SHARP EXOGEN POISONINGS

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SHARP EXOGEN POISONINGS
 
 
IFNMU Department of Anesthesiology and Intensive
Care
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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
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Classification of xenobiotics on toxicity 1.
Strong or extremely toxic - DL 50 lt50 mg/kg
of weight of a body 2. Highly toxic DL 50
50-200 mg/kg of weight 3. Average toxicity DL
50 200??-1 weight g/kg 4. Low toxic DL 50gt 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
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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
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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 )
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Clinical Classification of POISONS
Cardiac - glycoside, quinine, adrenoceptor
antagonist, ??lcium 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,
met??, ????) - 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
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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
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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. Toxic?genic - 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)
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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
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(No Transcript)
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STRENGTHENING OF NATURAL WAYS OF DETOXICATION
1. Forced alkali osmotic diur?sis 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
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2. STRENGTHENING OF DETOXICATION OF LIVER 1.
Indirect electrochemical oxidation of blood - i/v
sodium hypochloride for replacement of cytochrome
?-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 ??????, ???, enteral
introductions of oxygen, oxygen skins
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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 (???2 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
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EXTRACORPORAL METHODS OF DETOXICATION
1 cleaning of stomach 2 ALV 3 peritoneal
dialysis 4 oxygenation of the blood 5 hemo-
and ultra- filtration 6 hemodialysis
7-sorption
? hemosorption ? transfusion of the blood ?
???????? ? plasmophoresis, ? -
plasmosorption
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TIPES OF EXTRACORPORAL DETOXICATION
MEMBRANAL 1. Hemodialysis 2. Ultrafiltration 3. Hemofiltration 4. Hemodiafiltration 5. Plasmafiltration 6. Peritoneal dialysis THE GRAVITATIONAL 1. Plasmaphoresis ?) decretive ?) apparatus 2. Leukocytophoresis 3. Thrombocytphoresis 4.Erythrocytoephoresis
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CHEME OF HEMODIALISIS, HEMO- ULTRAFILTRATION

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TIPES OF EXTRACORPORAL DETOXICATION
SORPTION 1. Hemosorption 2. Plasmasorption 3. Limfosrption 4. Xenoperfusion ?) spleenperfusion ?) heparperfusion 5. Immunosorption THE REPLACEABLE 1. Replaceable blood transfusion 2. ALV 3. A lymph drainage 4. Hemooxygenation - Small line - Highly line
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CHEME OF HEMODIALISIS AND PLASMOFORESIS
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ANTIDOTES THERAPY

• Classification of antidotes
  (The international program
  from chemical safety ????, 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)

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3. Biochemical - change a metabolism of
poisons or a direction of biochemical reactions
in which they take part (lipoid acid - amanitini,
??????????? ????? - ?????, 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 hearts glycosides)
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ANTIDOTES
Poisons ANTIDOTES
Alcaloids ? permanganate. It is used in the form of a water solution 110000 for stomach washing. The solution prepares by dissolution 1 g (on a knife tip) in 100 ml of water and it is possible to 10 l. At solution preparation it is necessary to observe of carefulness of dissolution not to burn a mucous membrane crystals. Milk use in cultivation by water 11 for washing of a stomach or it is entered into a probe of 1-1,5 bottles of milk, and washing is then spent. Fiber of 10 eggs allows to drink or enter through a probe into a stomach, then necessarily spend stomach washing.
Amytriptillini Fyzostigmini (eserini, proserini) i\v slowly 0,5 - 2 mg. If it is needed, repeat two time in same doses with intervals 20 min.
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Atropine Fyzostigmini (look. Amytriptillini).
Bromides Na Cl 1 tea spoon in 1000 ml water for stomach washing, and after 100 ml of this solution per os every hours, till that time when all sings of poisoning disappear.
????????? oil Parafine butter per os 200300 ml before and after 100200 ml stomach washing.
????????? ????? Ethyl spirit per os 100 ml 30 solution every 4 hours during 13 dais or i\v in beginning 0,6 g/kg on 10 glucose, and after - 110,0 mg/kg/hours.
????????? ???? ???????? ????? (look poisoning by ????????? ???????)
Morphine and his group Naloxoni (narkanti, intrenoni) 1 mg naloxoni on 34 mg morphine or 0,42,0 mg i/v (i/m).
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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.
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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
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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.
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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 ??2 and ?2?.
?2?5?? gt ?????? gt ??????? gt ??2 ?2? Average
rate of ethanol oxidation in the human body is
0.1 g / kg / hr.
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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
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CLINIC
The first stage (euphoria) - following the
reception of 20-50 ml of ethanol concentration
and the last in the blood is 0,5-1,0 g / l
(0,5-1,0 )
The second stage (intoxication) - occurs after
administration of 50-100 ml of alcohol, and
poisons in the blood concentration of 1,0-2,0 g /
l (1,0-2,0 )
The third stage (drug) - occurs after consuming
100-200 ml of alcohol and its concentration in
blood is 2,0-3,0 g / l (2,0-3,0 )
The fourth stage (or comatose-asphyxia) - occurs
after receiving 200-400 ml of ethanol and its
concentration in the blood exceeds 3.0 g / l
(3,0-5,0 )
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INTENSIVE THERAPY

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

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

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

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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.
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Hemodialysis in 60 times speed up the
withdrawal of methanol in comparison with the
natural elimination Indications for urgent
hemodialysis Receptiongt 30 ml methanol The
concentration of methanol in blood 50-100
mg Severe acidosis (pH lt7,2, SB lt20 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
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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.
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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.
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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.
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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
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1. Resorpting action - hemolysis, changes in ABB
   (metabolic acidosis or alkalosis)
   nephrosis-nephritis, ARI, dystrophic changes and
   necrosis of liver slices, AHI, hemic hypoxia,
2. 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
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• 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 Hpgt 10 g / L (gt 1 g)

The content of free Hp 10 g / l 30 hemolysis
of red blood cells, and it appears in the urine
if the bloodgt 1 g / l (100 mg)
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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)

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INTENSIVE THERAPY

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

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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.
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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)
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POISONING by ??
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 gt 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
48
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 bloodgt 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 andgt following the death
49
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).
50
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.
51
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
52
CLINIC

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

53
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.

54

• 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.

55

1. 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.

56
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.
57
POISONING MUSHROOMS

• On the pathogenesis and toxicity of fungi are
  divided into
• Gastro-enteral action - gray and fake
  brick-pidpenok
• Neuro-vegetative action - fly agaric
• Hepato-nephritic action - a pale toadstool...

?????
??????
????
58

• 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.

59
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
60
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
61
Cholinergic (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
62
POISONING Pale Toadstool

• Pathogenesis poison pale toadstool
  (polypeptides) are divided into 2 groups
• Termolabil that destroyed at 70C - Falini and
  amanitohemolizyn
• Thermostable, are not destroyed during
  processing
• a) fast (6-12 hours). falotoxin (faloyin,
  faloyidyn, falotsydyn, falizyn)
• b) slow - amanitotoxin (a-, ß-, ?-amanityny,
  amanin, amanulin)

Amanitotoxin in 20 times toxic from
falotoxin Lethal dose of ß-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 diesgt 100 people.
63

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

64
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 therapy (buskopan, no-shpa forte,
  platifillin).
• Gastrocepin 10 mg 3 times daily i\m. Situational
  therapy

65

• When poisoning by mushrooms neuro-vegeto trophic
  
• When atropin syndrome
• Gastric lavage, enterosorbents, salt Laxatives,
  repeated cleansing enemas (regardless of whether
  diarrhea).
• 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)
• Symptomatic treatment
• When cholinergic syndrome
• Gastric lavage, enterosorbents saling Laxatives,
  repeated cleansing enemas (regardless of whether
  diarrhea).
• Against a background infusion therapy - atropine
  sulfate 0.1 1-2 ml in the disappearance of
  symptoms of poisoning . Symptomatic treatment

66
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.
67
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
68
POISONING chlorinated hydrocarbons
Most often found poisoned by organic solvents -
dyhloretanom (DHE - ?2?4??2) and carbon
tetrachloride (CTCH - ???4)
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 (???3, ??), 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
69

• Clinic in clinical course five syndromes are
  distinguished
• Neuropsychiatric - dizziness, intoxication,
  euphoria, agitation, seizures, hallucinations,
  consciousness up to coma (toxic encephalopathy)
• Respiratory disorder - hypersalivation,
  hyperbronhoreya, aspiration of gastric contents
  with the development of aspiration-obstructive
  syndrome
• Dysfunction C-V-S - tachycardia, hypotension,
  decreased bcc, increased permeability of blood
  vessels, circulatory hypoxia
• Kidney-liver - increased and morbidity of liver,
  reducing its functional capacity, jaundice,
  decreased daily diuresis until anuria, increase
  of uremic intoxication and disorder ABB
• Gastrointestinal - Clinic of acute
  gastro-enteritis

70
INTENSIVE THERAPY

1. 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.

71
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).
72
16. Hepatoprotectors Berlition (a-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.

73
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 contentgt 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 - HbCNgt 40 -
pronounced cyanosis, dyspnea, hypotension,
vomiting, convulsions, coma...
74
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 11000. 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
75
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.
76
POISONING Opiates
Codeine, morphine, opium, kodterpin, omnopon,
promedol, heroin, pentazocine (fortral, leksyr),
etc. Lethal dose gt 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
77
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
11000 or 0.2 solution of tannin. After rinsing
the stomach injected 50 ml of KMnO4,
enterosorbents salt and relaxed.
78

1. 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
2. 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.
3. Forced diuresis, peritoneal dialysis. Situational
   therapy.

79
POISONING CLONIDINE
Clonidin (hemiton, katapresan) refers to a
central presynapsis a2-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
80
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! a-blocker (fentolamin) and naloxone
under constant control of AT and heart rate 6.
Hemosorbtion, ultrafiltration.
81
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
• Cytolysis and tissue necrolysis
• Erythrocyte hemolysis
• Increased permeability of vascular wall
• Dismissal of the cascade of cytokines (histamine,
  bradykinin, inflammatory proteins, NO, serotonin
• Common toxicactions - violations of hemodynamic,
  respiratory, liver and kidneys, etc.

82
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
83
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

1. You can not make additional cuts in the site of
   the bite, enter any drugs, impose binder (except
   when cobra bite)
2. Process the morning with alcohol or iodine
   tincture and apply a clean bandage free
3. Dates patient hot drink and transport it to the
   hospital in supine position

84

1. Introduction antisnake specific serum
   (anti-gurza) at Bezredko first 1 ml diluted
   110, 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)
2. 250-500 mg hydrocortisone or prednisolone in
   equivalent doses
3. Heparin for 5 thousand units. every 6 hours.
   under the control clotting time
4. Preventing tetanus (toxoid)
5. Antibiotic
6. Situational symptomatic therapy

85
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,
andgt 100 - lethal.
86
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
87
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
• Tweezers or fingernails to remove stilet (sting)
  from the bite
• Place a bite to process alcohol, hydrogen
  peroxide, tincture of iodine and brilliant green
  or apply cold

88

1. When bitten of mucosal BP immediate entered
   hormons and be ready to tracheal intubation,
   konikotomiya, traheostomiya.
2. 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
89
 
 
 
 
 
 
 
Tarantul
Kara-Kurt
Phalanga
Spiders produce venom - toksoalbuminy.
Scorpion
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
90
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
• 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.
• Situational symptomatic therapy