Transcript Cirrhosis and Liver Failure

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
Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
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.
Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
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.
Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
4
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
Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
5
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.
Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
6
Etiology and Pathophysiology
 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
Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
7
Etiology and Pathophysiology
 Biliary cirrhosis
• Associated with chronic biliary
obstruction
• Diffuse fibrosis of liver with jaundice
 Cardiac cirrhosis
• From long-standing severe right-sided
heart failure
Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
8
Clinical Manifestations
Early manifestations
• Onset usually insidious
• GI disturbances:
 Anorexia
 Dyspepsia
 Flatulence
 Nausea/vomiting
 Change in bowel habits
Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
9
Clinical Manifestations
Early manifestations (cont’d)
• Abdominal pain
• Fever
• Lassitude
• Weight loss
• Enlarged liver or spleen
Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
10
Clinical Manifestations
Late manifestations
• Two causative mechanisms
 Hepatocellular failure
 Portal hypertension
Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
11
Pathophysiology of Cirrhosis
Fig. 44-5. Continuum of liver dysfunction in cirrhosis and resulting manifestations. ADH,
Antidiuretic hormone;ALT, alanine aminotransferase; AST, aspartate transaminase.
Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
12
Clinical Manifestations
Fig. 44-6. Systemic clinical manifestations of
liver cirrhosis.
Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
13
Clinical Manifestations
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
Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
14
Clinical Manifestations
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.
Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
15
Clinical Manifestations
• Skin lesions
 Due to increase in circulating estrogen
caused by inability of liver to
metabolize steroid hormones
Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
16
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
Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
17
Clinical Manifestations
• 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.
Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
18
Clinical Manifestations
• Hematologic disorders
 Splenomegaly
• From backup of blood from portal vein
 Bleeding tendencies
• Decreased production of hepatic clotting
factors
Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
19
Clinical Manifestations
• Peripheral neuropathy
 Dietary deficiencies of thiamine, folic
acid, and cobalamin (vitamin B12)
Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
20
Complications
•
•
•
•
•
Portal hypertension
Esophageal and gastric varices
Peripheral edema and ascites
Hepatic encephalopathy
Hepatorenal syndrome
Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
21
Complications
Portal hypertension
• Characterized by
 Increased venous pressure in portal
circulation
 Splenomegaly
 Ascites
 Large collateral veins
 Esophageal varices
 Systemic hypertension
Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
22
Complications
Portal hypertension (cont’d)
• Primary mechanism is increased
resistance to blood flow through the
liver.
Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
23
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
Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
24
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
Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
25
Complications
Portal hypertension (cont’d)
• Gastric varices
 Located in upper portion of stomach
 20% of variceal hemorrhages
Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
26
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
Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
27
Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
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
Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
29
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
Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
30
Ascites
Fig. 44-7. Mechanisms for development of ascites.
Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
31
Gross Ascites
Fig. 44-8. Gross ascites.
Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
32
Complications
• Ascites (cont’d)
 Factors involved in the pathogenesis
• ↓ Serum colloidal oncotic pressure
• ↑ Levels of aldosterone
• Portal hypertension
• ↑ Flow hepatic lymph
• Impaired water excretion
Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
33
Complications
Hepatic encephalopathy
• Neuropsychiatric manifestation
• Terminal complication in liver
disease
Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
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.
Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
35
Complications
Hepatic encephalopathy (cont’d)
• Etiologic factors (cont’d)
 Altered astrocyte function
• Regulate blood-brain barrier and
detoxification of ammonia
Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
36
Complications
Hepatic encephalopathy (cont’d)
• Clinical manifestations
 Changes in neurologic and mental
responsiveness
• Ranging from sleep disturbance to
lethargy to deep coma
Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
37
Complications
Hepatic encephalopathy (cont’d)
• Grading system used to classify stages
 Stages 0 through 4
 4 is most advanced.
• Asterixis
 Characteristic symptom
 Flapping tremors involving arms and hands
Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
38
Complications
Hepatic encephalopathy (cont’d)
• Fetor hepaticus
 Musty, sweet odor on patient’s breath
 Accumulation of digestive by-products
that liver is unable to degrade
Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
39
Complications
Hepatorenal syndrome
• Serious complication of cirrhosis
• Functional renal failure with
 Azotemia
 Oliguria
 Intractable ascites
Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
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.
Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
41
Diagnostic Studies
• History/physical examination
• Laboratory tests
 Liver function tests
 Serum electrolytes
 CBC
Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
42
Diagnostic Studies
• Laboratory tests (cont’d)
 Prothrombin time
 Serum albumin
 Stool for occult blood
 Analysis of ascitic fluid
• Liver biopsy
Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
43
Collaborative Care
• Rest
• Administration of B-complex
vitamins
• Avoidance of alcohol, aspirin,
acetaminophen, and NSAIDs
• Management of ascites
Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
44
Collaborative Care
• Prevention and management of
esophageal variceal bleeding
• Management of encephalopathy
Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
45
Collaborative Care
• Ascites
 High-carbohydrate, low-Na+ diet
(2 g/day)
 Diuretics
 Paracentesis
• Removes fluid from abdominal cavity
• Temporary measure
Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
46
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
Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
47
Collaborative Care
• Esophageal and gastric varices
 Goal: Avoid bleeding/hemorrhage
 Avoid alcohol, aspirin, and irritating
foods.
 Respiratory infection promptly treated
Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
48
Collaborative Care
 If bleeding occurs, stabilize patient,
manage airway, provide IV therapy.
 Drug therapy may include
• Octreotide (Sandostatin)
• Vasopressin (VP, Terlipressin)
• Nitroglycerin (NTG)
• β-adrenergic blockers
Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
49
Collaborative Care
• Endoscopic sclerotherapy
 Treatment for acute/chronic bleeding
varices
 Agent (morrhuate [Scleromate])
• Thromboses and obliterates distended
veins
Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
50
Collaborative Care
• Endoscopic ligation
 Banding of varices
 Fewer complications than
sclerotherapy
• Balloon tamponade
 Controls hemorrhage by compression
of varices
 Uses Sengstaken-Blakemore tube
Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
51
Sengstaken-Blakemore Tube
Fig. 44-9. A, Sengstaken-Blakemore tube. B, Tube inserted into esophagus and
stomach.
Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
52
Collaborative Care
• Supportive measures for acute bleed
 Fresh frozen plasma
 Packed RBCs
 Vitamin K
 Histamine receptor blockers
 Proton pump inhibitors
 Lactulose (Cephulac)
 Neomycin
Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
53
Collaborative Care
• Long-term management
 β-adrenergic blockers
 Repeated sclerotherapy/band ligation
 Portosystemic shunts
 Propranolol (Inderal)
Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
54
Collaborative Care
• Shunting procedures
 Used more after second major
bleeding episode
 Surgical vs. nonsurgical
Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
55
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
Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
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.
Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
57
Collaborative Care
• Surgical procedures
 Portacaval shunt
• Decreases bleeding episodes
• Does not prolong life; patient dies of
hepatic encephalopathy
Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
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.
Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
59
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 ↓
Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
60
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
 Treatment of precipitating cause
Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
61
Collaborative Care
• Drug therapy
 No specific drug therapy
 Drugs are used to treat symptoms and
complications of advanced liver
disease.
Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
62
Nutritional Therapy
• Diet for patient without
complications
 High in calories (3000 kcal/day)
 ↑ carbohydrate
 Moderate to low fat
 Protein restriction rarely justified
Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
63
Nutritional Therapy
• Protein supplements if proteincalorie malnutrition
• Low-sodium diet for patient with
ascites and edema
Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
64
Nursing Management
Nursing Assessment
• Past health history
 Chronic alcoholism
 Viral hepatitis
 Chronic biliary disease
•
•
•
•
Physical examination
Medications
Weight loss
Jaundice
Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
65
Nursing Management
Nursing Assessment
•
•
•
•
•
Abdominal distention
Nausea/vomiting
Altered mentation
RUQ pain
Abnormal laboratory values
Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
66
Nursing Management
Nursing Diagnoses
• Imbalanced nutrition: Less than
body requirements
• Impaired skin integrity
• Ineffective breathing pattern
• Excess fluid volume
• Dysfunctional family processes:
Alcoholism
Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
67
Nursing Management
Planning
• Overall goals
 Relief of discomfort
 Minimal to no complications
 Return to as normal a lifestyle as
possible
Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
68
Nursing Management
Nursing Implementation
• Health promotion
 Treat alcoholism.
 Identify hepatitis early and treat.
 Stress importance of adequate
nutrition.
 Identify biliary disease early and treat.
Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
69
Nursing Management
Nursing Implementation
• Acute intervention
 Rest
 Oral hygiene
 Between-meal nourishment
 Explanation of dietary restrictions
Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
70
Nursing Management
Nursing Implementation
• Acute intervention (cont’d)
 Accurate I/O
 Daily weights
 Abdominal girth
• Kneeling position, if possible
 Extremities measurement
Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
71
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.
Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
72
Nursing Management
Nursing Implementation
• Acute intervention (cont’d)
 Check respiratory status frequently.
• Semi- or high Fowler’s
 Skin care
• Turning schedule, at least every 2 hours
 ROM exercises
 Coughing/deep breathing exercises
Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
73
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 be a supportive listener.
Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
74
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
Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
75
Nursing Management
Nursing Implementation
• Acute intervention (cont’d)
• 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
Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
76
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
Effects of treatment measures
Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
77
Nursing Management
Nursing Implementation
• Acute intervention (cont’d)
 Hepatic encephalopathy (cont’d)
• Neurologic assessment every 2 hours
• Prevention of constipation
• Limited physical activity
• Control of hypokalemia
• Ensuring proper nutrition
Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
78
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
Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
79
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
Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
80
Nursing Management
Evaluation
• Maintenance of blood pressure and
urinary output
• Reports increased ease of breathing
• Experiences normal respiratory
rate/rhythm
Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
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.
Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
82
Case Study
Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
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
Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
84
Case Study
• Denies alcoholism and having more
than 3 oz of alcohol per day
 States “the girls and I have social
drinks”
Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
85
Case Study
• Review of old medical records shows
progressive weakness, weight loss,
anorexia, jaundice, edema, ascites,
and mental disorientation.
Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
86
Case Study
• Accepts treatment only during crises
• Upon admission, she is stuporous
and hypotensive, and has twitching
and asterixis.
Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
87
Case Study
• She is thin and malnourished with
marked edema on lower extremities
and ascites.
• Liver and spleen are both palpable.
Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
88
Case Study
• Jaundice and spider angiomas are
present.
• Evidence of bruising throughout
body
Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
89
Case Study
• Previous liver biopsies indicated
 At age 29, fatty liver
 At age 31, cirrhosis with hyaline
necrosis
Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
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%
Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
91
Discussion Questions
1. What clinical manifestations of
cirrhosis does she have?
2. Explain the results of her diagnostic
findings.
Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
92
Discussion Questions
3. What is the priority of care for her?
4. What patient and family teaching
is essential?
Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
93