Cirrhosis (cont.)
How is cirrhosis treated?
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.
Preventing further damage to the liver
- 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.
- 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).
- 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.
Treating the complications of cirrhosis
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).
Bleeding from varices. 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.
- 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.
- 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.
- 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.
Hepatic encephalopathy.
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.
Hypersplenism. The filtration of blood by an enlarged spleen usually results in
only mild reductions of red blood cells (anemia), white blood cells (leukopenia)
and platelets (thrombocytopenia) that do not require treatment. Severe anemia,
however, may require blood transfusions or treatment with erythropoietin or
epoetin alfa (Epogen, Procrit), hormones that stimulate the production of red
blood cells. If the numbers of white blood cells are severely reduced, another
hormone called granulocyte-colony stimulating factor is available to increase
the numbers of white blood cells. An example of one such factor is filgrastim
(Neupogen).
No approved medication is available yet to increase the
number of platelets. As a necessary precaution, patients with low platelets
should not use aspirin or
other nonsteroidal antiinflammatory drugs (NSAIDS) since these drugs can
hinder the function of platelets. If a low number of platelets is associated
with significant bleeding, transfusions of platelets usually should be given.
Surgical removal of the spleen (called splenectomy) should be avoided, if
possible, because of the risk of excessive bleeding during the operation and the
risk of anesthesia in advanced liver disease.
Spontaneous bacterial peritonitis (SBP). Patients suspected of having
spontaneous bacterial peritonitis
usually will undergo paracentesis. Fluid that is removed is examined for white
blood cells and cultured for bacteria. Culturing involves inoculating a sample
of the ascites into a bottle of nutrient-rich fluid that encourages the growth
of bacteria, thus facilitating the identification of even small numbers of
bacteria. Blood and urine samples often are obtained as well for culturing
because many patients with spontaneous bacterial peritonitis also will have infection in their blood and
urine. In fact, many doctors believe that infection may have begun in the blood
and the urine and spread to the ascitic fluid to cause spontaneous bacterial
peritonitis. Most patients with
spontaneous bacterial peritonitis are hospitalized and treated with intravenous antibiotics such as
ampicillin, gentamycin, and one of the newer generation cephalosporin. Patients
usually treated with antibiotics include:
- Patients with blood, urine, and/or ascites fluid
cultures that contain bacteria.
- Patients without bacteria in their blood, urine, and ascitic
fluid but who have elevated numbers of white blood cells (neutrophils) in
the asciticfluid(>250 neutrophils/cc). Elevated neutrophil numbers in ascitic fluid often means
that there is bacterial infection. Doctors believe that the lack of bacteria
with culturing in some patients with increased neutrophils is due either to a
very small number of bacteria or ineffective culturing techniques.
Spontaneous bacterial peritonitis is a serious infection. It often occurs in patients
with advanced cirrhosis whose immune systems are weak, but with modern
antibiotics and early detection and treatment, the prognosis of recovering from an episode of
spontaneous bacterial peritonitis is good.
In some patients oral antibiotics (such as
Cipro or
Septra) can be prescribed to
prevent spontaneous bacterial peritonitis. Not all patients with cirrhosis and ascites should be treated with
antibiotics to prevent spontaneous bacterial peritonitis, but some patients are at high risk for developing
spontaneous bacterial peritonitis and warrant preventive treatment:
- Patients with cirrhosis who are hospitalized for
bleeding varices have a high risk of developing
spontaneous bacterial peritonitis and should be started on antibiotics early
during the hospitalization to prevent spontaneous bacterial peritonitis
- Patients with recurring episodes of spontaneous bacterial peritonitis
- Patients with low protein levels in the ascitic fluid (Ascitic fluid with low
levels of protein is more likely to become infected.)
Prevention and early detection of liver cancer
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.
Liver transplantation
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.
Next: What is new and in the future for cirrhosis? »
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