Hepatic encephalopathy
Hepatic encephalopathy: Excerpt from Handbook of Diseases
Also known as hepatic coma, hepatic encephalopathy is a neurologic syndrome that results from the liver’s failure to detoxify noxious agents that arise from the GI tract. Most common in patients with cirrhosis, this syndrome is caused primarily by ammonia intoxication of the brain. It may be acute and self-limiting or chronic and progressive.
Treatment requires correction of the precipitating cause and reduction of blood ammonia levels. In advanced stages, the prognosis is extremely poor, despite vigorous treatment.
Causes
Hepatic encephalopathy develops as a result of rising blood ammonia levels. Several factors cause these levels to rise.
Improper shunting of blood
Normally, the ammonia produced by protein breakdown in the bowel is metabolized to urea in the liver. When portal blood shunts past the liver, ammonia directly enters the systemic circulation and is carried to the brain.
Such shunting may result from the collateral venous circulation that develops in portal hypertension or from surgically created portal-systemic shunts. Cirrhosis further compounds this problem because impaired hepatocellular function prevents conversion of ammonia that reaches the liver.
Other factors
Other factors that predispose to rising ammonia levels include excessive protein intake, sepsis, excessive accumulation of nitrogenous body wastes (from constipation or GI hemorrhage), and bacterial action on protein and urea to form ammonia.
Certain other factors heighten the brain’s sensitivity to ammonia intoxication, including fluid and electrolyte imbalances (especially metabolic alkalosis), hypoxia, azotemia, impaired glucose metabolism, infection, and administration of sedatives, narcotics, and general anesthetics.
Signs and symptoms
Clinical manifestations of hepatic encephalopathy vary, depending on the severity of neurologic involvement, and develop in four stages. Encephalopathy is usually graded by behavioral changes, the presence of asterixis, and EEG findings, with behavioral changes being the most apparent indicator.
❑ Grade or stage I (prodromal stage): mood fluctuation, sleep-wake reversal, forgetfulness; commonly overlooked because early symptoms, such as slight personality changes (disorientation, slurred speech) and a slight tremor, are subtle.
❑ Grade or stage II (impending stage): disorientation, confusion; may be incontinent; tremor progressing to asterixis, the hallmark of hepatic encephalopathy. Asterixis is characterized by quick, irregular extensions and flexions of the wrists and fingers when the wrists are held out straight and the hands flexed upward. Lethargy, aberrant behavior, and apraxia also occur.
❑ Grade or stage III (stuporous stage): hyperventilation; patient is stuporous but noisy and abusive when aroused.
❑ Grade or stage IV (comatose stage): hyperactive reflexes, a positive Babinski’s sign, fetor hepaticus (musty, sweet breath odor), and coma.
Diagnosis
Clinical features, a positive history of liver disease, and elevated serum ammonia levels in venous and arterial samples confirm hepatic encephalopathy. Other supportive test results include an EEG that slows as the disease progresses, an elevated bilirubin level, and prolonged prothrombin time.
Treatment
Effective treatment stops the progression of encephalopathy by reducing blood ammonia levels. Such treatment eliminates ammonia-producing substances from the GI tract by:
❑ administration of lactulose to reduce the blood ammonia levels and use of sorbitol-induced catharsis to produce osmotic diarrhea; neomycin therapy may be added if lactulose alone doesn’t reduce ammonia levels
❑ reduction of dietary protein intake
❑ continuous aspiration of blood from the stomach.
Lactulose
Lactulose traps ammonia in the bowel and promotes its excretion. It’s effective because bacterial enzymes change lactulose to lactic acid, thereby rendering the colon too acidic for bacterial growth. At the same time, the resulting increase in free hydrogen ions prevents diffusion of ammonia through the mucosa; lactulose promotes conversion of systemically absorbable ammonia to ammonium, which is poorly absorbed and can be excreted.
The usual dosage of lactulose syrup is 30 to 45 ml by mouth (P.O.) three or four times daily. For acute hepatic coma, 300 ml of lactulose syrup diluted with 700 ml of water may be administered by retention enema. Lactulose therapy requires careful monitoring of fluid and electrolyte balance.
Neomycin
Neomycin is usually given in a dose of 3 to 4 g daily P.O. or by retention enema. Although neomycin is nonabsorbable at the recommended dosage, an amount that exceeds 4 g daily may produce irreversible hearing loss and nephrotoxicity after prolonged use.
Other treatments
Treatment may also include potassium supplements to correct alkalosis (from increased ammonia levels), especially if the patient is taking diuretics.
Special considerations
❑ Frequently assess and record the patient’s level of consciousness and neurologic status. Continually orient him to place and time.
❑ Monitor intake and output and fluid and electrolyte balance. Check daily weight and measure abdominal girth. Immediately report signs of anemia (decreased hemoglobin), infection, alkalosis (increased serum bicarbonate levels), and GI bleeding (melena, hematemesis).
❑ Give prescribed drugs and watch for adverse effects.
❑ Consult with the dietitian to provide the specified low-protein diet, with carbohydrates supplying most of the calories. Provide good mouth care.
❑ Promote rest, comfort, and a quiet atmosphere. Discourage strenuous exercise.
❑ Use restraints if necessary, but avoid sedatives.
Clinical tip Protect the comatose patient’s eyes from corneal injury by using artificial tears or eye patches.
❑ Provide emotional support for the family of the patient with end-stage liver disease.
Book Source Details
- Book Title: Handbook of Diseases
- Author(s): Springhouse
- Year of Publication: 2003
- Copyright Details: Handbook of Diseases, Copyright © 2003 Lippincott Williams & Wilkins.
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Copyright notice for book excerpts: Copyright © 2008 Lippincott Williams & Wilkins. All rights reserved.
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More About This Book:
Title: Handbook of Diseases
Authors: Springhouse
Publisher: Lippincott Williams & Wilkins
Copyright: 2003
ISBN: 1-58255-266-5
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