Pathology of liver coma

2021-01-27 12:00 AM

Due to severe and widespread liver damage such as in acute hepatitis, toxic inorganic phosphorus, tetraclorure de Carbone, and Amanite phaloide

Outline

Liver coma is also known as hepatic encephalopathy, or brain-portal disease is defined as secondary brain disorders caused by a severe multifaceted hepatic failure or triggered after septal surgery. master.

Whole disease

In the case of liver failure too severe or due to the portal obstruction, blood from the portal vein to the liver is no longer metabolized by hepatocytes, becoming toxins that disturb tissue metabolism, especially in the brain. These metabolic toxins include ammonia, mercaptan, gamma-amino butyrium acid, and aromatic amino acids.

The causes of exogenous liver coma

Hepatic coma onset occurs on 1 cirrhosis or with a portal obstruction:

Eating too much Protide or passing protein.

Severe gastrointestinal bleeding.

Using strong diuretics causes dehydration and hypokalaemia.

Use of drugs for liver toxicity: Tetracycline, anti-tuberculosis drugs, sedatives, sleeping pills, antihypertensive drugs.

After surgery on 1 cirrhosis liver.

Infections of the liver, bile, kidneys, lungs, intestines.

Amputation: Often poked many times or 1 time too much to reduce the amount of circulation through the liver

Causes of endogenous liver coma

Due to severe and widespread liver damage such as acute hepatitis, inorganic phosphorus toxic hepatitis, tetraclorure de Carbone, Amanite phaloide, drug or liver cancer or end-stage cirrhosis.

Pathogenesis

The most important factor in the pathogenesis of hepatic coma is severely impaired hepatocytes and is also due to an internal or external obstruction, connecting portal blood to the general circulation. Consequently, many toxins absorbed from the intestine are not detoxified by the liver and lead to metabolic abnormalities in the central nervous system.

Current theories that explain the mechanism of hepatic coma are:

Ammonia Theory

It is assumed that ammonia from the digestive tract is not metabolized through the liver barrier to the brain, causing brain toxicity. It was found that in liver comatose patients the highest increase in blood ammonia was ammonia in the arterial blood. The last metabolite of ammonia, Glutamine, was also found to be elevated in cerebrospinal fluid and in the brain of patients with hepatic coma. However, there are also some studies that contradict this hypothesis.

Agonism theory

As proposed by Ziève, due to the synergism of ammonia to make some short chain fatty acids and Mercaptan is a toxic sulfur-based poison increase in the blood when liver failure.

Theory of fake neurotransmitters

Fisher et al suggest that the neurological manifestation in cirrhosis is due to the accumulation of false neurotransmitters. Dopamine, noradrenalin, tyrosine, and phenylalanine are released from protein breakdown in the colon. Increased plasma concentrations of these substances in patients with hepatic coma.

Theory of serotonin

Serotonin synthesized from L-Tryptophan is found in high concentrations in the brain in patients with hepatic coma.

Theory of GABA is a neurotransmitter inhibitor

In experiments on hepatic coma in animals, John demonstrated an increase in the concentration of GABA in the blood, an increase in the permeability of the meninges of GABA, inhibition of neurotransmitters causing drowsiness.

The theory of Benzodiazepines

In the brain, there are benzodiazepines receptors that facilitate GABA activity. Two substances found to be elevated in the blood in cirrhotic patients are Diazepam and N- dimethyl- diazepam.

Symptom

Clinical

Liver coma divided into 4 stages.

Stage 1:

Neurological manifestations are still mild and discreet, such as disorientation of space and time, drowsiness, drowsiness, irrational laugh, slurred speech, scribbled writing, possibly signs of flapping wings

Stage 2:

The symptoms became clearer. In particular, signs of flapping wings, pyramidal symptoms, hyper reflexes, Babinski mark or equivalent, hypertonia in the pyramids, a rabbit odour of liver.

Stage 3:

Real coma with loss of awareness, sensation and movement.

Stage 4:

Stage 4 A: Coma but pinching still responds.

Stage 4B: Deep coma can be accompanied by fertility disorders.

Subclinical

There are also tests for liver disease.

Ammonia in blood:

Usually tall but not entirely proportional to weight. Normally 60-80 mg. In a hepatic coma, an increase of over 160µg / L. Need to make ammonia in arterial blood.

Electrolyte and acid-base disorders:

Blood sodium usually decreases, potassium decreases, calcium is less affected, alkaline reserve increases, pCO2 decreases.

Cerebrospinal fluid:

Glutamine, glutamic acid increased.

Tests for impaired liver function.

EEG: High voltage, symmetry, slow delta wave.

CT scan and MRI: There may be cortical atrophy or cerebral oedema.

Diagnose

Mainly based on the following 4 main factors:

The patient has a history of acute or chronic liver disease, or after a door junction surgery.

Cognitive confusion: Confusion then coma.

There are neurological symptoms such as increased muscle tone, increased reflexes, fluttering wings, Babinski, sometimes signs of epilepsy.

EEG: High voltage, symmetry, slow-wave .

Other symptoms: The breath smells like liver, cerebrospinal fluid glutamine increases.

Prognosis and prevention

This is a serious complication of cirrhosis, a very severe prognosis, death 90- 95%, especially an endogenous liver coma. Particularly for exogenous coma, if the favourable factors are adjusted after 48- 72 hours, the patient can get out of the coma.

The prognosis depends on favourable factors for coma and the progression of cirrhosis.

Treatment

Identify and treat the cause of the onset.

Intervention to reduce the production and absorption of nitrogen and other toxins in the gut

Drugs that directly or indirectly alter the balance of neurotransmitters

Treatment of acute coma or acute hepatic encephalopathy

Diet: Reduce protein to 20 grams / day, 2000 calories / day. Increases with recovery by 10g / day for every few days, but with chronic liver coma, frequent protein restriction.

Enema to remove Nitrogen and Phosphate.

Use lactulose: 10-30ml x 3 times / day or lactitol 0, 3-0, 5g / kg / day.

Neomycin 1g x 4 times / day x 1 week, or Metronidazole 200mg x 4 times / day x 5-7 days.

Energy and fluid maintenance rely on water and electrolyte balance.

Diuretic discontinuation.

Sedatives: Oxazepam can be used.

Levodopa: Dopamine precursors cross the brain vessel barrier, only a few patients can tolerate.

Bromocriptine: A specific, long-acting dopamine receptor agonist.

Flumazenil: A benzodiazepine receptor antagonist may decrease conduction in 70% of cases.

Medicines that increase renal ammonia excretion: Benzoate de Sodium.

The amino acid branch: C promises to be agreed on and expensive drugs.

Close the branches connecting door-owner.

Liver transplantation.

For chronic liver encephalopathy

T groove medications containing nitrogen; vegetable protein 50gr / ng; defecation 2 times/day; taking lactulose or lactitol; If symptoms worsen then switch to treatment such as the acute coma regimen.