Hepatic encephalopathy (cont'd)

Focus on

Cirrhosis of the Liver

(Relates to Chapter 44,

“Nursing Management:

Liver, Pancreas, and Biliary Tract Problems” in the textbook)

Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.

Description

• A chronic progressive disease of the liver

 Extensive parenchymal cell degeneration

 Destruction of parenchymal cells


2

Cirrhosis

Fig. 44-4. Cirrhosis that developed secondary to alcoholism. The characteristic diffuse nodularity of the surface is due to the combination of regeneration and scarring of the liver.


3

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 result.


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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


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Etiology and Pathophysiology

• Factors that can lead to cirrhosis

 Chronic alcohol abuse

• Excessive alcohol ingestion is the single most common cause of cirrhosis.

• Alcohol has a direct hepatotoxic effect.

• First change from excessive alcohol intake is fat accumulation in liver cells.

• With continued abuse, scar formation occurs.


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 Nonalcohol fatty liver disease (NAFLD)

 Malnutrition that occurs concurrently with excessive alcohol intake, extreme dieting, malabsorption, and obesity

 Environmental factors, as well as a genetic predisposition

 Postnecrotic cirrhosis

• Complication of viral, toxic, or idiopathic hepatitis


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 Biliary cirrhosis

• Associated with chronic biliary obstruction

• Diffuse fibrosis of liver with jaundice

 Cardiac cirrhosis

• From long-standing severe right-sided heart failure


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Clinical Manifestations

Early manifestations

• Onset usually insidious

• GI disturbances:

 Anorexia

 Dyspepsia

 Flatulence

 Nausea/vomiting

 Change in bowel habits


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Early manifestations (cont’d)

• Abdominal pain

• Fever

• Lassitude

• Weight loss

• Enlarged liver or spleen


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Late manifestations

• Two causative mechanisms

 Hepatocellular failure

 Portal hypertension


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Pathophysiology of Cirrhosis

Fig. 44-5. Continuum of liver dysfunction in cirrhosis and resulting manifestations. ADH,

Antidiuretic hormone; ALT, alanine aminotransferase; AST, aspartate transaminase.


12


Fig. 44-6. Systemic clinical manifestations of liver cirrhosis.


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Late manifestations (cont’d)

• Jaundice

 Decreased ability of liver cells to conjugate and excrete bilirubin

 Functional derangement of liver cells

 Compression of bile ducts by overgrowth of connective tissue


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Jaundice (cont’d)

 Minimal or severe, depending on liver damage

 Late stages of cirrhosis

• Patient usually will be jaundiced.

 If biliary tract obstructed, pruritus can occur.


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• Skin lesions

 Due to increase in circulating estrogen caused by inability of liver to metabolize steroid hormones


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• 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


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• Endocrine disorders

 Steroid hormones of the adrenal cortex, testes, and ovaries are metabolized and inactivated by the normal liver.

 Damaged liver is unable to metabolize these hormones, and various manifestations occur.


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• Hematologic disorders

 Splenomegaly

• From backup of blood from portal vein

 Bleeding tendencies

• Decreased production of hepatic clotting factors


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• Peripheral neuropathy

 Dietary deficiencies of thiamine, folic acid, and cobalamin (vitamin B

12

)


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Complications

• Portal hypertension

• Esophageal and gastric varices

• Peripheral edema and ascites

• Hepatic encephalopathy

• Hepatorenal syndrome


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Complications

Portal hypertension

• Characterized by

 Increased venous pressure in portal circulation

 Splenomegaly

 Ascites

 Large collateral veins

 Esophageal varices

 Systemic hypertension


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Complications

Portal hypertension (cont’d)

• Primary mechanism is increased resistance to blood flow through the liver.


23

Complications


• Esophageal varices

 Complex of tortuous veins at lower end of esophagus

 Develop in areas where collateral and systemic circulations communicate


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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


25

Complications


• Gastric varices

 Located in upper portion of stomach

 20% of variceal hemorrhages


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Complications


• Internal hemorrhoids

 Occur because of the dilation of the mesenteric veins and rectal veins

• Caput medusae

 Ring of varices around the umbilicus


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28

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


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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


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Ascites

Fig. 44-7. Mechanisms for development of ascites.


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Gross Ascites

Fig. 44-8. Gross ascites.


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Complications

• Ascites (cont’d)

 Factors involved in the pathogenesis

• ↓ Serum colloidal oncotic pressure

• ↑ Levels of aldosterone

• Portal hypertension

• ↑ Flow hepatic lymph

• Impaired water excretion


33

Complications

Hepatic encephalopathy

• Neuropsychiatric manifestation

• Terminal complication in liver disease


34

Complications

Hepatic encephalopathy (cont’d)

• Etiologic factors

 Disorder of protein metabolism and excretion

• Liver unable to convert ammonia to urea, or blood shunted past liver through, so ammonia stays in systemic circulation

• Ammonia crosses blood-brain barrier and causes neurologic toxic manifestations.


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Complications


• Etiologic factors (cont’d)

 Altered astrocyte function

• Regulate blood-brain barrier and detoxification of ammonia


36

Complications


• Clinical manifestations

 Changes in neurologic and mental responsiveness

• Ranging from sleep disturbance to lethargy to deep coma


37

Complications


• Grading system used to classify stages

 Stages 0 through 4

 4 is most advanced.

• Asterixis

 Characteristic symptom

 Flapping tremors involving arms and hands


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Complications


• Fetor hepaticus

 Musty, sweet odor on patient’s breath

 Accumulation of digestive by-products that liver is unable to degrade


39

Complications

Hepatorenal syndrome

• Serious complication of cirrhosis

• Functional renal failure with

 Azotemia

 Oliguria

 Intractable ascites


40

Complications

Hepatorenal syndrome (cont’d)

• No structural abnormality of kidney

• Splanchnic and systemic vasodilation and ↓ arterial blood volume

 Renal vasoconstriction occurs with renal failure.


41

Diagnostic Studies

• History/physical examination

• Laboratory tests

 Liver function tests

 Serum electrolytes

 CBC


42

Diagnostic Studies

• Laboratory tests (cont’d)

 Prothrombin time

 Serum albumin

 Stool for occult blood

 Analysis of ascitic fluid

• Liver biopsy


43

Collaborative Care

• Rest

• Administration of B-complex vitamins

• Avoidance of alcohol, aspirin, acetaminophen, and NSAIDs

• Management of ascites


44


• Prevention and management of esophageal variceal bleeding

• Management of encephalopathy


45


• Ascites

 High-carbohydrate, low-Na + diet

(2 g/day)

 Diuretics

 Paracentesis

• Removes fluid from abdominal cavity

• Temporary measure


46


• 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


47


• Esophageal and gastric varices

 Goal: Avoid bleeding/hemorrhage

 Avoid alcohol, aspirin, and irritating foods.

 Respiratory infection promptly treated


48


 If bleeding occurs, stabilize patient, manage airway, provide IV therapy.

 Drug therapy may include

• Octreotide (Sandostatin)

• Vasopressin (VP, Terlipressin)

• Nitroglycerin (NTG)

• β-adrenergic blockers


49


• Endoscopic sclerotherapy

 Treatment for acute/chronic bleeding varices

 Agent (morrhuate [Scleromate])

• Thromboses and obliterates distended veins


50


• Endoscopic ligation

 Banding of varices

 Fewer complications than sclerotherapy

• Balloon tamponade

 Controls hemorrhage by compression of varices

 Uses Sengstaken-Blakemore tube


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Sengstaken-Blakemore Tube

Fig. 44-9. A, Sengstaken-Blakemore tube. B, Tube inserted into esophagus and stomach.


52


• Supportive measures for acute bleed

 Fresh frozen plasma

 Packed RBCs

 Vitamin K

 Histamine receptor blockers

 Proton pump inhibitors

 Lactulose (Cephulac)

 Neomycin


53


• Long-term management

 β-adrenergic blockers

 Repeated sclerotherapy/band ligation

 Portosystemic shunts

 Propranolol (Inderal)


54


• Shunting procedures

 Used more after second major bleeding episode

 Surgical vs. nonsurgical


55


• 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


56

Total Portal Division After TIPS

Fig. 44-10. Total portal diversion after transjugular intrahepatic portosystemic shunt (TIPS). A, Portal venogram before TIPS shows filling of large esophageal varices (arrows). B, After insertion of a TIPS, flow to varices is eliminated. Intrahepatic portal vein flow is now reversed, with the direction of intrahepatic flow toward the TIPS.


57


• Surgical procedures

 Portacaval shunt

• Decreases bleeding episodes

• Does not prolong life; patient dies of hepatic encephalopathy


58

Portosystemic Shunts

Fig. 44-11. Portosystemic shunts. A, Portacaval shunt. The portal vein is anastomosed to the inferior vena cava, diverting blood from the portal vein to the systemic circulation. B, Distal splenorenal shunt. The splenic vein is anastomosed to the renal vein. The portal venous flow remains intact while esophageal varices are selectively decompressed. (The short gastric veins are decompressed.) The spleen conducts blood from the high pressure of the esophageal and gastric varices to the low-pressure renal vein.


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• Surgical procedures (cont’d)

 Distal splenorenal shunt (Warren shunt)

• Leaves portal venous flow intact

• ↓ Incidence of hepatic encephalopathy

• With time, blood flow to liver ↓


60


• Hepatic encephalopathy

 Goal: Decrease ammonia formation

• Sterilization of GI tract with antibiotics

(e.g., neomycin)

• Lactulose (Cephulac) traps NH3 in gut.

• Cathartics/enemas

 Treatment of precipitating cause


61


• Drug therapy

 No specific drug therapy

 Drugs are used to treat symptoms and complications of advanced liver disease.


62

Nutritional Therapy

• Diet for patient without complications

 High in calories (3000 kcal/day)

 ↑ carbohydrate

 Moderate to low fat

 Protein restriction rarely justified


63

Nutritional Therapy

• Protein supplements if proteincalorie malnutrition

• Low-sodium diet for patient with ascites and edema


64

Nursing Management

Nursing Assessment

• Past health history

 Chronic alcoholism

 Viral hepatitis

 Chronic biliary disease

• Physical examination

• Medications

• Weight loss

• Jaundice


65


Nursing Assessment

• Abdominal distention

• Nausea/vomiting

• Altered mentation

• RUQ pain

• Abnormal laboratory values


66


Nursing Diagnoses

• Imbalanced nutrition: Less than body requirements

• Impaired skin integrity

• Ineffective breathing pattern

• Excess fluid volume

• Dysfunctional family processes:

Alcoholism


67


Planning

• Overall goals

 Relief of discomfort

 Minimal to no complications

 Return to as normal a lifestyle as possible


68


Nursing Implementation

• Health promotion

 Treat alcoholism.

 Identify hepatitis early and treat.

 Stress importance of adequate nutrition.

 Identify biliary disease early and treat.


69



• Acute intervention

 Rest

 Oral hygiene

 Between-meal nourishment

 Explanation of dietary restrictions


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• Acute intervention (cont’d)

 Accurate I/O

 Daily weights

 Abdominal girth

• Kneeling position, if possible

 Extremities measurement


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 Paracentesis

• Patient void immediately before

• High Fowler’s or side of bed

• Monitor for electrolyte imbalances.

• Monitor dressing for bleeding/leakage.


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 Check respiratory status frequently.

• Semi- or high Fowler’s

 Skin care

• Turning schedule, at least every 2 hours

 ROM exercises

 Coughing/deep breathing exercises


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 Monitor for electrolyte disturbances.

• Diuretic therapy alters electrolytes.

• Hypokalemia

• Cardiac dysrhythmias, hypotension, tachycardia, muscle weakness

 Observe for bleeding disorders.

 Always be a supportive listener.


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 Bleeding varices

• Close observation for signs of bleeding

• Balloon tamponade care

• Explanation of procedure

• Check for patency.

• Position of balloon verified by x-ray


75




• Balloon tamponade (cont’d)

• Saline lavage/NG suction to remove blood

• Monitor for complications (i.e., aspiration pneumonia).

• Scissors at bedside

• Semi-Fowler’s position

• Oral/nasal care


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 Hepatic encephalopathy

• Maintain safe environment.

• Assess carefully.

• Level of responsiveness

• Sensory and motor abnormalities

• Fluid/electrolyte imbalances

• Acid-base balance

• Effects of treatment measures


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 Hepatic encephalopathy (cont’d)

• Neurologic assessment every 2 hours

• Prevention of constipation

• Limited physical activity

• Control of hypokalemia

• Ensuring proper nutrition


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• 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


79


Evaluation

• Maintenance of food/fluid intake to meet needs

• Maintenance of muscle tone and energy

• Maintenance of skin integrity

• Normalization of fluid balance


80


Evaluation

• Maintenance of blood pressure and urinary output

• Reports increased ease of breathing

• Experiences normal respiratory rate/rhythm


81

Audience Response Question

A patient with advanced cirrhosis with ascites is short of breath and has an increased respiratory rate. The nurse should:

1. Initiate oxygen therapy at 2 L/min to increase gas exchange.

2. Notify the health care provider so a paracentesis can be performed.

3. Ask patient to cough and deep breathe to clear respiratory secretions.

4. Place the patient in Fowler’s position to relieve pressure on the diaphragm.


82

Case Study


83

Case Study

• 35-year-old woman was admitted with hepatic coma.

• History of numerous hospitalizations since age 19

 Usually for psychosomatic and nervous disorders


84

Case Study

• Denies alcoholism and having more than 3 oz of alcohol per day

 States “the girls and I have social drinks”


85

Case Study

• Review of old medical records shows progressive weakness, weight loss, anorexia, jaundice, edema, ascites, and mental disorientation.


86

Case Study

• Accepts treatment only during crises

• Upon admission, she is stuporous and hypotensive, and has twitching and asterixis.


87

Case Study

• She is thin and malnourished with marked edema on lower extremities and ascites.

• Liver and spleen are both palpable.


88

Case Study

• Jaundice and spider angiomas are present.

• Evidence of bruising throughout body


89

Case Study

• Previous liver biopsies indicated

 At age 29, fatty liver

 At age 31, cirrhosis with hyaline necrosis


90

Case Study

• Laboratory values

 Total bilirubin 11 mg/dL

 AST 80 U/mL

 ALT 70 U/mL

 LDH 700 U/mL

 Serum ammonia 220 mg/dL

 WBC 21,450/uL

 Hematocrit 24%


91

Discussion Questions

1.

What clinical manifestations of cirrhosis does she have?

2.

Explain the results of her diagnostic findings.


92

Discussion Questions

3.

What is the priority of care for her?

4.

What patient and family teaching is essential?


93

Hepatic encephalopathy (cont'd)

Nursing Assessment

Nursing Assessment

Nursing Diagnoses

Planning

Evaluation

Evaluation

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Hepatic encephalopathy (cont'd)

Nursing Assessment

Nursing Assessment

Nursing Diagnoses

Planning

Evaluation

Evaluation

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