Acute liver failure

Acute liver failure (ALF) (Video)  is a pathological condition that develops due to various etiological factors and in the pathogenesis of which there is inflammation and hepatocellular necrosis with subsequent impairment or loss of liver function.

Ваш браузер не поддерживает JWPlayer
 

Video. Acute liver failure

The main reasons for the development of ALF:

  • viral and bacterial infections: viral hepatitis B and C, adenoviruses, cytomegalovirus, Coxsackie virus, Epstein-Barr virus, toxoplasmosis, E. coli infection, etc .;
  • poisoning with hepatotropic toxins;
  • pathologies of other body systems with the presence of ischemia and hypoxia processes: acute respiratory failure, acute heart failure, malignant neoplasms, etc.;
  • hereditary metabolic liver diseases (Video): alpha-trypsin deficiency, Wilson disease, cystic fibrosis, glycogen storage disorder, galactosemia, tyrosinemia, hemochromatosis;

Ваш браузер не поддерживает JWPlayer

Video. Metabolic liver diseases

There are following types (forms) and stages of ALF:

Types (forms) ALF:

  • Acute hepatocellular (hepatocellular LF)
  • Acute portacaval LF
  • Mixed

Stages of ALF:

  • Initial (compensated)
  • Expressed (uncompensated)
  • Terminal (dystrophic)

Depending on the timing of symptoms, there are:

  • Lightning form (the main symptoms develop at least after 4 weeks);
  • Acute liver failure (develops on the background of various liver diseases within 1-6 months);
  • Chronic liver failure (develops gradually due to acute and chronic hepatic disease over a period of 6 months).

Hepatic insufficiency is acute, characteristic syndromes are dyspeptic disorders, nausea, vomiting, fever, CNS dysfunction, liver odor, increased hemorrhagic syndrome (presence of petechiae, nasal and uterine bleeding), varicose veins of the anterior abdominal wall, itchy skin and sclera.

In the initial stage of the disease, the liver may be enlarged, and in cirrhosis – reduced. Acute liver failure in children is mainly due to cirrhosis of the liver of various etiologies (most often due to genetic metabolic pathology), or in its final stage with the development of fulminant hepatitis.

At the pre-hospital stage, emergency care should be provided (assessment of the general condition, catheterization of the peripheral and, if possible, central vein, gastric tube, urinary catheter, maintenance of patency and adequate lung ventilation, non-invasive monitoring: pulse oximetry, measurement of RR, measurement of BP).

Emergency aid

  • Strict bed rest in the intensive care unit (ICU);
  • Diet therapy: in the stage of pre-coma restriction of protein to 0.3-0.5 g/kg/day, in the presence of coma - complete absence of protein;
  • Installation of a nasogastric tube (NGT) to provide enteral nutrition, avoid aspiration of gastric contents, remove any blood (bleeding varices) from the stomach; protect the airway with an endotracheal tube;
  • Maintenance of adequate pulmonary ventilation, if necessary use artificial lung ventilation;
  • Monitor temperature, pulse, RR, BP, urine output; daily weights, check blood glucose 1-4 hourly;
  • INR, U&E, LFT, blood cultures and ECG. The INR (or PT) is the best measure of liver synthetic function;
  • Nurse with a 20◦ head-up tilt in ICU;
  • Reduction of hyperthermia, use of mannitol (helps to reduce ICP);
  • Carrying out detoxification therapy with balanced crystalloid solutions (taking into account persperative and pathological losses): 50-100 ml/kg with correction of electrolytes and acid-base status;
  • Restoration of energy processes, infusion of 10%-20% glucose in a daily dose of 5-10 g/kg;
  • Correction of hypoalbuminemia (at the level of ≤30 g/l) – albumin solution of 5%-20% 10 ml/kg;
  • Correction of thrombocytopenia (at the level of ≤50 * 109) – platelet mass 5-10 ml/kg;
  • Reduction of hyperammonemia (reduction of production of ammonia, toxins and release of intestines from nitrogen-containing products):

-prescription of lactulose in age dosages (from 10 to 40 ml/day), gastric lavage, enemas with magnesium sulfate, enterosorbents;

-to reduce numbers of bowel organisms (amikacin, vancomycin, metonidazole);

  • Use of H2-receptor blockers, proton pump inhibitors in age doses (ranitidine hydrochloride, omeprazole, etc.) to reduce acid secretion and risk of gastric stress ulcers;
  • At bleeding the therapy is prescribed taking into account indicators of the coagulogram, factors of blood coagulation (tranexamic acid), 12.5% solution of etamsilat, 10% solution of calcium gluconate, if necessary – transfusion of erythrocyte mass, factors of blood coagulation;
  • At signs of a disseminated intravascular coagulation syndrome (DIC-syndrom)  without bleeding: prescription of heparins under the control of the coagulogram;
  • With the development of edema (ascites): limiting the amount of fluid, protein, saline solutions, the appointment of diuretics (furosemide, spironolactone); if necessary – conducting a pleural puncture, laparocentesis;
  • In hepatic encephalopathy and the presence of psychomotor agitation and/or seizures: anticonvulsant therapy (diazepam);
  • Antibacterial therapy is indicated in the presence of complications such as sepsis, pneumonia, etc .; treat sepsis aggressively and don’t forget the risk of spontaneous bacterial peritonitis;
  • Consider acetylcysteine, this can improve oxygenation and clotting profiles;
  • Watch renal function carefully. Terlipressin may help if deterioration is due to hepatorenal syndrome. Consider haemodialysis if water overload or acute renal failure develops;
  • Treat the cause if known (eg paracetamol overdose);
  • Avoid drugs with hepatic metabolism.

Approximately half of all children with acute liver failure need a liver transplant in order to survive.