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SHARP EXOGEN POISONINGS

SHARP EXOGEN POISONINGS. IFNMU Department of Anesthesiology and Intensive Care. POISONING Is a pathological process which arises in Consequence of influence on an organism of toxic substances Environment (chemical substances, p hytogenesis toxins).

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SHARP EXOGEN POISONINGS

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  1. SHARP EXOGEN POISONINGS IFNMU Department of Anesthesiology and Intensive Care

  2. POISONING Is a pathological process which arises in Consequence of influence on an organism of toxic substances Environment (chemical substances, phytogenesis toxins). All these substances are called xenobiotics and are characteristic that they do not accept participation in a power exchange and are not used by an organism with the plastic purpose POISON Is an alien chemical substance that breaks current of normal biochemical processes in an organism, owing to what there are infringements of physiological functions of different degree from the smallest displays of an intoxication to lethal consequences

  3. Classification of xenobiotics on toxicity: 1. Strong or extremely toxic - DL 50 <50 mg/kg of weight of a body 2. Highly toxic – DL 50 = 50-200 mg/kg of weight 3. Average toxicity – DL 50 = 200мг-1 weight g/kg 4. Low toxic – DL 50> 1 g/kg of weight of a body FREQUENCY OF POISONINGS: 1. In the USA - over 1 million cases a year, with what nearby 56 000 die 2. In the countries of Europe - in a year hospitalise in Average 1 person on 1 thousand population, that in 2 times More than with a myocardium heart attack 3. In region Iv.-Frankovsk - annually hospitalise about 1000 poisoned

  4. THE REASONS OF POISONINGS: 1. Casual or household - all 2/3 cases 2. Suicide attempts - 25 % 3. Professional - 10 % 4. Owing to extreme statuses and accidents - 2-3 % The reasons which increase amount of sharp exogenous poisonings: 1. Not supervised sale of various medicines (soporific, sedative, strong) 2. Self-treatment in connection with a medicine rise in price 3. Creation of stocks of medicines in house conditions (the first-aid set accessible to all members of families) 4. An alcoholism, a narcotism and glue sniffing 5. Use of toxic doses of preparations for interruptions of undesirable pregnancy

  5. Death rate from sharp poisonings: The general - 1 - 7 %, including: Alcohol and its(his) substitutes - 62,2 % Toxic gases (CO, hydrogen sulphide) - 15,4 % corrosive poisons (acids, alkalis) - 6,3 % Medicines - 4 % POS - 3,1 % Ways of receipt of poisons to an organism: 1. Oral - through GIT (85 %) 2. Inhalation - through breath bodies (11 %) 3. Percutaneal - through a skin and mucous (3 %) 4. Injections - u/s, i/m, i/v (1 %) 5. Through a rectum, genitals (0,1 %)

  6. Clinical Classification of POISONS Cardiac- glycoside, quinine, adrenoceptor antagonist, Саlcium channel inhibitor, clonidine, barium and potassium salts, tricyclic antidepressant, beladonna Nervous (a psychosis, spasms, a coma) - opiates, soporific, sedative, POS, CO, alcohol and its substitutes Hepatic (hepatopathy) - carbohydrates, poisonous mushrooms, phenols, aldehydes Blood (hemolisis, metНв, НвСО) - amonia, nitrates, nitrites, aniline marching Pulmonary (a hypostasis, fibrosis) - to a nitrogene oxide, CL, phosgene Nephritic (nephropathy, ANI) – ethylene glycol, salts of heavy metals, Gastroenteric (gastritis an enteritis) - corrosion poisons, heavy metals, arsen

  7. FACTORS THAT CAUSE DEGREE OF TOXICITY OF POISONS Concentration (quantitative) - dependence is directly-proportional to quantity of poison and its concentration in biological environments Time(Temporary)- dependence is directly-proportional to speed of receipt of poison in an organism and inversely proportional speeds of its neutralisation or removing Spatial - it is defined by receipt of poison and degree of blood supply of different bodies and fabrics (at per oral poisoning are amazed GIT, a liver, at inhalation - lungs) Ways of clarification of an organism from poison: 1. Liver biotransformation 2. Elimination through kidneys, GIT, a skin, lungs

  8. “LETHAL SYNTHESIS” - It is synthesis in an organism in the course of biotransformation Substances which own toxicity above in comparison with an initial product CLINICAL STAGES OF SHARP EXOGENOUS POISONINGS: 1. Toxicоgenic- the period of interaction of toxic substance with a human body, progressing of a clinical picture (average duration from several o'clock about 3 days) 2. Somatogenic- a clinical picture of consequences of a poisoning (duration is not defined and depends on depth of defeat)

  9. THE GENERAL PRINCIPLES OF TREATMENT SHARP EXOGENOUS POISONINGS: 1.A stop of receipt of toxic substance in an organism 2. Fast removing of poison from an organism 3. Use of antipillboxes (antidotes) 4. Strengthening of natural ways of detoxication, application of artificial methods of clarification of an organism from poisonous substances 5. Symptomatic syndromic therapy

  10. STRENGTHENING OF NATURAL WAYS OF DETOXICATION 1. Forced alkali osmotic diurеsis: The purpose - to increase amount of daily urine, to reduceconcentration toxic substances, to translate poisons in thedissociated form Carrying outtechnique: Water loading - throughout 1 hour i/v 500 ml 5 % of a solution of glucose + 300 ml of 4-5 % solution sodium hydrocarbonate + 700 ml of 5 % solution glucose Introductions of diuretics - throughout 15 minutes i/v 1 - 1,5 g/kg manitoli in the form of 15-20 % solution on 10 % solution glucose + 1-2 mg/kg lasicis + 240 mg eufilini . At decrease of diuretic effect all 3-4 times for days repeat The control over amount of urine - catheter Replaceable therapy - i/v solution of laktasoli, Ringera, Ringera-Lokka, 0,9 % of sodium of chloride, disolum,trisolum, qartasolum, in total and with speed of the allocated urine under control of CVP and electrolits of blood

  11. 2. STRENGTHENING OF DETOXICATION OF LIVER 1. Indirect electrochemical oxidation of blood - i/vsodium hypochloride for replacement of cytochrome Р-450 2. Heptral, Hepasterili - i/v 1-2 bottles for days 3. Hepatoprotectors, stabilizers of cellular membranes, antioxidants - glucocorticosteroides, inhibitor of proteolytic enzymes, essential lipids (berlitioni, lipostabili), silimarini, vitamins, chofitoli, ornicetili, glutargini, reamberini, hepedifi, tiotriasolini 4. Intestines sterilisation enterosorption – apple acid, lactulose, antibiotics, smekta, sillardi, gepa-merts (L-ornitini-L - aspartat) 5. Additional oxygenation of a liver - MT ТМОКВВ, ГБО, enteral introductions of oxygen, oxygen skins

  12. DETOXICATIONAL ALV It is used as a method of detoxication at poisonings with toxic substances which are removed through lungs are more often toxic gases (CO, NH3, H2S, methane, mine gas, butane, the prosir). ALV it is spent through intubation's tube in a mode of moderate hyperventilation (рСО2 = 34-36 mm hg) Operation of replaceable blood transfusion Is spent in volume from 0,5 to 1 V of B: spend catheterization of 2 veins, from them one - central. From it let out blood in measured ware, and in another with the same speed spend replaceable transfusion of crystals and colloid solutions. In a case when replace more than 30 % V of B, to them add erythrocytes. All operation is accompaniedby monitoring FHC, CVP, AP

  13. EXTRACORPORALMETHODS OF DETOXICATION 1 – cleaning of stomach ; 2 – ALV; 3 – peritoneal dialysis; 4 – oxygenation of the blood; 5 – hemo- andultra- filtration; 6 – hemodialysis; 7-sorption а – hemosorption; б – transfusion of the blood; в – МПТМОКВВ; г – plasmophoresis, д - plasmosorption

  14. TIPES OF EXTRACORPORAL DETOXICATION

  15. CHEME OF HEMODIALISIS, HEMO- ULTRAFILTRATION

  16. TIPES OF EXTRACORPORALDETOXICATION

  17. CHEME OF HEMODIALISISAND PLASMOFORESIS

  18. ANTIDOTES THERAPY • Classification of antidotes(The international program from chemical safety ВООЗ, 1993): • 1. Chemical which are sensitive to toxins - enter with poison the physicist-chemical bonds in GIP or in humoral environment of the organism : • Nonspecific- enterosorbents, the activated coal, white clay, KMgO4, NaHCO3 • Specific - unitioli, mercaptid - salts of heavy metals, protamini - heparin) • 2.Immunological - connect poisons reaction an antigene-antibody (antitoxic serum - poisons of insects and snakes, antidigoxiniserum, antidigoxini - heartglycosides)

  19. 3. Biochemical - change a metabolism of poisons or a direction of biochemical reactions in which they take part (lipoid acid - amanitini, метиленовий синій - метНв, ethanol - methanol, ethyleneglycolic, naloxoni - opiates, cytochrom - WITH, nitrates and sodium thiosulfates - cyanides, acetylcysteini - the chlorinated carbohydrates) 4. Pharmacological- own opposite pharmacological action on the same most functional systems of an organism (atropin - proserin, glucagon - insulin, proserin - pachicarpin, K chloride – heart”sglycosides)

  20. POISONING Sleeping pills (barbiturates) There are long barbiturates (phenobarbital), medium (barbital) and short (nembutal) actions. Lethal concentrations of = 10 half therapeutic doses of each drug or their mixtures. Pathogenesis: barbiturates cause blockage of oxidative phosphorylation in mitochondria, ATP synthesis, transport of ions across the cell membrane, and therefore - the violation of energy processes in cells mainly central nervous system, hypoxia, and their inability to function until the coma. Significantly inhibited the activity of respiratory centers and the motor vessel, leading to more respiratory and circulatory hypoxia.

  21. Stages of poisoning (by Reed): 0 - somnolentsiya, cough reflex is depressed I - loss of consciousness, is a reaction to pain stimuli, cough reflex is depressed II - loss of consciousness, painful response only to strong stimuli, suppressed cough reflex, orders decreased (hypoventilation) III - loss of consciousness, response to pain stimuli and absent cough reflex, expressed hypoventilation IV - same as III, an additional significant respiratory failure until it stops, wide pupil without fotoreaction, severe hypotension, anuria

  22. INTENSIVE THERAPY 1. Probe washing the stomach, diarrhea provocative saline laxative enterosorbents. 2. Maintenance-free airway, mechanical ventilation if necessary, stabilization of cardiac activity. 3. Analeptic in therapeutic doses: ephedrine hydrochloride 5% - 1-2 ml, 2-4 ml kordiamin, caffeine sodium benzoate 10% - 2-4 ml i\m, bemehryd i\v only 10-20 ml contamination with 0 - I severity. 4. Forced alkaline diuresis osmotic 5. Nicotinamide 1% - 20-100 ml i\v, drip under the control of BP 6. Cytomak, cytochrome C in 4.8 ml of 0.25%, sol i\v 7. Hemosorbtion, extended hemodialysis or a combination thereof.

  23. ETHANOL POISONING Lethal dose 96% ethanol = 4.12 g / kg Lethal concentrations in blood = 5-6 ‰ Pathogenesis: ethanol initially oxidized in the cytoplasm of cells, mainly the liver to acetaldehyde by 3m enzyme systems: alkoholdehydrohenase (80%), katalas (2%) and microsomes etanoloxidation (10-20%). In the second step in the mitochondria via enzyme aldehiddehidrohenazy acetaldehyde oxidized to acetate, which immediately goes into its biologically active form - acetyl-CoA and metabolized in the Krebs cycle toСО2and Н2О. С2Н5ОН>СНЗСНО>СНЗСООН>СО2+Н2О Average rate of ethanol oxidation in the human body is 0.1 g / kg / hr.

  24. If speed and enrollment ethanol capacity exceeds its enzymatic metabolism in the body accumulating in excessive concentrations of acetaldehyde, which causes and pathogenesis of poisoning. Acetaldehyde causes profound narcotic effect due to metabolism of neurons function mediated systems, utilization of oxygen by cells, the development of metabolic acidosis and as a result - CNS hypoxia with all negative consequences. Death of ethanol poisoning in most cases comes against a background of deep narcotic state of paralysis, respiratory and vascular-motor centers. Additional factors - miorenal syndrome, aspiration, hypoglycemia, mechanical asphyxia

  25. CLINIC The first stage (euphoria) - following the reception of 20-50 ml of ethanol concentration and the last in the blood is 0,5-1,0 g / l (0,5-1,0 ‰) The second stage (intoxication) - occurs after administration of 50-100 ml of alcohol, and poisons in the blood concentration of 1,0-2,0 g / l (1,0-2,0 ‰) The third stage (drug) - occurs after consuming 100-200 ml of alcohol and its concentration in blood is 2,0-3,0 g / l (2,0-3,0 ‰) The fourth stage (or comatose-asphyxia) - occurs after receiving 200-400 ml of ethanol and its concentration in the blood exceeds 3.0 g / l (3,0-5,0 ‰)

  26. INTENSIVE THERAPY • Therapy of poisoning, which corresponds to the first and second stages of severity: • If passed no more than 2 hours after receiving the last dose - gastric lavage 1-2% solution of sodium hydrogen carbonate (baking soda) in a total of 6.8 liters. Better use the microprobe method. When washing without probe should consider the possibility of aspiration of gastric contents. • 500 ml Glucose 20% solution of 24 OD insulin, then 500-1000 ml 5% glucose solution with vitamins C, B1, B6 by 500 mg every i\v. • Forced diuresis with osmo-and saluretyc (mannitol in doses of 1 g / kg, 80 mg lasix) eufillinum (10 ml 2.4% solution), aminomalu to 1 amp. 2-3 times a day, i\v slowly. • Control of body temperature and maintaining thermal conditions

  27. Therapy of poisoning of the third and fourth stages: Release and maintenance-free patency of upper airways. Violation of spontaneous breathing - tracheal intubation and transfer of patients on mechanical ventilation Introduction of permanent nazogastral probe and stomach lavage by sodium solution Hemodynamic stabilization and maintenance of vehicles of vasoactive and cardiotonic, infusion solutions on the level of central venous pressure Drip infusion therapy i\v glucose solution, sodium hydrogen carbonate, Refortan, balanced salt solutions in the total number equal to the daily diuresis + 1 l + abnormal fluid loss (vomiting, diarrhea, excessive sweating,)

  28. The method of forced osmotic diuresis using alkaline mannitol (1.0 g / kg) lasix (40-80 mg) and eufillinum (5-10 ml 2.4% solution) against a background infusion i\v listed in the preceding paragraph solution (until pH urine 7,5-8,0). • If possible, peritoneal or hemodialysis, especially in the comatose stage (11.4 in hemodialysis and peritoneal dialysis in 2,5 times more effective for natural elimination) • Prevention of pneumonia and hypothermia • Solution of glucose in the treatment of poisoning may be more effectively replaced by solutions of fructose in equivalent concentrations and doses. In this case, insulin is injected. WARNING! If carried out intensive care for several hours does not give effect to exclude injury or disease B!

  29. METHANOL POISONING Lethal dose = 100-150 ml (100 mg% in blood) Amaurosis can occur from 5-15 ml of methanol Pathogenesis: Methanol is metabolized by liver ADH to formaldehyde and formic acid (lethal synthesis) 5-7 times slower than ethanol. These products of metabolism cause toxic injury of neurons B, retinal ganglion cells of eyes and optic nerves, ending their degeneration, complete atrophy and irreversible loss of vision. Accumulation of formic acid causes severe decompensated metabolic acidosis, which increases by nonoxydated products of broken cellular metabolism (lactate, pyruvate, etc.) Death usually occurs from paralysis of respiratory and vascular-motor centers

  30. Clinic: speed of development of symptoms is directly proportional to the number-poison - headache, nausea, vomiting, pain in the epigastrium. Maybe a period of relative improvement, which after 6.10 pm. in severe cases ending coma. Gradually disturbed vision - blurring of vision and symptoms "before the eyes of butterflies" to complete blindness. Comatose state is accompanied by respiratory, cardiovascular and renal disease. INTENSIVE THERAPY 1. If the patient in mind, can cause vomiting (root irritation of the tongue or posterior pharynx) or wash the stomach without probeby 2-3% solution of sodium hydrogen carbonate. Better to do it (if violations of consciousness - always) with the probe. After rinsing the stomach enter the enteric (activated carbon, polisorb, silard, sorbent) and salt laxative.

  31. 2. Physiological antidote is ethanol, methanol, because it binds oxidase enzymes and alkoholdehydrogenase and this impedes the formation of toxic products of biotransformation of methanol (formaldehyde and formic acid). • If the patient in mind, the ethanol can be given inside satiating dose of 1.0 ml / kg 96% alcohol or other alcoholic beverages in equivalent amounts. In the future, provide alcohol to 0,15-0,20 ml / kg / h of alcohol per 96%. • If the patient in a comatose state or can not take alcohol into other reasons, then assign 10% ethanol solution of glucose in the satiating dose of 10 ml / kg i\v. Maintenance dose in the future is 1,5-2,0 ml / kg / h 10% solution. Above doses of ethanol concentration created in the blood of 1,0-2,0 g / L. Duration giving antidote 4-5 days or until disappearance of clinical manifestations of poisoning.

  32. 3. Antagonists alkoholdehydrogenase (ADH) - pyrazol or 4-metylpirazol in doses according to instructions. 4. Leykovoryn 1.0 mg / kg (maximum dose 50 mg) together with folic acid 1.0 mg / kg every 4 hours i\m (of 6 doses) or berlition i\v in a daily dose of 600 mg for 3 days to speed up the metabolism of formic acid . 5. The method of forced alkaline diuresis osmotic 6. Receiving more than 30 ml of methanol are shown extracorporeal detoxification in combination with ethyl alcohol antidote therapy. 7. Correction of acid-alkaline balance and water and electrolyte balance by general rules. 8. Symptomatic therapy.

  33. Hemodialysis in 60 times speed up the withdrawal of methanol in comparison with the natural elimination Indications for urgent hemodialysis: Reception> 30 ml methanol The concentration of methanol in blood 50-100 mg% Severe acidosis (pH <7,2, SB <20 mmol / l) Disorders of vision Peritoneal dialysis methanol output speed by 5-10 times and is recommended in cases when there are no conditions for dialysis or have contraindications to it (hemorrhagic syndrome) In disorders of view - retrobulbar novocaine blockade with prednisolon, SaSI2 10% - 10 ml / D in 200 ml 40% glucose solution with 20 units of insulin / D i\v

  34. POISONING ethylene glycol (EG) Lethal dose =  100 ml, which corresponds to 2-3 g oxalic acid Pathogenesis: EG hepatocytes under the influence of ADH becomes glycolaldegid first, then glyoksyl acid, and end - of oxalic acid. Last quickly reacts with ions of Ca + + and Ca oxalate forms, which crystallized and deposited in the kidney tubules, causing their mechanical obturation. Together with glyoksyl acid they lead to acute tubular necrosis, resulting in the development of ARI. In addition, EG and its metabolites pinch capillary bed of many organs (brain, myocardium, liver), leading to disturbances of microcirculation in them.

  35. Clinic: consists of symptoms of gastrointestinal tract, nervous and cardiovascular systems and kidney. Abdominal pain, vomiting, neurophysiology disorders, convulsive syndrome, coma, progressive bradycardia, hypotension, decreased diuresis until anuria. INTENSIVE THERAPY 1. Induce vomiting (if the patient in mind) or do gastric lavage suspension of activated charcoal in the first 1-2 hours. after taking poison. Manipulations finish entering the stomach enterosorbents and salt laxatives that contain magnesium salts (Na2SO4, karlsbadska salt) 2. As an antidote recommended doses of ethyl alcohol and methodology, as in methanol poisoning.

  36. 3. Thiamine and pyridoksyn in doses of 100 mg each i\v once a day. 4. To designate the development of oliguria alkaline osmotic diuresis forced by using large doses lazycis (up to 1 g per day) and replacement crystalloid infusion therapy alkaline solutions. 5. At a concentration of ethylene glycol levels above 50 mg% is shown hemodialysis to the disappearance of clinical symptoms of intoxication. 6. Correction of hypocalcemia i\v inputs 30-40 ml 10% solution of calcium chloride. If necessary, dose can be repeated or infusion of 1% solution of calcium chloride or gluconate in a daily dose of 300-400 ml. 7. Symptomatic treatment - antyspasm, decongestants, maintaining gas exchange and hemodynamic.

  37. POISONING CORROSIVE S Poison • Corrosives poison got the name from the English. corrosives - eating. These include: • 1. Acids: • Organic - vinegar (vinegar essence), oxalic • Inorganic - Sulfuric (battery fluid), nitric, hydrochloric • 2. Alkalis - ammonia, caustic soda, potassium carbonate, slaked lime Pathophysiologic changes during poisoning by these substances largely similar, with some features of each: 1. Chemical burn of gastrointestinal tract primary part - the mouth, pharynx, esophagus, stomach and small intestine less often with the development of burn shock (these burn units = 30% body surface) - coagulation from acid and colliquative from alkali

  38. Resorpting action - hemolysis, changes in ABB (metabolic acidosis or alkalosis) nephrosis-nephritis, ARI, dystrophic changes and necrosis of liver slices, AHI, hemic hypoxia, • Early complications - bleeding from the gastrointestinal tract, perforation of the esophagus, stomach, reactive peritonitis, pancreonecrosis, DIC syndrome In the clinical picture distinguish 5 main syndromes: Burn- signs skin burns around the mouth, pharynx and oral mucosa at FGS - esophageal and gastric Pain - pain when swallowing, along the esophagus, in the epigastrium, nausea, vomiting rarely Bleeding - esophageal-gastric bleeding due to burns and DIC syndrome Respiratory failure - due to edema and stenosis of the larynx, later - pneumonia Hemolytic - as a result of the venom on erythrocyte membranes and sudden changes of ABB

  39. Stages of burn disease: • Burn shock - to 1,5 days • Toxemia - to 4-th day • Infectious complications and late bleeding - up to 2 weeks • Scarring - to 2-3 months • Recovery • The degree of hemolysis: • Light - the content of free hemoglobin in the blood to = 5 g / l (500 mg%) • Moderate - the content of free hemoglobin = 10 g / l (1 g%) • Heavy - the content of free Hp> 10 g / L (> 1 g%) The content of free Hp 10 g / l = 30% hemolysis of red blood cells, and it appears in the urine if the blood> 1 g / l (100 mg%)

  40. FEATURES OF POISONING DIFFERENT CORROSIVE Poison • Organic acids- very deep penetration into the tissue, a burn more like a colliquative, much resorpting and hemolytic action • Oxalic acid - in the blood associated with Ca + + ions, forming insoluble compounds with oxalate, causing hypocalcemia and seizures, affects trophy of kidney • Inorganic acids - cause coagulation necrosis of tissues, superficial burn, slightly penetrate into the bloodstream and rarely lead to hemolysis, provide late gastrointestinal tract bleeding in the rejection of necrotic crust, often causing scar stricture • Alkalis - colliquative cause deep burns often result in perforation of the esophagus or stomach, rapidly penetrate the small intestine and affects it, while suffering less as a stomach (gastric neutralization of HCl)

  41. INTENSIVE THERAPY • Probe (only!) Ice water gastric lavage volume of 10.12 liters with the addition of magnesia, egg-protein mixture (protein 4.5 eggs) or cloth (25 grams of soap) contamination with acid or 2% milk solution acetic acid or alkali poisoning. 12 hours after poisoning washing the stomach - not shown. • Attention! Admixtures of blood in the washing fluid is not contraindications to gastric lavage • Analgesics (promedol, omnopon, tramal, no-foam, nubayin) and spasmolytics (buskopan, no-shpa, platifillin, halidor) in therapeutic doses or i\v i\m 3-4 times a day. • 3. Inside - maaloks, almagel, or fosfalugel sukralfat (1 g every 6 hours).

  42. 4. Inside of 20 ml mixture (200 ml 10% emulsion of sunflower oil or buck-thorn+ 2 g chloramphenicol + 2 g anesthesin) each hr. within 7-20 days. 5. Antishock therapy crystalloid and colloid (Refortan, Refortan plus stabizol, reopolyglukin) solutions under the control of central venous pressure, hourly diuresis to the stabilization of central hemodynamics. 6. Local gastric hypothermia 7. Prevention and treatment of hemolysis: Sodium hydrogen carbonate 1000-1500 mg / day i\v, drip to weak alkaline reaction of urine (with litmus paper), concentrated solutions of glucose, mannitol 2 g / kg + 40 mg lasix i\v every 2 hours. 8. In severe hemolysis - the operation of replacement blood volume in the bcc one.

  43. 9. Gastrocepin 10 mg 3 times daily i\v. 10. Fraxyparini 0,3 ml 1-2 times per day or thousand units of heparin 2,5-5. 4 times a day subcutaneously under control coagulograma and clotting time by Lee White. 11. Hemodialysis to include the path hemosorptional column. 12. When phenomena of acute respiratory failure - on transfer of mechanical ventilation, if necessary - tracheotomy. 13. Prednisolone 1 mg / kg for 7-10 days, then 15-20 mg for 2 months. (Prevention of scarring) Attention! When vinegar essence poisoning is strictly prohibited stomach wash sodium (risk of acute stomach expansion, strengthening of its gap and bleeding)

  44. POISONING by СО Source - the exhaust gases of internal combustion engines, products of incomplete combustion of fossil fuels as a component of natural gas. Toxic concentration of CO => 0,02 mg / l and in the ratio 1: 1000 with air transfers 50% Hp in carboxyhaemoglobin (NvSO) Pathogenesis: CO translates Hb in HbCO, which is unable to transport O2 and CO2. Besides blocking the enzyme cytochrome C-oxidase, ferrous and raises tissue respiration, and also connects with myoglobin and damages the myocardium. Thus, developing hemic and tissue hypoxia. CO affinity of Hp to 250 times greater than that of O2

  45. Clinic: distinguish 3 degree of poisoning Light - HbCO content in the blood by 30%. Headaches, dizziness, tachycardia, tachypnea, nausea, vomiting, totter Average - HbCO content in the blood of 30-50%. Short-term loss of consciousness, psycho-motor agitation, hallucinations, hypertension, squeezing headache, significant tachycardia, repeated vomiting, amnesia Heavy - HbCO content in blood> 50%. Persistent coma, abnormal reflexes, respiratory failure, unstable hemodynamics, hyperthermia, on ECG - Myocardial hypoxia, pink or carmine-red color of skin and upper half of body At a concentration NvSO 60% and> following the death

  46. INTENSIVE THERAPY 1. Take away the victim from the atmosphere that contains CO and thereby stop further get the gas into the body. 2. Inhalation of 100% oxygen via face mask with dense spontaneous breathing or through the endotracheal tube after intubation and transfer the victim to mechanical ventilation (with respiratory failure or lack of it) to reduce blood HbCO to 10%, and it usually is not less than 1,5-2 h, then inhalation of 40% oxygen-air mixture for 10-12 hours 3. At concentrations in the blood HbCO above 25-30% and neurological disorders recommended HBO at a pressure of 2.3 atm for 1.5 hours. 4 times a day (accelerated dissociation NvSO 10-15 times).

  47. 4. Antidote - Acyzol 6% solution of 1.0 ml / m, in severe cases - again in 1 hour. in the same dose 5. Prevention and treatment of edema of brain (diuretics, glycerol at 25.0 4-6 times a day inside, glucocorticosteroids). 6. Therapy hypoxia - tsytomak, cytochrome C in 4.8 ml 0.25% solution i\v drip. In severe cases the dose increased to 12-20 ml. 7. Fraxyparini 0.6 ml s/c 1 time per day, or heparin in 5000 D u/c every 4 hours 8. Magnesium Sulfate 25% of 10-20 ml per day i\v; instenon 2-4 ml i\v in 200 ml saline 2-3 times a day; Aktovegin in average daily dose to 800 mg d / in or / m for 5-7 days or until clinical recovery. 9. Removable or exchange blood transfusion of at least half of V of B.

  48. POISONING FOS Toxicity depends on the "lethal synthesis ", in which FOS converted in paraokson who have expressed toxic effects. Pathogenesis: Paraoksony have antiholinesterase action that leads to accumulation of endogenous ACh in the body and overexcited M-and H- holinoreactive structures M-holinoreactivesyndrome: miosis, tearing, salivation, blurred vision, diarrhea, laryngospazm, bronchospasm, bronhoreya, pouring sweat, arterial hypotension, bradycardia, urinary incontinence H-holinoreactivesyndrome: muscle cramps, convulsions, muscle weakness, paralysis (including respiratory muscles), arterial hypotension, disturbance of consciousness, coma

  49. CLINIC There are 3 clinical stages: Excitation - vertigo, dizziness, headache, decreased visual acuity, nausea, vomiting, abdominal pain, tenesmus, moderate miosis, hyperhidrosis, hipersalivation, hypertension Hyper kinesia and the spasm - psychomotor agitation, sopor, miois, absence of reaction of pupils, tonic seizures, mouth and nose with foam Palsy -a deep coma, absent of reflex, miosis, hyperhidrosis, bronchospasm, total paralysis of skeletal muscles (including respiratory), arterial hypertension, obstructive lung syndrome, severe combined hypoxia

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