• Biliary cirrhosis: Chronic biliary obstruction and infection leading to diffuse fibrosis; jaundice is main feature
• Cardiac cirrhosis: Longstanding, severe right-sided heart failure causing chronic hepatic congestion, resulting in fibrosis

• Usually insidious onset
• Liver has altered ability to metabolize carbs, fats, and proteins
• Abdominal pain - dull, heavy feeling in RUQ or epigastrium
• GI disturbances are common - Anorexia, dyspepsia, flatulence, nausea and vomiting, and changes in bowel habits (diarrhea or constipation)
• Other symptoms - Fever, lassitude, slight weight loss, hepatosplenomegaly (enlarged liver & spleen)

• Symptoms may be severe r/t liver failure and portal hypertension
• Jaundice, peripheral edema, and ascites
• Advanced stage, liver becomes small and nodular
• Jaundice - liver unable to conjugate and excrete bilirubin (hepatocellular jaundice)
• Pruritis - bile salts accumulate under skin
• Skin lesions - spider angiomas (nose, cheek, upper trunk, neck, shoulders) and palmar erythema; r/t liver's decreased ability to metabolize estrogen
• Thrombocytopenia, leukopenia, and anemia - splenomegaly (caused by backup of blood from portal vein into spleen) causes overactive spleen, increasing removal of blood cells from circulation
• Bleeding disorders - liver incapable of producing prothrombin and other clotting factors, causing decreased coagulation ability
• Endocrine - liver incapable of metabolizing adrenocortical hormones, estrogen, and testosterone; in men, gynecomastia, alopecia (axillary/pubic), testicular atrophy, loss of libido; in women, amenorrhea in menopausal women or vaginal bleeding in postmenopausal women; hyperaldosteronism causes sodium and water retention and potassium loss
• Lab values - high sodium, low potassium
• Peripheral neuropathy - dietary deficiency in thiamine, folic acid, and cobalamin

Portal hypertension resulting in esophageal varices, peripheral edema and ascites, hepatic encephalopathy (coma), and hepatorenal syndrome.

• Hypertension in the portal vein and its tributaries (veins from intestines to liver)
• Symptoms caused by blood being forced down alternate channels rather than into the portal system
• Symptoms include ascites, hepatic encephalopathy, bacterial peritonitis, hepatorenal syndrome, splenomegaly, caput medusae (distended paraumbilical veins), and esophageal, gastric, and anorectal varices

• Distention of esophageal veins; bleed easily
• Most life-threatening complication of cirrhosis
• Risk factors - ingesting poorly masticated or coarse foods or alcohol, acid reflux, increased pressure r/t nausea, vomiting, straining at stool, coughing, sneezing, lifting heavy object

• No aspirin, alcohol, or irritating foods; chew food 28 times or eat mechanical soft diet
• Avoid coughing, treat URI
• Prophylactic propanolol (Inderal) - lowers portal hypertension, prevents recurrent GI bleed
• Endoscopic sclerotherapy - endoscopic injection of sclerosing agent (e.g., morrhuate/Scleromate) into veins; NPO, conscious sedation; post procedure, check gag reflex, bleeding
• Balloon tamponade - tube-ballon down esophagus, inflate to put pressure against esophageal wall; keep scissors in reach if ballon slips to grab, cut, and pull tube to remove airway blockage
• Banding/ligation - tie off vessels to stop bleeding
• Shunt - shunting blood away from liver reduces pressure in esophageal veins
• Fresh frozen plasma and packed RBCs - for blood loss
• Vitamin K - blood clotting
• H2 histamine blockers and proton pump inhibitors - reduce reflux, reduce acidity and irritation
• Vasopresin (Pitressin) - potent vasoconstrictor
• Octreotide (Sandostatin) - decreases bleeding and pressure
• Nitroglycerine - vasodilator, lowers blood pressure, acts on heart to dilate heart arteries
• Neomycin and Lactulose - decease bacterial flora in the colon, which decreases ammonia production

• A&P: Some of the esophageal veins drain into the portal vein (esophageal veins -> left gastric vein -> portal vein)
• Problem: Hepatitis causes blood to congest in liver, back up into portal vein and cause venous distention and esophageal varices
• Solution: Create a bypass from the portal vein to the hepatic vein so that some blood is routed past the liver, relieving pressure in portal vein
• How: Using the jugular vein as an entrance, a shunt is guided down the superior to inferior vena cava and into the hepatic vein, punctured out the hepatic vein, and directed towards and anchored into the portal vein
• Contraindications: Severe hepatic encephalopathy, hepatic carcinoma, and portal vein thrombosis
• Complications: Increased levels of serum ammonia and resultant encephalopathy (ammonia is filtered by the liver, bypassing liver decreases filtering)

• Define: Neuropsychiatric manifestation of liver damage, caused by excess ammonia in systemic circulation (liver filters ammonia)
• How: Disorder of protein metabolism and excretion with nitrogenous
• Problem: Considered terminal complication of liver disease
• "Stop a Bus" Test: Put hands straight out, palms out, like hand signal to stop a bus, if high ammonia, hands will flap
• Nursing considerations: Seizure precautions, suction in room, lactulose for life (3-4x daily), neomycin to bring down bacterial load in gut
• Resolution: When ammonia levels decrease, mental state clears

• Define: Accumulation of serous fluid in the peritoneal or abdominal cavity causing increased weight, increased girth, striae, dehydration, decreased potassium, and decreased urine output
• How: Proteins move from blood vessels into capillaries and into lymph space; lymphatic system unable to carry off excess proteins and water; osmotic pressure of proteins pulls additional fluid into peritoneal cavity
• Treat: Paracentesis, shunting, salt restriction, diuretics, water restriction

• Define: Acute liver failure, severe impairment of liver function associated with hepatic encephalopathy
• Cause: Most commonly drug use, usually acetaminophen with alcohol; second most common is HBV; also mushroom poisoning ("death cap" mushroom)
• How: Drug disrupts essential intracellular processes or causes buildup of toxic metabolic products
• Treat: Liver transplant
• Nursing Considerations: Frequent mental status checks for decline in LOC; quiet environment to minimize agitation; seizure precautions; I&O for renal function; oral and skin care to avoid breakdown and infection; monitor renal function, glucose, F&E; watch for increased ICP; HOB at 30 degrees

• Metastatic carcinoma of the liver is more common than primary carcinoma
• 80% of liver cancer patients also have cirrhosis of liver
• Hep C responsible for 50-60% of liver cancers
• Hep B responsible for 20% of liver cancers
• Clinical manifestation similar to cirrhosis
• Liver biopsy is definitive test
• Management similar to cirrhosis; lobectomy or liver transplant
• If no signs of metastasis, treatment options may include radiofrequency ablation, cryoablation, percutaneous ethanol injection or percutaneous acetic acid injection
• Prognosis is poor; cancer grows rapidly, death within 4-7 months from hepatic encephalopathy or massive blood loss from GI bleed