SHARP EXOGEN POISONINGS

SHARP EXOGEN POISONINGS

SHARP EXOGEN POISONINGS

IFNMUDepartment of Anesthesiology and Intensive CareDepartment 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,

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

POISONIs 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

Classification of xenobiotics on toxicity:1. Strong or extremely toxic - DL 50 <50 mg/kg of weight of a body2. Highly toxic – DL 50 = 50-200 mg/kg of weight3. Average toxicity – DL 50 = 200мг-1 weight g/kg4. 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 die2. 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 attack3. In region Iv.-Frankovsk - annually hospitalise about 1000 poisoned

THE REASONS OF POISONINGS:1. Casual or household - all 2/3 cases2. 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 price3. 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 sniffing5. Use of toxic doses of preparations for interruptions of undesirable pregnancy

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 %)

Clinical Classification of POISONSClinical Classification of POISONSCardiac - 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

FACTORS THAT CAUSE DEGREE OF TOXICITY OF POISONS

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 biotransformation2. Elimination through kidneys, GIT, a skin, lungs

“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)

THE GENERAL PRINCIPLES OF TREATMENTSHARP EXOGENOUS POISONINGS:

1. A stop of receipt of toxic substance in an organism

2. Fast removing of poison from an organism3. 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

STRENGTHENING OF NATURAL WAYS OF DETOXICATION

STRENGTHENING OF NATURAL WAYS OF DETOXICATION

1. Forced alkali osmotic diurеsis:The purpose - to increase amount of daily urine, to reduce concentration toxic substances, to translate poisons in the dissociated formCarrying out technique: 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

2. STRENGTHENING OF DETOXICATION OF LIVER

1. Indirect electrochemical oxidation of blood - i/v sodium 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

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 accompanied by monitoring FHC,

CVP, AP

EXTRACORPORAL METHODS OF DETOXICATIONEXTRACORPORAL METHODS OF DETOXICATION

а – hemosorption; б – transfusion of the blood; в – МПТМОКВВ; г – plasmophoresis, д - plasmosorption

1 – cleaning of stomach ; 2 – ALV; 3 – peritoneal dialysis; 4 – oxygenation of the blood; 5 – hemo- and ultrafiltration; 6 – hemodialysis; 7-sorption

TIPES OF EXTRACORPORAL DETOXICATION


MEMBRANAL:

1. Hemodialysis

2. Ultrafiltration

3. Hemofiltration

4. Hemodiafiltration

5. Plasmafiltration

6. Peritoneal dialysis

THE GRAVITATIONAL

1. Plasmaphoresis:

а) decretive

б) apparatus

2. Leukocytophoresis

3. Thrombocytphoresis

4.Erythrocytoephoresis

CHEME OF HEMODIALISIS, HEMO- ULTRAFILTRATIONCHEME OF HEMODIALISIS, HEMO- ULTRAFILTRATION

SORPTION:

1. Hemosorption

2. Plasmasorption

3. Limfosrption

4. Xenoperfusion:

а) spleenperfusion

б) heparperfusion

5. Immunosorption

THE REPLACEABLE:

1. Replaceable blood transfusion

2. ALV

3. A lymph drainage

4. Hemooxygenation:

- Small line

- Highly line



CHEME OF HEMODIALISIS AND PLASMOFORESISCHEME OF HEMODIALISIS AND PLASMOFORESIS

ANTIDOTES THERAPYANTIDOTES 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, antidigoxini serum, antidigoxini - heart glycosides)

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”s glycosides)

POISONING Sleeping pills (barbiturates)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.

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

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.

ETHANOL POISONINGETHANOL POISONING

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 to СО2 and Н2О.

С2Н5ОН > СНЗСНО > СНЗСООН > СО2+ Н2О

Average rate of ethanol oxidation in the human body is 0.1 g / kg / hr.

Lethal dose 96% ethanol = 4.12 g / kgLethal concentrations in blood = 5-6 ‰

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

CLINICCLINIC

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 ‰)

INTENSIVE THERAPYINTENSIVE THERAPYTherapy of poisoning, which corresponds to the first and

second stages of severity:

1. 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.

2. 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.

3. 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.

4. Control of body temperature and maintaining thermal conditions

Therapy of poisoning of the third and fourth stages:

1. Release and maintenance-free patency of upper airways. Violation of spontaneous breathing - tracheal intubation and transfer of patients on mechanical ventilation

2. Introduction of permanent nazogastral probe and stomach lavage by sodium solution

3. Hemodynamic stabilization and maintenance of vehicles of vasoactive and cardiotonic, infusion solutions on the level of central venous pressure

4. 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,)

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!

METHANOL POISONINGMETHANOL 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

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 THERAPYINTENSIVE THERAPY1. If the patient in mind, can cause vomiting (root irritation of the tongue or posterior pharynx) or wash the stomach without probe by 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.

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.

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.

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

POISONING ethylene glycol (EG)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.

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 THERAPYINTENSIVE 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.

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.

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

POISONING CORROSIVE S PoisonPOISONING CORROSIVE S Poison

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

2. Resorpting action - hemolysis, changes in ABB (metabolic acidosis or alkalosis) nephrosis-nephritis, ARI, dystrophic changes and necrosis of liver slices, AHI, hemic hypoxia,

3. 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

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%)

FEATURES OF POISONING DIFFERENT CORROSIVE Poison

FEATURES OF POISONING DIFFERENT CORROSIVE Poison

1. Organic acids - very deep penetration into the tissue, a burn more like a colliquative, much resorpting and hemolytic action

2. Oxalic acid - in the blood associated with Ca + + ions, forming insoluble compounds with oxalate, causing hypocalcemia and seizures, affects trophy of kidney

3. 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

4. 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)

INTENSIVE THERAPYINTENSIVE THERAPY1. 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

2. 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. 3. Inside - maaloks, almagel, or fosfalugel sukralfat (1 g every 6 hours).

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.

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)

POISONING by СОPOISONING 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

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

INTENSIVE THERAPYINTENSIVE THERAPY1. 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).

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.

POISONING FOSPOISONING FOSToxicity 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-holinoreactive syndrome: miosis, tearing, salivation, blurred vision, diarrhea, laryngospazm, bronchospasm, bronhoreya, pouring sweat, arterial hypotension, bradycardia, urinary incontinence

H-holinoreactive syndrome: muscle cramps, convulsions, muscle weakness, paralysis (including respiratory muscles), arterial hypotension, disturbance of consciousness, coma

CLINICCLINIC

There are 3 clinical stages:

1. Excitation - vertigo, dizziness, headache, decreased visual acuity, nausea, vomiting, abdominal pain, tenesmus, moderate miosis, hyperhidrosis, hipersalivation, hypertension

2. Hyper kinesia and the spasm - psychomotor agitation, sopor, miois, absence of reaction of pupils, tonic seizures, mouth and nose with foam

3. 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


1. Hospitalization of victims in ITD or detoxification.

2. Gastric lavage (repeated every 4-6 hours during the day) 5% sodium hydrogen carbonate and activated charcoal following the introduction of the stomach and enterosorbents saline laxatives. Strictly prohibited to enter any fats, milk, butter.

3. When poisoning by contact - remove contaminated clothing, wipe the affected area 10-15% solution of ammonia, then wash the entire body with soap and warm water and sodium hydrogen carbonates within 15 minutes.

4. When ingested FOS in the eyes - rinse 1-2% solution of sodium hydrogen carbonate followed by instilling novocaine and 1% atropine.

6. Reactyvator cholinesterase highest performing prescribed in the first 72 hours of poisoning:

Dipiroksym 150 - 300 mg (1-2 ml 15% solution) i\m or i\v, but not more than 1.0 g per day;

At the same time impose on izonitrozyn 800-1200 mg (2-3 ml 40% solution) i\m or i\v, but not more than 4.0 grams per day.

7. Atropinization should complement the introduction of central M-holinolityc (amizil, metamizil), the central M-and N-holinolityc (aprofen, tsyklodol) and ganglionic blocker (benzoheksoniy, pentamin, imehin) in conventional doses. The latest cause hypotension, and they are not appointed in terms of low blood pressure.

5. Atropinization immediate to disappearance of symptoms of muscarinic action of FOS (the appearance of dry mouth, midriasis, warming and dry skin, mild tachycardia). The initial dose of atropine sulfate in benign or 1-2 mg i\m, i\v, with the average - 2-4 mg i\v when heavy - 5-10 mg i\v. Repeated doses and intervals of input set individually depending on the appearance of signs atropine action and their stability. Total dose of atropine sulfate in severe forms of poisoning can reach 100-150 mg per day and total time of its introduction - 3-4 days. Atropine action phenomena at medium to severe poisoning can achieve and maintain a constant infusion of atropine sulfate i\v 5% glucose solution (20 mg of atropine in 400 ml glucose), the frequency drops by adjusting the speed and effect of its introduction.

8. Oxygen, at expressed respiratory failure - ventilation.

9. If a cramps and psycho-motor excitation is removed antidote, use of benzodiazepines (seduksen, sibazon, diazepam, relanium, valium) 5-10 mg, 50-100 mg tranksen, thiopental sodium 2-3 mg / kg of sodium to 2 oxybutyrate -4 g i\v.

10. Forced diuresis, peritoneal dialysis, hemosorbtion, hemodialysis.

11. In cardiac arrest, before the introduction of adrenaline in the central vein or intracardiac, injected 300 mg dipiroksymu and dose of atropine sulfate increased to 10 mg.

12. Symptomatic treatment and prevention of infectious complications.

POISONING MUSHROOMSPOISONING MUSHROOMS

On the pathogenesis and toxicity of fungi are divided into:

1. Gastro-enteral action - gray and fake brick-pidpenok

2. Neuro-vegetative action - fly agaric

3. Hepato-nephritic action - a pale toadstool...

Жовта Зелена Біла

When using mushrooms may experience the following pathological conditions:

• Fatal poisoning amanital mushrooms - pale toadstool, some fly agaric

• Poisoning conditionally edible mushrooms that grow in areas of pollution and toxic substances accumulate

• Poisoning by mushrooms that were not enough cooking and kept toxins

• Food toxic that develop as a result of using mushrooms infected with pathogenic microflora

• Exacerbation of chronic digestive diseases.

POISONING MUSHROOMS Gastro-entero trophic ACTIONPOISONING MUSHROOMS Gastro-entero trophic ACTION

Pathogenesis: toxins are volatile chemicals with ketone groups, anhydrides of some acids or helvelov acid, which have sharply irritating effect on mucous membrane of the alimentary canal like some laxatives drugs

Clinic: incubation period is short and lasts for 2-3 hours. And then there are nausea, vomiting irresistible, abdominal pain, painful tenesmus, severe diarrhea. Quickly developing breach of ABB, which lead to hemodynamics (arterial hypotension, tachycardia, disturbances of microcirculation, metabolic acidosis). Helvelov acid can cause hemolysis, jaundice and ARI

POISONING MUSHROOMS neuro-vegeto trophic ACTIONPOISONING MUSHROOMS neuro-vegeto trophic ACTION

Depending on the type of toxins distinguish atropine or cholinergic syndrome

Atropine syndrome The toxins tiger toadstool and pantherina fly agaric, as

mustsymol, ibotenova acid and mushroom atropine, which excite the holinoreactive system mainly brain.

Clinic: develops within 2 hours. after taking mushrooms is characterized by a slight gastroenteritis, psycho-motor excitation, confusion, visual hallucinations, dry mucous membranes, and in severe cases - coma and convulsions. Symptoms last 12-24 hours., Mortality = 2%

Cholinergic (muscarin-like) syndromeCholinergic (muscarin-like) syndrome

Pathogenesis: toxins - alkaloids muscarin and muscaridin that have neurotoxic effect associated with excitation of the central and peripheral M-holinoreactive systems

Clinic: incubation = 2-3 hours. Then there hypersalivation, nausea, vomiting, profuse perspiration, bronhoreya, bronhiolospasm, pupil constriction, spasm of accommodation, myopia, bradycardia, arterial hypotension, spastic abdominal pain diarrhea, and in severe cases - collapse, pulmonary edema and hypoxia.

In 8-12 hr. symptoms gradually disappear.

Mortality rate = 4%

POISONING Pale ToadstoolPOISONING Pale ToadstoolPathogenesis: poison pale toadstool (polypeptides) are

divided into 2 groups:

• Termolabil that destroyed at 70°C - Falini and amanitohemolizyn

• Thermostable, are not destroyed during processing:

a) fast (6-12 hours). – falotoxin (faloyin, faloyidyn, falotsydyn, falizyn)

b) slow - amanitotoxin (α-, β-, γ-amanityny, amanin, amanulin)

Amanitotoxin in 20 times toxic from falotoxin

Lethal dose of β-amanityn = 0,1 mg / kg - for the child = 1 / 3 as an adult = 1 mushroom

Mortality = 60-70%, and the children = 90%. Only 1 year in Ukraine dies> 100 people.

1. Falotoksyny damage lipoprotein complexes of hepatocyte membrane and intracellular structures (mitochondria, lysosomes, endoplasmic mesh), inhibit oxidative phosphorylation and glycogen synthesis in them

2. Amanitotoksyny inhibit the formation of RNA and DNA, leading to cell autolysis

Clinic: in the course of intoxication distinguish 4 stages:

• Silent - lasts 12.6 hours., No symptoms

• Gastro-intestinal - lasts 2-3 days, weakness, abdominal pain, diarrhea with an admixture of blood, dehydration, hemodynamic disorders, metabolic acidosis, hallucinations

• Parenchymal - after a short-term stabilization of the liver increases, increasing jaundice and other symptoms AHI

• Final - 1-2 weeks following vyzdorovlennya or developing hepatargia, coma and death


When poisoning by mushrooms of the gastro-entero trophic action:

• Gastric lavage, enterosorbents

• Saling Laxatives, repeated cleansing enemas (regardless of whether diarrhea).

• Disintoxication infusion therapy (10-15 ml / kg body weight) glucose solution, Ringer-Locke and other balanced salt solution under the control of hemodynamic parameters (BP)

• Antispasmodic therapy (buskopan, no-shpa forte, platifillin).

• Gastrocepin 10 mg 3 times daily i\m. Situational therapy

When poisoning by mushrooms neuro-vegeto trophic : • When atropin syndrome

1. Gastric lavage, enterosorbents, salt Laxatives, repeated cleansing enemas (regardless of whether diarrhea).

2. Against the introduction of infusion therapy antidotes atropine (proserin 0,05% - 1 ml i/ v or u\c. to the disappearance of symptoms of poisoning)

3. Symptomatic treatment • When cholinergic syndrome

1. Gastric lavage, enterosorbents saling Laxatives, repeated cleansing enemas (regardless of whether diarrhea).

2. Against a background infusion therapy - atropine sulfate 0.1% 1-2 ml in the disappearance of symptoms of poisoning . Symptomatic treatment

When poisoning by mushrooms of hepatic- nephrite trophic action:

1. Gastric lavage, enterosorbents, salt Laxatives, repeated cleansing enemas (regardless of whether diarrhea).

2. Introduction antidote - benzylpenicillin sodium 250 mg / kg / day i\v during the first 3 days. From 3 to 10 days - the average daily dose

3. Early repeated plasmapheresis sessions, with the growth phenomena of hepatic-renal insufficiency and for detoxification - peritoneal dialysis, hemodialysis

4. Hepatoprotectors: berlition 600-900 mg Chophitol 5-10 ml 2-3 times, silibene 100 ml 3 times essentiale 10-20 ml ornitsetyl 1 g / kg, reamberine 400-800 ml, 200-250 mg lehalon, lactulose 45-60 ml Glutargin 5-10 ml / day.

5. Hydrocortisone 1 g / day i\v or other glucocorticosteroids in equivalent doses.

6. Inhibitors of proteolytic enzymes (kontrikal, trasilol, hordoks, antahozan, pantripin) in conventional doses.

Recanalization umbilical vein and catheterization portal vein for medication, intraportal infusion therapy (albumin, glucose, hepabene, hepasteryl, Glutargin), arterio-portal shunt blood transmembrane oxygenation portal vein.

Lipoic acid to 100-20 mg / d i/v or in lipamid 500-800 mg / day

Antagonists of proteins that carry the poison - chloramphenicol 4 g / day inside

POISONING chlorinated hydrocarbonsPOISONING chlorinated hydrocarbons

Most often found poisoned by organic solvents - dyhloretanom (DHE - С2Н4СІ2) and carbon tetrachloride (CTCH - ССІ4)

Pathogenesis: a volatile oil soluble substances, and may enter the body through the gastrointestinal tract, lungs and intact skin and mucous membranes. In liver subjected to metabolism involving cytochrome P-450 type of "lethal synthesis" with the formation of free radicals (ССІ3+, СІ¯), chloretanol, salt and monochloroacetic acid. Last prodused denaturation of cellular proteins, enzymes, metabolic cycle block, destroying cell membranes, activating LPO reaction.

Lethal dose = 20 - 40 ml

Mortality = 30-55%, and the development of shock = 90%

Clinic: in clinical course five syndromes are distinguished:

1. Neuropsychiatric - dizziness, intoxication, euphoria, agitation, seizures, hallucinations, consciousness up to coma (toxic encephalopathy)

2. Respiratory disorder - hypersalivation, hyperbronhoreya, aspiration of gastric contents with the development of aspiration-obstructive syndrome

3. Dysfunction C-V-S - tachycardia, hypotension, decreased bcc, increased permeability of blood vessels, circulatory hypoxia

4. Kidney-liver - increased and morbidity of liver, reducing its functional capacity, jaundice, decreased daily diuresis until anuria, increase of uremic intoxication and disorder ABB

5. Gastrointestinal - Clinic of acute gastro-enteritis

INTENSIVE THERAPYINTENSIVE THERAPY1. Probe gastric lavage 8.10 liters of warm water every 2 hours.

2. Provocative diarrhea using oil laxatives - petrolatum, glycerol or paraffin oil 150-200 ml probe, enterosorbents (smekta, silard, polisorb 9.12 g / day).

3. Hemosorption in first 3 hours after poisoning 2,5-3 bcc volume, lymphatic drainage.

4. Hemodialysis in the first 6 hours after the poisoning, duration 18-20 hours. Best combined with hemodialysis was on first in one manipulation.

5. Removable transfusion of at least 0,5 V of CB.

6. Osmotic diuresis induced alkaline.

7. Vitamin "E" 10% - 2 ml i\m 6 times a day.

8. Unitiol 5% - 5 ml 4 times a day i\v.

9. Acetylcysteine 5% solution 100 ml initially and then every subsequent 3 hours - 50 ml dovenno to 500 mg / kg in the first day and 300 mg / kg in the second period.

10. Tetacinum Calcium 10% - 40-60 ml per 500 ml 5% glucose i\v, drip.

11. Sodium hydrogen 4% - 1,5-2 l / day i\v, drip.

12. Treatment of shock (Refortan infusion, Refortan plus a dose of 20 ml / kg, stabizolu, perftoran, sorbilaktu, reosorbilact, crystalloid solutions).

13. Prednisolone 12-15 mg / kg / day i\v.

14. Fraxyparini 0,3 ml subcutaneously 1 time per day or in the abdomen around the navel area.

15. Protease inhibitors (kontrikal 50 000 units. i\v, drip 3-4 times a day).

16. Hepatoprotectors:

Berlition (α-lipoic acid) - 600 mg (2 ampoules) dissolved in 250 ml 0.9% sodium chloride, enter i\v, drip in doses of 600-900 mg per day.

Glutargin 500-1000 ml per day i\v, drip. In the development of a coma - 1000-1500 ml per day to improve.

Essentiale 5-10 ml 4 i\v times a day on autologous blood donation.

Silibene 100 ml 2-3 times a day i\v, drip.

Ornicetyl 1h/kh/d, i\v, drip in the development of hepatic coma.

Heptral 02.01 bottle a day i\m or i\v slowly for 2-3 weeks, then maintenance therapy of 2-4 tablets per day inside.

Glutargin - 40% - 5-10 ml per 400 ml 5% glucose solution i/v 1-2 times / day

Hepadyf - 1-2 vial. 200 ml 5% glucose i/v or 6 in the cap.

POISONING by METHEMOGLOBIN production substances (HbCN)

POISONING by METHEMOGLOBIN production substances (HbCN)

This group of substances which have in their molecule, nitro or amino group: aniline, benzene, toluene, toluyidyn, nitrates,

nitrites, nitroglycerin, sulfanilamides

Pathogenesis: Hp becomes HbCN (metNB), which loses the ability to transport O2, thus developing hemic hypoxia

Lethal dose = 1 g or NbCN content> 60%

Clinic: a) light level - HbCN = 15-20% - cyanosis of skin and mucous membranes, headache, shortness of breath, stun

b) average rank - HbCN = 20-40% - severe headache, cyanosis with chocolate shade, sopor state

c) severe degree - HbCN> 40% - pronounced cyanosis, dyspnea, hypotension, vomiting, convulsions, coma...

INTENSIVE THERAPYINTENSIVE THERAPY1. Probe washing the stomach with warm water and

adding salt at the end of manipulation is injected into the stomach 150 ml petrolatum oil, charcoal or other enterosorbents. When percutaneous poisoning should wash the affected area with water at room temperature with soap, and then process the 2-3% solution of acetic acid, diluted vinegar or potassium permanganate solution 1:1000.

2. Early and continuous oxygen therapy, if necessary - ventilation.

3. Methylene blue 1% - i/v drip in 5% glucose solution at a dose of 0,1-0,15 mg / kg body weight if necessary - again, the disappearance of cyanosis (total daily dose may reach 7.5 mg / kg) . Instead, the drug can be given hromosmon 20-30 ml / day

4. Ascorbic acid 5% dose of 1 - 1,5 g per day

5. Hyperbaric oxygen therapy using 1-1,5 ATM for 60 min. 2 times a day.

6. Osmotic alkaline forced diuresis, hemodialysis in the first 6 hours after intoxication, peritoneal dialysis.

7. Exchange blood transfusion (not less than 50% of BCC) at metgemoglobinaemia more than 30%.

8. Instenon 2-4 ml i\v, drip of 200 ml 5% glucose solution or isotonic sodium chloride 2-3 times a day for 5-7 days or until clinical recovery.

9. Aktovegin in average daily dose to 800 mg or i\v i\m.

10. Symptomatic treatment.

POISONING OpiatesPOISONING OpiatesCodeine, morphine, opium, kodterpin, omnopon,

promedol, heroin, pentazocine (fortral, leksyr), etc.

Lethal dose => 200 mg

Pathogenesis: acting on the central nervous system via opioid receptors, causing inhibition of pain sensitivity talamichnyh centers, break connection in B excite the vagus nerve centers and the gag, delaying vascular and respiratory motor centers trunk of B. With prolonged use causes phenomena of drug addiction.

Clinic: drowsiness, skin hyperemia, tinnitus, gradual loss of consciousness, miosis, shallow breathing, Cheyne Stokes breathing, bradycardia, hypotension, vomiting, cramping abdominal pain, pulmonary edema


1. In a coma to check patency of upper airway, breathing independently evaluate the effectiveness and degree of hypoxia. If necessary - tracheal intubation, artificial ventilation, toilet-tracheal bronchial tree, adrenomymetic circulatory support.

2. Repeated washing of the stomach in ways dear opioid hit in the body (in unconscience patients as usual only after prior intubation) solution of potassium permanganate 1:1000 or 0.2% solution of tannin. After rinsing the stomach injected 50 ml of KMnO4, enterosorbents salt and relaxed.

3. Naloxone hydrochloride (narkanti, intrenon) at a dose of 0,8-2,0 mg i\v. When inefficiency dose can be increased up to 10,0 mg i\v. The duration of these drugs is 1-2 hours, significantly less than morphine, so there is a need to repeat the dose of naloxone or long i\v its infusion of 5% glucose solution at the rate of 0.8 mg per hour. Naloxone in the absence of the vein can be entered under the tongue and endotracheal

4. Naltrexone - a drug similar to naloxone, but has a duration of 24-48 hours. He is appointed by 50.0 mg per day inside (or probe). Most often used to treat addiction to opiates.

5. Forced diuresis, peritoneal dialysis. Situational therapy.

POISONING CLONIDINEPOISONING CLONIDINE

Clonidin (hemiton, katapresan) refers to a central presynapsis α2-adrenostimulators, reduces AP and used to treat hypertension and also to reduce intraocular pressure in ophthalmology (1% solution). Significantly potentiates narcotic effect of alcohol and recently widely used for criminogenic purpose (especially the 1% region, which has no taste, no smell, no color)

Clinic: arterial hypotension, bradycardia, arrhythmia, colaps, dry mucous membranes, sweating, headache, consciousness even to fainting, adynamia retrograde amnesia, gastro-intestinal disorders

1. Permanent cardiomonitoring cardiac rhythm and conduction! (Risk of fatal arrhythmias!)

2. Itrop - 0,5 mg (1 ml) or atropine sulfate in 0,5-1,0 ml i\v, again under the control of heart rate.

3. Alupent 0,05% - 1-2 ml i\v, drip of isotonic sodium chloride solution, under the control of heart rate, again, proceed to normalize the rhythm and conduction or establishing temporary transvenous electro cardio stimulation.

4. Metoclopramide (tserukal, raglan) – i\v bolus dose of 0.5 mg / kg, then 0.25 mg / kg i\v drip in 400 ml 5% glucose solution at a speed of 2 ml / min. Average daily dose - 18-20 mg.

5. In severe poisoning with caution! α-blocker (fentolamin) and naloxone under constant control of AT and heart rate

6. Hemosorbtion, ultrafiltration.

SNAKE BITESNAKE BITE

In Ukraine there are steppe and forest adder, bites are poisonous.

Pathogenesis: in snakebite poison gets into the wound - viperotoksyn containing a mixture of bar - the enzymes (phospholipase, proteinase, Hyaluronidase, etc.), proteins, polypeptides hemolizyny, cytotoxin, coagulants.

They exhibit toxic effects due to: 1. Cytolysis and tissue necrolysis

2. Erythrocyte hemolysis

3. Increased permeability of vascular wall

4. Dismissal of the cascade of cytokines (histamine, bradykinin, inflammatory proteins, NO, serotonin

5. Common toxicactions - violations of hemodynamic, respiratory, liver and kidneys, etc.

b) the symptoms (especially when the poison gets into the bloodstream directly) - dizziness, weakness, nausea, sweating, shortness of breath, hypotension, syncope, collapse, sometimes seizures, hemolysis, DIC-syndrome

In the clinical picture is of great importance layers psycho-emotional stress, even to the manifestations

of shock

Clinic:

a) Local symptoms - pain, swelling, hemorrhage, venous thrombosis, bladder with hemorrhagic content, areas of necrosis, lymphadenitis phenomenon. Edema pronounced - the ending may deposited to 2-3 liters of fluid;

INTENSIVE THERAPYINTENSIVE THERAPY1. Limb immobilization

(splint, lonheta) because of faster movements poison spread by lymphatic routes

2. No later than within 10 minutes. absorption poison from the wound through the mouth if no damage to the mucous

3. You can not make additional cuts in the site of the bite, enter any drugs, impose binder (except when cobra bite)

4. Process the morning with alcohol or iodine tincture and apply a clean bandage free

5. Dates patient hot drink and transport it to the hospital in supine position

6. Introduction antisnake specific serum (anti-gurza) at Bezredko: first 1 ml diluted 1:10, then 1 ml of undiluted, and full dose - at a light form of 10-20 ml, with an average of 30-40 ml and 70 with severe -80 ml p / mizhlopatochnu school in the area or V / m. Only in very severe intoxication serum can enter slow i / v (10 ml = 500 AO)

7. 250-500 mg hydrocortisone or prednisolone in equivalent doses

8. Heparin for 5 thousand units. every 6 hours. under the control clotting time

9. Preventing tetanus (toxoid)

10.Antibiotic

11.Situational symptomatic therapy

Arthropod bite Arthropod bite Insect bites

By poisonous insects include bees, Hornets, wasps and bumblebees.

In the U.S. the number of deaths from insect bites 3 times more than from snake bites.

Stinging nettle insects apparatus located in the tail section. When they bite, they leave the body stiletto (sting)

with poison, and most within 2-4 hours. perish. The composition of venom include: apitoksyn, mellityn, phospholipase, hyaluronidase, kinins, histamine, apamin, ACh.

An insect bite in most cases cause allergic reactions, 5 bites - toxic, and> 100 - lethal.

Pathogenesis: single bite at developing a typical immediate type anaphylactic reactions due to antigen-antibody interaction with the release of a number of endogenous cytokines.

When multiple bite venom shows neurotoxic effect, acting as H-holinolityc, and hence ganglioplegic, central sedative and mioplegia effects. Death may occur as a result of acute disorders of circulation, coma and paralysis.

In addition, insect venom have a direct effect on neurons cytolitic efect and devastating result of activation of LPO

Clinic: Clinic with milder forms is fully consistent with allergic reactions from mild intensity to anaphylactic shock. Especially dangerous insect bites of mucosa BP that may end mechanical asphyxia.

Commontoxic manifestations characterized by tachycardia, arterial hypotension, shortness of breath, unconscious, muscle weakness, paralysis, and when bees sting more and intravascular hemolysis.

INTENSIVE THERAPY

1.Tweezers or fingernails to remove stilet (sting) from the bite

2.Place a bite to process alcohol, hydrogen peroxide, tincture of iodine and brilliant green or apply cold

INTENSIVE THERAPY

1.Tweezers or fingernails to remove stilet (sting) from the bite

2.Place a bite to process alcohol, hydrogen peroxide, tincture of iodine and brilliant green or apply cold

3. When bitten of mucosal BP immediate entered hormons and be ready to tracheal intubation, konikotomiya, traheostomiya.

4. All activities, as in anaphylactic reaction or anaphylactic shock (epinephrine, ß2-stimulants xantyni derivatives, ACS, antihistamines mullion, proteolytic enzyme inhibitors, infusion therapy, dopamine, dobutreks etc.)

Spider bite

Spider Kara-Kurt , scorpion, tarantula are toxic. Places to stay - mostly Central Asia, but they found

in the southern regions of Ukraine and Crimea

Poison Kara-Kurt is 15 times stronger than cobra but fatal bites rarely, because smaller dose

Scorpion

Phalanga

TarantulKara-Kurt

Spiders produce venom - toksoalbuminy.

Pathogenesis: It refers to neurotoxins and causes changes in membrane potential, sodium channels, mizhneyronalnyh synapses by releasing neurotransmitters (ACh, dopamine, etc.). This leads to dysfunctions of CNS and VNS

Clinic: local changes - pain, swelling, lymphangoitis.

General changes - toxic syndrome primarily involving the central nervous system - muscle pain, paresthesia, muscle weakness in the extremities and abdominal muscle tension, consciousness, hallucinations, manic depression, increased blood pressure, hyperthermia.

INTENSIVE THERAPY1.Place bite treated with antiseptic (alcohol)

2.Immobilization, cold, antipsychotics, analgesics

3.Calcium chloride (gluconate) Magnesium sulfate d / in

4.In loving bite Pauk - antykara-specific serum Kurtova 30-70 ml s/c, and in severe cases - i/v on Bezredko. Before that - hormons.

5.Situational symptomatic therapy

SHARP EXOGEN POISONINGS

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