Focus on Cirrhosis of the Liver (Relates to Chapter 44, “Nursing Management: Liver, Pancreas, and Biliary Tract Problems” in the textbook)

Cirrhosis Description A chronic progressive disease of the liver Extensive parenchymal cell degeneration Destruction of parenchymal cells

Cirrhosis Fig. 44-4

Cirrhosis Description Liver cells attempt to regenerate Regenerative process is disorganized Abnormal blood vessel and bile duct formation New fibrous connective tissue distorts liver’s normal structure, impedes blood flow Poor cellular nutrition and hypoxia results

Cirrhosis Description Insidious, prolonged course Ninth leading cause of death in United States Fourth leading cause of death in persons ages 35 to 54 Twice as common in men

Cirrhosis Etiology and Pathophysiology Four types of cirrhosis 1. Alcoholic cirrhosis Also called portal or nutritional Usually associated with alcohol abuse First change from excessive alcohol intake is fat accumulation in liver cells With continued abuse, scar formation occurs

Cirrhosis Etiology and Pathophysiology Four types (cont’d) 2. Postnecrotic cirrhosis Complication of viral, toxic, or idiopathic hepatitis Bands of scar tissue form

Cirrhosis Etiology and Pathophysiology Four types (cont’d) 3. Biliary cirrhosis Associated with chronic biliary obstruction Diffuse fibrosis of liver with jaundice 4. Cardiac cirrhosis From long-standing severe right-sided heart failure

Cirrhosis Etiology and Pathophysiology Cause may not be determined in all patients Most common cause: Excessive alcohol ingestion Environmental factors may lead to development Some may be predisposed, regardless of alcohol intake or diet

Manifestations of Liver Cirrhosis Fig. 44-6

Cirrhosis Clinical Manifestations Early manifestations Onset usually insidious GI disturbances: Anorexia Dyspepsia Flatulence Nausea/vomiting Change in bowel habits

Cirrhosis Clinical Manifestations Early manifestations (cont’d) Abdominal pain Fever Lassitude Weight loss Enlarged liver or spleen

Cirrhosis Clinical Manifestations Late manifestations Two causative mechanisms Hepatocellular failure Portal hypertension

Cirrhosis Clinical Manifestations Late manifestations (cont’d) Jaundice Decreased ability to conjugate and excrete bilirubin by liver cells Functional derangement of liver cells Compression of bile ducts by overgrowth of connective tissue

Cirrhosis Clinical Manifestations Jaundice (cont’d) Minimal or severe depending on liver damage Late stages of cirrhosis Patient will usually be jaundiced Pruritus from accumulation of bile salts

Cirrhosis Clinical Manifestations Skin lesions Due to increase in circulating estrogen from liver’s inability to metabolize steroid hormones

Cirrhosis Clinical Manifestations Skin lesions (cont’d) Spider angiomas Small dilated blood vessels with bright red center and spiderlike branches Nose, cheeks, upper trunk, neck, shoulders Palmar erythema Red area on palms of bands that blanches with pressure

Cirrhosis Clinical Manifestations Endocrine disorders Steroid hormones of the adrenal cortex (aldosterone), testes, and ovaries are metabolized and inactivated by the normal liver Damaged liver is unable to metabolize these hormones and various manifestations occur

Cirrhosis Clinical Manifestations Endocrine disturbances Alteration in hair distribution due to ↑ estrogen Hyperaldosterism Sodium retention/potassium loss

Cirrhosis Clinical Manifestations Hematologic disorders Splenomegaly From backup of blood from portal vein Bleeding tendencies Decreased production of hepatic clotting factors

Cirrhosis Clinical Manifestations Peripheral neuropathy Dietary deficiencies of thiamine, folic acid, and vitamin B12

Cirrhosis Complications Portal hypertension Esophageal and gastric varices Peripheral edema and ascites Hepatic encephalopathy Hepatorenal syndrome

Cirrhosis Complications Portal hypertension Characterized by Increased venous pressure in portal circulation Splenomegaly Ascites Large collateral veins Esophageal varices Systemic hypertension

Cirrhosis Complications Portal hypertension (cont’d) Primary mechanism is the increased resistance to blood flow through the liver

Cirrhosis Complications Portal hypertension (cont’d) Esophageal varices Complex of tortuous veins at lower end of esophagus Develop in areas where collateral and systemic circulations communicate

Cirrhosis Complications Esophageal varices (cont’d) Contain little elastic tissue and are fragile Bleeding esophageal varices Most life-threatening complication of cirrhosis 80% of variceal hemorrhages

Cirrhosis Complications Portal hypertension (cont’d) Gastric varices Located in upper portion of stomach 20% of variceal hemorrhages

Cirrhosis Complications Portal hypertension (cont’d) Internal hemorrhoids Occur because of the dilation of the mesenteric veins and rectal veins Caput medusae Ring of varices around the umbilicus

Cirrhosis Complications Peripheral edema and ascites Edema ↓ Colloidal oncotic pressure from impaired liver synthesis of albumin ↑ Portacaval pressure from portal hypertension Occurs as ankle/presacral edema

Cirrhosis Complications Peripheral edema and ascites (cont’d) Ascites Accumulation of serous fluid in peritoneal or abdominal cavity Abdominal distention with weight gain Common manifestation of cirrhosis

Ascites and Gynecomastia Fig. 44-8

Cirrhosis Complications Ascites (cont’d) Factors involved in the pathogenesis ↓ Serum colloidal oncotic pressure ↑ Levels of aldosterone Portal hypertension ↑ Flow hepatic lymph Impaired water excretion

Development of Ascites Fig. 44-7

Cirrhosis Complications Hepatic encephalopathy Neuropsychiatric manifestation Terminal complication in liver disease

Cirrhosis Complications Hepatic encephalopathy (cont’d) Etiologic factors Disorder of protein metabolism and excretion Liver unable to convert ammonia to urea or blood shunted pass liver through so ammonia stays in systemic circulation Ammonia crosses blood-brain barrier and causes neurologic toxic manifestations

Cirrhosis Complications Hepatic encephalopathy (cont’d) Etiologic factors (cont’d) Altered astrocyte function Regulate blood-brain barrier and detoxification of ammonia

Cirrhosis Complications Hepatic encephalopathy (cont’d) Clinical manifestations Changes in neurologic and mental responsiveness Ranging from sleep disturbance to lethargy to deep coma

Cirrhosis Complications Hepatic encephalopathy (cont’d) Grading system used to classify stages Stages 0–4 4 is most advanced Asterixis Characteristic symptom Flapping tremors involving arms and hands

Cirrhosis Complications Hepatic encephalopathy (cont’d) Fetor hepaticus Musty, sweet odor on patient’s breath Accumulation of digestive by-products liver is unable to degrade

Cirrhosis Complications Hepatorenal syndrome Serious complication of cirrhosis Functional renal failure with Azotemia Oliguria Intractable ascites

Cirrhosis Complications Hepatorenal syndrome (cont’d) No structural abnormality of kidney Splanchnic and systemic vasodilation and ↓ arterial blood volume Renal vasoconstriction occurs with renal failure

Cirrhosis Diagnostic Studies History/physical examination Laboratory tests Liver function tests Serum electrolytes CBC

Cirrhosis Diagnostic Studies Laboratory tests (cont’d) Prothrombin time Serum albumin Stool for occult blood Analysis of ascitic fluid

Cirrhosis Diagnostic Studies Esophagogastroduodenoscopy Liver biopsy Barium swallow Liver scan Liver ultrasound Angiography

Cirrhosis Collaborative Care Rest Administration of B-complex vitamins Avoidance of alcohol, aspirin, acetaminophen, and NSAIDs Management of ascites

Cirrhosis Collaborative Care Prevention and management of esophageal variceal bleeding Management of encephalopathy

Cirrhosis Collaborative Care Ascites High-carbohydrate, low-Na+ diet (2 g/day) Diuretics Paracentesis Removes fluid from abdominal cavity Temporary measure

Cirrhosis Collaborative Care Ascites (cont’d) Peritoneovenous shunt Continuous reinfusion of ascitic fluid from the abdomen to the vena cava Not first-line therapy Complications—thrombosis, infection, fluid overload, DIC

Peritoneovenous Shunt Fig. 44-9

Cirrhosis Collaborative Care Esophageal and gastric varices Goal: avoid bleeding/hemorrhage Avoid alcohol, aspirin, and irritating foods Respiratory infection promptly treated

Cirrhosis Collaborative Care If bleeding occurs, stabilize patient, manage the airway, IV therapy IV vasopressin to control bleeding Nitroglycerin to decrease side effects of vasopressin

Cirrhosis Collaborative Care Endoscopic sclerotherapy Treatment for acute/chronic bleeding varices Agent (morrhuate [Scleromate]) Thromboses and obliterates distended veins

Cirrhosis Collaborative Care Endoscopic ligation Banding of varices Fewer complications than sclerotherapy Balloon tamponade Controls hemorrhage by compression of varices Uses Sengstaken-Blakemore tube

Sengstaken-Blakemore Tube Fig. 44-10

Cirrhosis Collaborative Care Supportive measures for acute bleed Fresh frozen plasma Packed RBCs Vitamin K Histamine receptor blockers Proton pump inhibitors Neomycin

Cirrhosis Collaborative Care Long-term management Propranolol (Inderal) to prevent recurrent GI bleed High incidence of recurrent bleed with high mortality risk with each repeat

Cirrhosis Collaborative Care Shunting procedures Used more after second major bleeding episode Surgical versus nonsurgical

Cirrhosis Collaborative Care Nonsurgical procedure Transjugular intrahepatic portosystemic shunt (TIPS) Tract (shunt) between systemic and portal venous system Used to redirect portal blood flow Decreases portal venous pressure and decompresses varices

Total Portal Division After TIPS Fig. 44-11

Cirrhosis Collaborative Care Surgical procedures Used more in emergency situations Portacaval shunt Decreases bleeding episodes Does not prolong life; patient dies of hepatic encephalopathy

Cirrhosis Collaborative Care Surgical procedures (cont’d) Distal splenorenal shunt (Warren shunt) Leaves portal venous flow intact ↓ Incidence of hepatic encephalopathy With time blood flow to liver ↓

Portosystemic Shunts Fig. 44-12

Cirrhosis Collaborative Care Hepatic encephalopathy Goal: Decrease ammonia formation Sterilization of GI tract with antibiotics (e.g., neomycin) Lactulose (Cephulac) traps NH3 in gut Cathartics/enemas

Cirrhosis Collaborative Care Drug therapy No specific drug therapy Drugs are used to treat symptoms and complications of advanced liver disease

Nutritional Therapy Diet for patient without complications High in calories (3000 kcal/day) ↑ CHO Moderate to low fat Protein restriction rarely justified

Nutritional Therapy Protein supplements if protein-calorie malnutrition Low-sodium diet for patient with ascites and edema

Nursing Management Nursing Assessment Past health history Chronic alcoholism Viral hepatitis Physical examination Medications Weight loss Jaundice

Nursing Management Nursing Assessment Abdominal distention Nausea/vomiting Altered mentation RUQ pain Abnormal laboratory values

Nursing Management Nursing Diagnoses Imbalanced nutrition: Less than body requirements Impaired skin integrity Ineffective breathing pattern Excess fluid volume Dysfunctional family processes: Alcoholism

Nursing Management Planning Overall goals Relief of discomfort Minimal to no complications Return to as normal a lifestyle as possible

Nursing Management Nursing Implementation Health promotion Treat alcoholism Identify hepatitis early and treat Stress importance of adequate nutrition Identify biliary disease early and treat

Nursing Management Nursing Implementation Acute intervention Rest Oral hygiene Between-meal nourishment Dietary restrictions explained

Nursing Management Nursing Implementation Acute intervention (cont’d) Accurate I/O Daily weights Abdominal girth Kneeling position, if possible Extremities measurement

Nursing Management Nursing Implementation Acute intervention (cont’d) Paracentesis Patient void immediately before High Fowler’s or side of bed Monitor for electrolyte imbalances Monitor dressing for bleeding/leakage

Nursing Management Nursing Implementation Acute intervention (cont’d) Check respiratory status frequently Semi or high Fowler’s Skin care Turning schedule q2h ROM exercises Coughing/deep breathing exercises

Nursing Management Nursing Implementation Acute intervention (cont’d) Monitor for electrolyte disturbances Diuretic therapy alters electrolytes Hypokalemia Cardiac dysrhythmias, hypotension, tachycardia, muscle weakness Observe for bleeding disorders Always supportive listener

Nursing Management Nursing Implementation Acute intervention (cont’d) Bleeding varices Close observation for signs of bleeding Balloon tamponade care Explanation of procedure Check for patency Position of balloon verified by x-ray Deflation of balloon q8–12h Lumens labeled

Nursing Management Nursing Implementation Acute intervention (cont’d) Balloon tamponade (cont’d) Saline lavage/NG suction to remove blood Monitor for complications Most common—aspiration pneumonia Scissors at bedside Semi-Fowler’s position Oral/nasal care

Nursing Management Nursing Implementation Acute intervention (cont’d) Hepatic encephalopathy Maintain safe environment Assess carefully Level of responsiveness Sensory and motor abnormalities Fluid/electrolyte imbalances Acid–base balance Effect treatment measures

Nursing Management Nursing Implementation Acute intervention (cont’d) Hepatic encephalopathy (cont’d) Neurologic status q2h Prevention of constipation Limit physical activity Control hypokalemia Ensure proper nutrition

Nursing Management Nursing Implementation Ambulatory and home care Symptoms of complications Written instructions with adequate explanations for patient/family When to seek medical attention Remission maintenance Abstinence from alcohol Caring attitude always

Nursing Management Evaluation Maintenance of food/fluid intake to meet needs Maintenance of muscle tone and energy Maintenance of skin integrity Normalization of fluid balance Maintenance of blood pressure and urinary output Reports increased ease of breathing Experiences normal respiratory rate/rhythm