W12: Cirrhosis

• Chapter 46 in "Yim & Lee, 2023, pp. 1080-1090" covers nursing care for individuals living with cirrhosis.

The Liver

• The liver is the largest internal organ, weighing between 1200-1600g in adults.
• It has right and left lobes and is covered by Glisson's capsule, which contains blood vessels, lymphatics, and nerves.
• Hepatocytes are specialized liver cells.
• Kupffer cells are macrophages in the liver.
• The nerve supply to the liver is the left vagus nerve and the sympathetic celiac plexus.
• Its blood supply is 1/3 from the hepatic artery and 2/3 from the portal vein.

Functions of the Liver

• The liver performs carbohydrate metabolism.
• The liver performs protein metabolism.
• The liver performs fat metabolism.
• It is responsible for detoxification.
• Steroid metabolism occurs in the liver.
• Bile synthesis is a function of the liver.
• The liver functions with the mononuclear phagocyte system.

Jaundice

• Jaundice is the yellowish discoloration of the skin, sclera, and other body tissues.
• It is prompted by excessive bilirubin accumulation in the tissue and plasma fluids.
• Light-skinned individuals will first show it in their sclera, due to increased elastin.
• Dark-skinned individuals, it manifests in the hard palate and inner canthus of the eyes.
• Urine becomes dark brown or reddish-brown.
• Bilirubin levels are higher than 34 mcmol/L, compared to the normal adult range of 5.1-17 mcmol/L.
• Types of jaundice include prehepatic, hepatic, and posthepatic.
• Obstructive jaundice causes itchy skin due to bile salts accumulating in the skin.

Cirrhosis

• Cirrhosis is a chronic and progressive liver disease.
• It’s characterized by extensive parenchymal cell degeneration and destruction.
• Liver cells attempt to regenerate, leading to new fibrous scar tissue and regenerative nodules.
• Cirrhosis causes a distortion of lobular structure.
• Cirrhosis causes impeded vascular flow.
• Cirrhosis is the 11th leading cause of death in Canada.
• Cirrhosis incidence has increased in recent decades, especially among younger birth cohorts.
• The greatest increase in cirrhosis incidence is for women.

Types of Cirrhosis

• Alcoholic cirrhosis is the most common type .
• Postnecrotic cirrhosis is another type of cirrhosis.
• Biliary cirrhosis is another type of cirrhosis.
• Cardiac cirrhosis is another type of cirrhosis.
• Nonalcoholic steatohepatitis (NASH) is another type of cirrhosis.
• The precise cause of cirrhosis is not always known.
• Some individuals have a predisposition regardless of alcohol or dietary habits.
• Alcoholic cirrhosis is also called portal or nutritional cirrhosis.
• One of the most common causes for cirrhosis is alcohol misuse.
• This has a direct hepatotoxic effect from alcohol which causes necrosis and fat accumulation in the liver.
• Poor nutrition associated with excessive alcohol consumption contributes to liver damage.
• Uncomplicated fatty changes in the liver can be reversed with alcohol cessation.
• Widespread scar tissue will persist if alcohol consumption continues.
• Postnecrotic cirrhosis is a complication of viral, toxic, or idiopathic hepatitis.
• This form presents with broad bands of scar tissue which form within the liver.
• 20% of hepatitis C patients and 25% of chronic hepatitis B patients develop postnecrotic cirrhosis.
• Biliary cirrhosis is caused by chronic biliary obstruction, potentially from a stone, tumor, or infection.
• With this type of cirrhosis, diffuse fibrosis of the liver occurs.
• A key feature for biliary cirrhosis is jaundice from the chronic retention of bile and inflammation of bile ducts.
• Cardiac cirrhosis, also known as congestive hepatopathy, results from long-standing severe right-sided heart failure, constrictive pericarditis, and tricuspid insufficiency.
• Signs and symptoms of congestive heart failure are predominant.
• Decompensated right ventricular or biventricular heart failure elevates right atrial pressure which transmits to the liver via the inferior vena cava and hepatic veins.
• Nonalcoholic steatohepatitis (NASH) is characterized by fatty liver and hepatic inflammation.
• It occurs in nearly all morbidly obese adults and children.
• NASH is rising with the prevalence of obesity and diabetes.
• Changes due to NASH are reversible if a person loses weight.
• Progression from fatty liver to fibrosis to cirrhosis occurs in 30-60% of morbidly obese patients.
• Environmental and/or genetics can cause cirrhosis.
• Cell necrosis occurs, and destroyed cells are replaced by scar tissue during cirrhosis.
• The liver's lobular form becomes nodular.
• Liver function decreases due to disorganized regeneration, poor cellular nutrition, and hypoxia from inadequate blood flow and scar tissue.

Clinical Manifestations of Cirrhosis

• Early symptoms typically include GI disturbances, such as anorexia, dyspepsia, flatulence, nausea, vomiting, diarrhea, and/or constipation.
• Symptoms are caused by altered metabolism of carbohydrates, fats, and proteins.
• Patients may complain of a "dull, heavy feeling" in the right upper quadrant or epigastrium.
• Pain may be due to swelling or stretching of the liver capsule, spasm of biliary ducts, or intermittent vascular spasm.
• Other symptoms may include fever, lethargy, slight weight loss, and liver and spleen enlargement or shrinkage.
• A liver that is palpable is commonly found.
• Late-stage symptoms may include hepatocellular jaundice, characterized by a decreased ability to conjugate and excrete bilirubin.
• Patients may develop obstructive jaundice due to obstruction of the biliary tract and pruritis from bile salts accumulating under the skin.
• Skin lesions, such as spider angiomas and palmar erythema, appear.
• Liver issues diminishes the ability to metabolize steroids with increased circulating estrogen.
• The spider angiomas are small, dilated blood vessels with a bright red center point and spider-like branches over nose, cheeks, upper trunk, neck, and shoulders.
• Palmar erythema is a red area, that blanches with pressure, on the palms of the hands.
• Hematological issues in late-stage cirrhosis include thrombocytopenia, leukopenia, anemia, and coagulation disorders.
• Thrombocytopenia can stem from splenomegaly due to portal hypertension leading to platelet sequestration, and from a decrease in thrombopoietin production in the liver.
• Anemia can result from inadequate red blood cell production or survival, poor diet, poor folic acid absorption, and bleeding varices.
• Coagulation disorders- decreased production of Prothrombin and clotting factors, leading to epistaxis, purpura, petechiae, bruising, gingival bleeding, and heavy menstruation.
• Late-stage cirrhosis have endocrine disturbances due to altered metabolism and inactivation of adrenocortical hormones, estrogen, and testosterone.
• Estrogen accumulation in men can lead to gynecomastia, loss of axillary/pubic hair, testicular atrophy, impotence, and loss of libido.
• Women may experience amenorrhea if younger, or vaginal bleeding in older women.
• Hyperaldosteronism (hypo metabolism by liver-Na+ and water retention and potassium loss.
• Peripheral neuropathy in late stage cirrhosis can be due to dietary deficiency of thiamine, folic acid, and vitamin B12.
• Sensory symptoms are most common.
• Classification for compensated cirrhosis presents with normal liver functions despite cellular damage and lobular distortion.
• Typical lab values like albumin, bilirubin, and PT/INR are normal.
• Decompensated cirrhosis, presents with liver dysfunction along with overt signs and symptoms.
• Serum albumin, bilirubin, PT/INR are abnormal.

Complications of Cirrhosis

• Portal hypertension
• Esophageal and gastric varices
• Peripheral edema and ascites
• Hepatic encephalopathy
• Hepatorenal syndrome
• Portal hypertension is caused by destruction of portal and hepatic veins with obstruction of blood flow.
• Increased venous pressure in portal circulation prompts splenomegaly large collateral veins, ascites, systemic hypertension, esophageal varices, gastric varices, caput medusae and hemorrhoids.
• Esophageal varices are a complex of tortuous, enlarged, and swollen veins at the end of the esophagus which results from portal hypertension.
• Between 2/3 to 3/4 patients with cirrhosis develop esophageal varices.
• Esophageal varices consist of tissue with little elastic, thus, they are quite fragile and bleed easily.
• Bleeding esophageal varices are a life-threatening complication.
• Varices rupture and bleed from ulceration and irritation from alcohol, poorly chewed food, acid reflux, increased intra-abdominal pressure, nausea, vomiting, straining at stool, coughing, and sneezing.
• Melena and hematemesis may be present.
• Slow oozing or massive hemorrhage necessitates medical ER attention.
• Peripheral edema is due to decreased liver synthesis of albumin (decreased colloidal oncotic pressure).
• Filtration across the capillaries is increased from higher portacaval pressure from portal hypertension, thus promoting peripheral edema.
• Peripheral edema occurs in the ankles and presacral area.
• Ascites are an accumulation of serous fluid in the peritoneal or abdominal cavity.
• With portal hypertension, proteins enter the lymph space and leak through the liver capsule into the peritoneal cavity.
• Osmotic pressure pulls more fluid into the peritoneal cavity.
• Hypoalbuminemia (decreased liver synthesis of albumin) leads to reduced colloidal oncotic pressure.
• Hyperaldosteronism, due to it not being metabolized by the liver, can occur.
• Increased sodium retention, increased ADH, and increased water retention cause decreased intravascular volume, decreased renal blood flow, and decreased glomerular filtration.
• Severe ascites causes the umbilicus to evert, abdominal striae with distended abdominal wall veins develops.
• Further manifestations also include signs of dehydration, reduced GFR, reduced urinary output, and hypokalemia.
• Hepatic encephalopathy is a neuropsychiatric manifestation of liver damage
• The terminal complication in liver disease causes a high mortality rate.
• The main cause of hepatic encephalopathy elevated ammonia from metabolism of protein in the gut, not converted to urea and excreted by kidneys.
• Ammonia crosses the blood-brain barrier and is neurotoxic.
• Hepatic encephalopathy causes lethargy resulting in deep coma.
• Early HEP symptoms include emotional lability, apathy,irritability, memory loss, confusion, drowsiness, insomnia, agitation and slow/slurred speech,.
• Further signs include impaired judgment, hiccups, slow & deep respirations, hyperactive reflexes, and/or positive Babinski's reflex.
• Late HEP symptoms can present as disorientation, impairments in writing, hyperventilation, hypothermia, fetor hepaticus (musty, sweet breath), and asterixis aka flapping tremors.
• Hepatorenal syndrome (HRS) is functional kidney failure with azotemia (uremia), oliguria, and intractable ascites.
• No structural kidney abnormality occurs.
• Etiology is complex involving portal hypertension, liver decompensation, and splanchnic & systemic vasodilation with decreased arterial blood volume, renal vasoconstriction.
• Failure is reversible with liver transplant.
• HRS is common after diuretic therapy, GI hemorrhage, paracentesis.
• HRS is indicative of a poorer prognosis.
• Treatment: splanchnic vasoconstrictors; volume expanders; transjugular intrahepatic portosystemic shunt (TIPSS) or dialysis.

Interprofessional Care for Cirrhosis

• Rest the liver with conservative treatment.
• Lower liver metabolic demands.
• Avoid alcohol, ASA, sedatives, and NSAIDs.
• Na+ restriction to manage ascites.
• Diuretics-loop (e.g. furosemide) an aldosterone antagonist-K sparing (e.g. spironolactone).
• Restrict fluids if ascites is severe.
• Administer salt-poor albumin to maintain intravascular volume & urinary output.
• Fluid removal via abdominal paracentesis to for temporary relief.
• Transjugular intrahepatic portosystemic shunt (TIPSS)
• Bleeding Prevention and management is focused on esophageal varices.
• Screen patients with cirrhosis via endoscopy.
• Avoid alcohol, aspirin, and irritating foods.
• Control coughing.
• Prescribe prophylactic beta blockers to lower risk.
• Manage with sandostatin, vasopressin, nitroglycerin, B blockers.
• Perform endoscopic therapies like sclerotherapy, ligation/banding, or shunt therapy.
• In dire situations, use balloon tamponade by inserting sengstaken-Blakemore Tube to control hemorrhage.
• Administer fresh frozen plasma, packed red blood cells, vitamin K, and proton pump inhibitors.
• Monitor perrla orientation behaviour speech coordination reflexes , acidosis and NH3
• Encourage fluids laxatives and lactulose to produce 2-3 bm a day
• Administer antiobiotics
• Provide low protein diet to minimize Nh3 production.

Paracentesis

• Paracentesis involves a needle puncture of the abdominal cavity to remove ascitic fluid.
• It is indicated when diuretics fail or to relieve abdominal pain or difficulty breathing.
• Complications include hypotension, hyponatremia, ARF, hemorrhage, infection, persistent leaking, or organ and artery puncture.
• Withdrawing large volumes requires IV albumin replacement.

Nursing Management for Cirrhosis

• Obtain past health history.
• Collect medication history.
• Perform a physical examination, noting weakness, changes in sleep-wake pattern, anorexia, weight loss, gingival bleeding, dark urine, yellow sclera, epigastric pain, and/or sexual dysfunction.
• Note fever, muscle wasting, shallow respiration, jaundice, abdominal distension, altered mental state, gynecomastia in men, amenorrhea, or heavy bleeding in women.
• Monitor for anemia, thrombocytopenia, leukopenia.
• Monitor levels of serum albumin, serum potassium, ammonia, and bilirubin.
• Perform abnormal abdominal ultrasound and liver scan.
• A liver biopsy is preformed.
• Possible nursing diagnoses: Imbalanced nutrition for less than body requirements, impaired skin integrity, ineffective breathing pattern, risk for injury due to peripheral neuropathy, risk for infection due to leukopenia, potential for hepatic encephalopathy, and potential for hemorrhage.

Patient and Caregiver Teaching in the Home Setting

• Emphasize the importance of continuous health care and medical care.
• Instruct patient to look for and report symptoms of complications.
• Follow nutrition guidelines for low protein (preferably vegetable), high calorie, limited fat, and sodium restriction.
• Avoid hepatotoxic over the counter prescription drugs and acetaminophen.
• Avoid spicy & rough foods & activities that increase portal pressure ie Valsalva.
• The nurse is caring for a client with cirrhosis.
• Deficient vitamin K absorption due hepatic disease presents as purpura and petechiae.
• In managing hepatic encephalopathy, protein is restricted to 0-40g per day in order to decrease ammonia formation.
• Lactulose is the ideal drug of choice, splitting into lactic acid + acetic acid to lower colonic pH down to 5 to prevent bacterial growth
• Traps & expels ammonia from colon via, oral, retention enema, and NG tube.
• Administer antibiotics to reduce flora in the gut, which also reduces NH3 production.
• Administer cathartics and enemas to decrease bacterial action.
• Patient must prevent constipation.
• A patient with cirrhosis and changes to their neurological and mental responsiveness can be attributed to an increase in serum levels of ammonia.
• The nurse prescribes lactulose primarily for patients with advanced complications to prevent constipation.
• Liver cannot convert ammonia to rea for renal excretion-crosses BBB
• Daily Lactulose therapy titrated to 2-3 bms BMs decrease production/retention of NH3.
• Rifaximin-poorly absorbed antibioticis given ti reduce ammonia production eliminating ammonia-producing colonic bacteria.
• AVOID ASA NSAIDs as risk ℅ Bleeding increased.
• Teach to avoid straining /constipation heavylifting and vigorous noose blowing as increases PORTAL pressure.