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

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

3. Cirrhosis
Fig. 44-4

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

5. 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

6. 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

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

8. 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

9. 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

10. Manifestations of Liver Cirrhosis
Fig. 44-6

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

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

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

14. 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

15. 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

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

17. 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

18. 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

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

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

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

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

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

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

25. 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

26. 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

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

28. 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

30. 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

31. 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

32. Ascites and Gynecomastia
Fig. 44-8

33. 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

34. Development of Ascites
Fig. 44-7

35. Cirrhosis Complications
Hepatic encephalopathy
Neuropsychiatric manifestation
Terminal complication in liver disease

36. 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

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

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

39. 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

40. 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

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

42. 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

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

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

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

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

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

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

49. 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

50. Peritoneovenous Shunt
Fig. 44-9

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

52. 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

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

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

55. Sengstaken-Blakemore Tube
Fig

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

57. 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

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

59. 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

60. Total Portal Division After TIPS
Fig

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

62. 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 ↓

63. Portosystemic Shunts
Fig

64. 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

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

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

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

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

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

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

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

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

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

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

75. 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

76. 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

77. 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

78. 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

79. 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

80. 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

81. 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

82. 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

83. 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