Liver cirrhosis

BY: MR.J.G SAMBAD
M.SC.NURSING
IKDRC COLLEGE OF NURSING JG SAMBAD

"With ordinary talent and
extraordinary perseverance, all
things are attainable."
- Thomas E. Buxton
"Achievement is connected
with action, not in genes..…!”
- Conrad Hilton
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 1.5 kg, wedge
shape
 4 lobes, Right, left,
Caudate, Quadrate.
 Double blood
supply
 Hepatic arteries
 Portal – Venous
blood
 Acini / Portal triad.
 Lobules – central. V
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 Metabolism – Carbohydrate, Fat & Protein
 Secretory – bile, Bile acids, salts & pigments
 Excretory – Bilirubin, drugs, toxins
 Synthesis – Albumin, coagulation factors
 Storage – Vitamins, carbohydrates etc.
 Detoxification – toxins, ammonia, etc.
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•Blood
•Conjugated &
Conjugated
•Urine – Urobilinogen
•Stool – Stercobilin
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 The word "cirrhosis" is a neologism that derives from
Greek kirrhos, meaning "tawny" (the orange-yellow
colour of the diseased liver).
 While the clinical entity was known before, it was
René Laennec who gave it the name "cirrhosis" in his
1819 work in which he also describes the
stethoscope.
 Cirrhosis 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.
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 Cirrhosis of liver is a chronic, progressive
disease characterized by widespread fibrosis
(scaring) & nodule formation. Cirrhosis occurs
when the normal flow of blood, bile, & hepatic
metabolites is altered by fibrosis.
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1. Alcoholic cirrhosis- Most common, due to
chronic alcoholism. Scar tissue
characteristically surrounds the portal area.
2. Postnecrotic cirrhosis- There are broad
bands of scar tissue due to late results of
acute viral hepatitis, postintoxication with
industrial chemicals.
3. Biliary cirrhosis- Scaring occurs around bile
duct in liver, Results from chronic biliary
obstruction & infection.
4. Cardiac cirrhosis- Associated with severe
right sided long term heart failure, fairly
rare.
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 Primary event is injury to hepatocellular elements
 Initiates inflammatory response with cytokine
release->toxic substances
 Destruction of hepatocytes, bile duct cells, vascular
endothelial cells
 Repair through cellular proliferation and regeneration
 Formation of fibrous scar
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 Cirrhosis has many possible causes; sometimes more
than one cause is present in the same patient. In the
Western World, chronic alcoholism and hepatitis C are
the most common causes.
 1. Alcoholic liver disease (ALD).
Alcoholic cirrhosis develops in 15% of individuals who
drink heavily for more than a decade. There is great
variability in the amount of alcohol needed to cause
cirrhosis (as little as 3-4 drinks a day in some men and
2-3 in some women). Alcohol seems to injure the liver
by blocking the normal metabolism of protein, fats,
and carbohydrates.
 2 . Chronic hepatitis C.
Infection with this virus causes inflammation of and
low grade damage to the liver that over several
decades can lead to cirrhosis.
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 3. Chronic hepatitis B.
The hepatitis B virus is probably the most
common cause of cirrhosis worldwide,
especially South-East Asia, but it is less
common in the United States and the Western
world. Hepatitis B causes liver inflammation
and injury that over several decades can lead
to cirrhosis. Hepatitis D is dependent on the
presence of hepatitis B, but accelerates
cirrhosis in co-infection.
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 4.Non-alcoholic steatohepatitis (NASH)
In NASH, fat builds up in the liver and eventually
causes scar tissue. This type of hepatitis appears to
be associated with diabetes, protein malnutrition,
obesity, coronary artery disease, and treatment with
corticosteroid medications. This disorder is similar
to that of alcoholic liver disease but patient does not
have an alcohol history
 5.Primary biliary cirrhosis
May be asymptomatic or complain of fatigue,
pruritus, and non-jaundice skin hyperpigmentation
with hepatomegaly. There is prominent alkaline
phosphatase elevation as well as elevations in
cholesterol and bilirubin.
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 6. Primary sclerosing cholangitis
PSC is a progressive cholestatic disorder presenting with
pruritus, steatorrhea, fat soluble vitamin deficiencies, and
metabolic bone disease. There is a strong association with
inflammatory bowel disease (IBD).
 7. Autoimmune hepatitis
This disease is caused by the immunologic damage to the liver
causing inflammation and eventually scarring and cirrhosis
 8. Hereditary hemochromatosis
Usually presents with family history of cirrhosis, skin
hyperpigmentation, diabetes mellitus, pseudogout, and/or
cardiomyopathy, all due to signs of iron overload
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 9. Wilson's disease
Autosomal recessive disorder characterized by low serum
ceruloplasmin and increased hepatic copper content on
liver biopsy
 10. Alpha 1-antitrypsin deficiency
(AAT)
Autosomal recessive disorder. Patients may also have
COPD, especially if they have a history of tobacco smoking.
Serum AAT levels are low.
 11. Cardiac cirrhosis
Due to chronic right sided heart failure which leads to liver
congestion.
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 Galactosemia
 Cystic fibrosis
 Drugs or toxins
 Certain parasitic infections (such as
schistosomiasis)
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 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. These occur in about 1/3 of
cases.
 Palmar erythema
Exaggerations of normal speckled mottling of the
palm, due to altered sex hormone metabolism.
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 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.
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 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.
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 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.
 Other
Weakness, fatigue, anorexia, weight loss.
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 Nail changes.
◦ Muehrcke's nails - paired horizontal bands
separated by normal color due to
hypoalbuminemia (low production of albumin).
◦ Terry's nails - proximal two thirds of the nail
plate appears white with distal one-third red,
also due to hypoalbuminemia
◦ Clubbing - angle between the nail plate and
proximal nail fold > 180 degrees
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 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).
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 The gold standard for diagnosis of cirrhosis
is a liver biopsy
 Histologically cirrhosis can be classified as
micronodular, macronodular, or mixed, but
this classification has been abandoned since
it is nonspecific to the etiology
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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
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 Prothrombin time- increases since the liver synthesizes
clotting factors.
 Globulins - increased due to shunting of bacterial
antigens away from the liver to 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.
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Other laboratory studies performed in newly
diagnosed cirrhosis may include:
 Serology for hepatitis viruses, autoantibodies (ANA,
anti-smooth muscle, anti-mitochondria, anti-LKM)
 Ferritin and transferrin saturation (markers of iron
overload), copper and ceruloplasmin (markers of
copper overload)
 Immunoglobulin levels (IgG, IgM, IgA) - these are
non-specific but may assist in distinguishing
various causes
 Cholesterol and glucose
 Alpha 1-antitrypsin
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 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).
 Other tests performed in particular circumstances include
abdominal CT and liver/bile duct MRI (MRCP).
 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.
 Rarely diseases of the bile ducts, such as as primary sclerosing,
can be causes of cirrhosis. Imaging of the bile ducts, such as ERCP
or MRCP (MRI of biliary tract and pancreas) can show
abnormalities in these patients, and may aid in the diagnosis.
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As the disease progresses, complications may develop. In
some people, these may be the first signs of the disease.
 Bruising and bleeding due to decreased production of
coagulation factors.
 Jaundice due to decreased processing of bilirubin.
 Itching (pruritus) due to bile products deposited in the
skin.
 Hepatic encephalopathy - the liver does not clear
ammonia and related nitrogenous substances from the
blood, which are carried to the brain, affecting cerebral
functioning: neglect of personal appearance,
unresponsiveness, forgetfulness, trouble concentrating,
or changes in sleep habits.
 Sensitivity to medication due to decreased metabolism of
the active compounds.
 Hepatocellular carcinoma is primary liver cancer, a
frequent complication of cirrhosis. It has a high mortality
rate.
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 Portal hypertension - blood normally
carried from the intestines and spleen
through the hepatic portal vein flows more
slowly and the pressure increases; this
leads to the following complications:
◦ Ascites - fluid leaks through the vasculature into
the abdominal cavity.
◦ Esophageal varices - collateral portal blood flow
through vessels in the stomach and esophagus.
These blood vessels may become enlarged and
are more likely to burst.
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 Problems in other organs.
◦ Cirrhosis can cause immune system dysfunction,
leading to infection. Signs and symptoms of infection
may be aspecific are more difficult to recognize (e.g.
worsening encephalopathy but no fever).
◦ Fluid in the abdomen (ascites) may become infected
with bacteria normally present in the intestines
(spontaneous bacterial peritonitis).
◦ Hepatorenal syndrome - insufficient blood supply to
the kidneys, causing acute renal failure. This
complication has a very high mortality (over 50%).
◦ Hepatopulmonary syndrome - blood bypassing the
normal lung circulation (shunting), leading to cyanosis
and dyspnea (shortness of breath), characteristically
worse on sitting up.
◦ Portopulmonary hypertension - increased blood
pressure over the lungs as a consequence of portal
hypertension.
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 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. This accumulation of fluid is
called edema or pitting edema. (Pitting edema refers to the
fact that pressing a fingertip firmly against an ankle or leg
with edema causes an indentation in the skin that persists
for some time after release of the pressure. Actually, any
type of pressure, such as from the elastic band of a sock,
may be enough to cause pitting.) The swelling often is
worse at the end of a day after standing or sitting and may
lessen overnight as a result of the loss of the effects of
gravity when lying down. As cirrhosis worsens and more
salt and water are retained, fluid also may accumulate in
the abdominal cavity between the abdominal wall and the
abdominal organs. This accumulation of fluid (called
ascites) causes swelling of the abdomen, abdominal
discomfort, and increased weight.
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 Fluid in the abdominal cavity (ascites) is the perfect
place for bacteria to grow. Normally, the abdominal
cavity contains a very small amount of fluid that is able
to resist infection well, and bacteria that enter the
abdomen (usually from the intestine) are killed or find
their way into the portal vein and to the liver where
they are killed. 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. Therefore, infection within
the abdomen and the ascites, referred to as
spontaneous bacterial peritonitis or SBP, is likely to
occur. SBP is a life- threatening complication. Some
patients with SBP have no symptoms, while others have
fever, chills, abdominal pain and tenderness, diarrhea,
and worsening ascites.
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 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.
 As a result of the increased flow of blood and the resulting increase in
pressure, the veins in the lower esophagus and upper stomach expand and
then are referred to as esophageal and gastric varices; the higher the portal
pressure, the larger the varices and the more likely a patient is to bleed
from the varices into the esophagus or stomach.
 Bleeding from varices usually is severe and, without immediate treatment,
can be fatal. Symptoms of bleeding from varices include vomiting blood
(the vomitus can be red blood mixed with clots or "coffee grounds" in
appearance, the latter due to the effect of acid on the blood), passing stool
that is black and tarry due to changes in the blood as it passes through the
intestine (melena), and orthostatic dizziness or fainting (caused by a drop
in blood pressure especially when standing up from a lying position).
 Bleeding also may occur from varices that form elsewhere in the intestines,
for example, the colon, but this is rare. For reasons yet unknown, patients
hospitalized because of actively bleeding esophageal varices have a high
risk of developing spontaneous bacterial peritonitis.
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 Some of the protein in food that escapes digestion and
absorption is used by bacteria that are normally present in
the intestine. While using the protein for their own
purposes, the bacteria make substances that they release
into the intestine. These substances then can be absorbed
into the body. Some of these substances, for example,
ammonia, can have toxic effects on the brain. Ordinarily,
these toxic substances are carried from the intestine in the
portal vein to the liver where they are removed from the
blood and detoxified.
 As previously discussed, when cirrhosis is present, liver
cells cannot function normally either because they are
damaged or because they have lost their normal
relationship with the blood. In addition, some of the blood
in the portal vein bypasses the liver through other veins.
The result of these abnormalities is that toxic substances
cannot be removed by the liver cells, and, instead, the
toxic substances accumulate in the blood.
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 When the toxic substances accumulate sufficiently in the
blood, the function of the brain is impaired, a condition
called hepatic encephalopathy. Sleeping during the day
rather than at night (reversal of the normal sleep pattern) is
among the earliest symptoms of hepatic encephalopathy.
Other symptoms include irritability, inability to concentrate
or perform calculations, loss of memory, confusion, or
depressed levels of consciousness. Ultimately, severe hepatic
encephalopathy causes coma and death.
 The toxic substances also make the brains of patients with
cirrhosis very sensitive to drugs that are normally filtered
and detoxified by the liver. Doses of many drugs that
normally are detoxified by the liver have to be reduced to
avoid a toxic buildup in cirrhosis, particularly sedatives and
drugs that are used to promote sleep. Alternatively, drugs
may be used that do not need to be detoxified or eliminated
from the body by the liver, for example, drugs that are
eliminated by the kidneys.
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BRAIN
LIVER
Toxic N2 metabolites
From Intestines
Porta systemic
shunts
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 Patients with worsening cirrhosis can develop the
hepatorenal syndrome. This syndrome is a serious
complication in which the function of the kidneys is
reduced. It is a functional problem in the kidneys, that is,
there is no physical damage to the kidneys. Instead, the
reduced function is due to changes in the way the blood
flows through the kidneys themselves. The hepatorenal
syndrome is defined as progressive failure of the kidneys
to clear substances from the blood and produce adequate
amounts of urine even though some other important
functions of the kidney, such as retention of salt, are
maintained. If liver function improves or a healthy liver is
transplanted into a patient with hepatorenal syndrome, the
kidneys usually begin to work normally. This suggests that
the reduced function of the kidneys is the result of the
accumulation of toxic substances in the blood when the
liver fails. There are two types of hepatorenal syndrome.
One type occurs gradually over months. The other occurs
rapidly over a week or two.
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 Traditionally, 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.
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 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
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Treatment of cirrhosis includes
 1) preventing further damage to the liver,
 2) treating the complications of cirrhosis,
 3) preventing liver cancer or detecting it
early, and
 4) liver transplantation.
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 Consume a balanced diet and one multivitamin daily. Patients with
PBC with impaired absorption of fat soluble vitamins may need
additional vitamins D and K.
 Avoid drugs (including alcohol) that cause liver damage. All patients
with cirrhosis should avoid alcohol. Most patients with alcohol
induced cirrhosis experience an improvement in liver function with
abstinence from alcohol. Even patients with chronic hepatitis B and
C can substantially reduce liver damage and slow the progression
towards cirrhosis with abstinence from alcohol.
 Avoid nonsteroidal antiinflammatory drugs (NSAIDs, e.g.,
ibuprofen). Patients with cirrhosis can experience worsening of liver
and kidney function with NSAIDs.
 Eradicate hepatitis B and hepatitis C virus by using anti-viral
medications. Not all patients with cirrhosis due to chronic viral
hepatitis are candidates for drug treatment. Some patients may
experience serious deterioration in liver function and/or intolerable
side effects during treatment. Thus, decisions to treat viral hepatitis
have to be individualized, after consulting with doctors experienced
in treating liver diseases (hepatologists).
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 Remove blood from patients with hemochromatosis to reduce
the levels of iron and prevent further damage to the liver. In
Wilson's disease, medications can be used to increase the
excretion of copper in the urine to reduce the levels of copper in
the body and prevent further damage to the liver.
 Suppress the immune system with drugs such as prednisone and
azathioprine (Imuran) to decrease inflammation of the liver in
autoimmune hepatitis.
 Treat patients with PBC with a bile acid preparation,
ursodeoxycholic acid (UDCA), also called ursodiol (Actigall).
Results of an analysis that combined the results from several
clinical trials showed that UDCA increased survival among PBC
patients during 4 years of therapy. The development of portal
hypertension also was reduced by the UDCA. It is important to
note that despite producing clear benefits, UDCA treatment
primarily retards progression and does not cure PBC. Other
medications such as colchicine and methotrexate also may have
benefit in subsets of patients with PBC.
 Immunize patients with cirrhosis against infection with hepatitis
A and B to prevent a serious deterioration in liver function. There
are currently no vaccines available for immunizing against
hepatitis C.
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 Edema and ascites. Retention of salt and water can lead to swelling of the
ankles and legs (edema) or abdomen (ascites) in patients with cirrhosis.
Doctors often advise patients with cirrhosis to restrict dietary salt (sodium)
and fluid to decrease edema and ascites. The amount of salt in the diet
usually is restricted to 2 grams per day and fluid to 1.2 liters per day. In
most patients with cirrhosis, however, salt and fluid restriction is not
enough, and diuretics have to be added.
 Diuretics are medications that work in the kidneys to promote the
elimination of salt and water into the urine. A combination of the diuretics
spironolactone (Aldactone) and furosemide can reduce or eliminate the
edema and ascites in most patients. During treatment with diuretics, it is
important to monitor the function of the kidneys by measuring blood
levels of blood urea nitrogen (BUN) and creatinine to determine if too
much diuretic is being used. Too much diuretic can lead to kidney
dysfunction that is reflected in elevations of the BUN and creatinine levels
in the blood.
 Sometimes, when the diuretics do not work (in which case the ascites is
said to be refractory), a long needle or catheter is used to draw out the
ascitic fluid directly from the abdomen, a procedure called abdominal
paracentesis. It is common to withdraw large amounts (liters) of fluid from
the abdomen when the ascites is causing painful abdominal distension
and/or difficulty breathing because it limits the movements of the
diaphragms.
 Another treatment for refractory ascites is a procedure called transjugular
intravenous portosystemic shunting (TIPS, see below).
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 If large varices develop in the esophagus or upper stomach,
patients with cirrhosis are at risk for serious bleeding due to
rupture of these varices. Once varices have bled, they tend to
rebleed and the probability that a patient will die from each
bleeding episode is high (30%-35%). Therefore, treatment is
necessary to prevent the first (initial) bleeding episode as well as
rebleeding. Treatments include medications and procedures to
decrease the pressure in the portal vein and procedures to
destroy the varices.
 Propranolol (Inderal), a beta blocker, is effective in lowering
pressure in the portal vein and is used to prevent initial bleeding
and rebleeding from varices in patients with cirrhosis. Another
class of oral medications that lowers portal pressure is the
nitrates, for example, isosorbide dinitrate ( Isordil). Nitrates
often are added to propranolol if propranolol alone does not
adequately lower portal pressure or prevent bleeding.
 Octreotide (Sandostatin) also decreases portal vein pressure and
has been used to treat variceal bleeding.
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 During upper endoscopy (EGD), either sclerotherapy
or band ligation can be performed to obliterate
varices and stop active bleeding and prevent
rebleeding. Sclerotherapy involves infusing small
doses of sclerosing solutions into the varices. The
sclerosing solutions cause inflammation and then
scarring of the varices, obliterating them in the
process. Band ligation involves applying rubber bands
around the varices to obliterate them. (Band ligation
of the varices is analogous to rubber banding of
hemorrhoids.) Complications of sclerotherapy include
esophageal ulcers, bleeding from the esophageal
ulcers, esophageal perforation, esophageal stricture
(narrowing due to scarring that can cause dysphagia),
mediastinitis (inflammation in the chest that can
cause chest pain), pericarditis (inflammation around
the heart that can cause chest pain), and peritonitis
(infection in the abdominal cavity). Studies have
shown that band ligation may be slightly more
effective with fewer complications than sclerotherapy.
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 Transjugular intrahepatic portosystemic shunt (TIPS) is a non-
surgical procedure to decrease the pressure in the portal vein.
TIPS is performed by a radiologist who inserts a stent (tube)
through a neck vein, down the inferior vena cava and into the
hepatic vein within the liver. The stent then is placed so that one
end is in the high pressure portal vein and the other end is in the
low pressure hepatic vein. This tube shunts blood around the
liver and by so doing lowers the pressure in the portal vein and
varices and prevents bleeding from the varices. TIPS is
particularly useful in patients who fail to respond to beta
blockers, variceal sclerotherapy, or banding. (TIPS also is useful
in treating patients with ascites that do not respond to salt and
fluid restriction and diuretics.) TIPS can be used in patients with
cirrhosis to prevent variceal bleeding while the patients are
waiting for liver transplantation. The most common side effect of
TIPS is hepatic encephalopathy. Another major problem with TIPS
is the development of narrowing and occlusion of the stent,
causing recurrence of portal hypertension and variceal bleeding
and ascites. The estimated frequency of stent occlusion ranges
from 30%-50% in 12 months. Fortunately, there are methods to
open occluded stents. Other complications of TIPS include
bleeding due to inadvertent puncture of the liver capsule or a
bile duct, infection, heart failure, and liver failure
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 A surgical operation to create a shunt (passage)
from the high-pressure portal vein to veins with
lower pressure can lower blood flow and
pressure in the portal vein and prevent varices
from bleeding. One such surgical procedure is
called distal splenorenal shunt (DSRS). It is
appropriate to consider such a surgical shunt for
patients with portal hypertension who have early
cirrhosis. (The risks of major shunt surgery in
these patients is less than in patients with
advanced cirrhosis.) During DSRS, the surgeon
detaches the splenic vein from the portal vein,
and attaches it to the renal vein. Blood then is
shunted from the spleen around the liver,
lowering the pressure in the portal vein and
varices and preventing bleeding from the varices.
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 . Patients with an abnormal sleep cycle, impaired thinking,
odd behavior, or other signs of hepatic encephalopathy
usually should be treated with a low protein diet and oral
lactulose. Dietary protein is restricted because it is a source
of the toxic compounds that cause hepatic encephalopathy.
Lactulose, which is a liquid, traps the toxic compounds in
the colon. Consequently, they cannot be absorbed into the
blood stream and cause encephalopathy. To be sure that
adequate lactulose is present in the colon at all times, the
patient should adjust the dose to produce 2-3 semiformed
bowel movements a day. (Lactulose is a laxative, and the
adequacy of treatment can be judged by loosening or
increasing frequency of stools.) If symptoms of
encephalopathy persist, oral antibiotics such as neomycin
or metronidazole (Flagyl), can be added to the treatment
regimen. Antibiotics work by blocking the production of the
toxic compounds by the bacteria in the colon.
JG SAMBAD

 Several types of liver disease that cause cirrhosis
are associated with a particularly high incidence
of liver cancer, for example, hepatitis B and C,
and it would be useful to screen for liver cancer
since early surgical treatment or transplantation
of the liver can cure the patient of cancer. The
difficulty is that the methods available for
screening are only partially effective, identifying
at best only 50% of patients at a curable stage of
their cancer. Despite the partial effectiveness of
screening, most patients with cirrhosis,
particularly hepatitis B and C, are screened yearly
or every six months with ultrasound examination
of the liver and measurements of cancer-
produced proteins in the blood, e.g. alpha
fetoprotein.
JG SAMBAD

 Cirrhosis is irreversible. Many patients' liver function will
gradually worsen despite treatment and complications of
cirrhosis will increase and become difficult to treat. Therefore,
when cirrhosis is far advanced, liver transplantation often is the
only option for treatment. Recent advances in surgical
transplantation and medications to prevent infection and
rejection of the transplanted liver have greatly improved survival
after transplantation. On average, more than 80% of patients who
receive transplants are alive after five years. Not everyone with
cirrhosis is a candidate for transplantation. Furthermore, there is
a shortage of livers to transplant, and there usually is a long
(months to years) wait before a liver for transplanting becomes
available. Therefore, measures to retard the progression of liver
disease and treat and prevent complications of cirrhosis are
vitally important.
 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. Transplantation necessitates the use of immune
suppressants (ciclosporin or tacrolimus).
JG SAMBAD

Assessment-
History
Physical Examination
Mental Status
Nutritional status
JG SAMBAD

Activity intolerance R/T
fatigue
Altered nutrition
Impaired skin integrity
Risk for injury
JG SAMBAD

 Promoting rest
 Improving nutritional status
 Providing skin care
 Reducing risk of injury
 Monitoring & managing Potential complications
Bleeding & hemorrhage
Hepatic encephalopathy
Fluid Volume excess
 Promoting home & self care
 Client teaching.
JG SAMBAD

Learn from the
mistakes of others.
You can't live long
enough to make them
all yourself…!
JG SAMBAD

Liver cirrhosis

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