Lecture on diagnosis and treatment of hepatic coma

Define

Hepatic coma is a neuropsychiatric disorder occurring in patients with hepatocellular failure with or without association with the portal–host fusion.

It is a metabolic coma whose underlying lesion is CNS dysfunction.

Acute hepatic coma is a hepatic coma occurring within 8 weeks of the onset of symptoms of liver disease, which is an acute liver failure on the background of acute liver disease.

Chronic hepatic coma is seen in chronic liver disease (cirrhosis) with exacerbations with triggers.

Is a very serious complication of liver disease; It is a medical emergency requiring early diagnosis and prompt treatment.

Pathology

Acute hepatic coma

Cerebral edema increased intracranial pressure.

Chronic coma

The proliferation of Astrocytes (astrocytes).

Brain atrophy.

Pathophysiology

The pathogenesis has not yet been elucidated.

Nervous Toxicity

Including NH3, Phenol, short-chain fatty acids, Mercaptan... the outstanding multi-factor effect is NH3 causing hepatic coma related to cellular energy or nerve conduction.

Pseudo sympathetic neurotransmitter

Normally, nerve impulses are transmitted by biological substances acting on synapses. The biological substances that are Acetylcholine, catecholamine, Dopamine are true sympathomimetic neurotransmitters.

In a hepatic coma, there is an increase in aromatic amino acids in the blood such as Pheninalanin, Tyrosine, Tryptophan, Methionine, Glutamate, Aspartate that Phenylalanine and Tyrosine increase will lead to:

Inhibits Tyrosine Hydroxylase activity.

Increased synthesis of pseudo sympathetic neurotransmitters:

bphenyl ethanolamine and Octopamine.

Benzodiazepine gaba system

Benzodiazepines can be endogenous (present in the brain tissue of patients with hepatic coma) or exogenous (due to the use of benzodiazepines as sedatives).

GABA (Gamma Amino Butyric Acid): is an inhibitory nervous system formed in the gut.

Benzodiazepine binds to the GABA receptor, opening the chloride channel, chloride enters the CNS to generate an action potential, and the central nervous system is inhibited as the action of GABA.

Motivational factors

Occurs only in chronic liver disease, which can be classified into the following four groups:

Causes of increased blood NH3  

Gastrointestinal bleeding (due to rupture of dilated esophageal varices):

Blood enters the intestines due to the action of intestinal bacteria to form NH3 and then enters the blood, liver failure cannot convert it to urea.

Decrease blood flow to the kidney => increase BUN => increase NH3.

Blood transfusion, reserve blood with NH3 increased over time:

01 day => 170 mg%; 04 days => 330 mg%; 21 days => 900 mg%.

High protein intake also increases NH3.

Constipation: intestinal bacteria break down urea into NH3 which is put into the blood. Increases the production of Mercaptan, Indol, Scatol.

Renal failure: increase BUN => increase NH3. blood.

Electrolyte and metabolic disorders

 Lower blood potassium.

 Low blood sodium.

 Alkaline blood.

 Reduced blood oxygen.

 Reduced blood volume.

Using drugs that are toxic to the liver

 Sedative.

 Antipyretic.

 Diuretic...

Mixture

Infection.

Surgery.

There is also acute liver disease.

Progressive liver disease.

Connecting door - master.         

Symptom

Clinical

Consciousness disorder:

Poor memory, difficulty concentrating.

Change behavior, attitude: happy, sad, slurred speech, disorientation in space and time.

Comatose.

Neurological signs:

No localized nerve markers.

Shaking (an early sign).

Increased tendon reflexes.

Convulsions.

There may be Babinski marks on both sides.

Special signs:

Liver odor.

Pulmonary hyperventilation (rapid-deep).

Subclinical

Measure the amount of Glutamine in the cerebrospinal fluid (cannot be done).

NH3 in arterial blood (normal 75- 150 mg%):

NH3 increased in 90% of cases.

The increase in NH3 is not parallel to the severity of the disease.

There is a phenomenon of late arrival: when NH3 increases within 1-3 days after the patient is comatose and after NH3 returns to normal within 1-3 days, the patient will wake up.

EEG:

Valuable in the diagnosis of coma, manifesting:

Slow-wave is not stable.

Slow waves are interspersed with Theta waves.

Delta waves interspersed theta wave.

Delta Waves.

Slow waves have low amplitude.

The paraclinical need to do more:

Blood sugar.

Urea, ionogram, alkaline reserve.

Definite diagnosis

Clinical

Consciousness disorder.

Neurological signs.

Special signs.

Symptoms of liver failure.

Subclinical

Measure the concentration of NH3 in the blood.

Liver function tests.

Electroencephalogram.

Differential diagnosis

Mainly distinguished from cases of perceptual disorders such as:

Coma due to hypoglycemia.

Coma due to hyperglycemia.

Other metabolic coma: Hyperuricemia syndrome.

Level diagnosis

Team:

Exciting, inhibiting.

Confused speech is not clear.

Sleep disorders.

There may be tremors.

Normal EEG.

Level II:

Dull, moderately confused.

Shaking sign.

Abnormal EEG.

Grade III:

Doze off, doze off.

Incoherent speech.

Shaking sign.

Abnormal EEG.

Grade IV:

Coma, initially responsive to stimuli, later not.

No more shaking marks.

Abnormal EEG.

Evolution and prognosis

It is a serious complication of liver disease, high mortality rate, and poor prognosis.

More than 50% mortality.

Prognosis is mainly based on hepatocellular failure: the more severe the liver failure, the higher the mortality rate.

An appropriate prognostic assessment is based on:

Acute or chronic liver disease.

There is no cure for acute liver disease.

Is chronic liver disease a predisposing factor?

Treatment

Mainly aimed at two goals.

Limit or treat predisposing factors (chronic liver disease).

Reduces blood NH3 and other toxins.

Treatment of hepatic coma

Protein reduction diet 0.5-0.75g/kg/day (10-20g/day)

Plant protein is easier to tolerate than animal protein, when it is good, increase protein by 10g every 3 to 5 days, if there is improvement, it will continue to increase until fusion (acute liver coma needs to be increased more than normal people for the liver to recover; chronic hepatic coma 1g/kg/day).

A solution of amino acids with a high branching rate can be infused to keep NH3 and reduce NH3 in the blood.

Superior transmission

Expels waste products from the intestines

Lactulose turns NH3 into NH4 that is not absorbed into the blood and increases intestinal motility causing diarrhea.

Dosage: Lactulose 50% 15-30 ml 3 times/day, then reduce the dose to consume 2-3 times/day

Or enema is very effective in case of gastrointestinal bleeding.

Kills intestinal germs

Neomycin 2-4g/day divided into 4 times for 7-10 days.

Or Flagyl 0.25g x 3 times/day for 7-10 days.

Or enema with antibiotics dissolved in 200 ml of water with a concentration of 1-2%.

Amino acid solution with a high branching rate

 Morihepamine, Aminoplasmalhepa less effective.

Strong measures

Blood change.

Cross circulation.

Colon resection.

Liver transplant

Efficacy is unclear, still being studied.

Anti-cerebral edema (acute hepatic coma)

Mannitol 20% 1g/kg rapid infusion repeat 4-6 hours.

Barbituric or Thiopental.