Liver Cirrhosis - Document Transcript

1. LIVER CIRRHOSIS • The word \"cirrhosis\" derives from Greek kirrhos,

meaning \"tawny\" (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 • 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 \"backs-up\" 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) • Less common causes of cirrhosis include unusual
reactions to some drugs and • 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 • Glycogen storage disease type IV • Cystic

fibrosis • 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. • 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. 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 • 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 •
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. Provide low-sodium diet and restric Assess urine specific gravity.  Weight daily.
Assess for JVD, measure abdominal girth daily, and check for peripheral edema.
Monitor intake and output.  • 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 If possible, plan for consistent
nursing care assignments. Avoid factors that may precipitate hepatic
encephalopathy. Avoid hepatotoxic medications and CNS depressant drugs. 
Assess neurologic status, including level of consciousness, and mental status.
Observe for signs of early encephalopathy: changes in handwriting, speech, and
asterixis.  t fluids as ordered. • Disturbed thought processes

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