LECTURE NOTE ON LIVER CIRRHOSIS

Definition

Liver cirrhosis is a chronic disease characterized by the replacement of normal liver tissues
with diffuse degenerative changes and fibrosis that disrupt the structure and function of the
liver.

It is also known as hepatic cirrhosis.

Types

 Alcoholic cirrhosis: due to chronic alcohol ingestion. Here, scar tissue surrounds the
portal area mostly due to chronic alcoholism. It is the most common.
 Post necrotic cirrhosis: due to chronic necrosis possibly due to HB virus invasion.
This type is characterized by broad bands of scar tissue due to the late result of
previous acute viral hepatitis causing extreme necrosis.
 Biliary cirrhosis: may be due to cholestasis. here scaring occurs in the liver around
the bile duct, usually due to the chronic biliary obstruction and infection with lower
incidents than the first two

Chiefly affected in cirrhosis is a portion of the liver that consists of portal and peri portal
spaces. This is where the bile canaliculi of each lobule communicate to form the bile ducts,
these portal and peri portal spaces become sites of inflammation.

Occurrence

Liver cirrhosis is high in alcoholics, more common in men between 40 to 60 years

Causes

 Alcoholism 60 to 70% of all cases. Consumption of alcohol over several years can
produce fatty infiltration of the liver and liver dysfunction.

 Hepatitis especially severe type B viral hepatitis where there has been extensive
necrosis followed by considerable scaring (post necrotic cirrhosis).

 Chronic cholestasis (i.e. prolonged obstruction in the bile ducts causing arrest of bile
flow; this may cause degenerative changes. It may occur due to portal obstruction by
stone in the extra hepatic bile duct, but may also occur intra hepatic due to infection
or inflammation resulting in structure of small ducts (biliary cirrhosis).

 Non-alcoholic fatty liver disease: buildup of fat in the liver in individuals who are
overweight, obese or have other health conditions like metabolic syndrome or type -2
Diabetes Mellitus.

 Hepatic infiltration: infiltration of certain substances may cause fibrotic changes in

the liver e.g. conditions like Von-Gierke’s disease that causes excessive glycogen
accumulation, enlargement and fibrosis.
  Autoimmune hepatitis: this is a chronic disease in which the body’s immune system
attacks the liver cells, causing liver inflammation and damage.
 Inherited liver diseases like: Wilson disease which is a genetic disorder that prevents
the body from removing extra copper, resulting in accumulation of copper in the liver,
brain, eyes and other organs, causing life threatening damages. Other examples
include Gaucher’s disease, haemochromatosis (find out what these are)

Other Factors include

Exposure to certain chemical e.g. carbon tetrachloride

Long term use of certain drugs

Congestive heart failure resulting in liver congestion

Infection by schistosomiasis.

Pathophysiology

Cirrhosis denotes chronic diffuse degenerative tissue changes occurring in the liver.
Whatever is the cause of the cirrhosis, whether alcoholism, chronic hepatitis, hereditary
condition or any other cause results in inflammation of the hepatocytes. Excessive and
continuous or prolonged exposure of the liver to these hepatotoxic agents leads to fibrosis
(replacement of injured liver tissue by a collagenous scar) and nodule formation. Chronic
injury to the liver occurs, leading to alteration of the normal globular organization of the
liver.

Liver function decreases, resulting in accumulation of toxins. As toxins accumulate, the liver
becomes more fibrotic and liver functions reduce. The scar tissues blood flow through the
liver; reduced blood flow results in reduced blood supply to some hepatocytes, leading to
necrosis.

At this stage, complete recovery is still possible with medication and life style changes or
modification. This is the stage of compensated liver cirrhosis.

If recovery does not occur, severe scarring takes place due to necrosis and the liver can no
longer heal itself, leading to the stage of decompensated liver cirrhosis, with the sugns and
symptoms listed below.

Signs & Symptoms

The liver has considerable reserve; early cirrhotic changes generally go unrecognized without
apparent manifestation. However, signs & symptoms of cirrhosis increase in severity as the
disease progresses and worsens. The severity of the manifestation helps to categorize the
disorder into two groups:

i. Compensated
ii. Decompensated
Compensated Cirrhosis: This is the mild form of the disease, at this point, the patient may
be asymptomatic or have mild symptoms.

It comes from vague digestive disturbance problem, flatulence, dysphasia, nausea and
abdominal pain and sometimes intermitted mild fever, Palmar erythema, unexplained
epistaxis, firm, enlarged liver splenomegaly. (All these may be discovered on physical
examination).

Decompensated cirrhosis: here, scar tissues block flow through the portal vein leading to
portal hypertension. Symptoms are severe and are due to portal hypertension, impaired liver
function and hepato-renal symptoms. There is resultant inability of the liver to synthesize
protein, clotting Factor and other substance.

Signs at this stage include clubbing fingers, ascites, jaundice, muscle wasting, weight loss
and continuous wasting, purpura, spontaneous bruising, epistaxis, hypertension, white nails
and atrophy.

Other developments include:

 Liver enlargement: The liver tends to be large and loaded with fat (an early cause of
cirrhosis). The liver is firm and has a sharp end on palpation, there is abdominal pain
because of rapid enlargement of the liver producing tension on the fibrous coverage
of the liver (Glisson's Capsule). Later the liver decreases in size as the scar tissue
contracts it. The liver edge if palpable, is nodular.
 There is a portal obstruction secondary to the ascites i.e. all the blood from the
digestive organ collect in the portal vein and is carried to the liver. The cirrhosis does
not allow for free passage of this blood, which is packed up into the spleen and GIT,
causing congestion, indigestion and altered bowel function occurs.
 Fluid rich in protein accumulate in the peritoneal cavity causing ascites, there is
bacterial infection and peritonitis.
 GIT varices occurs, caused by obstruction to the blood flow in the liver.
 Prominent abdominal blood vessels become visible on abdominal inspection. The
vessel may rupture and cause bleeding into the intestinal tract.
 Concentration of plasma albumin predisposes to oedema
 Overproduction of aldosterone causes sodium (Na) and H 20 retention and potassium
(K) excretion.
 There is vitamin deficiency and weaknesses due to inadequate formation, use and
storage of vitamin A, C and K.
 Signs of anemia occur due to chronic ascites and impaired GIT function there is
mental deterioration with impending hepatic encephalopathy and hepatic coma.

Nursing management

 Health history
  Assessment

 Focus on signs & symptoms and precipitating factors alcohol and drugs

 Dietary intake

 Ask weather there is change in color of urine and stool,

 weight loss

 Mental status: assess ability to carry out household activities

Physical examination

General inspection: check for

 skin color and jaundice

 Flushing
 Decreased visual sight
 Hepatomegaly
 Abdominal tenderness
 Dry skin
 Neurological disorder
 Intellectual deterioration

Diagnostic Investigation

Serum bilirubin Test

AST and ALT

Prothrombin time.

In severe parenchyma destruction, serum Albumin levels, serum globulin.

Nursing management

 Provide rest: If there is no edema patient remains ambulatory but perform limited
amount of activities that does not produce excessive loss of energy.
 Observe for signs of edema daily
 Measure and chart intake and output

 Note response of orientation and awareness improve nutritional status of the patient if
the patient has no ascites, he should have 100 - 150 high protein diet which vitamin A,
C, K and folic acid supplement. Also a diet of 2500 to 3000 kcal high in carbohydrate
is recommended.
 If patient can tolerate fat or not jaundiced, give some fat to make diet palatable. small
meal and snack would be more tolerable than three large meals
  Reduce Sodium intake
 Ensure total abstinence in alcohol
 In severe cases of liver insufficiency, protein should be reduced and patient sustained
with CHO.
 In case of coma give IV infusion,
 Give skin care
 Change position frequently to prevent bed sore.
 Apply soothing location to irritated skin.
 Scratching should be minimized to reduce a risk of injury.
 Protect from Force and other injuries
 Place side rails.
 Patient should ask for assistance if he wants to come out of bed
 If there is injury, assess properly because of the tenderness for internal bleeding. Use
soft toothbrush to prevent bleeding from the gum.
 Prevent infections because resistance is lowered.
 Apply pressure to injection site.

Medication

 Multivitamins should be given, Parenteral vitamin K.

 In case of ascites and oedema – diuretic is given
 avoid toxic drug especially those inactivated by the liver.

 Monitor for complication such as haemorrhage or bleeding, melena stool, GIT

monitoring for bleeding.

 Equipment for hemorrhage control should easily be available in case of bleeding give
IV fluid and medication necessary to treat hemorrhage.

 In some cases, vasopressin is given I.V. to increase arterial vessel constriction and
also decrease puta venous pressure by reducing the volume of blood entering the
portal system.

Complications:

Ascites, varices, hepatic encephalopathy, hepatic failure

Continuous Assessment
(Identify 3 nursing diagnoses and develop nursing care plan for a patient with liver
cirrhosis- 10 marks.)