Cirrhosis of the Liver

Overview Treatment Options

Definition Treatment Strategy
Etiology Drug Therapies
Risk Factors Complementary and
Signs and Symptoms Alternative Therapies
Differential Diagnosis Patient Monitoring
Diagnosis Other Considerations
Physical Examination Prevention
Laboratory Tests Complications/Sequela
Pathology/Pathophysiolo e
gy Prognosis
Imaging Pregnancy
Other Diagnostic References
Procedures

Overview

Definition

Cirrhosis is characterized by irreversible chronic

injury of the liver manifested by hepatic fibrosis
and small regenerative nodules; it is often a
subclinical condition diagnosed on the basis of
the history, physical examination, and
biochemical and serologic tests. Approximately
10% of cases have no known etiology
(cryptogenic cirrhosis). Between 5% to 10% of
people in the U.S. are alcoholics; of these, 10%
to 15% will develop liver disease.

Etiology

Average daily consumption of alcohol (32 to

 48 oz. of beer, 4 to 8 oz. of liquor, 16 to 32
oz. of wine) for 10 years or more is
associated with an increased incidence of
alcoholic cirrhosis. The amount and duration
of alcohol ingestion are more important than
the type of alcoholic beverage ingested.
Drugs and toxins (e.g., alcohol,
methotrexate, isoniazid, methyldopa)
Infectious diseases (e.g., hepatitis B and C,
brucellosis, echinococcosis, schistosomiasis,
toxoplasmosis)
Inherited and metabolic disorders (e.g.,
Wilson's disease, hemochromatosis,
protoporphyria, galactosemia, glycogen
storage disease, alpha1-antitrypsin
deficiency, tyrosinosis, hereditary fructose
intolerance)
Biliary obstruction (e.g., carcinoma, chronic
pancreatitis, sclerosing cholangitis)
Cardiovascular diseases (e.g., chronic right
heart failure, Budd-Chiari syndrome, veno-
occlusive disease)
Miscellaneous causes (e.g., sarcoidosis,
jejunoileal bypass)

Risk Factors

Excessive ingestion of alcohol, exposure to toxins

and infectious agents

Signs and Symptoms

The clinical manifestations of cirrhosis can range

from an absence of symptoms (10% to 20% of
patients) to hepatic failure.
 Hepatomegaly and splenomegaly
Jaundice
Peripheral edema
Weakness, malaise
Anorexia and weight loss
Abdominal pain or gastrointestinal
complaints
Gastroesophageal varices and bleeding
Hepatic encephalopathy
Ascites with portal hypertension
Spider angiomas and palmar erythema
Testicular atrophy and gynecomastia (in
men)
Menstrual irregularities (in women)
Parotid enlargement

Differential Diagnosis

Nodular regenerative hyperplasia

Congenital hepatic fibrosis
Acute or chronic viral hepatitis
Diabetes mellitus
Biliary obstruction, lymphatic obstruction
Drug toxicity
Bacterial infections
Primary biliary or cardiac cirrhosis
Wilson's disease
Hemochromatosis
Hepatic schistosomiasis

Diagnosis

Physical Examination
The three most common hepatic findings in
alcoholics are fatty liver, alcoholic hepatitis, and
cirrhosis. Patients with fatty liver may have
abdominal pain, mild icterus, or gastrointestinal
symptoms but they may also present
asymptomatically. Patients with alcoholic hepatitis
may present with anorexia, nausea, vomiting,
weight loss, abdominal pain, hepatomegaly,
splenomegaly, ascites, and jaundice. Patients
with alcoholic cirrhosis may present
asymptomatically (10% to 20%) or with signs of
chronic liver disease such as ascites,
gastrointestinal bleeding, encephalopathy, spider
angiomas, palmar erythema, parotid
enlargement, testicular atrophy, gynecomastia,
menstrual disorders, and muscle wasting.

Laboratory Tests

A patient with significant liver injury may have

normal results.
Elevated serum aspartate aminotransferase
Hyperbilirubinemia, hypoalbuminemia, and
hyperglobulinemia
Elevated alkaline phosphatase
Prolonged prothrombin time
Hypomagnesemia, hypophosphatemia, and
hypokalemia
Respiratory alkalosis
Anemia (from folic acid and vitamin B12
deficiency), gastrointestinal blood loss, or
toxic effects of alcohol on bone marrow

Pathology/Pathophysiology
 Fibrosis and regenerative nodules
With fatty liverlarge droplets of fat in the
hepatocyte
With alcoholic hepatitishepatocellular
necrosis, alcoholic hyalin (Mallory bodies),
increased intralobular connective tissue in
the space of Disse, central vein sclerosis,
infiltration by polymorphonuclear leukocytes
With alcoholic cirrhosisportal and central
areas are linked by dense bands of
connective tissue, severe scarring in the
central areas, hypersplenism or bone marrow
suppression, leading to thrombocytopenia,
leukopenia, and anemia

Imaging

Ultrasonographyto exclude biliary

obstruction, confirm hepatosplenomegaly,
and detect textural abnormalities
Endoscopic retrograde
cholangiopancreatography (ERCP)to rule
out biliary tract disease by determining
patency of the biliary tree
Computed tomographyto determine
severity of hepatic encephalopathy, liver size,
and density in hemochromatosis

Other Diagnostic Procedures

Percutaneous needle biopsyto distinguish

the severity of the liver damage and to
evaluate patients who do not drink but
present with clinical manifestations of liver
disease
Paracentesisto diagnose cirrhotic ascites,
 ruling out other disorders
Cholangiography for duct obstruction
Laparoscopic liver biopsy

Treatment Options

Treatment Strategy

Remove/reduce the effects of the cause, prevent

further damage if possible, and prevent/manage
complications. Surgery is limited to procedures
for portal hypertension and complete liver
transplantation.
Well-balanced diet (2,000 to 3,000 kcal/day)
for malnutrition
Protein restrictionto reduce ammonia
production in colon in patients with hepatic
encephalopathy, yet ensure adequate protein
Salt and water restrictionto help manage
ascites (no more than 1.2 g of sodium and 1
liter of water per day)

Drug Therapies

Colchicine (0.6 mg bid)to slow progression

of disease
Diureticsfor ascites (e.g., spironolactone
[Aldactone] 100 to 400 mg/day; furosemide,
40 to 120 mg/day). Caution must be used
with diuretics so as not to cause electrolyte
abnormalities, hypovolemia, and death.
Neomycin (1 g every six hours)to reduce
ammonia production in intestine that causes
encephalopathy
 Lactulose (65 g/dL every two hours)to
reduce serum ammonia levels and improve
hepatic encephalopathy
Other specific drugs based on complications
and etiology

Complementary and Alternative Therapies

Effective either alone or as adjunctive therapy.

Nutrition

B-complex: B1 (50 to 100 mg), B2 (50 mg),

B3 (25 mg), B5 (100 mg), B6 (50 to 100 mg),
B12 (100 to 1,000 mcg), folate (400
mcg/day) to prevent deficiencies common in
liver disease
Antioxidants: vitamin C (1,000 to 3,000
mg/day), vitamin E (400 to 800 IU/day), and
selenium (200 mcg/day) reduce toxic effects
of alcohol/drugs and prevent fatty acid
oxidation.
Essential fatty acids are anti-inflammatory;
dietary manipulation includes reducing
animal fats and increasing fish and nuts. A
mix of omega-6 (evening primrose) and
omega-3 (flaxseed) may be best (1 tbsp.
oil/day or 1,000 to 1,500 mg/day). Watch
clotting times.
Choline, lecithin, methionine (1 g each/day)
for fat absorption
Carnitine (300 mg/day) prevents fatty liver
Glutathione (500 mg bid) helps remove
ammonia from the brain, a complication of
cirrhosis
Vitamin K is necessary for blood clotting;
 often depleted in cirrhosis.
Desiccated liver (500 mg tid) helps to provide
nutrition to promote liver repair.
Protein restriction to 45 g/day without
development of negative nitrogen balance as
long as a minimum of 400 g of carbohydrates
is ingested daily.
A change from animal to vegetable protein
may be helpful.

Herbs

Ascertain a diagnosis before pursuing treatment.

Herbs may be used as dried extracts (capsules,
powders, teas), glycerites (glycerine extracts), or
tinctures (alcohol extracts). Unless otherwise
indicated, teas should be made with 1 tsp. herb
per cup of hot water. Steep covered 5 to 10
minutes for leaf or flowers, and 10 to 20 minutes
for roots. Drink 2 to 4 cups/day. Tinctures may be
used singly or in combination as noted.
Due to the high doses required and the need to
avoid alcohol, the preferred form of these herbs is
powdered.
Milk thistle (Silybum marianum): 100 mg tid
prevents free radical damage in the liver,
stimulates regeneration of hepatocytes, aids
in digestion of fats, effective in treating
cirrhosis
Barberry (Berberis vulgaris): 250 to 500
mg/day corrects metabolic abnormalities in
liver cirrhosis
Catechin (Uncaria gambir): 400 mg tid, is
antioxidant, antiviral, and helps to regenerate
liver tissue
Homeopathy

May offer relief of symptoms, but needs to be

prescribed by an experienced practitioner.

Physical Medicine

Castor oil pack. Used externally, castor oil is a

powerful anti-inflammatory. Apply oil directly to
skin, cover with a clean soft cloth (e.g., flannel)
and plastic wrap. Place a heat source (hot water
bottle or heating pad) over the pack and let sit for
30 to 60 minutes. For best results, use for three
consecutive days. Apply pack over liver.
Preliminary study shows immune enhancement in
healthy patients, historic use to stimulate hepatic
function.

Acupuncture

May be helpful to alleviate symptoms and

increase physiological functioning.

Massage

May help alleviate stress and lymph congestion.

Patient Monitoring
Patients need long-term management because of
the serious life-threatening complications
associated with cirrhosis. Repeated liver tests are
necessary, with frequency based on the relative
stability of the patient.

Other Considerations

Prevention

The incidence of alcoholic cirrhosis is directly

related to the ingestion of alcohol. Approximately
10% to 20% of alcoholics develop cirrhosis. To
prevent some other forms of cirrhosis, patients
must practice safe sex and avoid IV drug use.

Complications/Sequelae

Portal hypertension and its subsequent

complications due to collateral flow from the
portal venous system
Bleeding esophageal varices
Hypersplenism
Ascites
Hepatorenal syndrome
Hepatic encephalopathy
Liver failure
Hepatocellular carcinoma
Bacterial peritonitis
Other infections
Prognosis

Dependent on etiology, extent of damage, and

success of intervention

Pregnancy

Cirrhosis can jeopardize the chances for a

healthy infant.

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