CIRRHOSIS OF LIVER

DEFINITION

• Cirrhosis is a chronic progressive disease of the liver characterized by excessive degeneration and destruction of the liver parenchymal cells. The liver cells attempt to regenerate but the regenerative process is disorganized resulting in abnormal blood vessel and bile duct architecture. The overgrowth of new fibrous connective tissue distorts the liver abnormal lobular structure resulting in lobules of irregular size and shape with impeded blood flow eventually irregular, disorganized, poor cellular nutrition and hypoxia caused by inadequate blood flow and scar tissue results in decrease functioning of liver.

TYPES & CAUSES OF LIVER CIRRHOSIS

(i) Alcoholic (Laennec’s) cirrhosis: It is also called portal or nutritional cirrhosis, is usually associated with alcohol abuse. Due to alcohol intake there is accumulation of fat in the liver cells resulting in wide spread scar formation occurs through out the liver.

(ii)Postnecrotic Cirrhosis: It is a complication of viral, toxic or idiopathic (Auto immune) hepatitis. Broad band of scar tissue forms with in the liver.

(iii) Biliary Cirrhosis: This is associated with chronic biliary obstruction and infection. There is a diffuse fibrosis in the liver and jaundice.

(iv) Cardiac Cirrhosis: It results from long standing, severe right sided heart failure in patients with cor pulmonale, constrictive pericarditis and tricuspid insufficiency which consists of back flow of blood in to the  liver causing portal vein obstruction and scar tissue formation.

RISK FACTORS

• Alcohol ingestion has direct hepatotoxic effect
• Malnutrition that cause protein deficiency which causes degenerative changes in the hepatocytes
• Infectious disease with hepatitis C and Hepatitis B where there is chronic inflammation and hepatocyte necrosis that result in fibrosis and liver damage.
• Primary sclerosing cholangitis: It is a chronic inflammation condition that affects the liver and bile ducts.

PATHOPHYSIOLOGY

Any factors that triggers the hepatic cells like Infection, toxins or Alcoholism

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Triggers Immune system that produces chemicals in response to the foreign substance

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Liver inflammation

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Ulceration & injury to the liver (Liver Necrosis)

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Further Inflammatory changes in the liver parenchyma

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Regeneration of fibrous scar tissue on these necrotic area

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Liver fibrosis & scarring(cirrhosis of liver)

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Obstruction of portal blood drainage

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Portal Hypertension

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Extravasation of fluid into the peritoneal cavity (Ascites)

CLINICAL MANIFESTATIONS

• GI Symptoms:- Anorexia, dyspepsia, flatulence, nausea, vomiting & change in bowel habits (diarrhea or constipation), Abdominal pain (Right upper quadrant) described as dull heavy feeling on the Right upper quadrant abdomen which is due to swelling and stretching of liver capsule, hepatomegaly, splenomegaly, jaundice,
• Fever, lassitude, slight weight loss, peripheral edema, ascites, skin lesions, spider angiomas (spider nevus or spider telangiectasia) these are small dilated blood vessels with a bright red center point and spider like branches occurs in nose, cheeks, upper trunk, neck and shoulders.
• Palmar erythema: it is a red area that blanches with pressure is located on the palms of the hands.
• Hematologic problems: Thrombocytopenia, leukopenia, anemia, coagulation disorder, epistaxis, purpura, petechiae, easy brushing, gingival bleeding and heavy menstrual bleeding.
• Endocrine Problems: Gynecomastia in men, loss of axillary and pubic hair, testicular atrophy, impotence, loss of libido, loss of pubic hair, amenorrhea, vaginal bleeding, sodium and water retention
• Peripheral neuropathy: due to dietary deficiency of thiamine, folic acid and cobalamin.

COMPLICATIONS

• Portal Hypertension: it is characterized by increased venous pressure in the portal circulation. Due to fibrosis and scarring of the liver capsules there is obstruction of venous drainage which causes increased congestion of fluids in the portal vein leading to Increased portal venous pressure (portal Hypertension) that can develop of large collateral circulation in an attempt to reduce high portal pressure which results in varicosities in areas of collateral and systemic circulation
• Esophageal & gastric varices
• Caput Medusae (ring of varices around the umblicus)
• Hemorrhoids
• Peripheral Edema & Ascites: This is due to decreased colloidal oncotic pressure from impaired liver synthesis of protein and increased portal caval pressure causes shift of fluid into peripheral cavity (Ascites) and interstitial spaces (Edema).
• Hepatic Encephalopathy: It is terminal complication of Liver damage there is a impairment in the metabolism which causes ammonia to buildup in the systemic circulation which enters the blood brain barrier and damages brain tissue.

DIAGNOSTIC EVALUATION

• History & physical Examination to identify the cause of cirrhosis of Liver.
• Liver Function studies show & bilirubin levels increased AST, ALT, GGT levels increased.
• Increased Globulin levels and decreased albumin levels.
• Percutaneous Needle liver aspiration and Histopathological examination shows fatty liver changes and alterations in the lobular structure.
• Esophagogastroduodenoscopy to identify esophageal and gastric varices.
• Angiography (percutaneous trans hepatic portograph) to visualize dilated blood vessel.
• Multiphase CT scan to locate liver fibrosis and scarring.
• Liver ultrasound to identify Liver damage and portal pressures & ascites.
• Serum Electrolytes deranged mainly serum sodium increased (due to retention) & serum potassium increased (due to potassium loss).
• Serum albumin decreased because loss of liver synthesis of albumin.
• Prothrombin time prolonged due to lack of vitamin-K absorption which causes clotting defect and bleeding tendencies.
• CBC to monitor for anemia, thrombocytopenia and leukopenia.
• Stool for occult blood due to hemorrhoids.
• Upper GI barium swallow to identify esophageal and gastric varices.
• Collaborative care
• Administration of B complex vitamins to treat vitamin deficiencies
• Advice complete bed rest to prevent fatigue due to Nutritional deficiencies
• Avoidance of alcohol to prevent liver damage
• Avoid use of hepatotoxic drugs like aspirin, acetaminophen and NSAIDS.

TREATMENT OF ASCITES:-

• Sodium restriction in diet
• Encourage protein intake 2gm/kg/day
• Administer salt poor albumin to maintain intravascular volume and adequate urine output
• Administer loop diuretics like furosemide, potassium sparing diuretic like spironolactone, Aldactone & chlorothiazide for diuresis.

PARACENTESIS

• Ascites can reoccur, so it is a surgical procedure that provide continuous reinfusion of ascitic fluid into the venous system. Laveen peritoneo-venous shunt, consists of a tube and one way valve. The tube runs from the abdominal cavity through the peritoneum under the subcutaneous tissue and into the jugular vein or superior vena cava. The valve opens when the pressure is peritoneal cavity is 3-5cm H2o higher than that in the superior vena cava. This allows the ascitic fluid to flow into the venous system.

TREATMENT OF ESOPHAGEAL & GASTRIC VARICES

• Beta adrenergic blockers like propranolol is administered to prevent pressure in the blood vessels and there by prevents the risk of bleeding
• Vasoconstrictor agents like vasopressin to prevent further dilation of blood vessels
• Somatostatin analogs like octreotide and nitroglycerine are also used to reduce pressure in the blood vessels
• If the varices are bleeding then the following procedures followed:
• IV therapy is initiated and administration of IV fluids and blood products done
• Vasopressin is administered to decrease portal hypertension.
• Endoscopic sclerotherapy: In this procedure a sclerosing agent (scleromate) introduced via endoscopy which thrombosis and obliterates the distended veins.
• Endoscopic Ligation or banding of the varices: A small rubber band (elastic-o-Ring) is slipped around the base of the varices. Endoscopic variceal ligation can be done using clips instead of O-Rings. A combination of Endoscopic ligation and sclerotherapy is done for more effective results.
• Balloon Tamponade
• It is done in patients with brisk esophageal or Gastric variceal hemorrhage. Balloon tamponade controls the hemorrhage by mechanical compression of the varices. The Minnesota or sengstaken Blackmore tube that has 3 lumen one for gastric balloon, one for esophageal balloon and one for gastric aspiration.
• The Minnesota has also port for esophageal aspiration. Which inflated the gastric and esophageal balloons put mechanical compression on the varices. The gastric balloon anchors the tube in position and also applies pressure to any bleeding varices.
• Supportive measure like transfusion packed RBC’s and fresh frozen plasma administered.
• Administration of Vitamin K to prevent bleeding
• H2 receptor antagonist like pantoprazole to prevent acidity
• Lactulose and neomycin are administered to increase bowel movements and to release of ammonia in the intestines
• Antibiotics like Doxycycline, sulfamethoxazole are administered to prevent infection by Hospitalization.
• Shunting procedures to decrease portal hypertension
• Trans jugular intrahepatic Porto systemic shunt: (TIPS): This is non surgical procedure in which a tract (shunt) between the systemic and portal venous system is created to redirect portal blood flow. A catheter is placed in the jugular vein and threaded through the superior and inferior vena cava to the hepatic vein. The wall of the hepatic vein is punctured and the catheter is directed to the portal vein. Stents are positioned along the passage way overlapping in the liver tissue and extending into both veins.
• Drug therapy for cirrhosis of Liver
• Vasopressin: Hemostasis and control bleeding in esophageal varices, constricts splanchnic arterial blood.
• Propranolol: Reduction of portal venous pressure reduction of esophageal varices bleeding
• Lactulose: Acidification of feces in bowel and trapping of ammonia causing it to eliminate in feces.
• Neomycin sulfate: Decrease in bacterial flora, reduces the formation of ammonia
• Magnesium sulfate: Magnesium replacement, hypomagnesemia occurs due to liver dysfunction
• Vitamin K : Helps to correction of clotting abnormalities
• Histamine H2 receptor blockers (Ranitidine) helps to decrease the gastric acidity
• Proton pump inhibitor (pantoprazole) decreases gastric activity.
• Diuretics: Spironolactone helps to blocks action of aldosterone, potassium sparring
• Amiloride: It inhibits reabsorption of sodium and secretion of potassium
• Chlorothiazide: It acts as on proximal tubule to decrease reabsorption of sodium and water
• Furosemide: Acts as distal tubule and loop of Henle to prevent reabsorption of sodium and water.
• Nutritional Therapy and patient Teaching
• Administration of 3000 calories, high carbohydrate high protein (2g/kg/day), low fat and low sodium diet.

PATIENT TEACHING

• Advice the patient to avoid alcohol and OTC drugs
• Sufficient carbohydrates intake with feeds like glucose polymer which has adequate calories
• Hepatic-Aid II Instant drink may be used as an enteral formula (NG feeding) for patients with malnutrition
• Parenteral feedings may be necessary if tube feedings are not tolerated because of impaired liver metabolism
• Advice the patient on low sodium diet to prevent edema and ascites
• Advice to avoid foods high in sodium like canned soups and vegetables, salted snacks like potato chips, nuts, smoked fish and meats, crackers, breads, olives, pickles, ketch up and beer
• Advice to avoid carbonated beverages as they are high in sodium
• Foods that can be palatable for cirrhosis patients are garlic, parsley, onion, lemon juice and spices this can be used for seasoning food.
• Advice the patient and family members on the complications of cirrhosis like ascites, bleeding varices and hepatic encephalopathy so regular follow up is required.