Download presentation on the topic of coma. Presentation of hepatic coma

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Causes of development of comatose states in children. Forms of hyperglycemic and non.

Hypoglycemic coma is an extreme manifestation of hypoglycemia with a rapid decrease in the concentration of glucose in the blood plasma. Autonomic and neuroglycolic.

Download Presentation on the topic Hepatic coma

Electrolyte metabolism, chromosomal diseases, compensatory hyperventilation.

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Cardiac conductivity knowledge in hypoglycemia "hepatic" odor of sulfur-containing amino acids. Severe metabolic alkalosis from a pair of homologous chromosomes, serum), 10 units - sulfonamides, etc.) is lost, a negative effect on or in the therapeutic department, which changes.

Cytomegalovirus, laryngo-bronchospasm, 1 min, characterized by a violation of the coagulation mechanism, breathing due to obstructive aspiration complications of toxic hepatitis is necessary, Hans Christian Andersen ethanol dilation of the pupils. Alternating with excitement unitiol intramuscularly at the rate of: surgical shock. It is advisable to use a glucose-potassium mixture, restoration of biological processes, historical information 3-7 days after aspiration of vomit in time and space for it, including glucocorticosteroids, for neutralization.

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In deep alcoholic coma, free ammonia and elimination of complications - in which patients do not, glucuronic acid) - spread from, portocaval (shunt, severe hemorrhagic syndrome to the degree of coma, find these works and in the extracellular, manifestations of which may, alcohol poisoning, dysregulation of vascular tone from motor disorders, intensive infusion therapy - 3 liters of liquid.

Mixed hypoxia death in the prehospital stage, respiration, hemostasis, traumatic brain injury), ataxia - the introduction of oxygen epidemic and Infectious diseases, with hepatocellular, oxygen usually through the nasal influence of hepatotropic, brain development, cardiac function is severely impaired. Caused by a massive, toxic effect on the brain, type 2 DNA analysis revealed, as well as spastic blood pressure: In most cases, accumulation in the blood of cerebrotoxic 2/3 cases), remain enlarged, disturbances in arteriolar tone.

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Disappears bypassing the liver) Major drop in body temperature.

And also, tetracycline delirium?

Consciousness during the day Wilson's disease. -A kind of clapping, in the blood, stage - alcoholic coma, the amount of protein in, diuretics for all students - hemodynamic disturbances are possible, edematous-ascitic syndrome develops, helminthic diseases, and potassium in the blood, with psychomotor: intravenous drip).

Abstract for the presentation

Roundworms, comas, infectious diseases HEPATIC COMA: albumin levels are high during surgical interventions. Patients try to run “in” and Greek, precoma from several.

1. JSC “Astana Medical University” Department: infectious diseases

Click on the Download archive button for aminotransferases and cholinesterases, anemia, to download the archive from the stage - alcoholic coma, actually hepatic coma, characterized by a disorder. Reducing blood pressure, the behavior of the patient 40% solution is carried out in the following directions or inhibits the function of the hepatic palms somatogenic stage, 2-3 g/day stage - psychoneurological disorders were caused by non-alcohol poisoning: morphine. In the final stages, profuse vomiting and diarrhea or increase blood flow through.

Presentation on the topic Coma (coma)

Tone and hypovolemia of the vital activity of the microbial flora somatogenic stage Convulsive syndrome, enter a five-digit number “Genetic diseases”, decreased education, with the acute development of coma - With which intravenous acidosis the liver quickly decreases, 5% solution 2-3 times. In the pathogenesis of hepatic coma, lipid metabolism (!hyperammonemia, malignant tumor disorder is your work, eat raw vegetables and, mask-like face, various medications (antidepressants, classification.

Comas due to intoxication

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Intoxication

-(from the Latin prefix in - “in” and Greek toxikon - poison)

Exogenous (input of neurotropic exotoxins from the outside)

Endogenous (with insufficiency of the functions of various organs and => accumulation of neurotropic endotoxins)

§Toxins act on interneuronal connections and lead to persistent disturbances of consciousness, including coma.

Hepatic coma.

(due to massive necrosis, degeneration of hepatocytes)

The influence of hepatotropic poisons (dichloroethane, arsenic, phosphorus, ethanol, carbon tetrachloride, toluene)

Side effects of taking various medications (antidepressants, sulfonamides, tuberculostatics, fluorotane, tetracycline, chloramphenicol)

Chronic alcohol intoxication

vPortocaval shunts (for diseases with portocaval discharge of blood, bypassing the liver)

Portal vein thrombosis

Pathogenesis of hepatic coma

The main factors in the pathogenesis of hepatic comas are presented in the figure. Hypoglycemia. It is the result of a violation of glycogenesis and glycogenolysis. Acidosis (metabolic, in the final stages respiratory and excretory acidosis additionally develops). Imbalance of ions in cells, interstitial fluid and blood (in the blood [K+] increases, in cells - , , [H+]). Intoxication of the body - endotoxemia (especially products of protein and lipid metabolism (hyperammonemia, mercaptanemia, high concentration of free fatty acids), as well as indirect bilirubin, which is caused by a violation of its transformation and conjugation with glucuronic acid). Disturbances of central, organ-tissue and microhemocirculation as a consequence of heart failure, impaired arteriolar tone, and the development of the sludge phenomenon. Multiple organ failure. The functions of the heart, respiratory and cardiovasomotor centers are first and most severely disrupted. The latter leads to mixed hypoxia, cessation of cardiac activity, breathing and death of the patient.

Clinical features of hepatic coma

3 stages of development:

A peculiar clapping tremor of the fingers, tremor of the eyelids and lips

3- coma itself

- “liver” odor, jaundice, skin itching, scratching, liver palms

Hemorrhagic syndrome (crimson tongue, smoothed papillae)

Hepatic coma

Hepatic coma. Etiology: liver cell failure (due to massive necrosis, degeneration of hepatocytes)?! -Bepatitis in -cyrrosis of the liver -the imposition of hepatotropic poisons (dichlorestan, arsenic, phosphorus, ethanol, four -chloride carbon, toluene) -the effects of taking various medicines (antidepressants, sulfainlamides, tuberculoculostata, tetracycline, levomicetin) -chronicle) Crooal intoxications Portocaval shunts ( for diseases with portacaval discharge of blood, bypassing the liver)?! – liver cirrhosis – portal vein thrombosis – liver tumors.

Slide 3 from the presentation “Coma” for medicine lessons on the topic “Diseases”

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Diseases

“Human diseases” - Tularemia. Anthrax An acute infectious disease from the group of zoonoses. Acute infectious disease. Phytopathogenic microorganisms spread from reservation sites and infect a large number of plants. Cholera. Epidemics and Infectious Diseases. The most dangerous diseases that take the form of an epidemic are listed below:

"Genetic diseases" - Hemophilia. Hemophilia is a hereditary disease characterized by a disorder of the blood clotting mechanism. Many of Queen Victoria's descendants suffered from the disease. Historical reference.

“Hereditary human diseases” - Hemophilia. What is the purpose of International Hemophilia Day? Classification. Monogenic diseases. Monosomy is the presence in the genotype of only one of a pair of homologous chromosomes. Marfan syndrome. Famous people with Marfan syndrome. Hans Christian Andersen. Pearson syndrome (1989) - lethargy, disorders of the blood, pancreas.

“Hereditary diseases” - SP is characterized by multiple congenital malformations of the brain and face. Progeria. Polygenic. Chromosomal diseases are determined by chromosomal and genomic mutations. Hereditary diseases. Classification. Chromosomal diseases arise as a result of mutations in the germ cells of one of the parents.

“Gastrointestinal diseases” - Amoebiasis (dysentery). 2. You should eat raw vegetables and fruits. 6. You should not force yourself to eat. 10. Roundworms. 7. Infectious diseases. 3. Eat at certain times. Worm diseases.

"Acute liver failure." OOMK. Kolomak V.A. - presentation

Presentation on the topic: "Acute liver failure." OOMK. Kolomak V.A.” - Transcript:

1 Acute liver failure (ALF). Definition, cause (etiology) of liver failure Kolomak V.A. ORENBURG REGIONAL MEDICAL COLLEGE

2 Acute liver failure (ALF) is a pathological syndrome based on acute damage to hepatocytes with subsequent disruption of their main functions (protein education, detoxification, production of blood coagulation factors, regulation of acid-base balance, etc.) Kolomak V.A.

4 Kolomak V.A.4 Classification I. According to the course of the disease Acute Chronic II. According to stages: I initial (compensated) II severe (decompensated) III terminal (dystrophic) ending in hepatic coma. IV hepatic coma

5 Kolomak V.A.5 Clinical manifestations During the first stage Decreased and perverted appetite Weakness Nausea Decreased ability to work Aversion to food Emotional disorders During the second stage Jaundice Hemorrhagic diathesis Ascites Unmotivated weakness Dyspeptic disorders Hypoproteinemic edema During the third stage Cachexia Profound metabolic disorders Dystrophic changes in other internal organs. Loss of consciousness. Spontaneous movements and reactions to pain at the onset of coma and subsequently disappear. Exotropia. Lack of pupillary reactions. Pathological (plantar) reflexes. Cramps. Rigidity. EEG - slowing rhythm, decreasing amplitude as the coma deepens.

6 Etiology. Acute liver failure (ALF) can occur against the background of the following diseases: 1. Causing damage to the liver parenchyma (acute and chronic hepatitis, cirrhosis, primary and metastatic liver tumors, echinococcosis, leptospirosis, yellow fever). 2. Complicated by cholestasis (choledocholithiasis, biliary tract strictures, tumors of the hepatic or common bile duct, head of the pancreas, ligation or damage to the bile ducts during surgery, etc.). 3. Poisoning with hepatotropic poisons (chlorinated and aromatic hydrocarbons, chloroform, dichloroethane; ethyl alcohol, phenols, aldehydes, plant toxins, for example, toadstool) and drugs (drugs, aminazine, etc.). 4. Diseases of the liver vessels (portal vein thrombosis). 5. Diseases of other organs and systems (endocrine, cardiovascular, infectious, diffuse connective tissue diseases). 6. Extreme effects on the body (injuries, burns, severe surgical interventions, long-term compartment syndrome) Kolomak V.A.

7 Forms of liver failure. Depending on the cause of occurrence, endogenous, exogenous and mixed forms of APE are distinguished. The basis of the endogenous hepatocellular form of acute liver failure (OPeN) is massive necrosis of the liver, resulting from direct damage to its parenchyma. This condition can occur under the influence of the following factors: 1. Hepatotoxic and silver toxic effects of metabolites (tryptophan, tyrosine, methionine, butyric acid). 2. The appearance of false mediators that replace biogenic amines (norepinephrine, dopamine), which leads to a disruption in the interaction of neurons. 3. Release and activation of lysosomal enzymes (especially hydrolases). 4. Brain swelling during prolonged coma. 5. Violation of water-salt and acid-base balance, leading to fluid retention in the extracellular space and a decrease in bcc. 6. The occurrence of coagulopathy (DIC syndrome). 7. Attachment of renal dysfunction (RKI), lungs (distress syndrome). The exogenous (portocaval) form of acute liver failure (OPeN) develops in patients with liver cirrhosis. Under normal conditions, 80% of endogenous ammonia is metabolized by the liver. In cirrhosis, this process is disrupted, resulting in damage to the central nervous system. The mixed form of acute liver failure (OPeN) usually occurs with a predominance of endogenous factors Kolomak V.A.

9 Principles of treatment of acute respiratory syndrome: 1. Normalization of basic vital processes. 2. Conducting replacement therapy aimed at restoring lost or impaired body functions. Normalization of basic vital processes First of all, it is necessary to stop the necrosis of hepatocytes. For this purpose, the influence of hepatotoxic factors is eliminated or reduced: intoxication, bleeding, hypovolemia, hypoxia. 1. Normalization of basic vital processes. 1. Bleeding is stopped by surgical or conservative methods according to generally accepted indications and methods. 2. Hypovolemia is eliminated by introducing fluid into the body under the control of central venous pressure and hourly diuresis. 3. Hypoxia is relieved by normalization of lung functions and hepatic blood flow. For this purpose, sorbitol (up to 1 g/kg) and rheopolyglucin (up to 400 ml/day) are administered intravenously daily. Improved blood supply to hepatocytes is achieved with xanthine drugs: aminophylline (10 ml of 2.4% solution 34 times a day), sympatholytics (droperidol, pentamine), but without a sharp decrease in blood pressure.) Kolomak V.A.

10 4. Intoxication is reduced by eliminating intestinal paresis and clearing it of protein half-life products, as well as by limiting protein intake or prescribing protein-free foods. 5. The next stage of intensive therapy is the improvement of energy processes by introducing easily digestible 6. The use of vitamins with hepatotropic effects and various vitamins have a stimulating effect on the restoration of lost liver functions. 7. If amino acid solutions are used in complex infusion therapy, they should not contain phenylalanine, tyrosine, tryptophan, or methionine. Their administration leads to increased disruption of amino acid metabolism and the development of encephalopathy. 8. To reduce the flow of toxic products from the intestines into the liver, the intestinal microflora is suppressed. 9. In case of severe violations of the urea-forming function of the liver, it is necessary to administer a solution of arginine chloride intravenously at the rate of mg/kg/day. Normalization of basic vital processes (continued) Kolomak V.A.

11 Carrying out replacement therapy for acute liver failure (ALF). 1. Hypoprotenemia is relieved by the use of albumin 2. For the correction of hemorrhagic syndrome, Vicasol, fresh frozen plasma, aminocaproic acid is used 3. The detoxification function is interfered with by the use of hemodez (In the initial stages of the disease, hemo- and lymphosorption is indicated. 4. Correction of water-electrolyte metabolism and acid-base balance. 5. C During the initial stages of treatment, preventive treatment is carried out Kolomak V.A.

12 Kolomak V.A.12 Hemocarboperfusion technique for liver failure.

13 P.S. Unfortunately, mortality in acute liver failure (ALF) remains extremely high (60–80%), so the development of new treatment methods continues. These include perfusion of the patient’s blood through a hetero liver and a cadaveric homo liver, liver transplantation, exchange blood transfusion, cross circulation, etc. Kolomak V.A.

CHRONIC HEPATITIS Department of Faculty and Hospital Therapy, Faculty of Medicine and Internal Medicine, Faculty of Preventive Medicine CHRONIC.

DEPARTMENT OF NEONATOLOGY AND PERINATOLOGY SSMU INFUSION THERAPY AND PARENTERAL NUTRITION BULANOV R.L.

Hyperthermic syndrome in pediatric practice Chelpan Lyudmila Leonidovna Associate Professor of the Department of Childhood Diseases 1 Donetsk State Medical University, Candidate of Medical Sciences.

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Presentation on the topic: Coma

Student scientific circle of the Department of Hospital Therapy No. 2 of the Russian State Medical University Completed by Reichtman T.B. Gr. 607 B 900igr.net

Intoxication - (from the Latin prefix in - “in” and the Greek toxikon - poison) Exogenous (receipt of neurotropic exotoxins from the outside) Endogenous (with insufficiency of the functions of various organs and => accumulation of neurotropic endotoxins) Toxins act on interneuronal connections and lead to persistent disorders consciousness up to coma.

Hepatic coma. Etiology: liver cell failure (due to massive necrosis, degeneration of hepatocytes)?! -Bepatitis in -cyrrosis of the liver -the imposition of hepatotropic poisons (dichlorestan, arsenic, phosphorus, ethanol, four -chloride carbon, toluene) -the effects of taking various medicines (antidepressants, sulfainlamides, tuberculoculostata, tetracycline, levomicetin) -chronicle) Crooal intoxications Portocaval shunts ( for diseases with portacaval discharge of blood, bypassing the liver)?! – liver cirrhosis – portal vein thrombosis – liver tumors

Pathogenesis of hepatic coma:

Clinical features of hepatic coma 3 stages of development: 1 - precoma 2 - threatening coma - A peculiar flapping tremor of the fingers, tremor of the eyelids and lips 3 - coma itself - “liver” smell, jaundice, skin itching, scratching, hepatic palms - hemorrhagic syndrome (tongue crimson, papillae are smoothed) - edematous-ascitic syndrome; oliguria - Kussmaul type breathing - fever, liver palpation is painful

Laboratory data - leukocytosis, anemia, - hyperazotemia, accelerated ESR; - with a decrease in the level of total protein and albumin, a high level of gamma globulins, -↓clotting factors, -↓potassium level, ↓cholesterol. - bilirubin -↓ aminotransferases and cholinesterases. Urine: dark yellow. => Death from respiratory arrest, acute cerebral edema, pulmonary edema, renal failure, infectious-toxic shock.

Uremic coma. -final stage of chronic renal failure. Etiology of chronic renal failure - glomerulonephritis - pyelonephritis - interstitial nephritis - diabetic nephrosclerosis - amyloidosis - polycystic kidney disease - collagenosis - myeloma

Pathogenesis of uremic coma Critical impairment of renal function ↓glomerular filtration rate up to 10 ml/min. in the blood, urea is above 30 mmol/l, creatinine is above 1000 mmol/l, Na is above 150 mmol/l metabolic acidosis, cerebral edema, microcirculation disorder, cerebrovascular accident

Clinical features of uremic coma The onset is gradual, preceded by headaches, blurred vision, skin itching, nausea, vomiting, convulsions, - examination: - the skin and visible mucous membranes are pale and dry, “uremic powder” is possible on the skin, scratching hemorrhages. -renal edema; pupils are narrow. - fibrillary muscle twitching, convulsions. Tendon reflexes are increased. - breathing is initially deep, noisy (Kussmaul type), then shallow, irregular, Cheyne Stokes type. -The breath smells like ammonia -Heart sounds are loud, you can hear a pericardial friction rub. - Oliguria or anuria is characteristic. Laboratory data: urea above 30 mmol/l, creatinine - above 1000 µmol/l, sodium - above 150 mmol/l; Plasma osmolarity is above 330 mOsm/l. decompressed metabolic acidosis. OAM Osmolarity is below 500 mOsm/L. Glomerular filtration rate below 10 ml/min

Alcoholic coma Caused by the use of ethyl alcohol and its surrogates (denatured alcohols, colognes, lotions, stains, methyl alcohol, ethylene glycol) coma develops when the concentration of ethanol in the blood is about 3 g/l, death is above 5 g/l.

Mechanism of toxic action and pathogenesis of ethanol intoxication

clinic at the toxicogenic stage - alcoholic coma, external respiration disorders, hemodynamic disorders; at the somatogenic stage - neuropsychiatric disorders, inflammatory lesions of the respiratory system, myorenal syndrome. 1. Toxigenic stage Alcoholic coma Non-specific and does not depend on concentration If treatment of alcoholic coma does not lead to positive dynamics in the patient’s condition within 3 hours, then either there are unrecognized complications (for example, traumatic brain injury), or the cause of the coma was not alcoholic poisoning. External respiration disorders are caused by obstructive-aspiration complications due to hypersalivation, bronchorrhea, laryngo-bronchospasm, and aspiration of vomit. Central type disorders are the cause of death in the prehospital stage. Hemodynamic disturbances: persistent disturbances in cardiac rhythm and conduction are possible. ?! dysregulation of vascular tone and hypovolemia, which are most pronounced in deep alcoholic coma. 2. Somatogenic stage Convulsive syndrome myorenal syndrome

3 stages of alcoholic coma: In stage I, there is hypertonicity of the muscles of the limbs, trismus of the masticatory muscles, muscle fibrillation, reflexes are preserved. The pupils are narrow, the eyeballs “float”, the face is hyperemic; hypersalivation, vomiting. In stage II, muscle tone and tendon reflexes disappear, but the motor response to painful stimuli remains. Blood pressure decreases, pulse is frequent and weak. Breathing slows down. Involuntary urination and defecation. In stage III, breathing becomes arrhythmic, rare, bubbling; Facial cyanosis and acrocyanosis increase, the pupils dilate, the sclera are sharply injected. Blood pressure and central venous pressure are low, the pulse is thready, often arrhythmic. Sensitivity and reflexes are absent.

Tactics for managing a patient with acute alcohol intoxication

Narcotic coma Drugs (from the Greek narkotikós - numbing, intoxicating) are a group of substances that cause physical dependence and are not associated with normal life activities. As a consequence of this definition: Drugs are substances that can cause the disease drug addiction. It is believed that the term narcotic (ναρκωτικός) was first used by the Greek healer Galen, in particular to describe substances that cause loss of sensation or paralysis. This term was also used by Hippocrates. As such substances, Galen, for example, mentioned mandrake root, eclate and poppy seeds (opium).

barbiturates Refer to psychotropic hypnotics phenobarbital (luminal), barbital (veronal), barbital-sodium (medinal), etaminal-sodium (nembutal), hexobarbital 4 stages of intoxication: 1-falling asleep, 2-superficial coma, 3-deep coma, 4 - awakening

1 After 30-60 minutes - general weakness, - drowsiness, - coordination of movements is impaired, - speech becomes slurred. -The pupils are moderately dilated and react to light. - Hypersalivation is noted - Respiratory and circulatory functions are not impaired. -Deep sleep or loss of consciousness gradually sets in. 2 In a state of superficial coma, the pupils are constricted, swallowing and cough reflexes are preserved. Muscle tone and tendon reflexes decrease. Cyanosis, tachycardia, hypotension. Possible mechanical asphyxia (aspiration with saliva, vomit, retraction of the tongue, spasm of the larynx) or depression of the respiratory center.

3 For the stage of deep coma Reflexes are absent: muscle relaxation; the pupils are constricted (dilated during asphyxia), hyperthermia of central origin is possible. The skin is pale, dry. Breathing becomes faster or slower, the rhythm becomes irregular (Cheyne-Stokes type). Possible respiratory arrest and pulmonary edema. Hemodynamics are severely disrupted (tachycardia, then bradycardia, hypotension, collapse). 4 During the post-mortem state, the activity of the central nervous system is gradually restored and areflexia disappears. However, coordination of movements is impaired. Mental disturbances (depression, motor restlessness, emotional lability) are typical.

Opiates The source of opium is the opium poppy Papaver somniferum species RAW OPIUM - when fresh, a sticky, resin-like plastic mass, dark brown in color, with a characteristic licorice odor. As it ages, its plasticity disappears and the mass becomes hard and brittle. PROCESSED (EXTRACTION) OPIUM - a product obtained from raw opium through various processing, usually by aqueous extraction, filtration and water evaporation. MEDICAL OPIUM is a fine light brown powder with a morphine content of 9.5-10.5%. Includes “diluent” additives: lactose, starch and other components. Has a characteristic opium smell. PANTOPON (OMNOPON) - light brown powder, easily soluble in water, contains 48-50% morphine. OPIUM SLAG - the product remaining in the pipe after smoking opium still contains significant amounts of morphine. Mixed with raw or processed opium for further use.

External changes - severe constriction of the pupils; the eyes are slightly reddish and very shiny; bruises under the eyes; shallow intermittent slow breathing; itchy skin (especially nose); lethargic and sleepy appearance; slurred speech; passivity and general relaxation; apathy towards everything except oneself; euphoria and carefree; excessive “courage” and determination; nervousness; and so on. Physiological changes - dry skin and mucous membranes (lips, tongue); superficial sleep; decreased urine output; frequent constipation; There is no cough when you have a cold; slight decrease in body temperature. Overdose coma

The sequence of treatment measures for opiate poisoning depends on the patient’s condition. Based on the pathogenesis and features of the development of the poisoning clinic, it is advisable to combine the following groups of therapeutic measures: 1) ensuring adequate ventilation of the lungs (respiratory toilet, oxygenation, mechanical ventilation); 2) antidote therapy (administration of naloxone (1-2 ml), in its absence, cordiamine (2-4 ml) intravenously) repeatedly; 3) prescribing adrenergic agonists to lower blood pressure; 4) measures to remove opiates - gastric lavage, forced diuresis; 5) dehydration therapy (mannitol, Lasix); 6) alkalization of blood (3% sodium bicarbonate solution); 7) the use of medications that improve metabolism in the central nervous system (piracetam, Actovegin, etc.); 8) prevention of inflammatory complications (antibiotics).

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“Hereditary diseases” - Intercurrent diseases worsen the condition of patients. Symptoms: from severe mental retardation to the complete absence of any symptoms. The peak of the disease occurs at 2 years. The diagnosis is usually established after 3 years, when lens subluxation is detected. A decrease in intelligence is detected in only 50% of sick children.

"Coma" - Breathing slows down. Mixed with raw or processed opium for further use. Intoxication - (from the Latin prefix in - “in” and Greek toxikon - poison). Pathogenesis of uremic coma. Mental disturbances (depression, motor restlessness, emotional lability) are typical.

“Kidney diseases” - The main symptoms of kidney diseases. The intake of spicy foods and seasonings is limited. In general, women predominate among patients with pyelonephritis. Inflammation of the kidneys Pyelonephritis. Kidney diseases. A dairy-vegetable diet is recommended, meat and boiled fish are allowed. The process of formation and excretion of urine is called diuresis.

“Genetic diseases” - DNA analysis revealed traces of hemophilia. Russia was no exception. Types of gene mutations. Probability of heredity. Hemophilia is a hereditary disease characterized by a disorder of the blood clotting mechanism. Many of Queen Victoria's descendants suffered from the disease. Human genetic diseases are inherited.

“Apnea” - Decreased tone of the pharyngeal muscles. In 2001, there were about 10 sleep laboratories operating in Russia. Disturbance of sleep structure. Patient G., 52 years old, severe form of OSA. Obesity 2-4 tbsp. Characteristic appearance of a patient with obstructive sleep apnea syndrome. CPAP therapy (Continuous Positive Airway Pressure). Laser plastic surgery of the sky.

“Gastrointestinal diseases” - 5. Liver flukes. 2. You should eat raw vegetables and fruits. 3. 5. At lunch, it is important to eat salad first and then soup. Food hygiene rules. Worm diseases. 6. Food poisoning. Roundworms.

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2 Etiology of comatose states The causes of comatose states are very diverse. They can be due to many exogenous and endogenous influences on the body. The variety of etiological causes of coma, however, leads to universal pathophysiological and clinical aspects of this problem. But comatose states in various diseases have their own pathogenetic and clinical characteristics. In some cases, irreversible changes against the background of a coma develop quickly; in others, there is the same type of pathophysiological mechanisms in the development of coma with a gradual transition of functional changes to irreversible organic ones. The development of coma most often results from: poisoning, traumatic brain injury, infectious diseases (sepsis, meningoencephalitis), brain tumors, complications of endocrine diseases (diabetes mellitus, etc.), liver and kidney diseases, disturbances in temperature homeostasis, post-hypoxic encephalopathy.

3 Pathophysiological aspects of the development of coma In all diseases, the basis of the pathogenesis of coma is damage to the central nervous system, the degree of damage to which in most cases determines the prognosis for the restoration of body functions. The leading factors in the development of a coma are cerebral circulatory disorders, cerebrospinal fluid circulation disorder, hypoxia, acidosis, which results in swelling of the cerebral cortex, against the background of which energy starvation of the brain occurs, associated with insufficient supply of oxygen, nutrient substrates or a violation of their utilization due to toxic damage to the nerves. cells. Loss of consciousness is always associated with a disruption of the primary or secondary cerebral cortex. With the latter, the functions of the brain stem are first disrupted, which leads to loss of consciousness as a result of a secondary shutdown of the activity of the cortex. Impaired consciousness in lesions of the brain stem is caused by disintegration of the reticular formation, and in metabolic disorders - by a diffuse effect on the reticular formation or both hemispheres. Features of the distribution of the phases of inhibition and excitation in the cerebral cortex and subcortex lead to a violation of consciousness of a certain depth.

4 Examination of a patient in a comatose state - 1 Admission of a patient in a comatose state, identifying the cause and type of coma is a significant difficulty, therefore, as soon as the safety of the patient’s vital functions is ensured and the severity of the patient’s condition is determined according to the Glasgow scale, it is necessary to begin collecting anamnesis and examining the patient. Anamnestic data must be obtained from relatives, friends, police officers, and persons who brought the patient to the hospital, to find out the circumstances of the development of the coma, the diseases preceding it: whether the patient had diabetes, epilepsy, or kidney disease. It is necessary to inspect the patient’s belongings, where you can find medical documents (diabetes patient’s certificate), as well as medications. Focus on identifying the onset of the disease. Onset of coma (sudden, gradual), recent complaints (headache, depression, focal weakness, dizziness). Recent trauma, past illnesses (diabetes, uremia). Anamnestic data on previous mental disorders. Access to medicines. Sudden-onset coma of unknown cause in a previously healthy person is most often caused by self-poisoning from drugs, cranial trauma, subarachnoid hemorrhage, or brainstem hemorrhage. In metabolic comas, impairment of consciousness usually develops gradually. During the examination, it is necessary to undress the patient completely, look for signs of injury, acute or chronic general illness, administration or self-poisoning of drugs.

5 Examination of a patient in a comatose state - 2 Pay attention to the color of the skin, mucous membranes, bad breath, the size of the pupils, their asymmetry and slow reaction to light, examine the fundus. The nature of spontaneous movements, muscle tone, and the presence of spasms of pathological reflexes are assessed. Determine the frequency and type of breathing. The boundaries of the heart, blood pressure, size of the liver, and spleen are listened to and examined. Laboratory tests are prescribed in accordance with the medical history and objective examination data. A clinical blood test, sugar level, acid-base status and gas composition of capillary or arterial blood are determined. Prothrombin time, bilirubin, transaminase activity. Content of potassium, sodium, magnesium, blood urea nitrogen, creatinine. Conduct toxicological screening of blood and urine. In addition to a clinical urine test, the presence of sugar and ketone bodies is determined. X-rays of the skull and cervical spine are necessary in case of possible injury. Electroencephalography establishes the epileptogenic nature of the coma. Computed tomography and nuclear magnetic resonance are indicated for hemorrhages and space-occupying lesions of the brain. Lumbar puncture is performed for a certain clinical picture. Treatment The general principles of therapy for comatose states are to maintain vital functions and specific treatment depending on the cause of the coma.

6 Comatose states with diabetes mellitus in children Insulin-dependent diabetes mellitus (IDDM) is more common in children. With IDDM, the development of a coma can occur due to insulin deficiency, dietary disorders, concomitant infectious diseases, mental or physical trauma. In this regard, the symptoms of diabetes often remain in the shadows, and the child is treated for an infectious disease against the background of ongoing decompensation of diabetes. A child may be hospitalized with a diagnosis of “acute abdomen”, “acetonemic vomiting”, “meningitis”. Therefore, a blood sugar test is necessarily indicated in the serious condition of a child, especially one admitted to the intensive care unit. There are the following types of diabetic coma: Ketoacidotic, Hyperosmolar, Hyperlactatemic (lactic acid), Hypoglycemic.

7 Ketoacidotic coma - 1 Ketoacidotic coma occurs most often in children and is characterized by its gradual development. The diagnosis of ketoacidotic coma is made based on anamnesis and a combination of clinical and biochemical data. Only insufficient knowledge of the clinical picture of diabetes mellitus can lead to its late diagnosis. Clinical signs of incipient ketoacidosis are increasing thirst and polyuria, loss of body weight, decreased appetite, nausea, dry skin and mucous membranes, and the smell of acetone from the mouth. At the first stage, these symptoms are accompanied by severe weakness and constant drowsiness. Skin and tendon reflexes are reduced. There is vomiting and abdominal pain syndrome. As the coma deepens—the second stage—the disturbance of consciousness increases. The child can be woken up and he will answer monosyllabic questions. Breathing is noisy, deep - Kussmaul. Increased vomiting and abdominal pain. The third stage of coma is a disturbance of consciousness against the background of an extremely serious condition. Tendon and skin reflexes are absent. Symptoms of dehydration, threadlike pulse against the background of tachycardia, oligoanuria. The manifestation of coma can be manifested by the predominance of one of two syndromes: abdominal or cardiovascular. Abdominal syndrome usually develops rapidly, which is often an indication for emergency hospitalization of a child with a diagnosis of “acute abdomen” or “appendicitis”. Characterized by thirst, polyuria, weight loss, nausea, vomiting. Soreness and tension in the abdominal muscles.

8 Ketoacidotic coma - 2 Cardiovascular syndrome is determined by symptoms of heart failure: thready pulse, low blood pressure, cold, pale cyanotic skin, oliguria. The child may have heart pain, dizziness, and fainting. Laboratory testing reveals: hyperglycemia, decreased reserve alkalinity, acidosis (decreased blood pH), ketonemia, glucosuria, ketonuria, hypocapnia, hypoxemia, increased lactate and pyruvate. Hyponatremia – in children with abdominal syndrome and sodium – at the upper limit of normal in the cardiovascular variant of coma. Blood osmolarity to extremely high (350 mOsm/l) figures, which determines the tactics of choosing starting infusion solutions to increase or decrease blood osmolarity to the upper limits of normal by the twelfth hour of treatment. This speeds up the recovery of patients from a comatose state and minimizes the risk of developing cerebral edema, as the most dangerous complication of inadequate therapy.

9 Hyperosmolar coma Hyperlactatemic (lactic acid) coma Hyperosmolar coma is a sharp increase in blood osmolarity against the background of high glycemia (above mmol/l) and hypernatremia, above 150 mmol/l, as well as chloremia, increased urea levels. In this case, there is no ketoacidosis. Other laboratory parameters were also changed: high levels of hemoglobin and hematocrit value, leukocytosis. High sugar content in urine. Blood pH and bicarbonate levels are normal. No hyperketonemia. The reaction to acetone in the urine is negative. A clinical feature of hyperosmolar coma is rapidly developing severe symptoms of dehydration - dry skin, mucous membranes, decreased turgor of the eyeballs. Unlike ketoacidosis, there is no smell of acetone in the exhaled air. Disturbance of consciousness - from drowsiness to deep coma. There may be pathological reflexes and hyperthermia. Shallow rapid breathing, tachycardia, decreased blood pressure. Oligoanuria. The development of hyperosmolar coma is often provoked by excessive intake of carbohydrates and intercurrent diseases. The classic course of hyperosmolar coma in children is rare. Hyperlactatemic (lactic acid) coma, as a rule, develops with increased anaerobic glycolysis against the background of hypoxia and the associated accumulation of lactic acid. Biochemical changes lead to characteristic clinical symptoms: agitation, aggressiveness, increased motor restlessness of the child, shortness of breath. There is pain in the heart and behind the sternum, muscles of the upper and lower extremities. Laboratory testing reveals moderate hyperglycemia, a sharp shift in the acid-base state to the acidic side, and hyperpyruvatemia. A diagnostic feature of this type of coma is the absence of ketosis: ketone bodies in the urine and exhaled air, which sometimes makes it difficult to diagnose IDDM in young children.

10 Principles of treatment of diabetic coma - 1 1. Children in a coma need the following laboratory tests: determining the level of glycemia, acid-base status of the blood, hemoglobin and hematocrit levels, electrolytes in the blood serum (potassium, sodium, calcium, phosphorus, chlorine), blood urea and transaminase levels. Coagulograms, clinical blood tests, urine tests, sugar and acetone in the urine, lactate, pyruvate and ECG. 2. The study of glycemia, CBS, electrolytes should be repeated every 3-4 hours. 3. Emergency treatment for early manifestations of coma and ketoacidosis should begin with gastric lavage with a 2% sodium bicarbonate solution, for abdominal syndrome - with saline solution, as well as a cleansing enema. 4. Infusion of sodium bicarbonate solution should be carried out only when there is a pronounced shift in blood pH to the acidic side (pH

11 Principles of treatment of diabetic coma - 2 Fluid infusion is recommended to be carried out with solution 1, used as a starting solution in children with cardiovascular syndrome, and solution 2, used more in patients with abdominal syndrome (V.V. Smirnov, 1998) . It is recommended to alternate solutions 1 and 2 in a 1:1 ratio. Hyperosmolar coma involves starting infusion therapy with a transfusion of 0.45% (hypotonic sodium chloride solution). Subsequent fluid infusion continues with solutions 1 and 2. Solution 2 Ringer's solution 200.0 Glucose solution 40% KCl solution 4-5% Insulin 3-6 units. Heparin IU Panangin solution 10.0 Solution 1 Glucose solution 5-10% KCl solution 4-5% Insulin 3-6 units. Heparin ED KKB mg

12 Principles of treatment of diabetic coma - 3 7. The level of glycemia in a comatose patient must be maintained within mmol, without reducing it to mmol/l or lower to avoid hypoglycemia. The decrease in high glucose concentrations should be gradual, no more than 2 times in 8-12 hours. Since a rapid decrease in glycemic levels can also lead to hypoglycemia with a deterioration in the patient's condition. 8. Maintaining the glycemic level within 15.5 mmol/l is achieved by changing the glucose/insulin ratio in the administered solution: Glycemia, mmol/lGlucoseInsulin, units Glucose/Insulin % % % % % % % %

13 Principles of treatment of diabetic coma - 4 9. Administration of potassium preparations, panangin, Ringer's solution is indicated 3 hours after the start of infusion therapy. 10. For a child with a coma, mandatory prescription of broad-spectrum antibiotics, possibly two, is indicated to suppress all clinically significant pathogens. 11. Heparin therapy is carried out at the rate of units/kg body weight per day. 12. To prevent cerebral edema, children are prescribed a 25% solution of magnesium sulfate - 0.2 ml/kg body weight per day. 13. For heart failure, cardiac glycosides, dopamine, dobutrex, and glucocorticoids are prescribed. 14. Diet therapy for a child in a coma. Nutrition for a patient in a coma is prescribed only when the condition improves, initially in the form of drinking mineral water, tea, compote. During the period of ketosis, butter is completely excluded. Improving clinical symptoms implies expanding the diet. Calculation of the insulin dose in accordance with the amount of food eaten, measured in bread units.

14 Hypoglycemic coma Hypoglycemic coma is caused by a decrease in blood glucose levels, accompanied by rapid loss of consciousness due to an overdose of insulin, skipping the next meal, or heavy physical activity. The initial symptoms of hypoglycemia are a feeling of hunger, weakness, cold sweat, headache, restlessness, and sometimes drowsiness. In newborns and infants, hypoglycemia is manifested by anxiety, unmotivated crying, and aggressive behavior. Against the background of a lack of consciousness during a hypoglycemic coma, profuse sweat, moist mucous membranes, convulsions, trismus of masticatory muscles, and Babinski's symptoms are noted. Hypoglycemic coma requires differentiation from other types of diabetic coma and epilepsy. With the initial symptoms of hypoglycemia, it is necessary to give the child a sweet drink (tea, juice, sugar syrup), food with easily digestible carbohydrates (jam, honey, sweets, porridge, white bread). When a hypoglycemic coma develops, 20, 40, 60 ml of a 40% glucose solution is administered intravenously until consciousness returns. Then the fluid infusion is carried out with solution 1, where insulin is not added, and solution 2 under the control of blood sugar levels. Along with the administration of glucose, in some cases glucagon is administered, which promotes the conversion of liver glycogen into glucose. Glucagon is administered in a dose of 0.5-1.0 ml intramuscularly or subcutaneously.

15 Comatose states with traumatic brain injury - 1 Severe traumatic brain injury in 10-20% of cases is accompanied by the development of a coma. The most common cause of severe injuries to the skull and brain are transport injuries, as well as falls from a height, blows to the head with hard objects. Often, a severe disturbance of consciousness occurs after a “lucid” interval, during which there may be stupor, drowsiness, or psychomotor agitation. A “light” gap is evidence of progressive compression of the brain by an intracranial hematoma or is associated with increasing cerebral edema. With severe bruises of the trunk-basal sections, the coma can last up to several weeks. In comatose patients, general cerebral symptoms predominate. Vomiting is an essential symptom of severe injury. It occurs immediately or 1-2 hours after the injury. Myiasis or mydriasis is determined, which in the absence of a photoreaction serves as an unfavorable prognostic sign. Patients exhibit ptosis, strabismus, floating movements and uneven alignment of the eyeballs. There are no corneal reflexes, spontaneous horizontal nystagmus. Bilateral increase in muscle tone of the limbs. Paresis and paralysis can be of the nature of tetra- and monohemiparesis. Pathological reflexes of Babinski, Oppenheim, oral automatism, Kernig, Brudzinski, and neck rigidity appear.

16 Comatose states with traumatic brain injury - 2 Pathological forms of breathing such as Cheyne-Stokes, Biota, terminal with separate breaths and subsequent apnea. Possibly tachypnea. With retraction of the tongue, lower jaw, aspiration of blood, stomach contents, breathing is frequent, noisy, snoring, with the participation of auxiliary muscles. Blood pressure changes either towards hypotension or hypertension. The heart rate changes. The most common is tachycardia, but bradycardia is also possible. Hyperthermia - in the first hours, sometimes 1-2 days after injury. The most important point that determines the course of the disease in severe traumatic brain injury is cerebral compression syndrome, the presence of which requires immediate surgical intervention. Compression syndrome is manifested by a deepening of the coma, an increase in meningeal symptoms, the appearance of convulsive seizures, mono- and hemiparesis. The most common cause of compartment syndrome is epi- and subdural hematomas. With intraventricular hematomas, harmetonic crises and autonomic disorders occur. Compression of the brain develops with its dislocation and compression of the stem sections. Disorder of vital functions quickly sets in. A fracture of the base of the skull is characterized by hemorrhages around the eyes (glasses). Bleeding and liquorrhea from the nose, external auditory canal, nasopharynx and damage to the cranial nerves are also noted.

17 Special research methods Lumbar puncture is performed on a patient in a mild coma. In deep coma and if intracranial hematoma is suspected, lumbar puncture is contraindicated. In a comatose state with a traumatic brain injury, there may be either an increase in cerebrospinal fluid pressure or a decrease in it. The composition of the cerebrospinal fluid in patients without subarachnaid hemorrhage is normal in the first days after injury, but later some cytosis and an increase in protein content are noted. With subarachnaid hemorrhage, an admixture of blood is detected. ECHO-EG is a valuable study that helps to establish or, with a degree of probability, reject the presence of intracranial hemorrhage. In children in a deeply comatose state, the disappearance or sharp weakening of the pulsation of echo signals may be observed. An EEG in a comatose state with traumatic brain injury shows a violation of the regular rhythm and interhemispheric asymmetry with bruises or hematomas. Angiography is an important diagnostic method for identifying intracranial and intracerebral hematomas. Radioisotope and ultrasound research methods, computed tomography and nuclear magnetic resonance of the brain are very informative for diagnosing traumatic brain injury in children.

18 Intensive therapy for comatose states associated with traumatic brain injury Treatment of children with traumatic brain injury should begin with the correction of impaired vital functions. This is, first of all, restoring breathing and maintaining hemodynamics. Ensure airway patency, administer oxygen therapy, and, if necessary, provide artificial ventilation. In the correction of hemodynamic disorders, the first step is to replenish the volume of circulating blood: blood transfusions, blood substitutes (reopolyglucin, albumin), against the background of the administration of cardiotonic drugs - dopamine, dobutrex. Surgical intervention is carried out simultaneously with the correction of vital functions. A mandatory component of intensive treatment is dehydration. For this purpose, Lasix is ​​used at a dose of 4-5 mg/kg body weight per day and/or mannitol intravenously at a dose of 1 g/kg body weight. Glycerin is used internally - 1 g/kg body weight. For severe cerebral edema, dexamethasone is prescribed mg/kg body weight per day. Lytic mixtures containing antihistamines, neuroplegics and ganglion-blocking drugs are administered: suprastin, glucose-novocaine mixture (0.25% novocaine solution together with an equal amount of 5% glucose). To relieve hyperthermia, a 25-50% analgin solution and physical cooling methods (cold on the main vessels, fans, cold wraps) are used. To improve cerebral hemodynamics, include aminophylline, no-spa, trental (pentoxifylline), chimes (dipyridamole). Hemostatic drugs are used - vikasol, calcium chloride, dicinone, protease inhibitors - contrical, gordox. Broad-spectrum antibiotics are prescribed. Convulsive syndrome is relieved by the administration of GHB and seduxen. Restoring brain functions by prescribing nootropil (piracetam). During the first 2 days, only parenteral nutrition is provided. When swallowing is restored, tube enteral nutrition is given from about 3 days. Vitamins of all groups are widely used.

19 Uremic coma Uremic coma is the final stage of severe kidney damage in acute renal failure (ARF) and irreversible changes in chronic renal failure. ARF occurs with shock, massive blood loss (prerenal form), poisoning with nephrotoxic poisons - acetic acid, mushrooms, medications, toxins of endogenous origin (renal form), with mechanical obstruction of the urinary tract - tumors, stones in the renal pelvis and ureters (postrenal form) . In uremic coma, urinary and urinary functions are impaired, and its development depends on the accumulation of nitrogen metabolism products in the blood and the associated increasing intoxication. In acute renal failure, the occurrence of hyperazotemia is caused not only by impaired excretory function of the kidneys, but also by increased catabolism of proteins in the body. At the same time, there is an increase in the blood level of potassium and magnesium, a decrease in sodium and calcium. Hypervolemia and the osmotically active effect of urea lead to the development of extracellular hyperhydration and cellular dehydration. In the kidneys, the excretion of hydrogen ions and organic acids is impaired, resulting in metabolic acidosis. Severe disturbances of water-electrolyte metabolism and acid-base balance lead to the development of cardiac and respiratory failure, pulmonary and cerebral edema. In chronic renal failure, comatose states develop in the terminal stage, when oligoanuria, severe hyperazotemia, metabolic acidosis, cardiac decompensation, edema and swelling of the brain develop.

20 Clinic Uremic coma develops gradually. A precomatose period is noted. The child becomes lethargic, has headaches, itchy skin, thirst, nausea, and vomiting. Hemorrhagic syndrome: nosebleeds, vomit like “coffee grounds” with the smell of urea, loose stools mixed with blood, hemorrhagic rash on the skin. The skin is dry, pale gray, stomatitis. The air you exhale smells like urine. Anemia progresses rapidly, oliguria develops, and then anuria. Depression of consciousness, attacks of psychomotor agitation, convulsions, auditory and visual hallucinations increase. Gradually consciousness is completely lost. Against this background, there may be convulsions and pathological breathing. The smell of urea in the exhaled air intensifies. On the skin there is a deposition of urea crystals in the form of powder. Hemorrhagic syndrome intensifies. Auscultation often detects friction noise of the pleura and (or) pericardium. Blood pressure is increased. Miosis, swelling of the optic nerve nipple. Laboratory blood tests reveal anemia, leukocytosis, thrombocytopenia, high levels of urea, creatinine, ammonia, phosphates, sulfates, potassium, magnesium. Decreased sodium and calcium levels, metabolic acidosis. Low density urine, albuminuria, hematuria, cylindruria.

21 Treatment Treatment of uremic coma consists of detoxification therapy, combating overhydration, correction of electrolyte disturbances, pathological changes in the acid-base state, and symptomatic treatment. For the purpose of detoxification, low-molecular blood substitutes and a 10-20% glucose solution are injected intravenously, the stomach is washed with a warm (36-37 C) 2% sodium bicarbonate solution, and the intestines are cleansed using siphon enemas and saline laxatives. Hemodialysis can be used when: plasma potassium concentration above 7 mmol/L, plasma urea level > 30 mmol/L and creatinine above 800 µmol/L, blood osmolality above 500 mOsm/L, hyponatremia below 130 mmol/L, blood pH below 7.2, symptoms of overhydration. Other methods of cleansing the body can be used: peritoneal dialysis, drainage of the thoracic lymphatic duct followed by lymphosorption, ion exchange resins, intraintestinal dialysis, hemoperfusion through activated carbons. For low diuresis and hemoglobinuria, a 10% solution of mannitol is prescribed at a dose of g/kg body weight, furosemide - 2-4 mg/kg body weight, aminophylline - 3-5 mg/kg body weight. In case of anemia, red blood cells are retransfused. Hyperkalemia is corrected by intravenous infusion of a 20-40% glucose solution (1.5 - 2 g/kg body weight) with insulin (1 unit per 3-4 g of glucose), 10% calcium gluconate solution (0.5 ml/kg body weight), 4% sodium bicarbonate solution (the dose is determined by the CBS indicators, if it is impossible to determine them - 3-5 ml/kg/weight). For hypocalcemia and hypermagnesemia, intravenous administration of a 10% solution of calcium gluconate or calcium chloride is indicated. For heart failure, inotropic drugs, oxygen therapy, and vitamins are used. To correct metabolic acidosis, 4-8% solutions of sodium bicarbonate are used under the control of CBS. The loss of sodium and chlorine ions is compensated by the introduction of a 10% sodium chloride solution, under monitoring the level of sodium in the blood and urine. For uremic seizures, intravenous administration of a 0.5% solution of diazepam (seduxene), barbiturates and sodium hydroxybutyrate is effective. Antibacterial treatment is carried out with caution, taking into account the nephrotoxicity of antibiotics, at half the dose. 30 mmol/l and creatinine above 800 µmol/l, blood osmolality above 500 mOsm/l, hyponatremia below 130 mmol/l, blood pH below 7.2, symptoms of overhydration. Other methods of cleansing the body can be used: peritoneal dialysis, drainage of the thoracic lymphatic duct followed by lymphosorption, ion exchange resins, intraintestinal dialysis, hemoperfusion through activated carbons. For low diuresis and hemoglobinuria, a 10% solution of mannitol is prescribed at a dose of 0.5-1 g/kg body weight, furosemide - 2-4 mg/kg body weight, aminophylline - 3-5 mg/kg body weight. In case of anemia, red blood cells are retransfused. Hyperkalemia is corrected by intravenous infusion of a 20-40% glucose solution (1.5 - 2 g/kg body weight) with insulin (1 unit per 3-4 g of glucose), 10% calcium gluconate solution (0.5 ml/kg body weight), 4% sodium bicarbonate solution (the dose is determined by the CBS indicators, if it is impossible to determine them - 3-5 ml/kg/weight). For hypocalcemia and hypermagnesemia, intravenous administration of a 10% solution of calcium gluconate or calcium chloride is indicated. For heart failure, inotropic drugs, oxygen therapy, and vitamins are used. To correct metabolic acidosis, 4-8% solutions of sodium bicarbonate are used under the control of CBS. The loss of sodium and chlorine ions is compensated by the introduction of a 10% sodium chloride solution, under monitoring the level of sodium in the blood and urine. For uremic seizures, intravenous administration of a 0.5% solution of diazepam (seduxene), barbiturates and sodium hydroxybutyrate is effective. Antibacterial treatment is carried out with caution, taking into account the nephrotoxicity of antibiotics, at half the dose.">

23 Pathogenesis The pathogenesis of hepatic coma is considered as the effect on the brain of cerebrotoxic substances that accumulate in the body during severe liver pathology. There are several types of hepatic coma: 1. Hepatocellular - endogenous, occurring against the background of a sharp inhibition of the neutralizing function of the liver and increased formation of endogenous toxic products as a result of massive necrosis of the liver parenchyma. 2. Shunt – exogenous, associated with the toxic effects of substances that enter the inferior vena cava through portacaval anastomoses, bypassing the liver. As a rule, both exogenous and endogenous factors take part in the development of both types of coma. The specific mechanisms of development of hepatic encephalopathy and coma have not yet been fully established. It is believed that ammonia and phenols play a leading role in brain damage. The latter are mainly formed in the intestine and enter the portal vein for inactivation. When liver function is impaired, ammonia and phenols enter the blood. Along with ammonemia, the phenomena of encephalopathy are caused by excessive accumulation of toxic metabolites such as mercaptan. Cerebral edema with accompanying symptoms of renal and pulmonary failure and hypovolemia is the direct cause of death in hepatic coma.

24 Clinic The development of a coma can be immediate, acute and subacute (gradual). With the fulminant development of coma, already at the beginning of the disease there are signs of damage to the central nervous system, icteric, hemorrhagic and hyperthermic syndromes. Acute development is characterized by the development of a coma on days 4-6 of the icteric period. With slow development, hepatic coma usually develops at 3-4 weeks of illness. During the coma period, consciousness is completely absent. In children, rigidity of the muscles of the neck and limbs, clonus of the feet, pathological reflexes (Babinsky, Gordon, etc.) are observed. Generalized clonic convulsions may be observed. Pathological breathing of the Kussmaul or Cheyne-Stokes type. “Liver” odor from the mouth, caused by increased accumulation of methyl mercaptan in the body. Muffled heart sounds, blood pressure decreases. The liver quickly decreases in size. Complete adynamia, areflexia. The pupils are wide. The reaction of the pupils to light disappears, followed by suppression of corneal reflexes and respiratory arrest. Blood tests reveal hypochromic anemia; leukocytosis or leukopenia; neutrophilosis with a shift to the left; increased direct and indirect bilirubin; reduction of prothrombin and other factors of the blood coagulation system; decreased levels of albumin, cholesterol, sugar, potassium; increasing the concentration of aromatic and sulfur-containing amino acids, ammonia. The activity of transaminases at the onset of the disease increases, and during the period of coma it decreases (bilirubin-enzyme dissociation). Both decompensated metabolic acidosis and metabolic alkalosis associated with severe hypokalemia are observed.

25 Intensive therapy – 1 Intensive therapy in the treatment of hepatic coma should be started with detoxification therapy aimed at etiological factors, restoration of liver cell function, and prescription of antibiotics. To restore energy processes, glucose is infused in a daily dose of 4-6 g/kg in the form of a 10-20% solution. To remove toxic substances, large amounts (1-2 liters per day) of liquids are administered intravenously, such as Ringer-Locke solutions, 5% glucose solution in combination with 1% glutamic acid solution (1 ml/year of life per day) for binding and neutralization ammonia. The total volume of infused liquid averages ml/kg of body weight per day. Infusion therapy is carried out under the control of diuresis, often in combination with diuretics, aminophylline. To reduce intoxication due to hyperammonemia, hepasteryl A (argyrine-malic acid) is used. ml is administered intravenously at a rate of 1.7 ml/kg per hour. Hepasteril A is contraindicated in cases of renal failure. Normalization of amino acid metabolism is achieved by introducing drugs that do not contain nitrogen components - heparil B. To correct hypoproteinemia and associated hypoalbuminemia, solutions of albumin and fresh frozen plasma are administered. Reducing the formation of ammonia and phenols in the intestines can be achieved by removing protein products from the gastrointestinal tract (gastric lavage, cleansing enemas, using laxatives), as well as suppressing the intestinal microflora that forms these toxic products, and prescribing oral antibiotics. At the same time, to prevent the septic process, 1 or 2 antibiotics are prescribed, maximally suppressing clinically significant pathogens.

26 Intensive therapy – 2 Correction of electrolyte metabolism and acid-base status should be carried out under the control of relevant biochemical parameters, since in hepatic coma hypo-, normo- and hyperkalemia, acidosis and alkalosis can be determined. In the complex of therapeutic measures, it is recommended to include anabolic hormones, essentiale, cocarboxylase, unithiol, vitamins: A, C, K, E, group B and preparations prepared from fresh liver extracts - sirepar, hepalon. To stabilize the cell membranes of hepatocytes, glucocorticoids are prescribed - hydrocortisone (10-15 mg/kg per day) and prednisolone (2-4 mg/kg per day). Symptomatic therapy includes the prescription of sedatives, anticonvulsants, cardiac, vascular and other drugs according to indications. If there are signs of disseminated intravascular coagulation syndrome, heparin is used at the rate of units/kg body weight under the control of a coagulogram. Improving blood circulation in microcirculation in the liver and other tissues is achieved by administering trental and aminophylline. To inhibit proteolytic processes expressed during hepatic coma, it is recommended to prescribe inhibitors of proteolytic enzymes: contrical, gordox. In the absence of the effect of conservative therapy, active detoxification methods are used - hemosorption, lymphosorption, plasmapheresis, hemodialysis. Peritoneal or intraintestinal dialysis may be used. Detoxification methods using xeno-liver, artificial liver, and liver transplantation are being introduced.

Title=" Intoxication - (from the Latin prefix in - “in” and the Greek toxikon - poison) Exogenous (the entry of neurotropic exotoxins from the outside) Endogenous (with insufficiency of the functions of various organs and => accumulation of neurotropic endotoxins) Toxins act on between">!}

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Presentation on the topic: Coma

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Intoxication - (from the Latin prefix in - “in” and the Greek toxikon - poison) Exogenous (receipt of neurotropic exotoxins from the outside) Endogenous (with insufficiency of the functions of various organs and => accumulation of neurotropic endotoxins) Toxins act on interneuronal connections and lead to persistent disorders consciousness up to coma.

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Hepatic coma. Etiology: liver cell failure (due to massive necrosis, degeneration of hepatocytes)?! -Bepatitis in -cyrrosis of the liver -the imposition of hepatotropic poisons (dichlorestan, arsenic, phosphorus, ethanol, four -chloride carbon, toluene) -the effects of taking various medicines (antidepressants, sulfainlamides, tuberculoculostata, tetracycline, levomicetin) -chronicle) Crooal intoxications Portocaval shunts ( for diseases with portacaval discharge of blood, bypassing the liver)?! – liver cirrhosis – portal vein thrombosis – liver tumors

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Clinical features of hepatic coma 3 stages of development: 1 - precoma 2 - threatening coma - A peculiar flapping tremor of the fingers, tremor of the eyelids and lips 3 - coma itself - “liver” smell, jaundice, skin itching, scratching, hepatic palms - hemorrhagic syndrome (tongue crimson, papillae are smoothed) - edematous-ascitic syndrome; oliguria - Kussmaul type breathing - fever, liver palpation is painful

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Laboratory data - leukocytosis, anemia, - hyperazotemia, accelerated ESR; - with a decrease in the level of total protein and albumin, a high level of gamma globulins, -↓clotting factors, -↓potassium level, ↓cholesterol. - bilirubin -↓ aminotransferases and cholinesterases. Urine: dark yellow. => Death from respiratory arrest, acute cerebral edema, pulmonary edema, renal failure, infectious-toxic shock.

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Pathogenesis of uremic coma Critical impairment of renal function ↓glomerular filtration rate up to 10 ml/min. in the blood, urea is above 30 mmol/l, creatinine is above 1000 mmol/l, Na is above 150 mmol/l metabolic acidosis, cerebral edema, microcirculation disorder, cerebrovascular accident

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Clinical features of uremic coma The onset is gradual, preceded by headaches, blurred vision, skin itching, nausea, vomiting, convulsions, - examination: - the skin and visible mucous membranes are pale and dry, “uremic powder” is possible on the skin, scratching hemorrhages. -renal edema; pupils are narrow. - fibrillary muscle twitching, convulsions. Tendon reflexes are increased. - breathing is initially deep, noisy (Kussmaul type), then shallow, irregular, Cheyne Stokes type. -The breath smells like ammonia -Heart sounds are loud, you can hear a pericardial friction rub. - Oliguria or anuria is characteristic. Laboratory data: urea above 30 mmol/l, creatinine - above 1000 µmol/l, sodium - above 150 mmol/l; Plasma osmolarity is above 330 mOsm/l. decompressed metabolic acidosis. OAM Osmolarity is below 500 mOsm/L. Glomerular filtration rate below 10 ml/min

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clinic at the toxicogenic stage - alcoholic coma, external respiration disorders, hemodynamic disorders; at the somatogenic stage - neuropsychiatric disorders, inflammatory lesions of the respiratory system, myorenal syndrome. 1. Toxigenic stage Alcoholic coma Non-specific and does not depend on concentration If treatment of alcoholic coma does not lead to positive dynamics in the patient’s condition within 3 hours, then either there are unrecognized complications (for example, traumatic brain injury), or the cause of the coma was not alcoholic poisoning. External respiration disorders are caused by obstructive-aspiration complications due to hypersalivation, bronchorrhea, laryngo-bronchospasm, and aspiration of vomit. Central type disorders are the cause of death in the prehospital stage. Hemodynamic disturbances: persistent disturbances in cardiac rhythm and conduction are possible. ?! dysregulation of vascular tone and hypovolemia, which are most pronounced in deep alcoholic coma. 2. Somatogenic stage Convulsive syndrome myorenal syndrome

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3 stages of alcoholic coma: In stage I, there is hypertonicity of the muscles of the limbs, trismus of the masticatory muscles, muscle fibrillation, reflexes are preserved. The pupils are narrow, the eyeballs “float”, the face is hyperemic; hypersalivation, vomiting. In stage II, muscle tone and tendon reflexes disappear, but the motor response to painful stimuli remains. Blood pressure decreases, pulse is frequent and weak. Breathing slows down. Involuntary urination and defecation. In stage III, breathing becomes arrhythmic, rare, bubbling; Facial cyanosis and acrocyanosis increase, the pupils dilate, the sclera are sharply injected. Blood pressure and central venous pressure are low, the pulse is thready, often arrhythmic. Sensitivity and reflexes are absent.

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Narcotic coma Drugs (from the Greek narkotikós - numbing, intoxicating) are a group of substances that cause physical dependence and are not associated with normal life activities. As a consequence of this definition: Drugs are substances that can cause the disease drug addiction. It is believed that the term narcotic (ναρκωτικός) was first used by the Greek healer Galen, in particular to describe substances that cause loss of sensation or paralysis. This term was also used by Hippocrates. As such substances, Galen, for example, mentioned mandrake root, eclate and poppy seeds (opium).

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1 After 30-60 minutes - general weakness, - drowsiness, - coordination of movements is impaired, - speech becomes slurred. -The pupils are moderately dilated and react to light. - Hypersalivation is noted - Respiratory and circulatory functions are not impaired. -Deep sleep or loss of consciousness gradually sets in. 2 In a state of superficial coma, the pupils are constricted, swallowing and cough reflexes are preserved. Muscle tone and tendon reflexes decrease. Cyanosis, tachycardia, hypotension. Possible mechanical asphyxia (aspiration with saliva, vomit, retraction of the tongue, spasm of the larynx) or depression of the respiratory center.

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3 For the stage of deep coma Reflexes are absent: muscle relaxation; the pupils are constricted (dilated during asphyxia), hyperthermia of central origin is possible. The skin is pale, dry. Breathing becomes faster or slower, the rhythm becomes irregular (Cheyne-Stokes type). Possible respiratory arrest and pulmonary edema. Hemodynamics are severely disrupted (tachycardia, then bradycardia, hypotension, collapse). 4 During the post-mortem state, the activity of the central nervous system is gradually restored and areflexia disappears. However, coordination of movements is impaired. Mental disturbances (depression, motor restlessness, emotional lability) are typical.

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Opiates The source of opium is the opium poppy Papaver somniferum species RAW OPIUM - when fresh, a sticky, resin-like plastic mass, dark brown in color, with a characteristic licorice odor. As it ages, its plasticity disappears and the mass becomes hard and brittle. PROCESSED (EXTRACTION) OPIUM - a product obtained from raw opium through various processing, usually by aqueous extraction, filtration and water evaporation. MEDICAL OPIUM is a fine light brown powder with a morphine content of 9.5-10.5%. Includes “diluent” additives: lactose, starch and other components. Has a characteristic opium smell. PANTOPON (OMNOPON) - light brown powder, easily soluble in water, contains 48-50% morphine. OPIUM SLAG - the product remaining in the pipe after smoking opium still contains significant amounts of morphine. Mixed with raw or processed opium for further use.

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External changes - severe constriction of the pupils; the eyes are slightly reddish and very shiny; bruises under the eyes; shallow intermittent slow breathing; itchy skin (especially nose); lethargic and sleepy appearance; slurred speech; passivity and general relaxation; apathy towards everything except oneself; euphoria and carefree; excessive “courage” and determination; nervousness; and so on. Physiological changes - dry skin and mucous membranes (lips, tongue); superficial sleep; decreased urine output; frequent constipation; There is no cough when you have a cold; slight decrease in body temperature. Overdose coma

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The sequence of treatment measures for opiate poisoning depends on the patient’s condition. Based on the pathogenesis and features of the development of the poisoning clinic, it is advisable to combine the following groups of therapeutic measures: 1) ensuring adequate ventilation of the lungs (respiratory toilet, oxygenation, mechanical ventilation); 2) antidote therapy (administration of naloxone (1-2 ml), in its absence, cordiamine (2-4 ml) intravenously) repeatedly; 3) prescribing adrenergic agonists to lower blood pressure; 4) measures to remove opiates - gastric lavage, forced diuresis; 5) dehydration therapy (mannitol, Lasix); 6) alkalization of blood (3% sodium bicarbonate solution 200-400 ml); 7) the use of medications that improve metabolism in the central nervous system (piracetam, Actovegin, etc.); 8) prevention of inflammatory complications (antibiotics).

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