Cirrhosis of the Liver
Prepared by: Dr. ahlam Said.
Be a Good Doctor
Description
•A chronic, progressive disease of the liver
–Extensive parenchymal cell
degeneration
–Destruction of parenchymal cells
Description
•Regenerative process is disorganized,
resulting in abnormal blood vessel and
bile duct relationships from fibrosis
Description
•Normal lobular structure distorted by
fibrotic connective tissue
•Lobules are irregular in size and shape
with impaired vascular flow
•Insidious, prolonged course
Statistics
•> 50% of liver disease in the US is directly
related to alcohol consumption
•Of the estimated 15 million alcoholics in the
USA 10-20% have or will develop cirrhosis
Statistics
•Growing number of cases related to chronic
hepatitis C
•4th leading cause of death in people between
35 and 54 years of age
Statistics
•Direct correlation between alcohol
consumption in any geographic area and the
death rate from cirrhosis in that area
Etiology and Pathophysiology
•Cell necrosis occurs
•Destroyed liver cells are replaced by
scar tissue
•Normal architecture becomes nodular
Etiology and Pathophysiology
•Four types of cirrhosis:
–Alcoholic (Laennec’s) cirrhosis
–Postnecrotic cirrhosis
–Biliary cirrhosis
–Cardiac cirrhosis
Etiology and Pathophysiology
•Alcoholic (Laennec’s) Cirrhosis
–Associated with alcohol abuse
–Preceded by a theoretically reversible
fatty infiltration of the liver cells
–Widespread scar formation
Etiology and Pathophysiology
•Postnecrotic Cirrhosis
–Complication of toxic or viral hepatitis
–Accounts for 20% of the cases of
cirrhosis
–Broad bands of scar tissue form within
the liver
Etiology and Pathophysiology
•Biliary Cirrhosis
–Associated with chronic biliary
obstruction and infection
–Accounts for 15% of all cases of
cirrhosis
Etiology and Pathophysiology
•Cardiac Cirrhosis
–Results from longstanding severe
right-sided heart failure
Manifestations of Liver Cirrhosis
Fig. 42-5
Clinical Manifestations
Early Manifestations
•Onset usually insidious
•GI disturbances:
–Anorexia
–Dyspepsia
–Flatulence
–N-V, change in bowel habits
Clinical Manifestations
Early Manifestations
•Abdominal pain
•Fever
•Lassitude
•Weight loss
•Enlarged liver or spleen
Clinical Manifestations
Jaundice
•Occurs because of insufficient
conjugation of bilirubin by the liver cells,
and local obstruction of biliary ducts by
scarring and regenerating tissue
Clinical Manifestations
Jaundice
•Intermittent jaundice is characteristic of
biliary cirrhosis
•Late stages of cirrhosis the patient will
usually be jaundiced
Clinical Manifestations
Endocrine Disturbances
•Steroid hormones of the adrenal cortex
(aldosterone), testes, and ovaries are
metabolized and inactivated by the
normal liver
Clinical Manifestations
Endocrine Disturbances
•Alteration in hair distribution
–Decreased amount of pubic hair
–Axillary and pectoral alopecia
Clinical Manifestations
Hematologic Disorders
•Bleeding tendencies as a result of
decreased production of hepatic clotting
factors (II, VII, IX, and X)
Clinical Manifestations
Hematologic Disorders
•Anemia, leukopenia, and
thrombocytopenia are believed to be
result of hypersplenism
Clinical Manifestations
Peripheral Neuropathy
•Dietary deficiencies of thiamine, folic
acid, and vitamin B
12
Complications
•Portal hypertension and esophageal
varices
•Peripheral edema and ascites
•Hepatic encephalopathy
•Fetor hepaticus
Complications
Portal Hypertension
•Primary mechanism is the increased
resistance to blood flow through the liver
Complications
Portal Hypertension
Splenomegaly
•Back pressure caused by portal
hypertension ® chronic passive congestion
as a result of increased pressure in the
splenic vein
Complications
Portal Hypertension
Esophageal Varices
•Increased blood flow through the
portal system results in dilation
and enlargement of the plexus
veins of the esophagus and
produces varices
Complications
Portal Hypertension
Esophageal Varices
•Varices have fragile vessel walls
which bleed easily
Complications
Portal Hypertension
Internal Hemorrhoids
•Occurs because of the dilation of
the mesenteric veins and rectal
veins
Complications
Portal Hypertension
Caput Medusae
•Collateral circulation involves the
superficial veins of the abdominal wall
leading to the development of dilated
veins around the umbilicus
Complications
Peripheral Edema and Ascites
•Ascites:
- - Intraperitoneal accumulation of
watery fluid containing small
amounts of protein
Complications
Peripheral Edema and Ascites
•Factors involved in the pathogenesis of
ascites:
-Hypoalbuminemia
- Levels of aldosterone
- Portal hypertension
Complications
Hepatic Encephalopathy
•Liver damage causes blood to enter
systemic circulation without liver
detoxification
Complications
Hepatic Encephalopathy
•Main pathogenic toxin is NH
3
although
other etiological factors have been
identified
•Frequently a terminal complication
Complications
Fetor Hepaticus
•Musty, sweetish odor detected on the
patient’s breath
•From accumulation of digested by-
products
Collaborative Care
Ascites
•Peritoneovenous shunt
–Provides for continuous reinfusion of
ascitic fluid from the abdomen to the
vena cava
Peritoneovenous Shunt
Fig. 42-8
Collaborative Care
Esophageal Varices
•Avoid alcohol, aspirin, and irritating
foods
•If bleeding occurs, stabilize patient and
manage the airway, administer
vasopressin (Pitressin)
Collaborative Care
Esophageal Varices
•Endoscopic sclerotherapy or ligation
•Balloon tamponade
•Surgical shunting procedures (e.g.,
portacaval shunt, TIPS)
Sengstaken-Blakemore Tube
Fig. 42-9
Portosystemic Shunts
Fig. 42-11
Collaborative Care
Hepatic Encephalopathy
•Goal: reduce NH
3
formation
–Protein restriction (0-40g/day)
–Sterilization of GI tract with antibiotics
(e.g., neomycin)
–lactulose (Cephulac) – traps NH
3
in gut
–levodopa
Drug Therapy
•There is no specific drug therapy for
cirrhosis
•Drugs are used to treat symptoms and
complications of advanced liver disease
Nutritional Therapy
•Diet for patient without complications:
–High in calories
F CHO
–Moderate to low fat
–Amount of protein varies with degree
of liver damage
Nutritional Therapy
•Patient with hepatic encephalopathy
–Very low to no-protein diet
•Low sodium diet for patient with ascites
and edema
Nursing Management
Nursing Assessment
•Past health history
•Medications
•Chronic alcoholism
•Weight loss
Nursing Management
Nursing Diagnoses
•Imbalanced nutrition: less than body
requirements
•Impaired skin integrity
•Ineffective breathing pattern
•Risk for injury
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
–Identify biliary disease early and treat
Nursing Management
Nursing Implementation
•Acute Intervention
–Rest
–Edema and ascites
–Paracentesis
–Skin care
–Dyspnea
–Nutrition
Nursing Management
Nursing Implementation
•Ambulatory and Home Care
–Symptoms of complications
–When to seek medical attention
–Remission maintenance
–Abstinence from alcohol
Nursing Management
Evaluation
•Maintenance of normal body weight
•Maintenance of skin integrity
•Effective breathing pattern
•No injury
•No signs of infection