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,
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
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
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
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 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
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
“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 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
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 form
Carrying 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 (Lornitini- 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 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 – hemoand ultra- filtration; 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- ULTRAFILTRATION
TIPES OF EXTRACORPORAL
DETOXICATION
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 PLASMOFORESIS
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, 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)
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 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 to СО2 and Н2О.
С2Н5ОН > СНЗСНО > СНЗСООН > СО2+ Н2О
Average rate of ethanol oxidation in the human body
is 0.1 g / kg / hr.
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
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 100200 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 THERAPY
1.
2.
3.
4.
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 5001000 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
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 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) 57 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 THERAPY
1. 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 4metylpirazol 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)
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 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.
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
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
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 THERAPY
1. 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 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 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).
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 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-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
CLINIC
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
INTENSIVE THERAPY
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 Mand 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 MUSHROOMS
On the pathogenesis and toxicity of fungi are divided into:
1. Gastro-enteral action - gray and fake brickpidpenok
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 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 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) syndrome
Pathogenesis: toxins - alkaloids muscarin and
muscaridin that have neurotoxic effect associated
with excitation of the central and peripheral Mholinoreactive 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 Toadstool
Pathogenesis: 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
INTENSIVE THERAPY
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
platifillin).
•
Gastrocepin 10 mg 3 times daily i\m. Situational therapy
therapy
(buskopan,
no-shpa
forte,
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, 200250 mg lehalon, lactulose 45-60 ml Glutargin 5-10 ml
/ day.
5.
Hydrocortisone 1 g / day i\v
glucocorticosteroids in equivalent doses.
or
other
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
chloramphenicol 4 g / day inside
the
poison
-
POISONING 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 THERAPY
1.
2.
3.
4.
Probe gastric lavage 8.10 liters of warm water every 2 hours.
Provocative diarrhea using oil laxatives - petrolatum,
glycerol or paraffin oil 150-200 ml probe, enterosorbents
(smekta, silard, polisorb 9.12 g / day).
Hemosorption in first 3 hours after poisoning 2,5-3 bcc
volume, lymphatic drainage.
5.
Hemodialysis in the first 6 hours after the poisoning,
duration 18-20 hours. Best combined with hemodialysis was
on first in one manipulation.
Removable transfusion of at least 0,5 V of CB.
6.
7.
Osmotic diuresis induced alkaline.
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 12 times / day
Hepadyf - 1-2 vial. 200 ml 5% glucose i/v or 6 in the cap.
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 THERAPY
1. 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 Opiates
Codeine, 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
INTENSIVE THERAPY
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,
therapy.
peritoneal
dialysis.
Situational
POISONING 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 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.
2.
3.
4.
Cytolysis and tissue necrolysis
Erythrocyte hemolysis
Increased permeability of vascular wall
Dismissal of the cascade of cytokines (histamine,
bradykinin, inflammatory proteins, NO, serotonin
5. Common toxicactions - violations of hemodynamic,
respiratory, liver and kidneys, etc.
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;
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
INTENSIVE THERAPY
1. 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
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
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
Tarantul
Phalanga
Scorpion
Kara-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 THERAPY
1.
2.
3.
4.
Place bite treated with antiseptic (alcohol)
Immobilization, cold, antipsychotics, analgesics
Calcium chloride (gluconate) Magnesium sulfate d / in
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