The blood bypasses the liver via the collaterals and the toxic metabolities (e.g ammonia, free fatty acids and mercapts ) pass directly to the brain to produce the encephalopathy. There is also an increased sensitivity of CNS neurons to the inhibitory neurotransmittor (GABA) and an increase in circulating levels of endogenous benzodiazepines. Cerebral edema is frequently present and contributes to the development of clinical features.
- Increased Nitrogen Load
- Gastrointestinal bleeding
- Excess dietray protein
- Electrolyte and Metabolic Imbalance
- Narcotics, Tranquilizers. sedatives
- Portosystemic shunt
- Superimposed acute liver failure
- Progressive liver disease
- Disturbance of sleep with sleeping during day and awaking in night is one of the earliest features.
- Alteration in personality, mood disturbances, confusion, deterioration of self care and deterioration of hand writing, slurring of speech, disorientation, drowsiness and eventually coma develop.
- Convulsions also sometimes develops.
- Hyperventilation, fever, nausea and vomiting are also common
- Fetor hepaticus: a sweet smell to the breath due to mercaptans
- Flapping tremor: is a non -rhythmic asymmetric lapse in voluntary sustained position of limbs , head and trunk. It is best demonstrated when the patient extends the arms and dorsiflexes the hands.
- Constructional Apraxia: patient is unable to do the already learnt things such as write or draw a five pointed star.
Stage 1: Euporia or depression, mild confusion, slurred speech, disoriented speech. Flapping tremor may or may not be present. EEG is usually normal.
Stage 2: Lethargy, moderate confusion and EEG is abnormal. Flapping tremor appears.
Stage 3: Marhed confusion, incoherent speech, sleeping but arousable.
Stage 4: Coma; initially responsive to noxious stimuli later becomes unresponsive.
Diagnosis of hepatic encephalopathy is usually made clinically if acute or chronic liver disease is evident. There is no confirmatory test available however following investigation help in the diagnosis:
1. Liver Biochemistry: such as LFT’s, PT, serym albumin – to confirm the presence of liver disease.
2. EEG: shows diffuse slowing of the normal alpha waves with eventual development of delta waves. Visual evoked potential also detect subclinical encephalopathy.
3. Arterial blood Ammonia: elevated levels of arterial blood ammonia is highly suggestive of diagnosis in the presence of clinical features of hepatic encephalopathy. However ammonia may be elevated in the absence of encephalopathy therefore it is not diagnostic.
- Identify and remove the precipitating factor.
- Stop or reduce diuretic therapy.
- Correct any electrolyte imbalance.
- Lower blood ammonia levels by decreasing the absorption of protein and nitrogenous products from the intestine .
- Constipation should be avoided.
- Give purgatives in order to empty the bowels of nitrogenous substances.
- Treat any infection if present.
- Flumazenil a benzodiazepine receptor antagonist can induce a transient improvement.
- Long term management includes low protein diet, Duphalac, an osmotic purgative 10-30 cc TDS and avoidance of precipitating factors.
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