CIRRHOSIS AND PORTAL HYPERTENSION

ASDN 228

ADULT MED-SURG

I.                     DEFINITION

A. End stage of chronic liver disease.  Progressive, irreversible disorder ,

 eventually leading to liver failure

B.      Pathophysiology

Functional liver tissue is destroyed and replaced by fibrous scar

tissue

Metabolic functions of the liver are lost

                        Bile statsis occurs due to constrictive bands

                        Blood does not flow freely through the liver to inferior vena cava

                        Increased  pressure in portal venous system  - congested veins result

 

II.                   CAUSES

A.      Alcoholic cirrhosis – most common cause

1.       Alcohol causes metabolic changes in liver

2.       Fatty infiltration of hepatocytes

3.       Inflammatory cells infiltrate the liver causing necrosis, fibrosis

         and destruction of functional liver tissue

4.       Liver shrinks and develops a nodular appearance

5.       Malnutrition commonly accompanies alcoholic cirrhosis

B.      Billary Cirrhosis

1.       Obstructed bile damages and destroys liver cells

2.       Leads to inflammation, fibrosis and formation of regenerative  nodules

C.      Posthepatic Cirrhosis

1.       Results from chronic hepatitis B or C  or unknown cause

2.       Liver is shrunken and nodular with cell loss and fibrosis

 

III.                  SIGNS AND SYMPTOMS

A.      Early – few symptoms

1.       Liver is usually enlarged and may be tender

2.       Dull ach in RUQ

3.       Weight loss, weakness and anorexia

4.       Bowel changes with diarrhea or constipation

B.      Late – related to liver cell failure and portal hypertension

1.       Malnutrition, muscle wasting

Impaired  nutrient metabolism

Impaired fat absorption

2.       Bleeding problems/bruising

Decreased clotting factor synthesis

Increased platelet destruction by enlarged spleen

Impaired vitamin K absorption and storage

3.       Ascites/edema

Impaired plasma protein synthesis

Increased pressure in portal venous system

4.       Jaundice

Impaired bilirubin metabolism and excretion

5.       Neurologic changes/encephalopathy

Accumulated metabolic toxins

Impaired ammonia metabolism and excretion

MULTISYSTEM EFFECTS OF CIRRHOSIS

 

Neurologic System

Agitation leading to lethargy, stupor, coma

Asterixis (liver flap) flapping tremor of hands when arms are extended

Endocrine system

Gynecomastia in males, possible diabetes

Respiratory system

Dyspnea

Cardiovascular system

Bounding pulses, pulmonary hypertension,

dysrhythmias

Hepatic system

Splenomegaly, possible liver cancer

Gastrointestinal System

Abdominal pain, anorexia, Nauses, Clay-colored

stools, peptic ulcers, GI bleeding, hemorrhoids

Hematologic System

thrombocytopenia, anemia

Reproductive System

Oligomenorrhea (female)

(testicular atrophy (male)

Integumentary System

Jaundice, erythemai of palsm, spider angioma, decreased body hair, pruritis, ecchymoses, caput medusae (dilated veins around the umbilicus)

Immune System

leukocytopenia, increased susceptibility to infection

 

                       

IV.                COMPLICATIONS

A.      Portal hypertension

1.       Normal blood flow returning to the heart from the abdominal

organs collects in the portal veins and travels through the liver

2.       Pressure increases in the portal vein due to restricted flow

3.       Collateral channels develop between the portal and systemic veins

that supply the lower rectum and esophagus and the umbilical veins

4.       Results in hemorrhoids, esophageal varices and caput medusae (dilated

veins around the umbilicus)

B.      Splenomegaly

1.       Spleen enlarges due to portal hypertension and shunting of blood into splenic

vein

2.       Increased destruction of red and white blood cells and platelets

3.       Leads to anemia, leukopenia and thrombocytopenia

C.      Ascites

1.       Accumulation of fluid in abdominal cavity

2.       Hypoalbuminemia – low serum albumin levels

D.      Esophageal Varices

1.       Enlarged, thin-walled veins in the esophagus due to portal hypertension

2.       May bleed, rupture causing massive hemorrhage

E.      Hepatic Encephalopathy

1.       Accumulation of neurotoxins in the blood

2.       Ammonia accumulation – destroys brain cells

F.      Hepatorenal Syndrome

1.       Renal failure with azotemia

2.       Sodium retention, oliguria, hypotension

 

V.                  TREATMENT

A.      Medications

1.Avoid known hepatotoxic drugs and alcohol (barbiturates, sedatives, hypnotics

, and     acetaminophen)

2. Diuretics – reduce fluid retention and ascites

            Spironolactone – lasix

3.Reduce nitrogenous load and lower serum ammonia levels

Lactulose and neomycin.  Reduce the number of ammonia forming organisms

in the bowel and ammonium is excreted in the feces

                        4. Lower hepatic venous pressure- prevent rebleeding of esophageal varices

                                    Corgard, Imdur, Monoket

5.       Ferrous sulfate and folic acid – treat anemia

6.       Vitamin K – reduce risk of bleeding

7.       Antacids are prescribed as indicated

8.       Serax  a benzodiazepine antianxiety/sedative drug, not metabolized by liver

to treat acute agitation

B.      Dietary and fluid management

1.       Sodium intake is restricted to under 2 g/day

2.       Fluids are limited to 1500mL/day

3.       Adequate calories 75-100g of protein per day

4.       With encephalopathy is present, 60-80 g/day

5.       Vitamins and mineral supplements.  Particularly B-complex

6.       Magnesium deficiency common in alcohol-induced cirrhosis

7.       TPN (total parenteral nutrition)  may be initiated through a Central line

Contains carbohydrates high concentration of dextrose), protein, e-lytes

vitamins, minerals and fat emulsion.

         New containers every 24 hours – procedure for checking similar to blood

checks.

         Solutions are mixed specifically for patient based on lab value

         Always infused with pump

         Blood glucose levels carefully monitored and insulin may be administered

as needed.  e-lytes also closely monitored and formula adjusted as needed

         High risk for infection due to disruption of skin barrier and high

glucose solution.  Monitor closely for S&S of infection

C.      Paracentesis

1.       Aspiration of fluid from peritoneal cavity to relieve respiratory distress

2.       Moderate withdrawal 500ml to 1L to reduce risk of fluid and electrolyte

imbalances

3.       4-6L of fluid may be done Albumin intravenously during large

 volume paracentesis

4.       Nursing care :

Informed consent

Weight prior to paracentesis

Vital signs for baseline

Have client void immediately prior to test to avoid bladder puncture

Position seated, on side of bed or in chair

Assess site for fluid leakage, change dressing prn

 

D.      Gastric Endoscopic

1.       Gastric lavage – saline  improve visualization; decrease bleeding

Nursing care during lavage

         Baseline assessment – VS, abdominal inspection, girth BS

         Pt teaching – gain cooperation during procedure

         Fowler’s or semi-fowlers position

         Verify placement - test

2.       Varices may be sclerosed to reduce risk of recurrent bleeding

3.       Banding – small rubber bands are placed on varices to occlude blood flow

4.       Balloon tamponade – Sengstaken-blakemore tube and balloons are

inflated to apply direct pressure on the bleeding varices

                                                ET tube inserted prior to support airway and reduce aspiration risk

                                                Short term measure only

E.      Transjugular intrahepatic portosystemic shunt (TIPS)

1.       Channel created through the liver tissue – shunt inserted to allow blood flow to

bypass the cirrhotic liver

2.       Relieves pressure in esophageal varices

3.       Stenosis and occlusion of shunt are frequent complications

4.       Increases the risk of developing hepatic encephalopathy

5.       Short term measure

F.      Surgery -  liver transplantation

Indicated for some clients with irreversible, progressive cirrhosis

G.     Central Venous Catheter

Placement confirmed by X-ray before use.

Triple lumen most common – administer meds, parenteral solutions, draw labs.

            Review nursing care of Central Venous Catheter care

VI.                NURSING DIAGNOSIS

Excess fluid volume

Disturbed thought process

Impaired skin integrity

Imbalanced nutrition:  less than body requirements

Ineffective health maintenance

Fatigue

 

VII HOME CARE

            A. Teaching

1.       Avoid alcohol and other hepatotoxic drugs

2.       Diet and fluid intake restriction and recommendations

3.       Medications – timing, adverse effects

4.       Bleeding precautions

5.       Manifestations of potential complications to be reported

6.       Skin care techniques to reduce pruritus and damage

7.       Ways to manage fatigue and conserve energy

B.  Referals

1.       Home health services, etc.

2.       Local support groups

3.       Hospice if indicated