Anesthesiology and resuscitation. Acute liver failure (lecture notes)

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Anesthesiology and resuscitation. Acute liver failure (lecture notes)

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Lecture number 8. Acute liver failure

Acute liver failure is a symptom complex characterized by a violation of one or more liver functions due to acute or chronic damage to its parenchyma.

Etiology

The causes of acute renal failure can be hepatitis viruses A, B, C, D, E, G, as well as herpes viruses, cytomegalovirus, infectious mononucleosis virus, simple and herpes zoster, Coxsackie, measles, septicemia that develops with liver abscesses and purulent cholangitis, drugs, alcohol, industrial toxins, heart failure. OPN always proceeds with multiple organ damage: the kidneys, the cardiovascular system, the lungs, the pancreas, and the brain are involved in the process. Impaired renal function manifests as acute tubular necrosis. Pulmonary complications - aspiration of gastric contents or blood, atelectasis, respiratory infections. Acute pancreatitis and pancreatic necrosis can cause death. A life-threatening disorder of homeostasis develops. Liver failure is explained by dystrophy and widespread necrobiosis of hepatocytes.

Clinic and diagnostics

The clinical manifestations of ARF are as follows.

1. Coagulopathy is caused by a deficiency of coagulation factors and an increase in fibrinolytic activity. It predisposes to spontaneous bleeding from the mucous membranes: gastrointestinal, uterine, nasal bleeding can be observed. Brain hemorrhages are possible. To assess the state of the hemostasis system, prothrombin time is determined.

2. Hypoglycemia is characterized by a high level of insulin in plasma, which is due to a decrease in its uptake by the liver. It leads to a rapid deterioration of the neurological status and death of patients.

3. Violations of water-electrolyte and acid-base balance. End-stage acute renal failure is characterized by hyponatremia, hypophosphatemia, hypocalcemia, and hypomagnesemia. The change in the acid-base state does not have an unambiguous direction. Respiratory alkalosis associated with stimulation of the respiratory center with toxic substances may be replaced by respiratory acidosis due to increased intracranial pressure and suppression of respiratory activity.

In the development of hepatic coma as a severe course of the disease, the stages of precoma, threatening coma and coma proper are distinguished. There are also hepatocellular (endogenous) coma, resulting from massive necrosis of the parenchyma, porto-caval (bypass, shunt, exogenous), due to a significant exclusion of the liver from metabolic processes due to the presence of pronounced porto-caval anastomoses, and mixed coma, occurring mainly with cirrhosis of the liver.

In the precomatous period, progressive anorexia, nausea, a decrease in the size of the liver, an increase in jaundice, hyperbilirubinemia, and an increase in the content of bile acids in the blood develop. In the future, neuropsychic disorders, slowing of thinking, depression, and sometimes euphoria increase. Characterized by instability of mood, irritability, memory is disturbed, sleep is disturbed. Tendon reflexes increase, a small tremor of the limbs is characteristic. Azotemia develops. With timely therapy, patients can get out of this state, but more often with severe irreversible changes in the liver, coma occurs.

During the period of coma, excitation is possible, which is then replaced by depression (stupor) and a progressive impairment of consciousness up to its complete loss. Meningeal phenomena, pathological reflexes, motor restlessness, convulsions develop. Breathing is disturbed (such as Kussmaul, Cheyne-Stokes); the pulse is small, arrhythmic; there is hypothermia. The patient's face is haggard, the extremities are cold, a characteristic sweet liver smell comes from the mouth and skin, hemorrhagic phenomena intensify (skin hemorrhages, bleeding from the nose, gums, varicose veins of the esophagus, etc.).

Acute liver failure develops quickly, within a few hours or days, and with timely therapy can be reversible.

Laboratory studies: bilirubin, urea and creatinine in blood and urine, parameters of the hemostasis system, complete blood count and urine, CVP, ECG, plasma and urine osmolarity, plasma electrolytes, free plasma and urine hemoglobin, ALT, AST, alkaline phosphatase, LDH, CPK, prothrombin time. Computed tomography of the liver can reveal a decrease in its size, but most clinicians focus on clinical and laboratory data.

Treatment

Timely inotropic support is an essential component of intensive care. Prevention of infectious complications - the appointment of cephalosporin antibiotics in combination with antifungal drugs (amphotericin-B). Hepatoprotectors and membrane stabilizing drugs: prednisolone up to 300 mg, vitamin C 500 mg, troxevasin 5 ml, sodium etamsylate 750 mg, Essentiale 30 ml, tocopherol 4 ml intramuscularly, cytomak 35 mg, cocarboxylase 300 mg, nicotinic acid 30-40 mg, complamin 900 mg, sirepar 5-10 ml, glutamic acid 1% 400 ml, vikasol 10 ml intravenously, B vitamins.

Protease inhibitors, which include cortrical 100 thousand units, trasilol 400 thousand units, antagonosan, gordox.

Stimulation of diuresis: reogluman 400 ml, mannitol, lasix up to 200 mg intravenously, eufillin 240 mg. To correct coagulopathy, intravenous administration of vitamin K (10 mg per day for 3 days) is used. The effect occurs after 3 hours. In this case, the elimination of hypoprothrombinemia associated with impaired absorption of vitamin K, resulting from a deficiency of bile acids. In case of bleeding or suspected invasive procedures (vascular catheterization, peritoneal dialysis), platelet mass or fresh frozen plasma is administered intravenously. Cerebral edema is a common cause of death. Mannitol is administered at the rate of 1 g/kg of body weight. In patients with renal insufficiency, mannitol is prescribed in combination with ultrafiltration to avoid hyperosmolarity and overhydration.

With the development of hepatic coma, potassium chloride is prescribed (0,4-0,5% solution in a 5% glucose solution with a volume of 500 ml intravenously drip) or sodium bicarbonate solution (with metabolic acidosis); Patients breathe humidified oxygen through a nasal catheter.

With a decrease in both arterial and venous pressure, polyglucin and albumin are administered intravenously. In the presence of massive bleeding, appropriate measures are taken to stop them, one-group blood is transfused, and drugs that contain blood clotting factors are administered. With significant signs of disseminated intravascular coagulation, heparin is administered intravenously at a dose of 10-000 IU bolus.

In case of renal failure, peritoneal hemodialysis and plasmapheresis are performed, which give a good result, but before carrying out these manipulations, the introduction of heparin is contraindicated. To stop psychomotor agitation and seizures, diprazine, haloperidol, sodium oxybutyrate are prescribed. In severe cases, resort to intubation and mechanical ventilation.

It is important to remember that the risk of bleeding is high, so all manipulations must be carried out with extreme caution. When removing the patient from a coma, the next step is to conduct intensive therapy for the underlying disease.

Author: Kolesnikova M.A.

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