Acute liver failure in a child 5.5 months old. and its etiological connection with infections with herpes group viruses: cytomegalovirus and human herpes virus type 6 St. Petersburg, Children's Hospital No. 1 2005.

Relevance of the problem Acute liver failure in children of the 1st year of life develops quite rarely, but the mortality rate for this suffering is 80-100% (Burdelski M., 1992). The etiological factors for acute liver failure in newborns and children of the 1st year of life are different. Viral infections in 15% of cases are the cause of its development (Durand P., Debrey D., Mandel R., et al., 2002). Approaches to the treatment of infants with acute liver failure differ from those for older children (Whittington P. F., 1994; Sokol R. J., 1995).

Cytomegalovirus infection is one of the possible causes of acute liver failure in children 1 year of life. Cytomegalovirus infection (CMV) is the most common intrauterine infection. The detection rate of CMV during examination of newborns is 1 in 1000-5000. CMV reproduces in lymphocytes, blood monocytes, and persists in lymphoid organs. The virus has a pronounced tropism for epithelial cells of the salivary gland ducts. Infection of the salivary glands with CMV occurs as a result of transepithelial migration of lymphocytes and histiocytes (Samokhin A.P., 1987). In children infected with CMV, any (or all) of the following conditions are possible: low birth weight, pneumonia, meningoencephalitis, hepatitis, jaundice, thrombocytopenia (purpura), chorioretinitis, microcephaly, inguinal hernia, biliary atresia, polycystic kidney disease, impaired formation of derivatives I embryonic arch (WHO Report, 1984). Late complications of CMV (at the end of the neonatal period): cerebral palsy, sensorineural deafness, optic nerve atrophy, VMR, pneumosclerosis, liver cirrhosis, nephrotic syndrome, diabetes mellitus, thyroid disease, etc. (Shabalov N.P., 2004).

Consequences of cytomegalovirus infection during pregnancy (Stagno S., 1985) Pregnant women with low income Pregnant women with high income 55% with recurrent CMV infection 45% of primary CMV infections 0.15% congenital infections 0 -1% of infected children may have manifest disease 1 - 4% of primary infections in 40% transmission of infection to the fetus 10 - 15% of infected children have a manifest disease in 10% normal development 15% of primary CMV infections in 90% develop complications 85% with recurrent CMV infection 0.5 - 1% congenital infections 0 -1% of infected children may have overt disease 85 - 90% of infected children do not have any symptoms of the disease 5 -15% develop complications 85 - 95% normal development

Infection with human herpes viruses type 6 (HHV-6) accounts for 5% of the causes of acute liver failure in infants. Studies in various regions of the world indicate a wide distribution of HHV-6 (85%) in the human population (Isakov V. A., 1991; Golubev A.G., 1998). A close relationship between HHV-6 and CMV has been established (Stasey E., at al., 1992). HHV-6 can persistently infect and be released from the salivary glands; HHV-6 can cause latent infection and persist in human monocytes and macrophages. The synergism of the pathogenic effects of HIV-1 and HHV-6 has been proven; it infects human T4 lymphocytes and is capable of killing them. But it does not cause general immunodeficiency. HHV-6 is capable of activating the latent HIV-1 provirus (Gallo R. C., 1990). Sudden exanthema in young children and chronic fatigue syndrome are associated with HHV-6 (Koichi J., 1995). HHV-6 is isolated from patients with lymphoproliferative diseases, in immunosuppressed patients with hematological malignancies (Gonchar V. A. et al., 2003). There is information about the involvement of HHV-6 in the development of acute hepatitis in adults and children, including malignant forms with a fulminant course (Asano Y., at al., 1990; Isakov V.A. et al., 1991).

Girl, 1 month 2 days 1st hospitalization in Children's Hospital No. 1 23.07.04 Referral diagnosis: Thrombocytopathy. Multiple hematomas. Diagnosis on admission: Coagulopathy? Complaints: The appearance of “bruises” in the back area against the background of normal health. Life history: Girl from first pregnancy with threat of miscarriage at 14 weeks. Delivery on time. Planned caesarean section (mother has myopia). Birth weight 2800 g, length 51 cm. She screamed immediately. Vaccinated with BCG and against hepatitis B in the maternity hospital. Discharged on the 6th day of life. Breastfed from birth. Heredity is not burdened. Objectively: Weight 3400. Slight yellowness of the skin and sclera against the background of general pallor. Hemorrhagic elements on the mucous membrane of the hard palate. Ecchymoses on the back 2.0 x 0.5 cm. Liver +1 cm; spleen +0.5 cm. Endothelial tests are negative. The chair is yellow.

Dynamics of clinical and biochemical blood tests Klin. blood tests 07.23.04 07.30.04 Hemoglobin, g/l 112 102 Erythrocytes, 1012/l 3.7 3.2 Reticulocytes, 0/00 22 Color. indicator, units 0, 91 210 240 Leukocytes, 109/l 12, 6 2 0 segmented, % 13 1 5 basophils, % 0 1 lymphocytes, % 71 13 10 1, 15 0, 61 1, 4 73 monocytes, % 05.08.10 eosinophils, % 07/29/10, 2 band, % ALT, mmol/l 07/26/0.95 Platelets, 109/l Biochemical blood tests ESR, mm/h 7 Dl. bleeding 2"00" MSC beginning 3"40" MSC end 4"00" AST, mmol/l 0.97 Total protein, g/l 56 Total bilirubin, µmol/l 114 118 91 Direct bilirubin, µmol/l 50 58 56 Indirect bilirubin, µmol/l 64 60 35

Dynamics of coagulogram parameters Indicators Norms Blood clotting time 5 - 10" 14" 40" 8" 6" 15" Kaolin time 60 - 90" 148" 73" 78" Thrombin time 14 ± 5" 13.5" 14" 18" Fibrinogen, g/l 2 – 4 g/l 2.7 2.5 2.4 Fibrinolysis 150 - 240" 180" APTT 0.8 - 1.1 1.95 0.98 0.99 Platelets, 109/l 180 - 320 230 320 Prothrombin index, % 80 -100 26.07.04 29.07.04 05.08.04 100

Results of additional ultrasound examinations of the abdominal organs: liver, IPD - 80 mm; portal vein - 6 mm; common bile duct - 2 mm; pancreas – 6 mm x 11 mm; splenic vein - 4 mm; spleen - 52 mm x 29 mm. Conclusion: Hepatosplenomegaly. Markers for HBV, HCV, HAV are negative. Neurologist's conclusion: Asymmetry of the palpebral fissures (D≥S). Slight smoothing of the nasolabial fold on the right. Varus position of the feet. Ultrasound of the brain: No pathology was detected. Ophthalmologist's conclusion: The anterior, middle and bottom parts of both eyes are without pathology. Coprograms (No. 3): fatty acids +++.

Treatment (1st hospitalization) Vikasol 0.5 ml, 1 time per day, 3 days. Allohol ¼ tablet. , 3 times a day. No-shpa ¼ tab. , 3 times a day. FTL. The main diagnosis at discharge: Hemorrhagic disease of the newborn, late form. Concomitant diagnosis: Protracted jaundice of newborns. Physiological anemia. Hyperfermentemia of unknown etiology. VUI?

Classification of hemorrhagic disorders of newborns (Shabalov N.P., 2004) Primary hemorrhagic disorders: - hemorrhagic disease of newborns (early and late forms); - hereditary coagulopathies; - thrombocytopenic purpura (congenital and hereditary); - thrombocytopathies (congenital, drug-induced, hereditary) Secondary hemorrhagic disorders: - decompensated DIC syndrome; - thrombocytopenic (symptomatic) hemorrhagic syndrome; - coagulopathic hemorrhagic syndrome during infections and hepatitis; - vitamin K deficiency hemorrhagic syndrome with obstructive jaundice; - drug-induced thrombocytopathic syndrome.

Laboratory data for the most common acquired hemorrhagic syndromes in newborns (Shabalov N.P., 2004) Indicators and their normal values ​​in healthy full-term newborns Hemorrhagic. newborn disease Liver pathology (hepatic coagulopath.) DIC, stage II-III. Thrombocytopenia Hemophilia Platelet count 150 - 400 · 109/l normal decreased normal increased normal increased normal increased Fibrinogen 1.5 - 3.0 g/l normal normal. or reduced norm Fibrin degradation products (FDP) 0 – 7 mg/ml norm norm. or increased more than 10 g/ml normal Prothrombin time 13 - 16" Thrombin time 0 - 16" Partial thromboplastin time 45 - 65"

Provoking factors for the detection and development of late forms of hemorrhagic disease of newborns (2-8 weeks of life, less often up to 6 months) Diarrhea with fat malabsorption lasting more than 1 week Biliary atresia Hepatitis Cholestatic jaundice of other origin Cystafibrosis of the pancreas Massive antibiotic therapy using broad-spectrum drugs α 1-antitrypsin deficiency Abetalipoproteinemia Celiac disease

Girl, 4 months. Day 1, 2nd hospitalization in Children's Hospital No. 1 10/22/04 Referral diagnosis: Jaundice of unknown etiology. Atresia of the gallbladder? VUI? Hepatolienal syndrome. Diagnosis upon admission: Intrauterine hepatitis? Atresia of the gallbladder? Portal hypertension? Complaints: Icterus, discolored stool, dark urine. Increase in abdominal size. Medical history: At 3 months. ALT 218 U/L (in N= 35 U/L); bilirubin 231 µmol/l (direct 158.6 µmol/l). From 3.5 months bottle-fed (Nutrilon). Objectively: The condition is serious. Lethargic. The sclera is icteric. Lemon-toned skin. The abdomen is increased in volume. The saphenous veins of the anterior abdominal wall are dilated. Liver + 4 - 5 cm, spleen + 3 - 4 cm. Urine is dark. The stool is light yellow.

Dynamics of clinical and biochemical blood tests Klin. blood tests 22.10.04 01.11.04 Biochemical blood tests 25.10.09.11 ALT, mmol/l 4.59 AST, mmol/l 2.0 Hemoglobin, g/l 117 94 Red blood cells, 1012/ l 3, 7 3, 35 Reticulocytes, 0/00 32 Color. indicator, units 0.95 0.84 Total protein, g/l 72 59 Platelets, 109/l 130 120 Total bilirubin, µmol/l 278 160 Leukocytes, 109/l 12.6 6.0 Direct bilirubin, µmol/l 152 89 band, % 9 5 segmented, % 10 14 Indirect bilirubin, µmol/l 126 71 eosinophils, % 1 3 Urea 2.8 2.4 basophils, % 0 0 Alkaline phosphatase µmol/l 14.0 lymphocytes, % 72 70 Cholesterol, mmol/ l 4, 56 monocytes, % 7 5 Lipoproteins, units. plasma cells , % 1 0 ESR, mm/h 30 44 Potassium 4.29 Sodium 136.2 Calcium++ 1.23

Coagulogram indicators Indicators Norms 09.11.04 Blood clotting time 5 - 10" 7" 00" Kaolin time 60 - 90" 81" Thrombin time 14 ± 5" 22" Fibrinogen, g/l 2 - 4 g/l 1, 4 Fibrinolysis 150 - 240" 180" APTT 0.8 – 1.1 0.97 Platelets, 109/l 180 - 320 160 80 -100 80 Prothrombin index, %

Diagnosis of IUI Markers for HBV, HCV, HAV are negative. Serological tests: 1) Ig M for CMV – negative. ; Ig G for CMV is positive. ; 2) Ig G for chlamydial inf. in a child - positive. ; mother's AT titer is 1:22; 3) AT titer to mycoplasma inf. - 1:13 in the child and 1:12 in the mother; 4) AT titer to rubella is 1:17 in the child and 1:21 in the mother. PCR of the child's and mother's blood for CMV - negative.

Girl, 5 months. 20 days 3rd hospitalization in Children's City Hospital No. 1 10.01.02 (in the intensive care unit) Complaints and anamnesis: Sharp deterioration in condition since December 2004, increase in abdominal volume, increased jaundice. An increase in ALT, AST, bilirubin, the appearance of ascites, fluid in the pleural cavity. Results of the examination in the hospital Changes in the clinical blood test: anemia, subthrombocytopenia, shift in the formula to promyelocytes. Changes in the biochemical blood test: ALT - 251 IU/l, AST - 311 IU/l, total bilirubin. - 538 µmol/l, direct - 364 µmol/l, indirect 174 µmol/l. Changes in the coagulogram: VSK 15", prothrombin index - 37.5%, fibrinogen - 0.8 g/l, CRP - 36. Ultrasound: the liver is compressed, homogeneous, the gallbladder is not visualized. A large amount of fluid in the pleural and abdominal cavities. There is no fluid in the pericardial cavity.

Dynamics of the patient's condition in the hospital The child's condition progressively worsened. On January 14, 05, laparocentesis was performed to evacuate ascitic fluid. There was an increase in neurological symptoms with transition to stupor. Ultrasound of the brain showed signs of hemorrhage in the right parietal region, initial signs of cerebral edema. 01/17/05. Terminal condition, signs of edema and swelling of the brain, coma III. At 20.15. lack of cardiac activity. At 20.30 death was registered. Clinical diagnosis: Intrauterine hepatitis of unspecified etiology with outcome in cirrhosis. Complications: Portal hypertension. Varicose veins of the esophagus. Ascites. Liver failure. Edema and swelling of the brain. Coma III.

Protocol of the pathoanatomical autopsy 01/18/05. Main diagnosis: Generalized cytomegalovirus infection with predominant damage to the salivary glands, liver (chronic hepatitis with outcome in small-nodular cirrhosis), lungs. Complications: Jaundice. Ascites. Bilateral hydrothorax. Dystrophic changes in internal organs. Respiratory distress syndrome. Pulmonary edema. Fibrinous thrombi in the vessels of the brain and kidneys. Focal hemorrhages in the myocardium, lungs, and adrenal medulla. Bullous emphysema of the right lung. Mediastinal emphysema, pneumopericardium. Edema and swelling of the brain. Concomitant diagnosis: O. respiratory RNA virus infection.

PCR of sectional material for IUI (liver) Hepatitis C - RNA: negative. Herpes virus type 6 (HHV 6) - DNA: positive. Herpes simplex virus types 1 and 2 - DNA: neg. Cytomegalovirus (HHV 5) - DNA: neg. Epstein-Barr virus (HHV 4) - DNA: neg.

Prospects and problems of management of patients with acute liver failure Treatment of children and adults with acute liver failure has improved significantly due to the emergence of the possibility of emergency orthotopic liver transplantation (Durand P., Debrey D., Mandel R., et al., 2002). In young children, such an operation is associated with problems of availability of a donor liver, the complexity of the surgical procedure and preoperative preparation of patients (Devictor D., Desplanques L., Debrey D., et al., 1992). However, the improvement in prognosis in patients with acute liver failure after emergency orthotopic liver transplantation remains doubtful. According to various authors, 1-year survival rate after such an operation ranges from 65 to 92% (Bismuth H., et al., 1995; Rivera-Penera T., et al., 1995). In addition, in children 1 year of life there are not always indications for orthotopic liver transplantation (Bonatti H., Muiesan P., Connolly S., et al., 1997).

Causes of acute liver failure in 80 children 1 year of life according to 14 years of experience at the Paris Liver Transplant Center (2002). Causes of acute liver failure Survived without surgery (24%) Operated (28%) Survived after surgery (52%) Died (48%) Mitochondrial disorders (n=34; 42, 5%) Tyrosinemia type 1 (n=12) 5 5 2 2 Mitochondrial cytopathy (n=17) 1 5 2 11 Urea cycle disorders (n=2) 1 0 0 1 Galactosemia (n=2) 2 0 0 0 Hereditary. fructose intolerance (n=1) 1 0 0 0 Neonatal hemochromatosis (n=13; 16, 2%) 2 1 0 10 Etiology unknown and Reye's syndrome (n=13; 16, 2%) 4 3 3 6

Causes of acute liver failure in 80 children 1 year of life according to 14 years of experience at the Paris Liver Transplant Center (2002). Causes of acute liver failure Survived without surgery (24%) Operated (28%) Survived after surgery (52%) Died (48%) Acute viral hepatitis (n=12; 15%) Hepatitis B (n=6) 1 2 2 3 Herpes simplex virus type 1 (n=2) 0 0 0 2 Herpes virus type 6 (n=4) 0 4 2 2 Paracetamol overdose (n=1) 1 0 0 0 Autoimmune hepatitis (n=3) 0 3 1 2 Neonatal leukemia (n=1) 0 0 0 1 Familial lymphohistiocytosis (n=2) 0 0 0 2 Nonfamilial hemophagocytosis (n=1) 1 0 0 0

Limitations of indications for orthotopic liver transplantation in children 1 year of life (Dubern B., et al., 2001; Dhawan A., et al., 2001; Goncalves I., et al., 1995) Rapid progression of liver failure with multiorgan failure or sepsis. High risk of vascular and infectious complications. Developmental delay, low head circumference growth, myoclonus-epilepsy, changes in the composition of cerebrospinal fluid, muscle changes. Familial hemophagocytic lymphohistiocytosis, neonatal leukemia.

Possibilities of liver transplantation in Russia Currently, there are 4 centers where such an intervention is possible. Since 1990, they have performed no more than 70 liver transplants. At the Russian Scientific Center of Surgery of the Russian Academy of Medical Sciences, along with the introduction into practice of orthotopic liver transplantation, prof. Gauthier S.V. performs operations on children, adolescents and adults to transplant part of the liver (right lobe) from a living donor, which is a priority for world practice and allows one to overcome the severe shortage of donor organs.

Acute liver failure in children (ALF) is a rapidly developing disorder of the synthetic function of the liver, characterized by severe coagulopathy and hepatic encephalopathy. The absence of a history of liver disease is a necessary condition for diagnosing acute liver failure. A decrease in PTI or an increase in prothrombin time is noted, as well as a decrease in the concentration of coagulation factor V by more than 50% of normal in combination with any stage of hepatic encephalopathy lasting less than 26 weeks.

The term “fulminant hepatic failure” was first introduced by Trey and Davidson in 1970 to define a clinical syndrome characterized by acute onset, coagulopathy, and hepatic encephalopathy occurring within 8 weeks of disease onset.

The diagnosis of subfulminant liver failure is established when liver failure develops without hepatic encephalopathy within 26 weeks.

In some cases, acute liver failure occurs against the background of previously undiagnosed liver disease. For example, AKI may be the first symptom of Wilson's disease or α1-antitrypsin deficiency. If previous diseases are detected, the term “acute liver failure” is not used (since the duration of the disease exceeds 26 weeks). However, sometimes it is impossible to establish the fact of chronic liver disease. The exception is patients with Wilson's disease, against the background of which infection with the hepatitis B virus occurs or the development of autoimmune hepatitis. These diseases are the direct causes of short-term liver failure (less than 26 weeks).

Concepts used taking into account the time of onset of hepatic encephalopathy after detection of jaundice:

• Hyperacute liver failure (less than 7 days).
• Acute liver failure (from 8 to 28 days).
• Subacute liver failure (from 4 to 12 weeks).

ICD-10 code

K 72 0 Acute and subacute liver failure.

K 72 9 Liver failure, unspecified.

Epidemiology of acute liver failure

The prevalence of acute liver failure is relatively low. Studies have shown that about 2,000 cases are diagnosed annually in the United States. There are no data on the incidence of acute renal failure in Russians in the literature. Mortality from acute liver failure averages 3-4 people per year per 1 million population and depends on many factors, primarily on the etiology and age of the patient. The most prognostically unfavorable causes of acute renal failure are considered to be viral hepatitis B and hepatitis delta, as well as age (younger than 10 and older than 40 years).

What causes acute kidney failure?

Viral and drug-induced hepatitis are the main causes of acute liver failure. According to data obtained in the USA, in more than half of cases, acute renal failure occurs due to drug-induced liver damage. Moreover, in 42% of cases, the development of acute renal failure is caused by an overdose of paracetamol. In Europe, paracetamol overdose also ranks first among the causes of acute renal failure. In developing countries, viral hepatitis B and delta viruses (in the form of coinfection or superinfection) predominate among the diseases that cause acute renal failure. Other viral hepatitis is less likely to cause the development of acute renal failure. In approximately 15% of patients, the cause of acute liver failure cannot be determined.

Causes of acute liver failure

Hepatitis viruses A, B (+5), C, E, G7	Impaired synthesis of bile acids
Cytomegalovirus	Galactosemia
Herpes simplex virus	Fructosemia
Epstein-Barr virus	Tyrosinemia
Paramyxovirus	Neonatal hemochromatosis
Adenovirus	Wilson's disease
Drugs and toxins	α-1-antitrypsin deficiency
Dose dependent	Neoplastic
Acetaminophen
	Metastases in the liver in breast or lung cancer, melanoma
Poisoning with mushrooms of the genus Amanita	Pregnancy related
Yellow phosphorus	Acute fatty liver of pregnancy
Bacillus cereus toxin	HELLP syndrome (hemolysis, elevated liver function tests, decreased platelet count)
Idiosyncratic	Other reasons
	Budd-Chiari syndrome
Isoniazid	Veno-occlusive disease
Rifampicin	Autoimmune hepatitis
Vapproic acid	Ischemic shock liver
Disulfiram	Heatstroke
Nonsteroidal anti-inflammatory drugs	Rejection reaction after liver transplantation
Nortriptylene	Cryptogenic
Reye's syndrome (salicylic acid)
Herbal medicine

Symptoms of acute liver failure

The main clinical symptoms of acute liver failure are jaundice (not always diagnosed) and pain in the right hypochondrium. The liver was not enlarged upon examination. The development of ascites and its combination in severe cases with peripheral edema and anasarca are characteristic. Hematomas are sometimes found on the surface of the skin. Bleeding from the mucous membranes of the gastrointestinal tract is often noted, and patients experience tarry stools (melena) or vomiting blood. Encephalopathy and increased ICP are determined to varying degrees of severity. When cerebral edema occurs, systemic hypertension, hyperventilation, altered pupillary reflexes, muscle rigidity, and in severe cases, decerebrate coma are noted.

After taking large doses of paracetamol, anorexia develops during the first day, the patient is bothered by nausea and vomiting (later disappearing). Then the symptoms of acute liver failure described above are detected.

In case of mushroom poisoning, severe abdominal pain and watery diarrhea are noted, occurring 6-24 hours after eating mushrooms and lasting for several days (usually from 1 to 4 days). PE occurs after 2-4 days.

Diagnosis of acute liver failure

Laboratory research

• Thrombocytopenia.
• Changes in indicators reflecting the synthetic function of the liver. Decrease in the concentration of albumin and cholesterol, coagulation factor V and fibrinogen, decrease in AChE activity, decrease in PTI (or prolongation of prothrombin time).
• Significant increase in the activity of ALT and AST transaminases. In case of an overdose of paracetamol, AST activity can exceed 10,000 U/l (the norm is up to 40 U/l). An increase in alkaline phosphatase activity is not always recorded.
• Increased concentrations of bilirubin and ammonia in the blood serum.
• Hypoglycemia.
• Increased lactate content in blood serum.
• Increased concentrations of creatinine and urea in the blood serum (with the development of hepatorenal syndrome).

Instrumental diagnosis of acute liver failure

Ultrasound and Doppler studies reveal nonspecific changes, depletion of the vascular pattern, disturbances of portal blood flow of varying degrees, and free fluid in the abdominal cavity. The liver is small.

Histological examination of a liver biopsy reveals necrosis of hepatocytes, which in most cases does not allow establishing the cause of the disease. In acute liver failure, a puncture biopsy is not performed due to the high probability of bleeding due to hypocoagulation. This study is carried out only if a liver transplant is necessary or during an autopsy.

Treatment of acute liver failure

The basis of treatment of acute liver failure is measures aimed at eliminating etiological factors (if they are detected), and syndromic therapy, which allows to correct complications.

In case of paracetamol poisoning, gastric lavage is performed through a wide tube. If a tablet is detected in the washing water, enterosorbents (for example, activated carbon) are prescribed. In the absence of a tablet in the lavage water, it is recommended to administer acetylcysteine ​​at a dose of 140 mg/kg (simultaneously through a nasogastric tube), and then prescribe 70 mg/kg orally every 4 hours for three days. Acetylcysteine ​​produces the greatest effect when used in the first 36 hours after paracetamol poisoning.

Most often, poisoning is caused by fungi of the genus Amatia and Galerina. Mushrooms of the genus Amatia contain a-amanitin, which has a toxic effect by irreversibly inhibiting RNA polymerase. Therapy for this condition includes the use of silibinin [orally at a dose of 20-50 mg/(kg/day)] and penicillin G [intravenously at a dose of 1 mg/(kg/day) or 1,800,000 units/(kg/day)]. The action of silibinin is based on its ability to prevent the uptake of a-amanitin by hepatocytes and increase antioxidant activity. This drug produces its maximum effect within the first 48 hours after poisoning. Penicillin G helps reduce the concentration of a-amanitin in bile by interrupting the hepatic-intestinal circulation of the toxin.

Measures taken when acute liver failure of any etiology is detected:

• Ensure adequate oxygenation. Provide additional oxygen and, if necessary, mechanical ventilation.
• Correction of metabolic disorders, electrolytes and CBS.
• Monitoring of hemodynamic parameters.
• ICP control.
• Parenteral administration of glucose to correct hypoglycemia.
• Administration of mannitol to reduce ICP.
• Parenteral administration of proton pump inhibitors or histamine type II receptor blockers to prevent gastrointestinal bleeding.

Treatment of complications of acute liver failure

Hepatic encephalopathy

To correct PE, it is necessary to limit the intake of protein from food and prescribe lactulose at a dose of 3-10 g/day orally (children under one year old - 3 g/day, from 1 to 6 years old - 3-7 g/day, 7-14 years old - 7 -10 mg/day).

Cerebral edema

General measures include ensuring rest and a certain position of the head (at an angle of 100 degrees to the horizontal surface), preventing arterial hypotension and hypoxemia. Specific therapy consists of prescribing mannitol at a dose of 0.4 g/kg every hour (intravenous bolus) until ICP normalizes. It should be noted that the use of this drug is ineffective in cases of renal failure and hyperosmolarity of blood serum. With the development of hepatic coma, hyperventilation often has a positive effect. In the treatment of cerebral edema caused by acute liver failure, the prescription of glucocorticoid drugs is inappropriate (due to the lack of effect).

Hypocoagulation

FFP is administered [intravenous drip at a dose of 10 ml/(kg day)] and Vikasol [intramuscular or intravenous at a dose of 1 mg/(kg day)]. If the drugs are insufficiently effective, blood coagulation factors are used (Feiba TIM-4 Immuno - blood coagulation factors II, VII, IX and X in combination 75-100 IU/kg). To prevent gastrointestinal bleeding against the background of hypocoagulation, parenteral administration of proton pump inhibitors or type 2 histamine receptor blockers is performed [for example, quamatel 1-2 mgDkgsut] in 2-3 doses, but not more than 300 mg/day].

Hepatorenal syndrome

Therapeutic measures include replenishment of blood volume in case of hypovolemia (infusion of 5% glucose solution), administration of dopamine [at a dose of 2-4 mcg/(kgh)], and if the drugs are ineffective, HD is performed. It is also recommended to use venovenous hemofiltration.

The development of sepsis is an indication for the use of antibacterial drugs. The drugs are prescribed taking into account the sensitivity of the sown microflora. The use of antibiotics is combined with passive immunization with pentaglobin. Newborns are prescribed 250 mg/kg, infants - 1.7 ml/(kgh) intravenously. For older children and adults, it is recommended to administer 0.4 ml/(kgh) until a total dose of 100 ml is reached, then over the next 72 hours a continuous infusion of pentaglobin4 [0.2 ml/(kgh) is carried out, increasing the rate of administration to 15 ml /(kghch)].

If conservative treatment is ineffective and there are no contraindications, liver transplantation is recommended. Determining indications for liver transplantation is an extremely difficult task. Even with severe forms of acute liver failure, there is a possibility of recovery. On the other hand, irreversible changes in other organs, including the brain, may occur at any time, which are considered a contraindication to liver transplantation.

With the development of acute liver failure, spontaneous recovery rarely occurs in patients with significantly reduced synthetic liver function (low albumin concentration, severe coagulopathy), high bilirubin levels, low ALT activity, and also with a longer period between the onset of the disease and the appearance of signs of encephalopathy.

What is the prognosis for acute liver failure?

In case of paracetamol overdose, additional criteria for assessing the severity of the patient’s condition are used:

• Hypoglycemia (less than 2.5 mmol/l).
• Increased creatinine concentration (more than 200 mmol/l).
• The presence of metabolic acidosis (pH less than 7.3).
• PE III degree.

The presence of these disorders in children indicates an increased likelihood of death and also indicates a worsening prognosis.

Adverse prognostic factors for the development of acute liver failure:

• Increased prothrombin time (more than 100 s).
• Decrease in the content of blood coagulation factor V (less than 20-30%).
• Prolonged jaundice (more than 7 days).
• Age (under 11 and over 40 years old).

Acute liver failure due to hepatitis A or after paracetamol poisoning has a good prognosis.

The survival rate of the organ after liver transplantation performed for acute liver failure, as a rule, is not too high (compared to surgery for chronic liver disease). According to the literature, the survival rate of patients after emergency transplantation during the first year is 66%, and within five years - 59%. After operations performed for chronic liver failure, depending on the diagnosis, an increase in survival rate of up to 82-90% in the first year and up to 71-86% within five years is recorded.

Disturbances in the functioning of these functions indicate liver problems.

What is liver failure

Viral hepatitis and poisoning, combined with uncontrolled use of medications, greatly harm the human body. The consequence of such phenomena is liver failure syndrome. The disease is accompanied by massive necrosis of organ cells and dystrophic changes in the parenchyma. EEG, hepatoscintigraphy, and biochemical analysis of blood parameters will help identify hepatocellular failure syndrome.

Liver failure - classification

According to the course of the disease, acute and chronic forms are distinguished. Acute liver encephalopathy has its own classification. It is divided into minor, acute and severe. These types of illness manifest themselves in different ways. With minor acute encephalopathy, mild liver cytolysis and cholecystitis are present in combination with signs of the underlying disease. The patient notices:

• drowsiness;
• mild nausea;
• decreased appetite.

If the cause of the disease is a decrease in the number of red blood cells or dilation of blood vessels, the patient is diagnosed with sleep disturbances, itching, and a decrease in urine volume. Severe encephalopathy develops due to viral hepatitis and hepatocellular cancer within three days. In 80% of cases it is fulminant and requires emergency care. Patients experience weakness, aversion to food, and decreased ability to work. Signs develop in stages.

Classification of liver failure according to the form of the disease includes endogenous and exogenous disease. In the endogenous form, massive cellular cytolysis of the liver is diagnosed. Exogenous disease is characterized by the release of toxic substances from an organ into the bloodstream. Acute liver failure is characterized by the simultaneous development of these forms with hepatargia.

Stages of liver failure

Clinical manifestations of the disease develop gradually and depend on the degree of intoxication of the body. The disease causes ascites, dyspeptic disorders, varicose veins/icteric disease. At the last stage of the disease, hepatargia with hepatic coma develops. There are 3 stages of liver failure:

The initial stage is characterized by insomnia, weakness, and changes in appetite. At an advanced stage, the patient begins to exhibit pathological reflexes and hypoproteinemic edema. During the terminal stage, the patient is diagnosed with cachexia, degenerative changes in tissues, loss of consciousness, divergent strabismus, and absence of pupillary reactions. The reaction to pain with spontaneous movements disappears.

Liver failure - symptoms

The nature of the disease is determined by two pathological processes: necrosis of organ tissue and cholestasis syndrome. With extensive liver damage, the patient develops fever, blood pressure rises, and tachycardia appears. Cholestasis is accompanied by jaundice. The color of the skin changes from green to orange, determined by the degree of biliary dyskinesia. The intensity of manifestations depends on the nature of tissue damage and the speed of development of the disease. Common signs of liver failure:

• lethargy or hyperexcitability;
• drowsiness;
• nausea;
• rigidity;
• convulsions/tremors of the limbs.

The filtering capacity of the kidneys gradually decreases, and the amount of decay products in the body increases. With rapidly developing hepatonecrosis, cellular metabolism is sharply disrupted. Protein fibers are destroyed, which leads to pulmonary edema, hemorrhagic diathesis, and cholelithiasis. A person develops plantar reflexes and hepatargia.

Symptoms of liver failure in women

The main symptom of the disease is menstrual irregularity. Also, symptoms of liver failure in women include emotional disorders, sleep disturbances, degenerative changes in the pelvic and abdominal organs. If the patient is pregnant, the disease is accompanied by jaundice, cirrhosis, hepatitis E, and fatty hepatosis.

Symptoms of liver failure in men

The first manifestation of the disease is a sharp decrease in libido and mental instability. The patient's taste preferences change, an aversion to alcohol and nicotine develops, and the face becomes grayish. Lethargy and apathy are replaced by surges in working capacity and cramps of the limbs. Symptoms of liver failure appear more quickly in men than in women.

The symptom complex of the disease is the same as in adults. The child becomes inactive, sleeps a lot, and has a perversion of appetite. Liver failure in children can be diagnosed using CT, EEG and biochemical blood tests. After the disease is detected, the child is prescribed lactulose, folic acid, antibiotics, interferon, vitamin D. Diet is mandatory.

Treatment of liver failure

Therapy is carried out in a hospital setting. Patients' blood and urine are regularly tested. Treatment of liver failure is aimed at eliminating the underlying disease that affected the functionality of the organ and eliminating encephalopathy. Patients are given daily antibiotics, anabolic steroids, preparations from extracts of fresh liver, glucose, insulin, methionine, and glucocorticoid hormones are administered. If a sharp decrease in the number of protein fractions in the blood is detected, patients are prescribed albumin injections or plasma transfusions.

Liver failure - diet

The patient's menu should contain a lot of carbohydrates. Proteins and fats are completely removed from the diet. The diet for liver failure consists of a large amount of vegetables, fruits, and dairy products. Marinated, fried, spicy, smoked dishes are excluded from the menu. If the body’s condition improves after therapy, 40 grams of protein are added to the diet.

Video: liver failure - what is it

The information presented in the article is for informational purposes only. The materials in the article do not encourage self-treatment. Only a qualified doctor can make a diagnosis and give treatment recommendations based on the individual characteristics of a particular patient.

Liver failure – life is at risk!

Classification

Acute and chronic insufficiency differ in nature.

The acute form develops with an acute form of hepatitis, poisoning or subacute liver dystrophy.

The chronic form is characteristic of liver cirrhosis and chronic hepatitis. Both forms of failure can result in hepatic coma.

There are different stages: compensated, decompensated, dystrophic and hepatic coma.

Endogenous - is a complication of the death or degeneration of liver tissue and is characteristic of cirrhosis and hepatitis.

Exogenous is self-poisoning of the body with metabolic products and substances produced by intestinal microflora. This happens if the above substances enter the blood through the intestinal walls and do not pass through the liver, for example, if the portal vein is blocked. This form of failure does not cause changes in the quality of liver tissue.

Reasons

Hepatogenic: diseases and phenomena that directly affect liver tissue.

Extrahepatic: processes affecting liver functions indirectly.

• Dystrophies ( use of drugs, sulfonamides, antibiotics, poisoning with toxic substances, alcohol, mushrooms)
• Hepatitis
• Cirrhosis.

Symptoms

• Aversion to food
• Aversion to alcohol ( in former drinkers)
• Aversion to nicotine ( in former smokers)
• Lethargy
• Weakness
• Mood instability
• The complexion becomes grayish or yellowish
• Night blindness appears
• The menstrual cycle in women, libido in men are disrupted, and other hormonal disorders appear
• There is a tendency to bleed
• Swelling.

The exogenous form is characterized by:

• Mental instability of a temporary nature up to mental disorders
• Bad sleep
• Neurological symptoms.

Acute liver failure

The main symptom of acute liver failure is hepatic encephalopathy.

The condition causes death in 50–90% of cases.

1. Viral hepatitis

3. Poisoning with poisons that destroy liver cells ( adulterated alcohol, mushrooms)

5. Liver dystrophy during pregnancy, occurring in acute form.

• General deterioration in health
• Yellowing of sclera, skin
• Breath smells like rotten meat
• Trembling limbs
• Swelling.

Go to the hospital immediately.

Diagnostics

5. Blood biochemistry

6. Alpha-fetoprotein test

7. Ultrasound of the abdominal cavity

9. Radionuclide scanning

In children

In newborns under 15 days of age, liver failure is often caused by immaturity in the production of certain enzymes.

In addition, in children the cause of this condition may be hypoxia and an increased amount of proteins in the body.

If you do not provide urgent help to the baby, he falls into a coma.

Treatment of a baby with liver failure is carried out only in the hospital. Subsequently, after being discharged home, the child must adhere to a special diet for a long time and take increased doses of vitamins B, A, C, K.

Treatment

It is necessary to maintain the vital functions of the patient’s body and at the same time fight the main illness that caused this condition.

If the cause of deficiency is poisoning, toxins are removed from the body using laxatives. Intravenous injections are used to cleanse the body of ammonia. glutamic acid twice or thrice a day for 3 to 4 days.

The use of oxygen installations and oxygen pillows is mandatory.

In chronic cases of insufficiency, drugs are prescribed to alleviate the patient’s condition, the proportion of protein in food is reduced, enemas are indicated to cleanse the intestines, as well as from time to time antibiotics and vitamins IN in the form of injections, vitohepat.

Diet

2. The basis of the diet is plant foods ( juices from vegetables and fruits, honey, puree soups, compotes with boiled fruits, rosehip decoction, jelly, jelly).

3. Eat food once every 2 hours in semi-liquid or liquid form.

4. Avoid salt completely.

5. Drink up to 1.5 liters of fluid per day in the absence of edema.

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Liver failure: symptoms and treatment of the disease

Our body is an incredibly complex mechanism. Thousands of established processes ensure stable functioning of the whole organism. A failure in one of the organs can lead to disruption of all vital processes. One of the common diseases is liver failure, its symptoms depend on the type and nature of the disease. Necrosis of liver tissue or cholestasis syndrome.

Why does liver failure occur?

There are a lot of reasons for this. The most common ones should be highlighted:

• acute and chronic hepatitis;
• malignant formations;
• diseases of the heart, blood vessels and other organs;
• infectious diseases;
• poisoning (food products, medications);
• past stress (extensive burns, serious injuries, septic shock, major blood loss).

Types and symptoms

Cholestasis syndrome. The disease consists of poor excretion of bile from liver tissue. The symptoms are:

• with functional cholestasis. Decreased normal movement of bile, water, bilirubin, acids through the liver tubules;
• with morphological cholistasis. Accumulation of bile compounds in the bile ducts;
• with clinical cholestasis. Accumulation in the blood of components translated into bile. Itching of the skin, jaundice, and an increase in bilirubin levels in the blood appear.

Necrosis syndrome. This disease destroys the structure of the liver, as a result of various factors. A very dangerous disease. Often leads to complications and death. Symptoms are divided depending on the type:

• yellow skin tone;
• weight loss;
• increase in temperature;
• skin itching, appearance of vascular networks;
• diarrhea, vomiting, pain in the liver;
• emotional instability;
• the liver and spleen are enlarged.

• skin itching, peeling;
• dark urine;
• uncharacteristic, light-colored stool;
• increased levels of cholesterol and bilirubin in the blood.

Attention! If you experience at least a few of these symptoms, you should immediately consult a doctor.

Acute liver failure

Severe liver disease is divided into three stages of severity:

• light. It occurs without visible symptoms and can be detected by special tests;
• medium-heavy. Pain in the liver area, colic, yellow discoloration of the skin and mucous membranes;
• difficult stage. Can cause serious disruptions in the body, leading to hepatic coma.

Chronic form of the disease

In the process of long-term destruction of liver cells due to various influences, a chronic form of liver failure occurs. The consequence may be the onset of encephalopathy, mental disorder of behavior and consciousness.

Symptoms:

• nausea, vomiting, diarrhea;
• insomnia, or vice versa drowsiness;
• eczema;
• edema, ascites;
• infertility.
• anorexia;
• heart failure;
• constant feeling of thirst;
• memory impairment.

Liver failure in children

Liver diseases often occur in children. In most cases, they are difficult and require immediate specialist intervention. There are many causes of liver disease in children, here are some of them:

• congenital liver pathologies. Sometimes abnormal liver development begins in the womb. This could be a liver cyst, hernia, liver lobulation disorder;
• introduction of the hepatitis virus during blood transfusion;
• intoxication after poisoning, extensive burns;
• excessive protein intake;
• heavy blood loss.

Remember! Timely visit to the hospital and appropriate behavior will help preserve the life and health of your child.

Treatment at home

If you decide to be treated at home, the course of medications is still only prescribed by a doctor. The process of treating liver failure directly depends on the type of disease and its complexity.

In particularly difficult cases with a severe and dangerous course of the disease, treatment should only be inpatient. In milder forms, the fight against the disease can be carried out at home, under the close supervision of a doctor. Taking medications and vitamins aimed at combating the disease gives good results in our time. By following a course of treatment and a special diet, you can get rid of the disease in a certain period of time.

Interesting to know! The human liver has half a thousand functions. 20 million chemical reactions take place in this small organ per minute.

Use of drugs

Treatment often follows a certain pattern:

• The patient's intake of protein and table salt is sharply limited;
• antibacterial drugs such as ciprofloxacin are administered;
• drip infusions of drugs such as ornithine, glucose, sodium chloride;
• lactulose injections;
• Be sure to use B vitamins;
• calcium, magnesium;

This is just an approximate, primitive treatment regimen. Do not under any circumstances try to prescribe treatment for yourself. This is extremely dangerous to life and health. The consequences may be irreversible. Only specialists with clear knowledge can prescribe the correct treatment.

Folk remedies for treatment

As with many other diseases, some folk remedies can help with liver-related diseases. Their variety is very great. Of course, there is no certainty that such tools will help you with a 100% guarantee. In addition, the use of some traditional methods can cause complications and irreversible harm to health. Allergies, drop in blood pressure and other phenomena are not excluded when treated with folk remedies. Before using any prescriptions, be sure to consult your physician. Such treatment is only auxiliary to drug treatment. Let's try to figure it out in more detail.

Recipes for cleansing the liver

1. Pour boiling water over corn silk (use only ripe cobs) and cook for 10 - 15 minutes. Take 200 grams of decoction in the morning and evening.
2. St. John's wort herb (1 tablespoon) pour milk (200 grams). Boil for 10 minutes, strain, let settle. Take 50 grams 3-4 times a day.
3. Grate the peeled beets and boil in water for 15 minutes. The product should be taken a quarter glass 3-4 times a day.

Treatment of cirrhosis

• dissolve turmeric (1 tablespoon) in a glass of water. You can add a little honey or sugar for taste. Drink half a glass several times a day;
• Chop a clove of garlic and mix with a glass of kefir or yogurt. Drink every morning before meals;
• Chop two cloves of garlic, pour boiling water (one glass). Leave to brew for a day. Drink in the morning on an empty stomach before meals;
• Boil the oats for an hour, let them brew. Take half a glass 2-3 times a day;
• lemon, honey, garlic. Mix the ingredients in a ratio of 2:2:1. Take a teaspoon 2 times a day;
• take half a glass of carrot juice 2 times a day for cirrhosis;
• Fresh potato juice can be taken in half a glass for cirrhosis.

Herbs

Since ancient times, our ancestors have noticed and appreciated the extremely beneficial properties of some herbs. Plants can relieve inflammation, normalize blood pressure, energize, rejuvenate, soothe, heal wounds and much more. Nowadays, doctors themselves often prescribe herbal recipes as adjuvant therapy for many diseases.

To help treat liver diseases, there are the following recipes:

• St. John's wort, dandelion root, sandy immortelle mixed in a ratio of 2:2:1. Brew 500 grams of boiling water. Take a glass morning and evening;
• Mix nettle, rose hips, wheatgrass in a ratio of 1:1:1. Brew a glass of boiling water and leave for 2-3 hours. Take 2-3 doses per day for cirrhosis;
• Mix lingonberry leaves, corn silk, dandelion root, linden blossom, and motherwort herb in equal quantities. Pour a liter of boiling water and leave for 5-6 hours. Take half a glass 2 times a day;
• Mix yarrow, St. John's wort, juniper fruits in a ratio of 2:2:1. Fill with a liter of water. Boil for 10 minutes, strain, let sit for 12 hours. Take half a glass 2-3 times a day;
• mint herb, bearberry, knotweed, St. John's wort, dill seeds, Kuril tea, mix everything in equal proportions, chop well. Boil in a liter of water for a minute, strain. Let sit for hours. Take a quarter glass 2-3 times a day.

Diet for liver failure

For liver diseases, a special diet is absolutely necessary. There are products that can aggravate the course of the disease, and vice versa, help in healing.

Remember! The goal of any diet is to alleviate the disease and avoid complications.

Dietary rules for liver diseases:

• food should be easily digestible and light;
• exclude spicy, salty, sour, smoked, fatty, fried foods;
• porridge should be well cooked. It is better to rub large-grain porridges on a sieve;
• include foods that have choleretic properties in your food. These are corn, sunflower, peanut oils. Greens: dill, spinach, celery. Fruits include oranges, lemons, grapefruits. Dried apricots, cauliflower, artichokes are useful;
• limit protein intake, no more than grams per day;
• Have a fasting day once a week.

Prohibited products:

• mushrooms;
• fatty meat;
• alcohol;
• chocolates;
• fatty dairy products;
• strong black tea;
• radishes, sorrel;
• rye breads, fresh pastries.

© 2017 Treatment with folk remedies - the best recipes

The information is provided for informational purposes.

Liver failure: symptoms and treatment

Liver failure - main symptoms:

• Headache
• Dizziness
• Fever
• Nausea
• Loss of appetite
• Hair loss
• Pain in the right hypochondrium
• Heaviness in the right hypochondrium
• Bad breath
• Swelling of the legs
• Fever
• Aggressiveness
• Increase in abdominal volume
• Trembling limbs
• Varicose veins
• Yellowing of the skin
• Facial swelling
• Redness of the palms
• Nail splitting
• Breast atrophy

A disease characterized by a violation of the integrity of liver tissue due to acute or chronic damage is called liver failure. This disease is considered complex, due to the fact that after liver damage, metabolic processes are disrupted. If appropriate measures are not taken to cure the disease, then under certain conditions liver failure can develop quickly and rapidly and lead to death.

Classification

The disease is classified according to two criteria: the nature of the course and stages.

Based on the nature of the disease, there are two stages of the disease:

Acute liver failure occurs due to the loss of the liver's ability to perform its functions. The disease manifests itself predominantly within a few days and is characterized by a severe form of symptoms. Often the acute form is fatal, so it is very important to know the symptoms in order to recognize the disease at an early stage.

Acute liver failure is divided, in turn, into major and minor. Large is the classic form of manifestation of the disease, which is quite clearly visible in clinical and laboratory studies. Minor acute liver failure occurs more often in children against the background of serious illnesses (poisoning, intestinal infections, pneumonia, etc.). This subspecies is very difficult to diagnose due to the absence of symptoms of the disease. The small species can develop either rapidly or over several years.

Chronic liver failure develops through a slow progression of the disease. Due to the gradual dysfunction of the liver with the progressive course of a chronic disease of the parenchyma, a chronic type of disease is formed. Diseases such as liver cirrhosis or chronic hepatitis are a consequence of chronic liver failure. Both manifestations end in hepatic coma followed by death.

Additionally, there are two types of liver failure:

The endogenous species is characterized by the manifestation of complications due to death or dystrophic changes in the liver tissue. This type is characteristic of liver cirrhosis and chronic hepatitis.

The exogenous species is formed as a result of self-poisoning of the body, which is caused by metabolic products and substances produced by the intestinal microflora. It occurs due to the entry of these substances into the blood through the intestinal walls when they stop in the liver. The reason for the stop may be blockage of the veins, so as a result, self-destruction of the liver is observed.

According to degrees of severity, four stages are distinguished:

1. Initial or compensated, which is characterized by an asymptomatic course of the disease. At the initial stage, the liver begins to actively react to toxins.
2. Decompensated. The first signs of the disease appear. At this stage, a blood test indicates the development of the disease.
3. Dystrophic or terminal. The pre-final stage, upon the onset of which the patient experiences serious liver dysfunction. Against this background, there is also a disruption in the functioning of the entire body from the central nervous system to metabolism.
4. Stage of hepatic coma. It is characterized by deepening liver damage, which ultimately leads to death. The last stage is characterized by the complexity of treatment, as the liver enters the stage of death.

Causes of the disease

The disease “liver failure” is diagnosed in both men and women; moreover, it has no age restrictions, so you can get sick both in childhood and in the elderly. The causes of liver failure are varied and unpredictable. It is important to know them in order to be able to make a premature diagnosis and speedy treatment. So, the reasons that can provoke liver failure in a person are as follows:

1. Liver diseases, which include: malignant tumors and other neoplasms, cirrhosis, acute and chronic hepatitis, echinococcus, etc. Any of these signs can serve as an impetus for the development of a fatal disease. Cirrhosis and hepatitis can be both the cause of the disease and its consequences.
2. Blockage of the bile ducts, as a result of which an increase in the pressure of biliary hypertension is predicted. Failure of hypertension disrupts blood circulation in the liver, which causes the development of dystrophic abnormalities in the cells of this organ.
3. Diseases of the heart, blood vessels, infectious infections of the body, insufficiency of the endocrine glands, autoimmune diseases. Any disorder in the body can cause the development of a serious disease, so it is much easier to eliminate signs of abnormalities at an early stage than to try to cure serious diseases.
4. Taking medications (especially over a long period of time) can leave their mark on the liver. As you know, any medicine affects the liver, so it is very important to maintain the correct dosages of drugs and not violate the frequency of administration.
5. Poisoning with various organic and inorganic substances: poisonous mushrooms, alcohol, tobacco, chemicals, etc.
6. Extreme influences. The cause of a fatal disease can be even a minor burn on the skin, for which appropriate treatment measures are simply not taken. In addition: injuries, blood loss, allergies, septic shock and other factors can become the root cause of liver failure.
7. Deviation of kidney function, tuberculosis, urolithiasis, pyelonephritis, congenital anomalies and much more are the causes of such a disease as renal-hepatic malaise.

The main cause of renal-liver disease is the lack of balance between the narrowing and dilation of blood vessels. The reason for the lack of balance can be the banal cause of alcohol abuse, as well as food and respiratory poisoning. The disease of renal-liver failure is no less serious than damage to the liver alone, since there is an annual increase in mortality from this type of disease.

Based on all the reasons, a complex of symptoms of the disease appears. Let’s take a closer look at what these symptoms are and their main features.

Symptoms of the disease

The symptoms of liver failure are very diverse, but they are the first factors, after detection of which you need to rush to the doctor. The initial stages of the disease manifest themselves in the form of general malaise of the body, the appearance of mania and other motor disturbances. During flexion/extension of the fingers, a symptom of tremor may be observed, that is, lateral signs or trembling, often occurring with sudden movements.

Liver failure and its symptoms are always accompanied by the development of jaundice and neuritis. The patient experiences a rise in temperature to 40 degrees with an exacerbation of the disease, as well as swelling of the legs. An unpleasant but specific odor appears from the mouth, indicating the beginning of the formation of trimethylamine and dimethyl sulfide. A disorder of the endocrine system occurs, there is an increase in hair loss, up to baldness, libido decreases, atrophy of the uterus and mammary glands in women occurs, and nails split and crumble. In women, liver failure at an early age can negatively affect fertility, that is, provoke the development of infertility.

In addition, throughout the entire period of the disease, the patient experiences an increase in headaches, feverish manifestations, dizziness, even fainting, and an aggressive state. Let us consider in more detail what symptoms are characteristic of the three stages of the disease.

Stages of chronic liver failure

Often, chronic liver failure is characterized by four stages, which have their own symptoms.

1. The compensated stage often manifests itself asymptomatically, but the following negative processes are observed inside the body: increased pressure in the hepatic system, overflow of the venous plexuses in the abdomen, varicose veins. At the initial stage, you can notice the indistinct appearance of spider veins on the patient’s body and redness of the palms. The patient refuses to eat food due to disgust. There is a slight weight loss.
2. The decompensated stage is caused by increased symptoms of the disease. The first signs of the disease begin to appear: aggression, disorientation in the area, slurred speech, trembling of the limbs. Relatives may observe a significant change in a person's behavior.
3. The dystrophic stage is caused by the occurrence of stupor. The patient becomes inadequate, it is very difficult to wake him up, and during moments of wakefulness, apathy is periodically replaced by excitement. Swelling of the face, legs, and fluid accumulation in the abdominal cavity appear. The patient may also experience bleeding from the nose or gastrointestinal tract in the morning or evening.
4. At the final stage, the patient experiences the appearance of hepatic coma, as a result of which the patient is unconscious, and there is no reaction to external painful stimuli. The patient's vision decreases, strabismus develops, brain swelling and fluid accumulation occur. Chronic liver failure develops differently in each individual case, often over decades.

Acute symptoms

Acute liver failure occurs predominantly rapidly with a pronounced pattern of symptoms. This type has the following symptoms:

• sudden onset of weakness;
• nausea, vomiting and other signs similar to poisoning;
• increase in body temperature;
• an increase in jaundice, and you can observe a change in skin color to yellow. The patient's eyeballs also become yellow;
• bad breath;
• a decrease in the size of the liver, which manifests itself in the form of pain;
• lethargy, anxiety and speech impairment.

Acute liver failure is characterized by a change in blood composition: an increase in bilirubin occurs, which indicates the breakdown of hemoglobin and its decrease, as well as a decrease in the prothrombin index.

It is very important to deliver the patient to the clinic on time in order to be able to administer medication. Otherwise, acute liver failure can lead to death in a very short time.

Symptoms of renal-liver disease

The symptoms of renal-liver disease are almost identical to those above, the only difference is kidney damage, which indicates their pain and the manifestation of the following symptoms:

1. The presence of pain first in the liver, and then in the kidney area.
2. Increase in temperature.
3. Signs of jaundice.
4. Red blood cells, protein and bile compounds are found in the urine.
5. A hemorrhagic diathesis is formed, the cause of which is intoxication of the body.

The main danger of renal-liver disease is the involvement of other organs and systems in the pathology process: gastrointestinal tract, central nervous system, respiratory organs, etc. In the chronic form, the functioning of the liver tissues stops, as a result of which toxins begin to be eliminated through the gastrointestinal tract and lungs. This is an abnormal condition, so the body experiences severe stress.

Before starting treatment, it is important to correctly diagnose the disease. What is needed for diagnosis can be found in the next section.

Diagnostics

If all of the above symptoms are detected, you must immediately go to the hospital or call an ambulance. The clinic will require diagnostics to be able to make a correct diagnosis. First of all, diagnosis begins with interviewing and examining the patient. Often this is not enough to make a correct diagnosis, so the doctor will prescribe clinical measures.

Clinical activities include donating blood to identify biochemical data for bilirubin, alkaline photosphase, LDH, AST and ALT. Using these indicators, the doctor identifies not only the presence of signs of the disease, but also at what stage the liver disease is. The higher the indicators, the correspondingly more active the process of liver cell breakdown.

Additionally, an ultrasound may be required, on the basis of which it is possible to determine the nature of the disease (acute or chronic), identify the size of the liver and the presence of structural and degenerative changes.

The following diagnostic measures cannot be ruled out:

These additional tests and data will give an idea of ​​how other human organs and systems are involved in the disease process.

Treatment

Treatment of liver failure is a rather complex and lengthy procedure, which depends, first of all, on the stage of the disease.

An important place in the treatment process is given to infusion therapy, through which proper nutrition is ensured and the body is detoxified. It is also necessary to improve liver microcirculation, normalize or restore the acid-base balance.

The patient is prescribed laxatives and enemas to cleanse the gastrointestinal tract of toxins and relieve constipation. A drip with a solution of glucose, vitamins B6, B12, and lipoic acid is administered daily.

If the disease has progressed to the stage of hepatic coma, then intensive drug interventions are resorted to. The purpose of these measures is to maintain the patient’s life so that the functioning of the liver can be normalized. A solution of sodium or potassium bicarbonate is injected, and humidified oxygen is inhaled through a nasal catheter. If the pressure decreases, then albumin is administered intravenously.

The patient must be in hospital and under the supervision of nurses. In addition to medication procedures, the following conditions are observed:

• daily monitoring of a blood test to determine the composition of albumin;
• urinary monitoring;
• prevention of bedsores;
• carrying out weigh-ins daily.

Hypoammonemic drugs can reduce the level of ammonia in the body.

If the patient has associated renal failure, then additional hemodialysis will be required in order to remove ammonia and other toxins from the blood, which under normal conditions are neutralized by the liver. In case of edema or ascites, paracentesis is necessary to help remove excess fluid from the body.

In addition to all of the above, normalizing the liver will require maintaining proper nutrition, or rather, following a diet.

Diet

Diet in the treatment of liver disease is a mandatory procedure, since the liver receives a significant blow precisely from improper nutrition. The diet includes compliance with the following procedures:

1. Reducing the level of protein and fat to 30 grams per day, and carbohydrates to 300.
2. It is preferable to eat plant foods, which include: fruits, vegetables, honey, compotes, jelly.
3. Consume food only in liquid or semi-liquid form. At the same time, you need to eat little by little, but every 2 hours.
4. Eliminate salt from your diet completely.
5. If there is no swelling, then you need to drink about 1.5 liters of fluid per day.

Diet plays an important role in the treatment of liver failure, so a combined effect will help you get rid of the symptoms of the disease and return to your previous healthy life.

If you think that you have liver failure and symptoms characteristic of this disease, then doctors can help you: hepatologist, gastroenterologist, therapist.

We also suggest using our online disease diagnostic service, which selects probable diseases based on the entered symptoms.

Jaundice is a pathological process, the formation of which is influenced by a high concentration of bilirubin in the blood. The disease can be diagnosed in both adults and children. Any disease can cause such a pathological condition, and they are all completely different.

Viral hepatitis B is an inflammatory viral disease that primarily affects liver tissue. After a person recovers from this disease, he develops lasting, lifelong immunity. But it is possible for the acute form of hepatitis B to transform into a chronic progressive form. Carriage of the virus is also possible.

Thrombocytopenic purpura or Werlhof's disease is a disease that occurs against the background of a decrease in the number of platelets and their pathological tendency to stick together, and is characterized by the appearance of multiple hemorrhages on the surface of the skin and mucous membranes. The disease belongs to the group of hemorrhagic diathesis and is quite rare (according to statistics, 10–100 people fall ill with it per year). It was first described in 1735 by the famous German physician Paul Werlhof, in whose honor it received its name. Most often, it manifests itself before the age of 10 years, while it affects both sexes with equal frequency, and if we talk about statistics among adults (after 10 years of age), women get sick twice as often as men.

With the help of exercise and abstinence, most people can do without medicine.

Symptoms and treatment of human diseases

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Obert A.S., Morozova O.P., Yakob L.E., Zinovieva L.I., Ivanov I.V., Pershin O.V.

Acute hepatocellular failure is a clinical concept equivalent to the morphological concept of “massive” or “submassive liver necrosis”. Hepatocellular failure is usually characterized by encephalopathy - a disorder of consciousness, a change in the consistency and reduction in the size of the liver, hemorrhagic syndrome, and often progressive jaundice.

In the literature, the terms “hepatodystrophy”, “malignant” or “fulminant” forms are used as synonyms. The main morphological substrate of these conditions is early acute massive necrosis of the liver. In the future, when presenting the material, the terms “acute hepatic cell failure” (ALF) and “acute hepatic encephalopathy” (AHE) are more often used.

The main etiological factors of acute renal failure in children include viral hepatitis B. An important comatogenic factor is superinfection with the D virus. The provoking role of the addition of HAV and HCV has been confirmed. In recent years, much attention has been attracted in the literature by indications of the predominant frequency of detection of mutant HBV strains, in particular the e-minus strain, in patients with fulminant HBV (Nakayama I. et al., 1995; Sato Sh. et al., 1995; Baymert T.F., Liang T.I. , 1996). ARF occurs predominantly in children of the first year of life in 0.7-1% (Drobinsky N.R., Dokuchaeva K.D., 1972; Nisevich N.I., Uchaikin V.F., 1982, 1990). Mortality, according to N.I. Nisevich, V.F. Uchaikin (1982), is 11.6%. AKI in children, in addition to viral hepatitis, can develop due to drug-induced, toxic liver damage.

Pathogenesis

The most important factors causing acute massive liver necrosis in viral hepatitis are: the high immunogenicity of the pathogen, the massiveness of the infecting dose, and a genetically determined strong type of immune cell reaction. Rapid, super-intensive synthesis and secretion of antibodies in excess develops. The forming antigen-antibody complexes cause massive immune cytolysis, and can also contribute to increased fragility of lysosomal membranes of hepatocytes, release of proteolytic enzymes, and massive necrosis of hepatocytes (A.F. Bluger et al., 1988).

Hepatic coma is the most striking manifestation of acute hepatic cellular failure, its final stage and is clinically characterized by impaired mental activity up to complete loss of consciousness. Disorder of consciousness occurs as a result of the accumulation in the blood serum of numerous cerebrotoxic substances formed as a result of progressive functional inferiority of the liver and autolytic breakdown of the hepatic parenchyma. Among the direct cerebrotoxic substances, products of free radical oxidation of hepatocyte membranes are important, which can increase the permeability of brain cell membranes and have a direct toxic effect on the central nervous system. Products of protein metabolism (phenylpyruvate, ammonia, etc.), carbohydrates (pyruvic, lactic, alpha-ketoglutaric acids), and fat (low-molecular fatty acids butyric, valeric, caproic) also have a toxic effect. A sharp drop in the detoxification function of the liver also underlies a significant increase in the blood content of intestinal toxins phenol, indole, skatole, indican, mercaptan and a number of others.

As a direct cause of hepatic coma, the decisive importance is given to the inhibition of oxidative phosphorylation processes with a sharp decrease in the synthesis of high-energy bonds of phosphorus compounds and a drop in the bioenergetic potential of cerebral cells. This is accompanied by a violation of oxidative processes, a decrease in glucose and oxygen consumption, and the development of cerebral hypoxia and hypoglycemia. Hypoglycemia associated with inhibition of gluconeogenesis in the liver can aggravate functional disorders of the central nervous system (deficiency of the main substrate for energy production). An increase in the permeability of neuronal membranes leads to the accumulation of Na and Ca in subcellular structures and a decrease in the K content. The accumulation of hydrogen ions, pyruvic, lactic and tricarboxylic acids of the Krebs cycle inside neurons leads to the development of intracellular metabolic acidosis. The result of these processes is edema-swelling of brain cells.

With APE, the coagulation potential of the blood is depleted, the synthesis of coagulation factors decreases, the enzymes of proteolysis and fibrinolysis are activated, and the activity of their inhibitors is catastrophically reduced. The implementation of various forms of hemostasis pathology occurs in the presence of hypocoagulation and depletion of blood coagulation factors, leading to disruption of microcirculation in the liver with the formation of intravascular blood clots and the occurrence of hemorrhagic syndrome. The synergism of toxic substances increases due to the violation of CBS, the redistribution of electrolytes and contributes to the development of hepatic coma.

Clinic

The clinical picture of acute renal failure is far from clear and varies widely depending on the duration of the disease and the rate of progression of the process.

Manifestations of liver failure are fundamentally the same as in severe forms of the disease, but differ in a more significant degree of severity and rapid dynamics of development: severe weakness, headaches, anorexia, constant nausea, repeated vomiting. Hemorrhagic syndrome progresses: skin petechiae, ecchymoses, and sometimes profuse hemorrhagic rash, melena, bloody urine, bleeding from injection sites, vomiting “coffee grounds”. There is a rapid increase in jaundice. Hypotension, muffled heart sounds, decreased diuresis, and slowed ESR are characteristic.

For acute renal failure, the presence of clinical signs of massive liver necrosis is mandatory. They are characterized by a rapidly progressive decrease in the size of the liver (symptom of “melting liver” or “empty hypochondrium”); the consistency of the liver becomes flabby, doughy, and the lower edge can no longer be felt. A distinct liver odor appears from the mouth. Repeated recording of liver size according to percussion and palpation data, carried out at short intervals, makes it possible to assess the rate of progression of the necrotic process. Indirect signs of beginning massive liver necrosis are spontaneous pain and tenderness on palpation in the right hypochondrium due to necrosis and autolytic breakdown of the liver parenchyma. Characterized by tachycardia, pronounced temperature reaction (T 38-39 ° C), neutrophilic leukocytosis, leukemoid reactions.

In parallel with the clinical signs of acute renal failure and massive liver necrosis, the neurological symptoms of hepatic precoma, which is the highest manifestation of hepatic cellular failure, are increasing. The development of precoma-coma characterizes the transformation of “pure” liver failure into hepatocerebral failure. It is the emergence and rapid progression of impaired consciousness that serve as the main criterion for distinguishing severe non-comatose forms of HBV with a cyclic course from the fulminant variant of the disease (early acute massive liver necrosis).

There are 4 successive stages of progressive neuropsychiatric disorders: acute hepatic encephalopathy (AHE) I-II (precoma); OPE III-IV (coma). This division is of great practical interest, since it allows a more objective assessment of the effectiveness of the therapy and to judge the prognosis; there are no pathognomic symptoms indicating a threat of developing hepatic coma. The totality of clinical data is informative, especially when providing dynamic monitoring of patients.

It is customary to distinguish 4 stages of progression of neuropsychiatric disorders. In this case, an integral assessment of the depression of consciousness can be used, based on taking into account the patient’s reaction to verbal commands and painful stimulation. According to this system, in the precoma stage, the reaction to verbal treatment is slowed down, but purposeful, and to painful stimulation it is preserved. In the first stage of coma, there is no reaction to a cry; pain is characterized by a short-term awakening, sometimes with inadequate speech reactions (moaning, incoherent words) and unfocused movements. In stage II coma, there are no targeted verbal and motor reactions; in response to pain, only undifferentiated movements of the body and limbs occur. Clinical monitoring is supplemented by repeated EEG registration, which is considered as the most objective criterion for assessing the depth of coma.

OPE I (precoma I) in older children is characterized by a change in the child’s behavior and usually begins gradually: euphoria is often observed, in other cases there is a feeling of anxiety, melancholy, depression or apathy, memory “gaps”, handwriting disorder, deterioration of orientation in time and space . A slowdown in thinking (slow responses to simple questions) is detected quite early. An important symptom is sleep disturbance. The patient may doze during the day and become noisy at night. Handwriting impairment should be considered as an objective, and most importantly, early-onset sign of acute liver failure. Changes in the EEG are inconsistent and weakly expressed.

OPE II (precoma II) is manifested by more pronounced disturbances of consciousness: confusion becomes more distinct, disorientation in time, space, and personality is observed. Speech is slow. Attacks of excitement, sometimes with delirium, are replaced by depression and drowsiness. The reaction to painful stimuli is preserved. Control of the sphincters is also maintained. One of the most characteristic movement disorders is flapping tremor. In precoma II, clinical signs may appear indicating cerebral edema: facial flushing and sweating, hiccups, hallucinations, yawning, increased blood pressure. Patients carry out the simplest commands with difficulty, periodically completely “switching off”, which corresponds to repeated short-term loss of consciousness. The EEG records an increase in amplitude and a slowdown in rhythm.

OPE III (coma I) corresponds to a shallow coma. Consciousness is absent, but the reaction to strong stimuli (pain, cold, heat) is preserved. The neurological status is characterized by wide pupils with an almost complete lack of reaction to light, a symptom of “floating” eyeballs; pronounced pathological reflexes of Babinsky, Gordon, clonus of the foot muscles. The face becomes amicable, the limbs are rigid, and paroxysmal clonic convulsions are observed. Paresis of smooth muscles leads to intestinal atony with progressive bloating and cessation of urination with a full bladder. EEG changes are characterized by a decrease in amplitude with a rare rhythm. Duration of OPE III is 1-2 days.

OPE IV (coma II) - deep coma, differs from the previous stage in complete areflexia, loss of response to any stimuli. Basically the same abnormalities are recorded in the neurological status. The pupils are wide, their reaction to light disappears, corneal reflexes fade, and sphincter paralysis occurs. The appearance of periodic breathing of the Kussmaul or Cheyne-Stokes type is characteristic. The EEG shows a decrease in cerebral activity up to its complete absence. The duration of OPE IV ranges from several hours to a day, on average 17 hours.

Based on the nature of the initial manifestations of liver failure and the rate of development of clinical symptoms of massive liver necrosis, it is customary to distinguish between the acute and subacute course of acute renal failure. Morphologically, this corresponds to acute and subacute massive liver necrosis. In addition, there is also a fulminant variant of the course of acute liver failure - this is the most rare form. A feature of the fulminant course is the development of massive liver necrosis, acute liver failure with a fatal outcome in the prodromal period, even before the appearance of distinct jaundice (usually in the first 3-4 days from the onset of the disease). In the acute course, the clinical manifestations are the same as in the severe form of the disease, but differ in a more significant degree of severity. Signs of massive liver necrosis and hepatic coma usually develop on the 5th-6th day of the icteric period. The subacute course of APE is characterized by a gradual, wave-like progression of clinical symptoms of liver failure and the development of massive liver necrosis and hepatic coma at 3-5 weeks of the disease. When macronodular cirrhosis develops, hepatic coma occurs at a later date (after 3-6 months).

Features of fulminant forms of viral hepatitis in children of the first year of life

APE is more common in children 1 year of life (up to 20%). The development of acute liver failure with a fatal outcome is 6 times higher in them than in children older than one year.

In children of the first year of life in the first stages of disease development, the clinical diagnosis of APE is difficult. Intoxication is often mild for a long time. Appetite is often preserved, regurgitation and vomiting are episodic. Certain information is provided by a change in the child's behavior - unmotivated restlessness, lethargy, change in sleep rhythm. An objective criterion for the severity of the disease is intense jaundice, especially in combination with a small liver. At the same time, one should remember about the possible discrepancy between the degree of skin icterus and bilirubinemia, as well as the initial stages of acute liver failure in some children with low levels of bilirubin in the blood. During this period, children of the 1st year of life, as well as in the older age group, are characterized by an increase in hemorrhagic syndrome in the form of petechial rash, ecchymoses, bleeding from injection sites, and nosebleeds. Tachycardia, muffled heart sounds, decreased diuresis, leukocytosis, and slowed ESR are noted.

Further development of massive liver necrosis, as in older children, is characterized by a rapidly progressive decrease in its size, pain on palpation, doughy consistency, and hepatic odor from the mouth. Intoxication increases, hemorrhagic syndrome intensifies, which together leads to increased vomiting of “coffee grounds”. Along with this, body temperature rises to febrile levels, tachycardia, toxic shortness of breath, oligoanuria and edematous ascitic syndrome often develop. A significant indicator of the severity of the condition is flatulence, followed by intestinal paresis.

It is very difficult to assess the degree of mental disorders in children in the first year of life; they can be distinguished as OPE II (precoma), OPE III (coma I) and OPE IV (coma II). In addition, it is not always possible to note a gradual increase in the severity of the disease and a clear transition from one stage of coma to another.

OPE II (precoma) is a condition with a predominance of symptoms of a disorder of the central nervous system. Attacks of psychomotor agitation are replaced by attacks of adynamia, drowsiness, children cannot fix their gaze on toys, periodically do not recognize their mother, but react to painful stimuli by crying. The reaction of the pupils to light is preserved, abdominal reflexes are usually not evoked. 50% of children experience convulsive twitching in certain muscle groups, sometimes trembling of the upper extremities, and some children have clonic-tonic convulsions. Constant symptoms are the clinical manifestations of massive liver necrosis described above.

OPE III (coma I) is characterized by a persistent lack of consciousness, the child is restless, does not respond to examination, the pupils are constricted, with a sluggish reaction to light, tremor increases, and convulsions become more frequent. However, at this stage the reaction to strong painful stimuli remains, and swallowing is not impaired.

After 1-2 days, OPE III turns into OPE IV (coma II), the distinctive signs of which are a complete lack of response to painful stimuli, dilated pupils without reaction to light, disappearance of the corneal reflex, respiratory distress of the Kussmaul or Cheyne-Stokes type, which occurs periodically convulsions.

Complications OPE

The clinical picture of APE changes significantly with the addition of additional pathological processes. These include the development of cerebral edema, renal failure, massive gastrointestinal bleeding, and the addition of a secondary infection. These pathological conditions, for the most part, can only conditionally be classified as complications. Rather, we are talking about different options for a particularly severe course of hepatitis B. The exception is a generalized secondary infection, which is a true complication of the underlying disease. Their development further complicates the already extremely difficult prognosis. Timely recognition of these conditions is necessary for adequate intensive care.

The most common complication is edema-swelling of the brain. Clinically, this is manifested by symptoms of cerebral hypertension and irritation of the meninges, intense headaches, dizziness, repeated “cerebral” vomiting that does not bring relief; Characterized by hyperemia and sweating of the face, convulsive twitching, the appearance of oculomotor disorders, increased blood pressure, and progressive disturbances in breathing rhythm.

Massive gastrointestinal bleeding, clinically manifested by vomiting “coffee grounds”, blood clots, dark tarry stools, sometimes with the presence of unchanged blood. Anemia is progressively increasing.

Acute renal failure. For early recognition of renal failure and subsequent monitoring of patients, it is important to take into account hourly urine output. Diuresis less than 35-45 ml/h corresponds to oliguria, less than 15-20 ml/h oligoanuria. With such a volume of urine, even at its maximum concentration, complete excretion of metabolic products is not ensured. Despite such a significant decrease in diuresis, the relative density of urine is sharply reduced (1003-1010), which confirms a violation of the concentration function of the kidneys. Characterized by a rapid increase in body weight due to pulmonary and cerebral edema.

Secondary infection. Most often, pneumonia occurs; a septic process may occur, which is facilitated by prolonged catheterization of the venous vessels. In patients with fulminant hepatitis, the body's resistance is sharply reduced, which facilitates the addition of a secondary infection.

Diagnostics

The main clinical criteria for fulminant forms of viral hepatitis are the combined development of two symptom complexes: hepatic coma and massive liver necrosis. The intensity of jaundice is diagnostically uninformative, since with a truly lightning-fast course it does not have time to reach its maximum development. The main diagnostic difficulties arise at an early stage, before the onset of coma and in the absence of classical signs of massive liver necrosis. Below are the clinical and laboratory signs that are precursors of early acute massive liver necrosis of fulminant hepatitis (S.N. Sorinson, 1997):

- progressive increase in the severity of the patient’s condition;

- pain and tenderness in the right hypochondrium;

- progressive reduction in liver size; temperature reaction;

- manifestation of hemorrhagic syndrome;

- the appearance of a slight liver odor in the patient’s breathing zone;

Tachycardia;

- increased breathing and increased blood pressure (with the development of cerebral edema);

- neutrophilic leukocytosis;

- changes in neuropsychic status with the sequential development of a phase of excitation and a phase of inhibition;

- during the excitement phase, euphoria, headaches, autonomic disorders, vomiting;

- against the background of drowsiness, lethargy, attacks of psychomotor agitation;

- impaired coordination of small movements (autograph test, handwriting impairment);

- mistakes when counting out loud;

- change in Romberg's posture, "flapping tremor";

- changes in the EEG with an increase in the amplitude of the waves and a tendency to slow down the rhythm.

In a general blood test in patients with acute renal failure, there are signs of anemia, especially severe in hemorrhagic syndrome, leukocytosis from moderate to severe. ESR is normal or reduced, but acceleration is also noted in some cases.

Biochemical studies occupy an exceptional place in the diagnosis of acute renal failure. Of the numerous tests, the most informative are the so-called bilirubin-protein and bilirubin-enzyme dissociations. Their essence lies in the fact that with a high content of bilirubin in the blood serum, the level of protein complexes and enzyme activity decrease sharply. The level of total bilirubin increases due to the direct fraction in the first days, then, as the process progresses, the proportion of the indirect fraction increases due to impaired uptake and conjugation of bilirubin by liver cells (massive necrosis of hepatocytes).

Very important in the diagnosis of massive liver necrosis is the blood coagulation indicator prothrombin, the content of which is less than 10% indicating a hopeless prognosis of the disease. Particularly valuable is the study of the levels of proaccelerin and proconvertin, the decrease of which precedes the manifestations of massive liver necrosis. As a result of a sharp disruption of the protein-synthetic function of hepatocytes, the content of β-lipoproteins and total protein decreases due to the albumin fraction, and the sublimate titer decreases. The activity of enzymes (ALT, AST) is different at different stages of acute liver failure. In the early periods, there is usually a significant increase in transaminase activity. Subsequently, as hepatic cell failure increases, enzyme activity decreases. When monitoring patients with severe forms of viral hepatitis, dynamic monitoring of acid-base status (ABS) and water-electrolyte balance is necessary. Characterized by a decrease in potassium content and, conversely, an increase in sodium. Regular changes take place in the ratio of CBS. In the stage of precoma and coma, extracellular alkalosis and intracellular acidosis are detected, which increases the content of free ammonia in brain tissue, disrupts the metabolism of neurocytes and contributes to the deepening of coma.

To identify the etiological factor, it is necessary to test the patient’s blood for markers of viral hepatitis (HBsAg, HBeAg, antiHBcor IgM, antiHBs, antiHBe, antiHCV, antiHDV), PCR (polymerase chain reaction) is informative, with which you can detect HBV DNA, HCV RNA. Taking into account clinical data and the dynamics of HBV markers makes it possible to distinguish between hyperimmune (hyperreactive) and immunotolerant (replicative) variants of fulminant hepatitis B. Early (in the first 7-10) appearance of antiHBe, antiHBs is characteristic of the hyperimmune variant, and the continued circulation of HBeAg, HBsAg, antiHBcor IgM ( without the above-mentioned seroconversion at the same time) for replicative.

For early recognition of acute renal failure, it is important to take into account the level of urea and creatinine.

Treatment

In the treatment of acute renal failure, the use of a therapeutic complex as early as possible plays an extremely important role, i.e. at the first signs of liver failure.

The intensive care program includes a set of therapeutic measures aimed at maintaining vital functions, stabilizing blood circulation, adequate oxygenation, and reducing intracranial pressure.

Emergency measures are carried out immediately upon admission of the patient. These include: ensuring airway patency, gastric lavage, catheterization of the subclavian vein, catheterization of the bladder to measure daily urine output. It is important to insert a permanent nasogastric tube, which allows bile to be sucked out repeatedly.

Considering the sharp impairment of the detoxification function of the liver, protein unloading is absolutely mandatory. At an early age, a water-tea break is prescribed for 8-12 hours, followed by dosed feeding, expressed breast milk or fermented milk mixtures of 20.0 ml every 2 hours with a 6-hour night break. Older children are prescribed sugar-fruit fasting days, then kefir 100.0 after 3 hours. The expansion of the diet depends on the dynamics of liver failure; if positive, table No. 5 according to Pevzner is subsequently prescribed.

With progressive disorders of consciousness, natural nutrition becomes impossible. In this case, feeding is carried out with infant formula through a nasogastric tube in combination with parenteral administration of energy solutions. You can introduce fruit juices, jelly, infusions, liquid semolina porridge, mashed potatoes. Feeding through a tube is carried out fractionally, in small portions of 20-30 ml, and for children over 3 years old, 50-100 ml every 2.5-3 hours.

Overloading the body with products of perverted metabolism requires active detoxification therapy, which is carried out by administering fluids enterally and parenterally. The calculation of liquid is carried out according to the generally accepted scheme, taking into account the daily need for water and its possible losses:

Age-related fluid requirement per 1 kg/weight/day;

With body temperature for each degree above 37 0 C for a duration of more than 8 hours, 10 ml/kg;

For every 20 respiratory movements above normal, 15 ml/kg.

60-70% of the total amount of liquid is administered intravenously. Colloidal preparations (reopolyglucin, albumin, fresh frozen plasma) make up 25% of the infusate. The remaining amount of liquid consists of glucose solutions to which medications are added (trental, contrical, GHB, potassium chloride, etc.). Specific recommendations for the dose and route of administration of individual drugs are presented in the table below.

Dosages and route of administration of drugs used in treatment

acute liver failure

Drugs	Doses, route and frequency of administration	Note
Prednisolone	15 mg/kg per day. IV, infusion every 4 hours without an overnight break
Claforan	100 mg/kg per day. IV, stream in 2 doses
Kanamycin	50 mg/kg per day. by mouth in 4 doses
Trichopolum	30 mg/kg per day. by mouth in 4 doses
Normaze	5-10 ml 2 times through the mouth
Reopoliglyukin	10-15 ml/kg per day. IV, drip
Albumen	10 ml/kg per day. IV, drip
Fresh frozen plasma	up to 20 ml/kg per day. IV, drip
GHB, 20%	100 mg/kg per day. IV, drip in 2 doses
Contrikal	3 thousand units/kg per day. IV, drip in 2 doses	administered in 5% glucose solution
KCl, 7.5%	2-3 ml/kg per day. IV, drip	administered as part of a polarizing and hyperinsular mixture
Polarizing mixture	10% glucose, insulin 1 unit per 5 g of glucose, 7.5% KCl in volume, the final concentration of which in glucose is not > 1%, 25% magnesium sulfate 0.2 ml/kg, 10% calcium chloride 0.2 ml/ kg
Hyperinsular mixture	glucose 20% 5 ml/kg; insulin 1.5 units/kg; KCl 7.5% 0.3 ml/kg; everything is administered intravenously
Heparin	100-150 units/kg per day. s/c, after 6 hours	first portion (1/4 of the daily dose) IV drip with fresh frozen plasma, subsequent s.c.
Trental, 2%	1-3 mg/kg per day. IV, drip	administered in 5% glucose solution
Curantil, 0.5%	0.5-1 mg/kg per day. IV, drip	administered in 5% glucose solution
Complamin 20 %	10-20 mg/kg per day. IV, drip	administered in 5% glucose solution
Droperidol, 0.25%	0.1 ml/kg, IM, 2-3 times
Solcoseryl	1-2 ml per day. IV, drip 2 times	administered in 5% glucose solution
Ascorbic acid, 5%	1-2 ml per day. i/v, stream	administered in 5% glucose solution
Cocarboxylase	50-100 mg per day. i/v, stream	administered in 5% glucose solution
Riboxin, 2%	0.5-2.0 ml per day. IV, stream or drip	administered in 5-10% glucose solution
Lasix	1-2 mg/kg, IV, bolus 1-2 times

Infusion therapy is carried out evenly throughout the day in combination with diuretics (Lasix, Veroshpiron). Drip administration of fluid continues throughout the entire period of acute renal failure. When carrying out infusion therapy, it is necessary to carry out constant monitoring: temperature, pulse, respiration, diuresis are measured hourly, the child is weighed 2 times a day. An increase in weight indicates fluid retention in the body, which requires additional correction, both the volume of fluid administered and the dose, or a change in prescribed diuretics. Maintaining energy balance is one of the main directions of intensive care for patients with acute renal failure. The most frequently used amino acid mixtures in recent years are aminosteril, aminoped, hepatamin, hepasteril. In children, aminoped is more often used, which contains 18 essential and non-essential amino acids. Available in the form of 5% and 10% solutions. The energy value is 200 and 400 kcal/l. The daily dose of 5% solution for newborns is 20-30 ml/kg, for children over 1 year old - insert table 6 10-20 ml/kg. The infusion rate should not exceed 2 ml/kg/hour. When using a 10% solution, appropriate adjustments are made.

In case of acute renal failure, it is necessary to use large doses of corticosteroids (glucocorticoids prednisolone), which, by suppressing the transformation of lymphocytes and antibody formation, reduce the destruction of liver cells caused by cytotoxic and autoimmune mechanisms, stabilize the membranes of lysosomes and, by blocking the release of histamine, serotonin, and kinins, reduce inflammatory and allergic reactions. The need for early use of hormonal drugs in children with massive liver necrosis is emphasized by all researchers. It is preferable to prescribe prednisolone in a short course of up to 7-10 days, since the clinical effect, regardless of the duration of the course of treatment, appears in the first 3-10 days. Longer administration of prednisolone increases adverse reactions, in 60% drug intolerance develops (hemodeza, albumin, etc.), possibly due to the competitive interaction of drugs for binding centers on serum proteins and disruption of their pharmacokinetics (D.K. Bashirova, G. F. Muklisova, A.P. Zvereva, 1988).

The loss of potassium by hepatocytes, as well as increased hypokalemia due to the use of large doses of glucocorticoids, require the prescription of its drugs. Potassium is prescribed in the form of a 7.5% KCl solution and is administered as part of a polarizing and hyperinsular mixture. The latter also contributes to the rehabilitation of neuroglia and the reduction of cell edema. It should be borne in mind that in case of anuria, potassium supplements are contraindicated.

According to the results of our research (L.E. Yakob, N.A. Dolgova, 1989), as well as according to literature data, with acute renal failure in young children, the coagulation potential of the blood is depleted, the synthesis of coagulation factors decreases, and the enzymes of proteolysis and fibrinolysis are activated. All this served as the basis for the use of heparin in combination with fresh frozen plasma and contrical as a pathogenetic agent in the treatment of acute renal failure. The main methods for monitoring heparin therapy are the Lee and White clotting time, ethanol and autocoagulation tests.

Impaired microcirculation in the liver and the manifestation of portal vasculitis are the basis for the use of trental, complamin, and chimes in a complex of therapeutic agents.

Removing psychomotor agitation is of great importance in the treatment of patients with APE. The following drugs are used: sodium hydroxybutyrate (GHB), droperidol.

To correct hypoxia, solcoseryl is used, which is a deproteinized extract of calf blood with high RES activity. Solcoseryl contains factors that increase the absorption of oxygen in tissues and accelerate recovery processes. For the same purposes, hyperbaric oxygenation is used (pressure 1.1-1.5 atm., exposure 45-60 minutes, 1-2 times a day, course duration 7-10 days). In the absence of opportunities for HBOT, oxygen therapy is used by the usual inhalation route, i.e., humidified oxygen. Ascorbic acid and cocarboxylase should be a mandatory component of therapy.

To suppress intestinal microflora, patients with APE are recommended to administer orally poorly absorbed antibacterial drugs (kanamycin or trichopolum) and enterosorbents. To suppress putrefactive microflora, it is advisable to use lactulose (normase), an artificial disaccharide consumed by anaerobic lactobacilli, which sharply increases their reproduction and thereby reduces the number of ammonia-forming phenol bacteria. To cleanse the intestines and reduce autointoxication, daily enemas and gastric lavage are indicated.

The use of large doses of glucocorticoids, under conditions of which activation of secondary flora is possible, dictates the need for antibiotic therapy to suppress it. The most effective and frequently used are cephalosporins.

Hemosorption, plasmapheresis, exchange transfusions (20-30% of blood volume), hemoperfusion through a suspension of living hepatocytes should be considered as additional methods of treating acute renal failure.

The most accessible method for children is exchange blood transfusion (EBT), which does not require special equipment and can be performed in any intensive care unit or infectious diseases department. Its principle is to remove cerebrotoxic metabolites from the patient’s blood and deliver essential substances that are not synthesized by the affected liver with the donor’s blood. The indication for APE is the ineffectiveness of intensive therapy for 1-2 days and an increase in symptoms of APE. The multiplicity of OPCs depends on their effectiveness. The volume of replaced blood is determined at the rate of 70 ml per 1 kg of body weight, which approximately corresponds to one volume of bcc. Freshly collected, less often heparinized blood is used with strict adherence to the instructions for blood transfusions. Stop OPC when you come out of a coma and improve biochemical parameters.

Exit from the specified intensive care complex is carried out as follows. When biochemical tests indicating the severity of hepatic cellular failure (an increase in total bilirubin, a decrease in the level of β-lipoproteins and prothrombin index) stabilize and the first signs of their positive dynamics appear, immediately remove half of the intravenously administered dose of prednisolone, and after 2-3 days another half is removed, which should be completely discontinued after another 2-3 days, and the last 2-3 days the drug can be administered intramuscularly. Contrical and plasma are prescribed until the pain and hemorrhagic syndromes are relieved, intoxication is reduced, and the liver becomes thick and enlarged (3-4 days). Infusion therapy is completed when intoxication disappears and the level of total bilirubin decreases to at least 90-100 µmol/l. The duration of the course of antibiotic therapy is 5-7 days.

Treatment of complications of hepatic coma

Edema-swelling of the brain is associated with the cerebrotoxic effect of liver autolysis products and impaired cellular metabolism on the neuron. A paranecrotic process develops in the neuron with swelling of the neuroglia and disruption of its function.

Treatment includes drugs that improve neuroglial function and dehydration therapy. Hormone therapy for acute renal failure continues. The volume of infusion therapy is reduced to 30-40% of the daily physiological (excluding losses) fluid requirement. With good diuresis, up to 30% of the fluid is replenished orally or administered nasogastrically in the form of glucose-saline solutions. Dehydration is carried out with concentrated solutions of plasma, 15% albumin solution, Lasix; Mannitol is used as an osmodiuretic. To improve the function of neuroglia, the following drugs are prescribed: GHB, seduxen, polarizing mixture, hyperinsular mixture. Dopamine administration at a dose of 6-8 mcg/kg/min is effective. Barbiturates are contraindicated in cases of acute renal failure. Oxygen therapy is indicated. If signs of cerebral edema or swelling increase, a lumbar puncture is necessary. With the development of severe external respiratory disorders associated with cerebral edema, patients are transferred to mechanical ventilation.

In acute renal failure, it is advisable to sharply limit or completely eliminate protein to reduce the accumulation of nitrogenous waste; the dose of antibiotics is reduced to 1/5 of the daily dose, administered 2 times a day. For oliganuria, the amount of fluid administered (enterally and parenterally) should correspond to a volume of fluid equal to daily diuresis, loss with perspiration (25 ml/kg). In the absence of vomiting, 60-70% of this volume is administered orally, the rest intravenously. The administration of a hyperinsular mixture and calcium chloride is indicated (do not prescribe additional potassium!). It is necessary to periodically rinse the stomach and intestines. To stimulate diuresis, large doses of furosemide 5-10 mg/kg are indicated; in the absence of a diuretic effect, it can be repeated 2-3 times. Dopmin is important, providing vasodilation of the renal vessels, at a dose of 1-2 mcg/kg/min. In the absence of a therapeutic effect, it is necessary to connect extracorporeal hemodialysis or perform peritoneal hemodialysis.

The main directions of treatment for massive gastrointestinal bleeding are to compensate for the deficiency of coagulation factors (under the control of a coagulogram) and protect the gastric mucosa. For the purpose of replacement therapy, repeated direct blood transfusions, administration of fresh frozen plasma, and hemoconcentrates are indicated. The protection of the gastric mucosa is facilitated by suction of spilled blood, cold on the stomach, ingestion (sucking) of a frozen solution of aminocaproic acid, administration of hemostatics (gelatin, dicinone), Almagel, Maalox, Venter, H2 receptor blockers - cimetidine, ranitidine. In this case, antacids and H2 receptor blockers are taken at intervals of at least 1 hour.

A disease characterized by a violation of the integrity of liver tissue due to acute or chronic damage is called liver failure. This disease is considered complex, due to the fact that after liver damage, metabolic processes are disrupted. If appropriate measures are not taken to cure the disease, then under certain conditions liver failure can develop quickly and rapidly and lead to death.

Classification

The disease is classified according to two criteria: the nature of the course and stages.

Based on the nature of the disease, there are two stages of the disease:

• Acute;
• Chronic.

Acute liver failure occurs due to the liver losing its ability to perform its functions. The disease manifests itself predominantly within a few days and is characterized by a severe form of symptoms. Often the acute form is fatal, so it is very important to know the symptoms in order to recognize the disease at an early stage.

Acute liver failure is divided, in turn, into big and small. Big is a classic form of manifestation of the disease, which can be seen quite clearly in clinical and laboratory studies. Small Acute liver failure occurs more often in children against the background of serious illnesses (poisoning, intestinal infections, etc.). This subspecies is very difficult to diagnose due to the absence of symptoms of the disease. The small species can develop either rapidly or over several years.

Chronic liver failure develops through a slow progression of the disease. Due to the gradual dysfunction of the liver with the progressive course of a chronic disease of the parenchyma, a chronic type of disease is formed. Diseases such as or are a consequence of chronic liver failure. Both manifestations end in hepatic coma followed by death.

Additionally, there are two types of liver failure:

• endogenous;
• exogenous.

For endogenous species The manifestation of complications due to death or dystrophic changes in liver tissue is typical. This type is characteristic of liver cirrhosis and chronic hepatitis.

Exogenous species is formed as a result of self-poisoning of the body, which is caused by metabolic products and substances produced by the intestinal microflora. It occurs due to the entry of these substances into the blood through the intestinal walls when they stop in the liver. The reason for the stop may be blockage of the veins, so as a result, self-destruction of the liver is observed.

According to degrees of severity, four stages are distinguished:

1. Initial or compensated, which is characterized by an asymptomatic course of the disease. At the initial stage, the liver begins to actively react to toxins.
2. Decompensated. The first signs of the disease appear. At this stage, a blood test indicates the development of the disease.
3. Dystrophic or terminal. The pre-final stage, upon the onset of which the patient experiences serious liver dysfunction. Against this background, there is also a disruption in the functioning of the entire body from the central nervous system to metabolism.
4. Stage of hepatic coma. It is characterized by deepening liver damage, which ultimately leads to death. The last stage is characterized by the complexity of treatment, as the liver enters the stage of death.

Causes of the disease

The disease “liver failure” is diagnosed in both men and women; moreover, it has no age restrictions, so you can get sick both in childhood and in the elderly. The causes of liver failure are varied and unpredictable. It is important to know them in order to be able to make a premature diagnosis and speedy treatment. So, the reasons that can provoke liver failure in a person are as follows:

1. Liver diseases, which include: malignant tumors and other neoplasms, cirrhosis, acute and chronic hepatitis, echinococcus, etc. Any of these signs can serve as an impetus for the development of a fatal disease. Cirrhosis and hepatitis can be both the cause of the disease and its consequences.
2. Blocked bile ducts, as a result of which an increase in biliary hypertension pressure is predicted. Failure of hypertension disrupts blood circulation in the liver, which causes the development of dystrophic abnormalities in the cells of this organ.
3. Diseases of the heart and blood vessels, infectious infections of the body, insufficiency of the endocrine glands, autoimmune diseases. Any disorder in the body can cause the development of a serious disease, so it is much easier to eliminate signs of abnormalities at an early stage than to try to cure serious diseases.
4. Taking medications(especially for a long time) can leave its mark on the liver. As you know, any medicine affects the liver, so it is very important to maintain the correct dosages of drugs and not violate the frequency of administration.
5. Poisoning with various substances organic and inorganic: poisonous mushrooms, alcohol, tobacco, chemicals, etc.
6. Extreme influences. The cause of a fatal disease can be even a minor burn on the skin, for which appropriate treatment measures are simply not taken. In addition: injuries, blood loss, allergies, septic shock and other factors can become the root cause of liver failure.
7. Deviation of kidney function, urolithiasis, congenital anomalies and much more, are the causes of such a disease as renal-hepatic malaise.

The main cause of renal-liver disease is the lack of balance between the narrowing and dilation of blood vessels. The reason for the lack of balance can be the banal cause of alcohol abuse, as well as food and respiratory poisoning. The disease of renal-liver failure is no less serious than damage to the liver alone, since there is an annual increase in mortality from this type of disease.

Based on all the reasons, a complex of symptoms of the disease appears. Let’s take a closer look at what these symptoms are and their main features.

Symptoms of the disease

The symptoms of liver failure are very diverse, but they are the first factors, after detection of which you need to rush to the doctor. The initial stages of the disease manifest themselves in the form of general malaise of the body, the appearance of mania and other motor disturbances. During flexion/extension of the fingers, a symptom of tremor may be observed, that is, lateral signs or trembling, often occurring with sudden movements.

Liver failure and its symptoms are always accompanied by the development of neuritis. The patient experiences a rise in temperature to 40 degrees with an exacerbation of the disease, as well as swelling of the legs. An unpleasant but specific odor appears from the mouth, indicating the beginning of the formation of trimethylamine and dimethyl sulfide. A disorder of the endocrine system occurs, there is an increase in hair loss, up to baldness, libido decreases, atrophy of the uterus and mammary glands in women occurs, and nails split and crumble. In women, liver failure at an early age can negatively affect fertility, that is, provoke the development.

In addition, throughout the entire period of the disease, the patient experiences an increase in headaches, feverish manifestations, dizziness, even fainting, and an aggressive state. Let us consider in more detail what symptoms are characteristic of the three stages of the disease.

Stages of chronic liver failure

Often, chronic liver failure is characterized by four stages, which have their own symptoms.

1. Compensated stage It often manifests itself asymptomatically, but the following negative processes are observed inside the body: increased pressure in the hepatic system, overflow of the venous plexuses in the abdomen, . At the initial stage, you can notice an indistinct appearance on the patient’s body and redness of the palms. The patient refuses to eat food due to disgust. There is a slight weight loss.
2. Decompensated stage due to increased symptoms of the disease. The first signs of the disease begin to appear: aggression, disorientation in the area, slurred speech, trembling of the limbs. Relatives may observe a significant change in a person's behavior.
3. Dystrophic stage caused by the occurrence of stupor. The patient becomes inadequate, it is very difficult to wake him up, and during moments of wakefulness, apathy is periodically replaced by excitement. Swelling of the face, legs, and fluid accumulation in the abdominal cavity appear. The patient may also experience bleeding from the nose or gastrointestinal tract in the morning or evening.
4. At the final stage the patient experiences the appearance of hepatic coma, as a result of which the patient is unconscious, and there is no reaction to external painful stimuli. The patient's vision decreases, strabismus develops, brain swelling and fluid accumulation occur. Chronic liver failure develops differently in each individual case, often over decades.

Acute symptoms

Acute liver failure occurs predominantly rapidly with a pronounced pattern of symptoms. This type has the following symptoms:

• sudden onset of weakness;
• nausea, vomiting and other signs similar to poisoning;
• increase in body temperature;
• an increase in jaundice, and you can observe a change in skin color to yellow. The patient's eyeballs also become yellow;
• bad breath;
• a decrease in the size of the liver, which manifests itself in the form of pain;
• lethargy, anxiety and speech impairment.

Acute liver failure is characterized by a change in blood composition: an increase in bilirubin occurs, which indicates its breakdown and decrease, as well as a decrease in the prothrombin index.

It is very important to deliver the patient to the clinic on time in order to be able to administer medication. Otherwise, acute liver failure can lead to death in a very short time.

Symptoms of renal-liver disease

The symptoms of renal-liver disease are almost identical to those above, the only difference is kidney damage, which indicates their pain and the manifestation of the following symptoms:

1. The presence of pain first in the liver, and then in the kidney area.
2. Increase in temperature.
3. Signs of jaundice.
4. Red blood cells, protein and bile compounds are found in the urine.
5. A hemorrhagic diathesis is formed, the cause of which is intoxication of the body.

The main danger of renal-liver disease is the involvement of other organs and systems in the pathology process: gastrointestinal tract, central nervous system, respiratory organs, etc. In the chronic form, the functioning of the liver tissues stops, as a result of which toxins begin to be eliminated through the gastrointestinal tract and lungs. This is an abnormal condition, so the body experiences severe stress.

Before starting treatment, it is important to correctly diagnose the disease. What is needed for diagnosis can be found in the next section.

Diagnostics

If all of the above symptoms are detected, you must immediately go to the hospital or call an ambulance. The clinic will require diagnostics to be able to make a correct diagnosis. First of all, diagnosis begins with interviewing and examining the patient. Often this is not enough to make a correct diagnosis, so the doctor will prescribe clinical measures.

Clinical activities include donating blood to identify biochemical data for bilirubin, alkaline photosphase, LDH, AST and ALT. Using these indicators, the doctor identifies not only the presence of signs of the disease, but also at what stage the liver disease is. The higher the indicators, the correspondingly more active the process of liver cell breakdown.

An important place in the treatment process is given to infusion therapy, through which proper nutrition is ensured and the body is detoxified. It is also necessary to improve liver microcirculation, normalize or restore the acid-base balance.

The patient is prescribed laxatives and enemas to cleanse the gastrointestinal tract of toxins and relieve constipation. A drip with a solution of glucose, vitamins B6, B12, and lipoic acid is administered daily.

If the disease has progressed to the stage of hepatic coma, then intensive drug interventions are resorted to. The purpose of these measures is to maintain the patient’s life so that the functioning of the liver can be normalized. A solution of sodium or potassium bicarbonate is injected, and humidified oxygen is inhaled through a nasal catheter. If the pressure decreases, then albumin is administered intravenously.

The patient must be in hospital and under the supervision of nurses. In addition to medication procedures, the following conditions are observed:

• daily monitoring of a blood test to determine the composition of albumin;
• urinary monitoring;
• prevention of bedsores;
• carrying out weigh-ins daily.

Hypoammonemic drugs can reduce the level of ammonia in the body.

If the patient has associated renal failure, then additional hemodialysis will be required in order to remove ammonia and other toxins from the blood, which under normal conditions are neutralized by the liver. In case of edema or ascites, paracentesis is necessary to help remove excess fluid from the body.

In addition to all of the above, normalizing the liver will require maintaining proper nutrition, or rather, following a diet.

Diet

Diet in the treatment of liver disease is a mandatory procedure, since the liver receives a significant blow precisely from improper nutrition. The diet includes compliance with the following procedures:

1. Reducing the level of protein and fat to 30 grams per day, and carbohydrates to 300.
2. It is preferable to eat plant foods, which include: fruits, vegetables, honey, compotes, jelly.
3. Consume food only in liquid or semi-liquid form. At the same time, you need to eat little by little, but every 2 hours.
4. Eliminate salt from your diet completely.
5. If there is no swelling, then you need to drink about 1.5 liters of fluid per day.

Diet plays an important role in the treatment of liver failure, so a combined effect will help you get rid of the symptoms of the disease and return to your previous healthy life.