1. LIVER CIRRHOSIS
• The word quot;cirrhosisquot; derives from Greek kirrhos, meaning quot;tawnyquot; (the orange-
yellow colour of the diseased liver).
• It is a consequence of chronic liver disease characterized by replacement of liver
tissue by fibrous scar tissue as well as regenerative nodules (lumps that occur as a
result of a process in which damaged tissue is regenerated), leading to progressive
loss of liver function.
• It is most commonly caused by alcoholism, hepatitis B and C and fatty liver disease
but has many other possible causes.
• Some cases are of unknown cause, but most of these are probably due to previously
unrecognized fatty liver disease.
• The diseases that lead to cirrhosis do so because they injure and kill liver cells and
the inflammation and repair that is associated with the dying liver cells causes scar
tissue to.
• Cirrhosis is generally irreversible once it occurs, and treatment generally focuses on
preventing progression and complications.
Signs and symptoms
Patients with cirrhosis may have few or no symptoms and signs of liver disease. Some
of the symptoms may be nonspecific, that is, they don't suggest that the liver is their cause.
Some of the more common symptoms and signs of cirrhosis include:
Yellowing of the skin (jaundice)
•
Fatigue
•
Weakness
•
Loss of appetite
•
Itching
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Easy bruising from decreased production of blood clotting factors by the diseased
•
liver.
Some of the following signs and symptoms may occur in the presence of cirrhosis or as a
result of the complications of cirrhosis. Many are nonspecific and may occur in other
diseases and do not necessarily point to cirrhosis. Likewise, the absence of any does not
rule out the possibility of cirrhosis.
Spider angiomata or spider nevi - vascular lesions consisting of a central arteriole
•
surrounded by many smaller vessels due to an increase in estradiol.
Palmar erythema. Exaggerations of normal speckled mottling of the palm, due to
•
altered sex hormone metabolism.
Nail changes.
•
o Muehrcke's nails - paired horizontal bands separated by normal color due to
hypoalbuminemia (low production of albumin).

2. Terry's nails - proximal two thirds of the nail plate appears white with distal
o
one-third red, also due to hypoalbuminemia
o Clubbing - angle between the nail plate and proximal nail fold > 180
degrees
Hypertrophic osteoarthropathy. Chronic proliferative periostitis of the long bones
•
that can cause considerable pain.
Dupuytren's contracture. Thickening and shortening of palmar fascia that leads to
•
flexion deformities of the fingers. Thought to be due to fibroblastic proliferation
and disorderly collagen deposition. It is relatively common (33% of patients).
Gynecomastia. Benign proliferation of glandular tissue of male breasts presenting
•
with a rubbery or firm mass extending concentrically from the nipples. This is due
to increased estradiol and can occur in up to 66% of patients.
Hypogonadism. Manifested as impotence, infertility, loss of sexual drive, and
•
testicular atrophy due to primary gonadal injury or suppression of hypothalamic or
pituitary function.
Liver size. Can be enlarged, normal, or shrunken.
•
Splenomegaly (increase in size of the spleen). Due to congestion of the red pulp as a
•
result of portal hypertension.
Ascites. Accumulation of fluid in the peritoneal cavity giving rise to flank dullness
•
(needs about 1500 mL to detect flank dullness). It may be associated with hydrocele
and penile flomation (swelling of the penile shaft) in men.
Caput medusa. In portal hypertension, the umbilical vein may open. Blood from the
•
portal venous system may be shunted through the periumbilical veins into the
umbilical vein and ultimately to the abdominal wall veins, manifesting as caput
medusa.
Cruveilhier-Baumgarten murmur. Venous hum heard in epigastric region (on
•
examination by stethoscope) due to collateral connections between portal system
and the remnant of the umbilical vein in portal hypertension.
Fetor hepaticus. Musty odor in breath due to increased dimethyl sulfide.
•
Jaundice. Yellow discoloring of the skin, eye, and mucus membranes due to
•
increased bilirubin (at least 2-3 mg/dL or 30 mmol/L). Urine may also appear dark.
Asterixis. Bilateral asynchronous flapping of outstretched, dorsiflexed hands seen in
•
patients with hepatic encephalopathy.
Others. Weakness, fatigue, anorexia, weight loss.
•
4 major types of Liver Cirrhosis
Definition Etiology
1. Post Necrotic Cirrhosis - most common worldwide - post acute viral hepatitis
- most massive loss of liver
cells, wit irregular patterns
of regenerating cells
2. Biliary Cirrhosis - bile flow decreased with Primary:
concurrent cell damage to Chronic stasis of the bile in
hepatocytes around the bile intrahepatic ducts
ductules -autoimmune process

3. implicated
Secondary:
- Obstruction of bile ducts
outside the liver.
3. Cardiac Cirrhosis Chronic liver disease - Atriventricular valve dse
associated with right sided - prolonged constructive
heart failure. peritonitis
- decompensated core
pulmonale
4. Alcoholic Cirrhosis Small nodules form as a Associated with alcohol
result of persistence of some abuse
aoffending agents.
Complications
Edema and ascites
• As cirrhosis of the liver becomes severe, signals are sent to the kidneys to retain salt
and water in the body. The excess salt and water first accumulates in the tissue
beneath the skin of the ankles and legs because of the effect of gravity when
standing or sitting.
• Spontaneous bacterial peritonitis (SBP)
Fluid in the abdominal cavity (ascites) is the perfect place for bacteria to grow. In
cirrhosis, the fluid that collects in the abdomen is unable to resist infection normally. In
addition, more bacteria find their way from the intestine into the ascites.
• Bleeding from esophageal varices
In the cirrhotic liver, the scar tissue blocks the flow of blood returning to the heart
from the intestines and raises the pressure in the portal vein (portal hypertension). When
pressure in the portal vein becomes high enough, it causes blood to flow around the liver
through veins with lower pressure to reach the heart. The most common veins through
which blood bypasses the liver are the veins lining the lower part of the esophagus and the
upper part of the stomach.
• Hepatic encephalopathy

4. When the toxic substances accumulate sufficiently in the blood, the function of the
brain is impaired, a condition called hepatic encephalopathy.
• Hepatorenal syndrome
Patients with worsening cirrhosis can develop the hepatorenal syndrome. This
syndrome is a serious complication in which the function of the kidneys is reduced.
• Hepatopulmonary syndrome
These patients can experience difficulty breathing because certain hormones
released in advanced cirrhosis cause the lungs to function abnormally. Blood flowing
through the lungs is shunted around the alveoli and cannot pick up enough oxygen from the
air in the alveoli.
• Hypersplenism
As the pressure in the portal vein rises in cirrhosis, it increasingly blocks the flow
of blood from the spleen. The blood quot;backs-upquot; and accumulates in the spleen, and the
spleen swells in size, a condition referred to as splenomegaly. As the spleen enlarges, it
filters out more and more of the blood cells and platelets until their numbers in the blood
are reduced. Hypersplenism is the term used to describe this condition.
• Liver cancer (hepatocellular carcinoma)
Cirrhosis due to any cause increases the risk of primary liver cancer (hepatocellular
carcinoma). Primary refers to the fact that the tumor originates in the liver. A secondary
liver cancer is one that originates elsewhere in the body and spreads (metastasizes) to the
liver.
Causes
Alcohol
•
Nonalcoholic fatty liver disease (NAFLD)
•
Cryptogenic cirrhosis (cirrhosis due to unidentified causes)
•
Chronic viral hepatitis
•
Inherited (genetic) disorders
•
Primary biliary cirrhosis (PBC
•
Primary sclerosing cholangitis (PSC
•
Autoimmune
•
Infants can be born without bile ducts (biliary atresia)
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Less common causes of cirrhosis include unusual reactions to some drugs and
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prolonged exposure to toxins, as well as chronic heart failure (cardiac cirrhosis).
Hereditary hemochromatosis.
•
Wilson's disease.
•
Alpha 1-antitrypsin deficiency (AAT).
•

5. Cardiac cirrhosis
•
Galactosemia
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Glycogen storage disease type IV
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Cystic fibrosis
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Drugs or toxins
•
Certain parasitic infections (such as schistosomiasis)
•
Etiology
INCIDENCE
Cirrhosis has a worldwide prevalence of approximately 5/100,000 and an annual
incidence of approximately 6/1,000,000. The prevalence and incidence appear to be similar
in different regions of the world. About 90% of patients with PBC are women. Most
commonly, the disease is diagnosed in patients between the ages of 40 and 60 years.
• United States
Using statistics from 1976-1980, the National Digestive Diseases Information
Clearinghouse (NDDIC) quotes a prevalence of 400,000 persons in the United States who
have cirrhosis or some other type of chronic liver disease.2
• International
Cirrhosis is among the leading causes of death, and a disturbing epidemic of hepatitis has
contributed to a rising incidence of HCCA, a serious complication of chronic hepatitis and
cirrhosis. Using official death certification data from 1955-1990, derived from the World
Health Organization (WHO) database, an analysis was made of cirrhosis-related trends in
mortality rates in 38 countries (2 countries from North America, 6 from Latin America, 5
from Asia, 23 from Europe, 1 each from Australia and New Zealand). 3 The study found
that the highest reported death rates occurred in Chile and Mexico (60 deaths per 100,000
males; 15 deaths per 100,000 females) during the late 1980s.
Race
Generally, the regions of highest prevalence of HCCA occur in Asia, South Africa, and
some areas of the Middle East. Susceptibility to the disease is believed to be based not on
race but rather on prevalent environmental factors, including epidemiologic factors and
exposure to environmental toxins (such as aflatoxin). In the United States, death rates from
HCCA between 1980 and 1989 were 50% higher in the black population than in the white
population.

6. Sex
The male-to-female ratio for cirrhosis is 1.5-3:1 (see Frequency/International), based on
etiologic differences. Ethanol-related cirrhosis has a male predominance, but primary
biliary cirrhosis (accounting for only 1.5% of deaths from cirrhosis) has a female
predominance.
Age
Age-specific death rates in the United States tend to be the highest in the older age ranges,
peaking at 49 per 100,000 in males aged 65-74 years and at 26.7 per 100,000 in women
aged 75-84 years.

7. Pathophysiology
Predisposing Factors Precipitating Factors
acetaldehyde
Injury to stromal cells
Abnormal damage of
the injured tissue with
Liver inflammation Parengchymal damage fibrotic tissues
Dec
Decrease Dec Liver Failure
detoxification
bilirubin metabolism
metabolism of CHON
Dec ADH &
or biliary
Dec androgen aldosterone
tree damage
and estrogen detoxification
detoxification
Dec
plasma
Conjugat Inc Waste
CHON
Fluid
ed & products
retenti
unconjug
on
ated
Ascites/
Palmar Renal
edema
Jaundice Erythema, Hepatic Ascites
/edema
spider Syndrom
angiomas, loss e
body hair,
Dec bile
Testicular Inability to
in GIT
atrophy, metabolized
and inc
Gynecomastia, ammonia to urea
azotemia
urobilino
Menstrual
gen
changes
Hepatic
azotemia
Clay Dark enceph
-colored urine
urine
Hepatic
coma
Diffuse fibrosis
Obstruction of normal blood flow
Portal hypertension

8. splenomegaly
Superficial Esophageal Rectal vein engorgement
abdominal engorgement
Destruction of
varices
blood cell
hemorrhoids
bleeding Ruptured of
esophageal
pancetopenia
vein
bleeding
UGI bleeding
Dec RBC Dec WBC Dec plt
hypovolemia
Anemia Infection Bleeding
shock
Dec. CHON synthesis
hypoalbuminemia infection Dec. Fibrogen Dec. vit. K
synthesis
Dec. Dec. clotting mech
colloidal
oncotic
pressure
bleeding
Fluid
shifting
Ascites/
edema
Mgt:
Bleeding Precautions
Tx:
Diuretics, fluid
restriction

9. Diagnosis
The gold standard for diagnosis of cirrhosis is a liver biopsy, through a
percutaneous, transjugular, laparoscopic, or fine-needle approach. Histologically cirrhosis
can be classified as micronodular, macronodular, or mixed, but this classification has been
abandoned since it is nonspecific to the etiology, it may change as the disease progresses,
and serological markers are much more specific. However, a biopsy is not necessary if the
clinical, laboratory, and radiologic data suggests cirrhosis. Furthermore, there is a small but
significant risk to liver biopsy, and cirrhosis itself predisposes for complications due to
liver biopsy.
Lab findings
The following findings are typical in cirrhosis:
Aminotransferases - AST and ALT are moderately elevated, with AST > ALT.
•
However, normal aminotransferases do not preclude cirrhosis.
Alkaline phosphatase - usually slightly elevated.
•
GGT – correlates with AP levels. Typically much higher in chronic liver disease
•
from alcohol.
Bilirubin - may elevate as cirrhosis progresses.
•
Albumin - levels fall as the synthetic function of the liver declines with worsening
•
cirrhosis since albumin is exclusively synthesized in the liver
Prothrombin time - increases since the liver synthesizes clotting factors.
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Globulins - increased due to shunting of bacterial antigens away from the liver to
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lymphoid tissue.
Serum sodium - hyponatremia due to inability to excrete free water resulting from
•
high levels of ADH and aldosterone.
Thrombocytopenia - due to both congestive splenomegaly as well as decreased
•
thrombopoietin from the liver. However, this rarely results in platelet count <
50,000/mL.
Leukopenia and neutropenia - due to splenomegaly with splenic margination.
•
Coagulation defects - the liver produces most of the coagulation factors and thus
•
coagulopathy correlates with worsening liver disease.
Other laboratory studies performed in newly diagnosed cirrhosis may include:

10. Serology for hepatitis viruses, autoantibodies (ANA, anti-smooth muscle, anti-
•
mitochondria, anti-LKM)
Ferritin and transferrin saturation (markers of iron overload), copper and
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ceruloplasmin (markers of copper overload)
Immunoglobulin levels (IgG, IgM, IgA) - these are non-specific but may assist in
•
distinguishing various causes
Cholesterol and glucose
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Alpha 1-antitrypsin
•
Imaging
Ultrasound is routinely used in the evaluation of cirrhosis, where it may show a
small and nodular liver in advanced cirrhosis along with increased echogenicity with
irregular appearing areas. Ultrasound may also screen for hepatocellular carcinoma, portal
hypertension and Budd-Chiari syndrome (by assessing flow in the hepatic vein).
Endoscopy
Gastroscopy (endoscopic examination of the esophagus, stomach and duodenum) is
performed in patients with established cirrhosis to exclude the possibility of esophageal
varices. If these are found, prophylactic local therapy may be applied (sclerotherapy or
banding) and beta blocker treatment may be commenced.
MEDICAL MANAGEMENT
Medications are used to treat the complications and effects of cirrhosis; they do not
reverse or slow the process of cirrhosis itself. Known hepatotoxic drugs and alcohol are
avoided, as are drugs metabolized by the liver (e.g. barbiturates, sedatives, hypnotics, and
acetaminophen).
• Diuretics reduce fluid retention and ascites. Spironolactone is frequently the drug of
choice because it addresses one of the causes of ascites- increased aldosterone
levels.
• Medications to reduce the nitrogenous load and lower serum ammonia levels are
added when manifestations of hepatic encephalopathy develop. The commonly
administered medications are lactulose and neomycin.
• The beta-blocker nadolol (Corgard) may be given together with isosorbide
mononitrate to prevent rebleeding of esophageal varices. This drug combination
also lowers hepatic venous pressure.
• Ferrous sulfate and folic acid are given as indicated to treat anemia. Vitamin K may
be ordered to reduce the risk of bleeding. When bleeding is acute, packed RBCs,
fresh frozen plasma, or platelets may be administered to restore blood components
and promote hemostasis.
• Antacids are prescribed as indicated.

11. • Oxazepam (Serax), a benzodiazepine antianxiety/ sedative drug, is not metabolized
by the liver, and may be used to treat acute agitation.
Generally, liver damage from cirrhosis cannot be reversed, but treatment could stop or
delay further progression and reduce complications. A healthy diet is encouraged, as
cirrhosis may be an energy-consuming process. Close follow-up is often necessary.
Antibiotics will be prescribed for infections, and various medications can help with itching.
Laxatives, such as lactulose, decrease risk of constipation; their role in preventing
encephalopathy is limited.
Alcoholic cirrhosis caused by alcohol abuse is treated by abstaining from alcohol.
Treatment for hepatitis-related cirrhosis involves medications used to treat the different
types of hepatitis, such as interferon for viral hepatitis and corticosteroids for autoimmune
hepatitis. Cirrhosis caused by Wilson's disease, in which copper builds up in organs, is
treated with chelation therapy (e.g. penicillamine) to remove the copper.
SURGICAL MANAGEMENT
• Transplantation
If complications cannot be controlled or when the liver ceases functioning, liver
transplantation is necessary. Survival from liver transplantation has been improving over
the 1990s, and the five-year survival rate is now around 80%, depending largely on the
severity of disease and other medical problems in the recipient. In the United States, the
MELD score (online calculator) is used to prioritize patients for transplantation.
Transplantation necessitates the use of immune suppressants (cyclosporine or tacrolimus).
NURSING MANAGEMENT
• Excess fluid volume
 Weight daily. Assess for JVD, measure abdominal girth daily, and check for
peripheral edema. Monitor intake and output.
 Assess urine specific gravity.
 Provide low-sodium diet and restrict fluids as ordered.
• Disturbed thought processes
 Assess neurologic status, including level of consciousness, and mental
status. Observe for signs of early encephalopathy: changes in handwriting,
speech, and asterixis.
 Avoid factors that may precipitate hepatic encephalopathy. Avoid
hepatotoxic medications and CNS depressant drugs.
 If possible, plan for consistent nursing care assignments.

12.  Provide low-protein diet as prescribed; teach the family the importance of
maintaining diet restrictions.
 Administer medications or enemas as ordered to reduce nitrogenous
products. Monitor bowel function and provide measures to promote regular
elimination and prevent constipation.
 Orient to surroundings, person, and place; provide simple explanations and
reassurance.
• Ineffective protection
 Monitor VS; report tachycardia or hypotension
 Institute bleeding precautions
 Monitor coagulation studies and platelet count. Report abnormal results.
 Carefully monitor the client who has had bleeding esophageal varices for
evidence of rebleeding: hematemesis, hematochezia or tarry stools, signs
and symptoms of hypovolemia or shock.
• Impaired skin integrity
 Use warm water rather than hot water when bathing.
 Use measures to prevent dry skin
 If indicated, apply mittens to hands to prevent scratching.
 Institute measures to prevent skin and tissue breakdown
 Administer prescribed antihistamine cautiously.
• Imbalanced nutrition: less than body requirements
 Weight daily
 Provide small meals with between meal snacks
 Unless protein is restricted due to impending hepatic encephalopathy,
promote protein and nutrient intake by providing nutritional supplements
such as Ensure or instant breakfast.
 Arrange for consultation with a dietician for diet planning while
hospitalized and at home.