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Saturday, 8 October 2011

How to Diagnose and Treatment Encephalopathy Hepaticum

Diagnosis is made on the basis of anamnesis history physical examination and laboratory disease.
1. history
History of liver disease
History of the possibility of trigger factors.
Is there a neuropsychiatric disorder: changes in Hepatic Encelopathy behavior, personality, intelligence, speech and so on. 

2. physical examination
Determine level of consciousness / level of encephalopathy.
Stigmata of liver disease (signs of liver failure and portal hypertension physiology).
The abnormalities neurologic: incoordination tremor, pathological reflexes, rigidity.
Convulsions, dysarthria.
Symptoms of severe infection / septicemia.
Signs of Hepatic Encelopathy dehydration.
There gastrointestinal bleeding.
3. laboratory tests
a. hematology
Hemoglobin, hematocrit, erythrocyte count, leukocyte-platelet, leukocyte counts.
If necessary: physiology of blood clotting.
b. blood biochemistry
Test the liver physiology: transaminase, billirubin, protein electrophoresis, cholesterol, alkaline phosphatase.
Test renal physiology: Urea nitrogen (BNU), serum creatinine.
Levels of blood ammonia.
Top indication: HBsAg, anti-HCV, AFP, electrolytes, blood gas analysis.
c. Urine and stool routine test
4. Other tests (not routine).
a. EEG with potential trigger visual (visual evoked potential) is a new method for assessing subtle early changes in mental status in cirrhosis.
b. CT scan of the head, usually done in stages to assess encephalopathy severe brain edema and get rid of structural lesions (especially subdural hematoma in alcoholics).
c. Lumbar puncture, generally reveal normal results, except for an increase in glutamine. Cerebrospinal fluid can be colored xantochrome due to increased levels of bilirubin. White blood cell count increased spinal fluid showed the presence of infection. Brain edema may lead to increased pressure.

Algorithm how to treatment Encephalopathy Hepatic

1. Acute type
Management of type either / or types of secondary endogenous / exogenous, on the same principle that is comprised of general and specific measures. For the type of secondary / exogenous factors necessary management originators.
a. common actions
1. Patients with stage III-IV need intensive supportive care nyang: note the position of lying down, free the airway, oxygen administration, catheter forley pairs.
2. Monitoring awareness, neuropsychiatric conditions, cardiopulmonary and renal systems of fluid balance, electrolyte and acid and alkaline.
3. Giving calories 2000 cal / day or more in the acute phase protein-free gram / ​​day (orally, via nasogastric tube or parental)
b. special Treatment
1. Reduce protein intake
  § A diet without protein for stage III-IV
  § A diet low in protein (vegetable) (20gram/hari) for stage I-II. Immediately after the acute phase is exceeded, protein intake increased from the starting load of 10 grams of protein is then added gradually until the need maintanance (40-60 grams / day).
2. Reduce colonic bacterial populations (urea splitting organisms).
  § lactulose orally for stage I-II or nasogastric tube for stage III-IV, 30-50 cc per hour, given enough until there is mild diarrhea.
Lacticol (Beta Galactoside Sorbitol), dose: 0.3 to 0.5 grams / day.
  § intestinal emptying with lavement 1-2x / day: can be used such as MgSO4 or osmotic cathartic laveman (using 20% solution of lactulose or neomycin solution of 1% in order to get pH = 4)
Antibiotics: neomycin 4x1-2gram / ​​day, orally, for stage I-II, or
  § through a nasogastric tube for stage III-IV.
Rifaximin (derifat Rimycin), dose: 1200 mg per day for 5 days is said to be quite effective.
3. Other medicines
  § Patients with hepatic coma, need to get parenteral nutrition. As a first step can be given fluids dektrose 10% or 10% maltose, because the carbohydrate needs should be met first. The next step may be given fluids containing AARC (Comafusin liver) or a mixture slightly in the AARC AAA (Aminoleban): 1000 cc / day. The purpose of AARC is to prevent the entry of AAA into the brain barrier, decrease protein catabolism, and reduced blood ammonia concentration. This fluid is much discussed lately.
L-DOPA: 0.5 grams orally for stage I-II or through a nasogastric tube for stage III-IV every 4 hours.
  § Avoid sedativa or hipnotic, unless the patient is very anxious to be given diimenhidrimat (Dramamine) 50 mg im: if necessary, repeated every 6-8 hours. Choice of other drugs: phenobarbital, which is mainly through renal excretion. Vit K 10-20 mg / day im or orally or nasogastric tube  .
  §   Drugs in the experimental stage:
o Bromocriptine (dopamine receptor antagonist) in doses of 15 mg / day may provide improved clinical, psychometric and EEG.
o benzodiaepin receptor antagonist (flumazenil), gave satisfactory results, especially for stage I-II.
4. radical treatment
Tranfusio exchange, plasmapheresis, dialysis, charcoal hemoperfusion, transplant liver.
c. radical treatment
1. Correction of fluid balance disturbances, electrolyte, acid-base.
2. Penggulangan gastrointestinal bleeding
3. Overcome the infection with appropriate antibiotic in adequate doses.
4. Stop the originator medicines Hepatic encephalopathy; hepatotoxic drugs, diuretics, or which cause constipation.

2. Chronic type
The principles of treatment of chronic type Hepatic encephalopathy.
a. Low-protein diet, a maximum of 1 g / kg mainly vegetable protein.
b. Avoid constipation by giving lactulose in sufficient doses (2-3 x 10 cc / day).
c. When symptoms of encephalopathy increased, plus neomycin 4x1 grams / day.
d. When arising acute exacerbation, the same as the type of acute Hepatic encephalopathy.
e. Need long-term monitoring for the assessment of mental and neuromuscular conditions.
f. Elective surgery: colony by pasis, liver transplantation, particularly for chronic Hepatic encephalopathy stage III-IV.

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