Cirrhosis PDF

# Cirrhosis - A chronic disease in which there has been diffuse destruction and fibrotic regeneration of hepatic cells; necrotic tissue is replaced by fibrotic tissue resulting to alteration in the normal structure and vasculature impairing blood and lymph flow causing hepatic insufficiency and por...

# Cirrhosis - A chronic disease in which there has been diffuse destruction and fibrotic regeneration of hepatic cells; necrotic tissue is replaced by fibrotic tissue resulting to alteration in the normal structure and vasculature impairing blood and lymph flow causing hepatic insufficiency and portal hypertension. - chronic liver disorder characterized by fibrotic changes, the formation of dense connective tissue within the liver, subsequent degenerative changes, and loss of functional liver tissue - A chronic, progressive, irreversible disease - **CLASSIFICATION OF CIRRHOSIS:** - **Laennec's/Alcoholic/Portal Cirrhosis** ← The most frequent cause of death related to long-term, high-risk alcohol consumption. The end result of alcoholic liver disease. - or micronodular cirrhosis caused by chronic alcoholism, nutritional deficiencies or both - **Biliary cirrhosis** ← Bile flow is obstructed within the liver or in the biliary system, retained bile damages and destroys liver cells close to the interlobular bile ducts. Fibrosis, ductul cell destruction and inflammation makes the liver enlarged, firm and green. - Early in the disease: jaundice, pruritus and steatorhea - **Post-hepatic cirrhosis** ← Advanced progressive liver disease resulting from chronic hepatitis B or C or from an unknown cause. The liver is shrunken and nodular, with extensive liver cell loss and fibrosis. - or macronodular cirrhosis - **Cardiac cirrhosis** ← Can stem from liver congestion caused by severe chronic right sided heart failure, mitral or tricuspid valvular diseases. The liver becomes congested with blood and hepatic cells become anoxic and die causing fibrotic scarring. - **STAGES OF LAENNAEC'S CIRRHOSIS:** - Alcohol causes metabolic changes in the liver. - **1st STAGE** ← accumulation of fats; triglyceride and fatty acid synthesis increases and the formation and release of lipoproteins decrease, leading to fatty infiltration of hepatocytes (causing fatty liver). At this stage, abstinence from alcohol can allow the liver to heal. - **2nd STAGE** ← **ALCOHOLIC HEPATITIS**. Inflammatory cells infiltrate the liver, causing necrosis, fibrosis and destruction of functional liver tissue. - **3rd STAGE** ← **ALCOHOLIC (END STAGE)**. Fibrotic tissue replaces normal tissue, significantly altering basic liver structure to the extent that little normal function remains. - Early indicators of this stage: signs of portal hypertension, impaired digestion and absorption. - **PATHOPHYSIOLOGY: CIRRHOSIS** - The functional liver tissue is gradually destroyed and replaced by fibrous scar tissue - Abnormal nodules encircled by connective tissue forming constricting bands. - **PATHOPHYSIOLOGIC EFFECT OF CIRRHOSIS:** - Loss of liver function - Interference with blood, lymph and bile flow in the liver. - **CLINICAL MANIFESTATIONS: CIRRHOSIS** - Onset is insidious; may take years to develop - **Early Stage:** liver usually is enlarged and may be tender; vague symptoms such as a dull, aching pain in the RUQ along with fever, nausea, vomiting, diarrhoea, anorexia and malaise - **Later complaints:** - **Edema, ascites** - Impaired plasma protein synthesis (hypoalbuminaemia), Disrupted hormone balance and fluid retention, Increased pressure in portal venous system - **Bleeding, bruising** - due to Decreased clotting factor synthesis, Increased platelet destruction by enlarged spleen, Impaired vitamin K absorption and storage - **Esophageal varices, haemorrhoids** - due to Increased pressure in portal venous system with collateral vessel development - **Gastritis, anorexia, diarrhea** - due to Engorged veins in gastrointestinal system, Alcohol ingestion, Impaired bile synthesis and fat absorption - **Abdominal wall vein distension (caput medusae)** - due Portal hypertension - **Jaundice** - due to Impaired bilirubin metabolism and excretion - **Malnutrition, muscle wasting** - due to Impaired nutrient metabolism, Impaired fat absorption, Impaired hormone metabolis, - **Anemia, leucopenia, increased risk of infection** - due to Bleeding, Increased blood cell destruction by spleen - **Asterixis, encephalopathy** - due to Accumulated metabolic toxins, Impaired ammonia metabolism and excretion - **Gynecomastia, infertility, impotence** - due to Altered sex hormone metabolism - **MAJOR COMPLICATIONS: CIRRHOSIS** - **PORTAL HYPERTENSION** ← is a result of impaired blood flow caused by tissue damage and fibrosis - Increased pressure within the portal circulation; impaired blood flow to the liver; and slowed, congested circulation from the portal vein. - The veins are easily torn by passage of food - **massive hemorrhage** - the first sign of the major complication. - Characterized by: bleeding esophageal varices, hemorrhoids, collateral veins on the abdominal wall (caput medusa), peripheral edema (feet, ankle, pre-sacral area), ascites. - **FLUID RETENTION:** in the form of ascites and edema - Ascites may result from disturbances in both the local and systemic mechanism that govern the movement of fluid and electrolytes. - **Local factors:** - Portal hypertension - Increased hepatic lymph flow - **Systemic factors:** - Decreased colloid oncotic pressure - Hyperaldosteronism - Impaired water excretion - **HEPATIC ENCEPHALOPATHY** ← A metabolic disorder of the nervous system that may occur as cirrhosis progresses, resulting from the inability of the liver to convert ammonia to urea. Results from accumulation of neurotoxins in the blood and cerebral edema. - Cerebral edema that leads to increased intracranial pressure and cerebral hypoxia ← is the leading cause of death in people with portal systemic encephalopathy and liver failure. - **CLINICAL SIGNS OF HEPATIC ENCEPHALOPATHY:** - **STAGES OF HEPATIC ENCEPHALOPATHY:** - **STAGE I** ← Tremors, slurred speech, impaired decision making - **STAGE II** + Drowsiness, loss of sphincter control, asterixis - Asterixis (liver flap) is an early sign of portal systemic encephalopathy - **STAGE III** ← Dramatic confusion, somnolence - **STAGE IV** ← Coma, unresponsiveness - **DIAGNOSTIC TEST: CIRRHOSIS** - Liver function studies - may be elevated in cirrhosis - FBC with platelets - A low RBC count, hemoglobin and hematocrit - Platelets are low - Leucopenia - Coagulation studies - show a **prolonged prothrombin time** - Serum electrolytes - Hyponatremia ← common - Hypokalemia, hypophosphatemia and hypomagnesemia - Bilirubin levels are elevated in severe cirrhosis - Serum albumin levels - hypoalbuminemia - Serum ammonia levels - Elevated - Serum glucose and cholesterol levels frequently are abnormal in people with cirrhosis. - **Abdominal ultrasound** ← is to evaluate liver size; detect ascites and identify liver nodules. - **Liver biopsy under ultrasound** ← is useful to aid diagnosis - **Endoscopy** may be done to determine the presence of esophageal varices. - **MEDICAL MANAGEMENT: Cirrhosis** - **Nutritional measures:** - Diet modification – encourage client to eat **high-calorie moderate protein meals** and to have supplementary feedings - Abstinence from alcohol - 2000-3000 kcal/day, low protein at least 10-20 g/day, low Na <2g/day - Vitamin supplementation - Vit A, B-complex, C and K - Needed for healing of the damaged liver cells and to improve nutritional status - Anorexic → Parenteral Nutrition - **Management of variceal hemorrhage** - Diet: soft, non-irritating foods or parenteral nutrition - **EMERGENCY TREATMENT:** - **Restoration of circulating blood volume** with blood and IV fluids -for massive hematemesis and melena - **Infusion with Vasoconstrictors** with the use of: - Sandostatin (Ocreotide) I.V. ← drug of choice - Pitressin (Vasopressin) I.V. ← urgent condition - Beta-blocker - Nadolol (Corgard) may be given together with Isosorbide Mononitrate (Imdur, Monodur) – to prevent re-bleeding of the esophageal varices. This drug combination lowers the hepatic venous pressure. - Gastric lavage - **Esophageal balloon tamponade** - with the use of Sengstaken-Blakemore tube; to apply direct pressure on the bleeding varices; used only when conservative therapy would fail - **Complications:** esophageal necrosis, perforation, aspiration, asphyxiation, stricture - 3 lumen balloon↓ - Inflation of the esophageal balloon - Inflation of the gastric balloon - Gastric aspiration - L Gastric vein occlusion - **Endoscopic sclerotherapy** ← injection of sclerosing agent; use of epinephrine to promote inflammation and cause the development of scar tissue - **Complications** may include: esophageal ulceration, stricture and perforation - **Endoscopic esophageal ligation (variceal banding)** - **Emergency surgical shunting:** PORTOSYSTEMIC SHUNT/ PORTACAVAL SHUNT - **Management of ascites/fluid retention:** - Bedrest - Strict fluid and sodium restriction - Na - 2 gms/day - High in kilojoules, moderate protein, moderate fat intake - Limit fluid intake to 1-1.5L/day - Weigh OD - **Diuretics** ← reduce fluid retention and ascites - Spironolactone (Aldactone) ← first diuretic of choice; potassium-sparing diuretic that reduces ascites by increasing renal excretion of fluid and decreasing aldosterone levels. - Furosemide (Lasix) - **Albumin infusion** ← to maintain osmotic pressure. - **Therapeutic Paracentesis** ← Aspiration of fluid from the peritoneal cavity. To relieve severe ascites that does not respond to diuretic therapy. The goal is to relieve respiratory distress caused by excess fluid in the abdomen. - Moderate amount withdrawn: 500 mL to 1 L daily - Large-volume paracentesis - withdrawal of 4 to 6 L of fluid at one time - **Nursing Responsibilities: PARACENTESIS** - Weight before and after the procedure - Obtain baseline VS; monitor during and after every 15 minutes until stable - Let client void before the procedure - Obtained signed consent - Position client - Drain fluid slowly; limit to 1-2L - Apply dressing when needle is removed; record amount and characteristics - **Peritoneovenous shunt** ← a surgical implantation of a plastic shunt between the peritoneal cavity to the superior vena cava. Also referred to as Le Veen or Denver shunt. - **TIPS (Transjugular intrahepatic portosystemic shunt)** ← used to relieve portal hypertension and its complications of esophageal varices and ascites. - **Complications:** Stenosis and occlusion of the shunt and it increases the risk of developing hepatic encephalopathy - **Management of hepatic encephalopathy:** - **Neomycin/Lactulose p.o** ← **cornerstone** of treatment for increased ammonia level - **No/LOW protein in the diet temporarily** - until ammonia level decreases - **Neomycin** ← non-systemic aminoglycoside antibiotic that reduces intestinal bacteria and decreases ammonia production in the bowel lumen. - **Lactulose** ← can be give per orem or by enema; helps in elimination of ammonia from the Gl tract. - Reduces the number of ammonia forming organism in the bowel and increases the acidity of the colon contents - Convert ammonia into ammonium ion and is not absorbed and excreted in the stool thereby it decreases the ammonia level - **Other drugs: for relief measures:** - Pain medication – opioids, barbiturates and sedatives are used with caution - Antiemetics - Metoclopromide IV PRN for nausea and vomiting - Antacid - Vit. K (Aquamephyton) ← reduce the risk of bleeding - Ferrous sulfate and folic acid ← to treat anemia; for patients with biliary cirrhosis - Ursodeoxycholic acid ← to improve the liver function - Oxazepam (Serepax), a benzodiazepine antianxiety/sedative drug - Vitamin and mineral supplements are ordered based on laboratory values. - Liver transplantation ← is indicated for some people with irreversible, progressive cirrhosis. - **Indications** for liver transplantation: A decline in functional status, increasing bilirubin levels, falling albumin levels and increasing problems with complications that respond poorly to treatment - **NURSING MANAGEMENT: Cirrhosis** - **NURSING DIAGNOSIS:** - Activity intolerance R/T fatigue, general debility and discomfort. - Altered nutrition: less than body requirement R/T anorexia and GI disturbances. 3. Risk for injury R/T altered clotting mechanism 4. Disturbed thought processes R/T deterioration of liver function and increased serum ammonia level. 5. Risk for Impaired skin integrity R/T edema, jaundice and compromised immunologic status 6. Risk for fluid volume excess R/T ascites and sodium retention. - **NURSING INTERVENTION: Cirrhosis** - Promote activity tolerance - Encourage alternate periods of rest and ambulation. - Maintain some period of bed rest with legs elevated to mobilized edema an ascites. - Encourage and assist with gradual increasing periods of exercise. - Improve nutritional status - Encourage to eat high-calorie, moderate protein and to have supplementary feedings. - Suggest small frequent feedings - Encourage oral hygiene before meals - Administer antiemetic as ordered - Prevent injury through bleeding - Observe stools and emesis; send stool for occult test - Be alert for symptoms of anxiety; epigastric fullness, weakness, restlessness – may indicate → **GI bleeding.** - Keep client quiet and limit activity if signs of bleeding is exhibited. - Administer Vit. K as ordered. - Teach client to prevent trauma: maintain safe environment; gentle blowing of nose; use soft toothbrush - Use small gauge needles for injections and maintain pressure over site until bleeding stops. - **Avoid** rectal manipulation - Assess oral cavity for bleeding gums - Monitor the coagulation studies including platelet count, prothrombin time, and partial thromboplastin time - Assess the skin of the client for presence of bruising, hematoma, purpura or petechiae. - Promote improve thought processes - Restrict high-protein load in diet if serum ammonia is elevated; monitor ammonia levels. - Protect from sepsis through good hand washing and prompt recognition and management of infection. - Monitor fluid intake and output; serum electrolytes to prevent dehydration and hypokalemia which may precipitate hepatic coma. - Keep environment warm and limit visitors - Pad side rails and provide careful nursing surveillance to ensure safety. - Assess LOC/NVS and reorient client frequently. - Administer lactulose/neomycin as ordered - For fluid volume excess: - Measure weight, abdominal girth OD; MIO strictly - Restrict fluid intake; provide low sodium diet - For impaired gas exchange R/T ascites and fatigue: Promote gas exchange - Place in **semi-fowler's with feet elevated** - Administer O2, monitor O2 sat and ABG level - Promote skin integrity - Use warm water; hot water stimulates pruritus - Prevent dry skin; avoid soap or preparations with alcohol and do not rub the skin - Apply mittens to protect skin from injury - Turn every 2 hours. Assess for skin breakdown - For clients with bleeding esophageal varices: - Maintain adequate tissue perfusion - Assess vital signs; monitor for hypovolemia - Monitor clients with vasopressin infusion for complications such as hypertension, bradycardia, abdominal cramps, chest pain or water intoxication. - Observe for straining, gagging or vomiting – these increases portal pressure and increase risk of further bleeding. - Check Gl secretions and feces for occult and frank bleeding. - Monitor infusion of blood products - Administer vitamin K as ordered. - Prevent aspiration - Assess respiration/monitor O2 saturation - Note for signs of obstructed airway or ruptured esophagus from esophageal balloon such as changes in skin color, RR, breath sounds, LOC, chest pain and vital signs - Check location and inflation of balloon, maintain traction on tubes if applicable - Have scissors readily available, cut tubing and remove balloon immediately if with respiratory distress - Keep head of the bed elevated to avoid gastric regurgitation and aspiration of gastric contents - If with Sengstaken-blakemore tube, ensure removal of gastric secretion above the esophageal balloon; position NGT for suctioning purposes; provide intermittent oropharyngeal suctioning. - Inspect nares for skin irritation; clean and lubricate frequently to prevent bleeding - Reduce anxiety and fear - **HEPATIC COMA** ← a neurologic syndrome that develops as a complication of hepatic encephalopathy-CEREBRAL AMMONIA INTOXICATION. In advanced stage, the prognosis is poor despite vigorous treatment. - **ASSESSMENT FINDINGS: HEPATIC COMA** - **PRODROMAL STAGE** ← Slight personality changes such as disorientation, forgetfulness, slurred speech, slight tremor - **IMPENDING STAGE** ← asterixis, lethargy, aberrant behavior, apraxia (inability to perform or carry out skilled movements and gestures) - **STUPOROUS STAGE** ← hyperventilation, noisy and abusive when aroused - **COMATOSE** ← hyperactive reflexes, (+) babinski reflex, fetor hepaticas, coma, possibly decorticate or decerebrate posture. - **INTERVENTION:** directed to reduce ammonia level - **Medications** - Neomycin - side effect of neomycin/lactulose: **DIARRHEA** - Sorbitol ← produce osmotic diarrhea - Lactulose - Salt-poor albumin (Albuminar) ← to improve colloidal pressure to prevent the third spacing to occur thereby reducing ascites - Potassium supplement - Reduce dietary proteins - **NURSING DIAGNOSIS: HEPATIC COMA** - Potential/Actual alteration in cerebral tissue perfusion R/T ammonia intoxication - Alteration in nutrition: less than body requirement - Potential for injury R/T decreasing levels of consciousness - Knowledge deficit R/T lack of information regarding treatment options - **NURSING INTERVENTION: HEPATIC COMA** - Assess LOC; reorient continually to place and time. - MIO; monitor electrolyte; check daily weights, measure abdominal girth - Provide specified low protein with carbohydrates - Provide good oral hygiene - Provide rest, comfort and quiet atmosphere - Avoid sedatives, use restraints only as necessary 7. If comatose, use protection to the cornea by instilling artificial tears 8. Provide emotional support to the family INTRA-ABDOMINAL HYPERTENSION AN - **Notes from ma'am:** - Diet for patient with liver problem → low protein diet - Bile - digests fat - Beer - lesser evil, Whiskey - lead to blood clots → **aneurysm** - Circle of willis - a lot of bifurcation - **Assessment** - sclera - tongue (the lower part) - skin - Banana bag - yellow IV; mixture of high dose of multivitamins - Later on, liver is doorknob-sized - Rigid board like abdomen an **EMERGENCY** → bleeding (due to rupture of varices) - upon auscultation: trickling sounds - **REMEMBER:** **ANY GI BLEEDING IS AN EMERGENCY** - CSF - increased, ICP - increased - Sphincter wink ← means patient is starting to regain continence - bowel & bladder training every 4 hours - Low albumin = low BP - **3 Compartments of the Body** - Intracellular - Extracellular - Interstitial - Vasopressin for DI - oral or inhaled - Peritoneal venous shunt - superior vena cava - **REMEMBER:** No oral vit K - 2 disorders to think of when there is fresh red blood in the stool: **hemorrhoids** & cancer - **REMEMBER:** ⚠️ **DON'T** give acetaminophen to liver patient - **Room assignment:** - Pneumonia & liver patient ⇒ NO - TB & liver patient ⇒ NO - Appendectomy and liver patient ⇒ YES - AIDS and liver patient ⇒ YES - Is the patient at risk for falls? YES. Because of hepatic encephalopathy - **Type / for options**