HEPATIC ENCEPHALOPATHY AND COMA

Hepatic encephalopathy, is a life-threatening complication of liver disease, occurs with

profound liver failure and may result from the acculmulation of ammonia and other toxic
metabolites in the blood. Hepatic coma represents the most advanced stage of hepatic
encephalopathy. Some researchers describe a false or weak neurotransmitter as a
cause, but the exact mecahnism is not fully understood. These false neurotransmitters
may be generated from an intestinal source and result in the precipitation of
encephalopathy.Many other theories exist about the causes of encephalopathy,
including excess tryptophan and its metabolites, and endogenous benzodiazepines or
opiates. Benzodiazepine-like chemicals (compounds) have been detected in the
plasmaAnd cerebrospinal fluid of patients with hepatic encephalopathy due to cirrhosis
(Bacon & Di Bisceglie, 2000).

Portal-systemic encephalopathy, most common type of hepatic encephalopathy,

occurs primary in patients with cirrhosis with portal hypertension and portal-systemic
shunting.

PATHOPHYSIOLOGY

Ammonia accumulates because damaged liver cells fail to detoxify and convert to
urea the ammonia that is constantly entering the bloodstream. Ammonia enters the
bloodstream as a result of its absorption from the GI tract and its liberation from kidney
and muscles cells. That increased ammonia concentration in the blood causes brain
dysfunction and damage, resulting in hepatic encephalophaty.

Circumtances that increase serum ammonia levels tends to aggravate or precipitate

hepatic encephalophaty. The largest source of ammonia is the enzymatic and bacterial
digestion of dietary and blood proteins in the GI tract. Ammonia from these sources is
increased as a result of GI bleeding (ie, bleeding esophageal varices or chronic GI
bleeding), a high- protein diet, bacterial infections and uremia. The indigestion of
ammonium salts also increases the blood ammonia level. In the presence of alkalosis or
hypokalemia, increased amounts of ammonia are absorbed from the renal tubular fluid.

Conversely,serum ammonia is decreased by elimination of protein from the diet and by

the administration of antibiotic agents, such as neomycin sulfate, that reduce the
number of intestinal bacteria capable of converting urea to ammonia (Dudek,2001).

Other factors unrelated to incresed serum ammonia levels that may cause hepatic
encephalopathy in susceptible patients include excessive diuresis, dehydration,
infections, surgery,fever, and some medications (sedative agents tranquilizers,
analgesic agents, and diuretic medications that cause potassium loss). Table 39-3
presents the stages of hepatic encephalopathy, common signs and symptoms, and
potential nursing diagnoses for each stage.

CLINICAL MANIFESTATIONS

The earliest symptoms of hepatic encephalopathy include minor mental changes and
motor disturbances. The patients appears slightly confused, has alterations in mood,
becomes unkempt, and has altered sleep paterns The patients tends to sleep during
the day and have restless and insomia at night. As hepatic encephalopathy
progress,the patient may be difficult to awaken. ASTERIXIS (flapping tremor of the
hands) may occur (fig. 39-12).

Simple tasks, such as handwriting, become difficult. A hand writing or a drawing

sample (e.g star figure), taken daily may provide graphic evidence of progression or
reversal of hepatic encephalophaty. In ability to reproduce a simple (Fig.39-13) is
referred to as structional apraxia. In the early stages of hepatic encephalopathy. The
deep tendon reflexes are hyperactive; with worsening of hepatic encephalopathy,
these reflexes disappear and the extremities may become flaccid.

ASSESSMENT AND DIAGNOSTIC FINDINGS

The electroencephalogram (EEG) shows generalized slowing , an increase in the

amplitude of brain waves, characteristics triphasic waves.Occasionally, FETOR
HEPATICUS, a sweet,slightly fecal odor to the breath presumed to be of intestinal
origin may be noticed. Also been described as a similar to that of freshly mowed
grass, acetone , or old wine.Fetor hepaticus is prevalent with extensive collateral
portal circulation in chronic liver disease. In a more advanced stage, there are gross
disturbances of consciousness and the patients is completely disoriented with respect to
time and place. With further progression of the disorder, the patient lapses into frank
coma and may have seizures. Approximately 35% of all patients with cirrhosis of liver
die in hepatic coma.

MEDICAL MANAGEMENTS

Lactulose (Cephulac) is administered to reduce serum ammonia levels.It acts by

several mechanisms that promote the excretion of ammonia in the stool: (1) ammonia is
kept in the ionized state, resulting in a fall in colon to the pH, reversing the normal
passage of ammonia from the colon to the blood;(2) evacuation of the bowel takes
place, which decreases the ammonia
Absorbed from the colon; and (3) the fecal flora are changed to organisms that do not
produce ammonia from urea. Two or three soft stools per day are desirable; this
indicates that lactulose is performing as intended.

Possible side effects include intestinal bloating and cramps, which usually disappear
within a week. To mask the seewt taste, to which some patients object, lactulose can be
diluted with fruit juice. The patient is closely monitored for hypokalemia and dehydration.
Other laxatives are not prescribed during lactulose administration because their effects
would disturb dosage regulation. Lactulose can be administered by nasogastric tube or
enema for patients who are comatose or in whom oral administration is contraindicated
or impossible.

Other aspects of management include intravenous administration of glucose to

minimize protein breakdown, administration of vitamins to correct deficiencies, and
correction of electrolyte imbalances (especially potassium). Additional principles of
management of hepatic encephalopathy include the following:

• Therapy is directed toward treating or removing the cause

• Neurologic status is assessed frequently. A daily record is kept of handwriting

and performance in arithmetic to monitor mental status.

• Fluid intake and output and body weight are recorded each day.

• Vital signs are measured and recorded every 4 hours

• Potential sites of infection (peritoneum, lungs) are assessed frequently, and

abnormal findings are reported promptly.

• Serum ammonia level is monitored daily.

• Protein intake is restricted inpatients who are comatose or who have

encephalopathy that is refractory to lactulose and antibiotic therapy

• Reduction in the absorption of ammonia from the GI tract is accomplished by the

use of gastric suction, enemas, or oral antibiotics.

• Electrolyte status is monitored and corrected if abnormal.

• Sedatives, tranquilizers, and analgesic medications are discontinued.

• Benzodiazepine antagonists (flumazenil {Romazicon} may be administered to

improve encephalopathy whether or not the patient has previously taken
benzodiazepines.
NURSING MANAGEMENT

The nurse is responsible for maintaining a safe environment to prevent injury, bleeding,
and infection. The nurse administers the prescribed treatments and monitors the patient
for the many potentila complications. The nurse also communicates with the patients
family to keep them informed about the patients status, and supports them by expalining
the procedures and treatments that are part of the patients care. If the patient recovers
from the hepatic encephalopathy and coma, rehabilitation is likely to be prolonged.
Thus, the patient and family will require assistance to understand the causes of this
severe complication and to recognize that it amy recur.

PROMOTING HOME AND COMMUNITY-BASED CARE

Teaching Patients Self-Care. If the patient has recovered from hepatic encephalopathy
and is to be discharged home, the nurse instructs the family to watch for subtle signs of
recurrent encephalopathy. In the acute phase of hepatic encephalopathy, dietary protein
may be reduced to 0.8 to 1.0 g/kg per day. During recovery, and in the home situation, it
is important to instruct the patient in maintenance of a low-protein, high-calorie diet.
Protein may then be added in 10-g incrments every 3-5 days. Any relapse is treated by
a return to the previous level. The limits of tolerance are usually 40 to 60 g/day (1.0 to
1.5 g/kg per day). Continued use of lactulose in the home environment is not
uncommon, and the patient and family should monitor its efficacy and side-effects
closely. Use of vegetable rather than animal protein may be indicated in patients whose
total daly protein tolerance is less than 1 g/kg. Vegetable protein intake may result in
improved nitrogen balance without precipitating or advancing hepatic encephalopathy.

Continuing Care. Referral for home care is warranted for the patient who returns home
after recovery from hepatic encephalopathy. The home care nurse assesses the
patients physical and mental status and collaborates closely with the physician. The
home visit also provides an opportunity for the nurse to assess the home environment
and the ability of the patient and family to monitor signs and symptoms and to follow the
treatment regimen. Home care visits are particularly important if the patient lives alone,
because encephalopathy may affect the patients ability to follow the treatment regimen.
The nurse reinforces previous teaching and reminds the patient and family about the
importance of dietary restrictions, close monitoring, and follow-up.

OTHER MANIFESTATION OF LIVER DYSFUNCTION

Edema and Bleeding

Many patients with liver dysfunction develop generalized edema from hypoalbuminemia
tha results from decreased hepatic production of albumin. The production of blood
clotting factors by the liver is also reduced, leading to an increased incidence of
bruising, epistaxis, bleeding from wounds, and as described above, GI bleeding.

Vitamin Deficiency.

Decreased production of several clotting factors may be due, in part, to deficient

absorption of Vitamin K from the GI tract. This probably is caused by the inability of liver
cells to use vitamin K to make prothrombin. Absorption of the other fat-soluble vitamins
(Vitamins A,D and E) as well as dietary fats may also be impaired because odf
decreased secretion of bile salts into the intestine.

Another group of problems common to patients with severe chronic liver dysfunction
results from inadequate intake of sufficient vitamins. Among the specific deficiency
states that occur on this basis are:

• Viatmin A deficiency, resulting in night blindness and eye and skin changes.

• Thiamine deficiency, leading to beriberi, polyneuritis, and Wernicke-Korsakoff

psychosis.

• Riboflavin deficiency, resulting in characteristic skin and mucous membrane

lesions.

• Pyroxidine deficiency, resluting in skin and mucous membrane lesions and

neurologic changes.

• Vitamin C deficiency, resulting in the hemorrhagic lesions of scurvy.

• Vitamin K deficiency, resulting in hypoprothrombinemia, characterized by

spontaneous bleeding and ecchymoses

• Folic acid deficiency, resulting in macrocytic anemia

The treat of these avitaminoses provides the rationale for supplementing the diet of
every patient with chronic liver disease (especially if alcohol-related) with ample
quantities of vitamins A,B complex, and K and folic acid.

Metabolic Abnormalities

Abnormanlities of glucose metabolism also occur; the blood glucose level may be
abnormally high shortly after a meal (a diabetic type glucose tolerance test result), but
hypoglycemia may occur during fasting because of decreased hepatic glycogen
reserves and decreased gluconeogenesis. Because the ability to metabolize
medications is decreased, medication dosages must be reduced for the patient with
liver failure.
Many endocrine abnormalities also occur with liver dysfunction because the liver cannot
metabolize hormones normally, including androgens or sex hormones. Gynecomastia,
amenorrhea, testicular atrophy, loss of pubic hair in the male, and menstrual
irregularities in the female and other disturbances of sexual function and sex
characteristics are thought to result from failure of the damaged liver to inactivate
estrogens normally.

Pruritus and Other Skin Changes

Patients with liver dysfunction resulting from biliary obstruction commonly develop
severe itching (pruritus) due to retention of bile salts. Patients may develop vascular (or
arterial) spider angiomas on the skin, generally above the waistline. These are
numerous small vessels resembling a spider’s legs. These are most frequently
associated with cirrhosis, especially in alcoholic liver disease. Patients may also
develop reddened palms (liver palms or palmar edema).

Chronic Renal Failure

- a progressive irreversible deterioration in renal function in which the body’s

ability to maintain metabolic and fluid and electrolyte balance fails resulting
from uremia or azotemia ( retention of urea and other nitrogenous wastes in
the blood)
- may be caused by systemic dse. Such as diabetes mellitus, hypertension,
chronic glomerulonephrotis, pyelonephritis, obstruction of urinary tract,
infections
- Environmental and occupational agents are lead, cadmium, mercury,
chromium

Pathopysiology

- end product of protein metabolism accumulate in the blood

- Uremia develops and affects the body

Clinical manifestation

Uremic frost- the deposits of urea crystals on the skin

Hypertension Kussmaul respiration

Pitting edema uremic pneumonia

Periorbital edema uremic fetor ammonia breath

Pericardial friction rub metallic taste

Distended neck veins mouth ulceration

Pericarditis anorexia

Pericardial effusion nausea and vomiting

Pericardial tamponade hiccups

Hyperkalemia constipation and diarrhea

Hyperlipidimia

Weakness and fatigue bleeding of GI

Confusion inability to concentrate Anemia

Disoriented

Tremors thrombocytopenia

Seizure

Restlessness

Burning of soles anf feet

Gray bronze skin

Pruritus dry and flaky skin

Ecchymosis

Purpura

Thin brittle nails

Thinning of hair

Crackles

Thick tenacious sputum

Depressed cough

Pleuritic pian

Shortness of breath

Tachypnea

Diagnostic test

BUN

Creatinine

- check for
o glomerular filtration rate
o sodium and water retention
o acidosis
o anemia
o calcium and phosphorus imbalance

Complications

- Hyperkalemia due to decrease excretion, metabolic acidosis

- Pericarditis, pericardial effusion, pericardial tamponade due to retention of
uremic waste products
- Hypertension due to sodium and water retention and malfunction of the rennin
angiotensin and aldosterone system
- Anemia due to decrease erythropoietin

Medical management

1. Pharmacologic therapy administer antihypertensive and erythopoetin (epogen)

iron supplement calcium and phosphate binding agents
2. Antacids
3. Antihypertensive agents
4. eryhtropoetin- to treat anemia EPOGEN
5. Nutritional therapy
6. dialysis