Acute liver failure

Description:

The acute liver failure represents the clinical syndrome which is developing at bystry injury of a liver and shown hepatic encephalopathy (up to a coma) and a hemorrhagic syndrome.

Symptoms of the Acute liver failure:

In a clinical picture it is possible to allocate 2 leading syndromes.
1. Syndrome of a massive necrosis of a liver.
1.1. The increasing general weakness.
1.2. Anorexia.
1.3. The constant nausea passing into vomiting.
1.4. Temperature increase.
1.5. Increase of jaundice.
1.6. Emergence of a specific sweetish and luscious "hepatic" smell.
1.7. Reduction of the sizes of a liver (symptom of empty hypochondrium).
1.8. Emergence in the general blood test of a leukocytosis, the accelerated SOE, decrease in a protrombinokvy index to 0,50
1.9. Increase in biochemical analysis of blood of the general bilirubin at the expense of indirect fraction against the background of falling of the ALT level (a syndrome of bilirubino-fermental dissociation.
2. Encephalopathy syndrome (hepatic prekoma and coma)
Allocate 4 stages of encephalopathy.
2.1. Prekoma 1 (phase of harbingers).
2.1.1. There is an adynamia, block, a hypophrasia, orientation disturbance, forgetfulness.
2.1.2. Inversion of a dream (drowsiness in the afternoon, sleeplessness at night), nightmares is noted.
2.1.3. There are vegetative frustration (faints, dizziness, "front sights" before eyes, a sonitus, a hiccups, yawning, the increased perspiration).
2.1.4. Neurologic disturbances accrue:
2.1.4.1. Coordination of movements is broken.
2.1.4.2. There is a non-constant and not sharply expressed "clapping" tremor of hands, language.
Patients keep orientation in time and space, give the adequate, but slowed-down answers to questions, execute simple commands.
2.3. Prekoma 2.
2.3.1. Patients are sleepy, the most part of time doze or sleep, when awakening a dezkoriyentirovana. Stereotype of the speech and behavior are characteristic reaction to verbal irritation (address) is slowed down, but is purposeful, on pain stimulations – is kept
2.2.1. Neurologic disturbances amplify:
2.3.1.1. The "clapping" tremor of hands.
2.2.1.1. Decrease in tendon jerks.
2.3.1.2. Decrease in pupillary tests
2.2.1.2. Diskoordination of movements.
2.3.1.3. Breath increase
2.2.1.3. Quite often there are frustration of pelvic bodies – an involuntary urination and defecation.
During this period there can be an acute psychomotor excitement reminding a tremens - a hepatic delirium. In this state patients lose orientation, jump from a bed, shout, become aggressive, the convulsive syndrome appears.
2.4. Coma 1 (superficial coma).
2.4.1. Consciousness is oppressed, reaction to a hail is absent, on strong irritants (pain, cold, heat) – is kept.
2.4.2. Neurologic changes: wide pupils with almost total absence of a photoharmose, a symptom of floating eyeglobes, pathological Babinski's reflexes, Gordon, a clonus of muscles of feet; the person becomes masklike, extremities rigid, there are attacks of clonic spasms.
2.4.3. Paresis of smooth muscles leads to an intestines atony with the progressing intestines swelling, the termination of a mocheotdeleniye at a full bladder - "ischuria paradoxa".
2.5. Coma 2 (deep coma).
Full loss of reaction to any irritations is characteristic of it.
As additional syndromes allocate:
1. Swelled - swelling of a brain.
2. Hemorrhagic syndrome.
3. Acute renal failure.
4. Accession is purulent - a septic infection.
5. Pain syndrome.

Reasons of the Acute liver failure:

Allocate the following pathogenetic kinds of an acute liver failure.
1. Theory of false neurotransmitters.
The main reason – a fulminantny viral hepatitis.
Owing to destruction of hepatocytes tserbrotoksichesky substances and patologicheksky metabolites are formed. Level of the aromatic amino acids (tyrosine, tryptophane, phenylalanine) which are well getting through a blood-brain barrier increases. To pathological metakbolita carry октопамин and фенилэтаноламин, relatives on structure to adrenergic mediaktor to a dopamine and noradrenaline, so-called "false neurotransmitters". They break proktsessa of nervous transfer in synapses, in particular in a reticular formation, as defines komaktogenny effect. Igibitorny effect also the serotonin which is formed of a triptokfan has.
2. Theory of toxic effect of ammonia.
Arises at cirrhosis.
The liver serves as the highly effective filter for intestinal autotoksin in physiological conditions. Cirrhosis promotes opening of porto-caval shunts on which blood from intestines gets to the general blood stream, passing a liver. The main toxin which is formed in intestines of protein when splitting by bacterial enzymes is ammonia. Ammonia, getting to mitochondrions of neurocytes, connects to α-ketoglutarate with formation of a glutamine. The α-ketoglutarate and a glutamate flowing from a citrate cycle reduce glucose oxidation speed that leads to insufficient formation of ATP. Thereof there is a power starvation of cells of a brain that reduces their activity. The glutamine which is formed in neurocytes of ammonia under the influence of a glutamatsintetaza and ATP promotes osmotic hypostasis of a cell.
Except ammonia as autotoksin phenol, an indole, an indican, mercaptans, korotkotsepochechny fatty acids act (oil, valerian, kapron, caprylic). In nastoyakshchy time important diagnostic significance is attached to concentration definition γ-aminobutirovy acid as to intoxication indicator.
Increase of portosistemny encephalopathy can be provoked by the unlimited use of proteinaceous products, and also disintegration and absorption of blood protein at massive hemorrhages.
3. The theory of the strengthened GABA-ergic transfer.
It is established that some colibacilli are capable to synthesize γ-aminonomasklyanny acid which in the conditions of decrease in its hepatic clearance collects in TsNS and causes komatogenny effect.
4. Gipokaliyemichesky theory.
The main reasons – stimulation of a diuresis and loss of ascitic liquid at which there is a potassium loss. Reduction of potassium in neurocytes increases their vulnerability in connection with simplification of penetration in them of ammonia and other toxic substances.

Treatment of the Acute liver failure:

Patients observe a high bed rest. In a diet limit the use of animal protein.
Appoint massive disintoxication therapy:
1) Enterosorbtion:
a) High cleansing enemas;
b) Enterodesum: on 15,0 – 20,0 3 time a day;
c) Absorbent carbon in a dose of 1 g/kg/days;
d) Lactulose – 1 ml/kg;
2) Infusional therapy (30мл/кг/сут). For this purpose use glyukozo-saline solutions in the ratio 1:1 and colloids (реополиглюкин, Haemodesum, albumine) in the ratio to glyukozo-saline solutions 1:1.
3) Extracorporal methods (the most optimum the plasmapheresis is).
Antibacterial therapy is used on purpose:
1. Suppression of intestinal microflora:
Metronidazole (7,5mg/kg) in 3 receptions.
Monomycinum (20mg/kg) in 2 receptions.
Lactulose.
2. Fight against bacterial superinfection – appoint non-toxic antibiotics of a broad spectrum of activity (cephalosporins)
Glucocorticoid therapy. Hormones in a dose 10 – 15mg/kg in days ravnokmerno in 4 – 6 receptions are used. The course of treatment makes 5 – 6 days. Glucocorticoids with care appoint at a viral hepatitis E against the background of pregnancy.
Inhibitors of proteolysis use for the purpose of suppression of activity of enzymes of kallikkrein-kinin system. Use Contrykal of 500000 - 1000000 PIECES in 2 – 3 receptions, овомин - 5000 ATE/kg/days.
Metabolic therapy:
1. Inosine of 2% - 10 ml a day.
2. Pyridoxal phosphate 0,005 - 0,03/days.
3. Cytochrome C or cytopoppy of 0,25% - 4 – 8 ml intramusculary or intravenously 1 – 2 time a day.
Correction of water and electrolytic balance is carried out under laboratory control.
At decrease in a diuresis use diuretic drugs (lasixum – 2 – 4 mg/kg, Mannitolum – 0,5 – 1,5 mg/kg).
For correction of a hypoproteinemia appoint albumine, freshly frozen plasma.
Correction of a hemostasis is carried out:
1. Cryoplasma of 10 - 15 mg/kg/days.
2. Dicynonum of 2 - 4 ml each 4 hours.
3. Adroxonum of 0,5 ml 2 – 4 times a day.
4. Troxevasinum of 5% - 5 ml a day.
5. Vikasolum of 1% - 2 ml a day.
If necessary appoint parenteral food, stop a convulsive syndrome.
At an opportunity use hyperbaric oxygenation.
Efficiency of parenteral interferon is not proved.