CIRRHOSIS

Hepatitis C and alcohol abuse the most common causes of liver cirrhosis.
Develops over time, causes alterations in the structure of the liver and function of
its cells hepatocytes.
Changes characterized by inflammation and liver cell necrosis.
The necrosis followed by abnormal regeneration, where fibrous tissue and
regenerative nodules distort the normality of the liver lobule and alter blood flow.
Changes are irreversible, result in chronic liver dysfunction and liver failure
Eventually all liver metabolic processes are altered

Inflammation, fibrotic changes and increased intrahepatic vascular resistance

cause compression of the liver lobule leading to obstructed blood flow.

This portal hypertension results in venous congestion and dilation

Blood from the GI tract is shunted away from the liver

Pressure builds in the systemic venous circulation causing congestion where the
portal and systemic venous systems connect, the esophagus, stomach and
rectum.

Results in varicose veins in the rectum and in the esophagus called esophageal
varices

Rupture from the varices can be life threatening

Splenomegaly results from the trapped blood from portal hypertension which
traps platelets

Bleeding from esophageal and gastric varices can cause melena

Portal hypertension results in ascites

Cirrhosis develops and causes cardiac dysfunction seen as hypotension, tachycardia

and cardiac flow murmurs

Altered protein metabolism results in decreased synthesis of albumin which leads

to interstitial tissue edema and decreased plasma volume.

Decreased globulin, another protein, alters blood clotting leading to bruising or

hemorrhage and a low grade DIC may develop
Fluid accumulates in the peritoneum causing respiratory distress due to pressure on the
diaphragm

Ascites is managed with bed rest, low sodium diet, fluid restriction and diuretic
therapy with spironolactone which is the first line therapy for ascites.

Paracentesis used to treat ascites that is unresponsive to other therapies.

A nonsurgical approach is preferred to manage ascites and acute variceal

hemorrhage called the transjugular intrahepatic portosystemic shunt
(TIPS). A stent is placed using an angiographic catheter to create a
conduit between the hepatic and portal vein to decrease portal pressure.

Fairly successful as a procedure but recent meta-analysis

concluded that it is associated with development of increased
encephalopathy and offers no survival benefit.

Nursing interventions include monitoring nutrition, fluid balance, urinary output,

electrolyte and blood chemistries, drug type, dosing requirements, bleeding times,
hematocrit, platelet function, bowel regimens and above all, monitoring for the signs of
liver failure: changes in neurological and mental status, increasing ascites, and
hepatorenal syndrome