HEPATIC ENCEPHALOPATHY AND COMA AND END STAGE RENAL DSE

HEPATIC ENCEPHALOPATHY AND COMA

Hepatic encephalopathy, is a lifethreatening 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

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 portalsystemic 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

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 breath 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
glomerular

filtration rate sodium and water retention acidosis anemia 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.

2. 3. 4. 5. 6.

Pharmacologic therapy administer antihypertensive and erythopoetin (epogen) iron supplement calcium and phosphate binding agents Antacids Antihypertensive agents eryhtropoetin- to treat anemia EPOGEN Nutritional therapy dialysis

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