General principles of intensive  therapy of the acute poisonings

Acute poisoning is a chemical injury, which occurs when chemical

substance gets to the organism and violates its vital functions. If the

substance is aggressive enough and proper treatment is not provided

on time poisoning will bring death.

Although there are over 500 toxic substances which may cause

acute poisoning, clinical picture is made up of quite similar syndromes.

Proper diagnostics of these syndromes allows avoiding life_

threatening complications and gets the chance to make correct

preliminary conclusions about the nature of poisoning.

Main clinical syndromes of poisonings

Affection of central nervous system manifests as excitation or

depression of patient’s mental activity. Depression of CNS has

different stages: confusion, stupor, sopor and toxic coma. One of the

coma’s deepness criteria is reaction of the patient to the painful

stimuli (you can also check reaction to smell of ammonium chloride).

Lack of reaction is a sign of coma. Don’t leave such patient without

observation, because his condition is severe and at any moment life_

threatening complications may appear: those patients have tendency

to bradypnoea up to complete respiratory arrest. Also you should

not forget that decreased tone of soft palate and tongue in a supine

position will violate patency of the airways and patient can die of

asphyxia. In addition comatose condition influences reflexes and lack

of swallowing can leads to getting of the saline and gastric contents

into the airways (and thus to development of aspiration pneumonia).

Usually CNS depression is caused by excessive alcohol

consumption or admission of its surrogates, overdose of neuroleptics,

sleeping pills, drugs, sedative medicines, antidepressants and carbon

monoxide poisoning. You can remind intensive treatment of comatose

patients in chapter 5.

Some poisoning are followed with acute intoxication psychosis

(mental disorders, hallucinations, time and space disorientation,

inadequate behavior). This clinical picture you can observe in case of

atropine poisoning (and also atropine_like agents: tincture of dope,

henbane, amanita) or cocaine, tubazid, antihistaminic drugs and

organophosphates poisoning.

In case of psychosis you will have to immobilize patient in the

bed for his own good and safety (to avoid injuries both patient’s and

those of the staff). You will also have to do this in order to maintain

i/v lines for antidotes and sedative infusions (aggressive patient will

try to remove everything he or she considers irritating). Constantly

observe the patient’s vital functions.

Toxic affection of the respiratory system can progress as the

violation of:

a. external respiration – neurogenic form, aspirations and

obstructions of the airways which bring hypoxic hypoxia;

b. hemoglobin’s function – aniline and nitrobenzene create

methmoglobin, carbon monoxide connected with hemoglobin creates

carboxyhemoglobin and neither the first nor the second is capable of

normal oxygen transportation; heavy metal, organic acids and arsenic

poisonings lead to destruction of the red blood cells and emission of

the free hemoglobin into the plasma;

c. oxygen transportation due to the decrease of circulating blood

volumeexotoxic shock;

d. cellular respiration – tissue hypoxia occurs when cytochromes

are blocked with toxins like cyanides.

Practically all severe poisonings earlier or later lead to hypoxia,

because they violate oxygen supply, transportation and consumption.

Your immediate treatment actions in this situation will be:

to assess the respiratory system (described above);

to provide the airways patency (cleaning of the oral cavity,

aspiration of the saline and gastric contents, conicotomy if necessary,


to begin oxygen supply (face mask, nasal catheter);

to start artificial ventilation if necessary;

to prescribe antidotes if they are available (methylene_blue in

case of nitro compounds poisonings, unithiolum in case of heavy

metals and arsenic poisonings, cytochrome c in case of tissue hypoxia);

to start hyperbaric oxygenation in case of carbon monoxide


to begin infusion therapy in order to stabilize the


to start general detoxification;

to prescribe symptomatic treatment and provide prevention

of the complications (for example prescription of antibiotics).

Affection of the cardiovascular system manifests as inability of

the heart and vascular bed to provide adequate blood supply of the

organs, which leads to metabolic disorders and in the worst case to

death. Severe toxic damage of cardiovascular system brings acute

cardiovascular failure: primary toxic collapse, exotoxic shock,

secondary somatogenic collapse.

Primary toxic collapse appears in case of massive poison

admission, when compensatory mechanisms are not quick enough

to resist the chemical aggression. Immediately or minutes after

poisoning patients begin to suffer from reduced cardiac output

and thus from decreased blood flow in the tissues. Peripheral pulse

is weak or absent, blood pressure critically lowers and cardiac

arrest may appear. In most cases of primary toxic collapse

ambulance is not able to save the life of the patient due to the

fulminant development of life_threatening complication. However

you should remember that such collapse occurs only in 5 % of the


Exotoxic shock is the reason of death for 70 % of poisoning

victims. Violations of hemodynamics on one hand are caused by direct

heart and vessels damage and on the other hand by compensatory

sympathetic and adrenal reactions. On the background of CNS and

gastrointestinal system violations you will observe disorders of

systemic hemodynamics and microcirculation: arrhythmias, decrease

of blood pressure, central venous pressure, cardiac output and

diuresis. The peripheral vascular tone changes: toxins induce spasm

or dilation of arterioles with the ischemia of one and hyperemia of

other tissues. Depending on the body reaction to intensive treatment

shock can be compensated, decompensated reversible and

decompensated irreversible.

In case of toxic shock you should:

get an i/v line (preferably several, including central venous access);

– start infusions of colloids (albumin, rheopolyglucin,

hydroxyethylstarch solutions) and crystalloids (saline, glucose solutions,

polarizing solution) in order to normalize blood pressure, heart rate and

diuresis; sometimes infusion dose is up to 100_150 ml/kg, (7_10 l/day);

constantly control patient’s condition: monitor the heart

action, blood pressure and central venous pressure;

– provide antidote treatment and detoxification; remember that

extracorporeal detoxification is possible only after the stabilization

of the hemodynamics (systolic blood pressure >90 mm Hg ).

Secondary somatogenic collapse is the reason of death in 25% of

the cases. It can occur few days after poisoning, when the toxin is

already eliminated from the body, however the tissue changes (in the

lungs, liver, kidneys, heart) are irreversible. Necessary treatment:

hemodynamics stabilization, improvement of microcirculation,

intensive therapy of functional disorders and organic changes

(artificial lung ventilation, hemodialysis, cardiac support, etc.).

Toxic affection of gastrointestinal tract.

Usually poisoning provokes typical protective reactions: nausea,

vomiting, diarrhoea. Chemically aggressive agents can cause

corrosive” effects: concentrated acids and bases can burn the mucous

membrane of oral cavity, oesophagus and stomach (vomit is coloured

with blood). Profuse vomiting and diarrhoea bring dehydration,

electrolytes loss and acid_base imbalance. Especially rapid those

complications appear in children.

After recovery patients with chemical burns of gastrointestinal

mucous membranes may suffer from cicatrisation and stenosis of

digestive tract.

Be aware of the fact, that intensive usage of narcotic pain killers

and sleeping pills can lead to inhibition of peristalsis and thus to

constipation and slow elimination of toxins.

Immediate aid actions:

– clean the stomach. If the patient is conscious stimulate

vomiting pressing on the root of the tongue or giving 2_4 liters of

slightly salted fluid. Don’t you ever do this in case of chemical burns!

if you have the skills and possibility insert the gastric tube and

evacuate gastric contents with the help of 10_15 liters of water; if

necessary give also antidotes through the tube; you can also use tubes

with several channels;

after the gastric lavage in order to bind toxins use

enterosorbents (activated charcoal for example);

– stimulate stool with saline laxatives (150_200 ml of 33%

magnesium sulfate solution) in order to remove connected with the

toxin sorbent from the intestines;

cleansing enemas also help to eliminate toxins from the body.

Toxic injury of liver and kidneys.

This syndrome is caused by primary toxic damage of the liver

and kidneys (nephrotoxic and hepatotoxic poisons) or by the

secondary disorders of their functions due to violations of blood flow

and oxygenation.

Liver is the main detoxification and biotransformation center of

the organism, so it takes the “main blow” during intoxication.

Intensive detoxification increases metabolic activity and oxygen

consumption of the liver several times. Hepatocytes become very

sensitive to hypoxia.

Light forms of toxic and hypoxic affections can develop without

clinical manifestation. However they will be noticeable in laboratory

tests (elevation of transaminases, bilirubin, phosphates). Severe

poisoning will lead to toxic hepatitis and even hepatic coma.

Among the hepatotoxic substances are: heavy metals salts,

dichloroethane, ethylene glycol, deadly amanita toxins.

To protect the liver you should:

– eliminate the toxic substance from the gastrointestinal tract;

– give antidotes if they exist (unithiol for heavy metals salts,

lipoic acid for deadly amanita);

– prescribe cleansing enemas 2_4 times a day (to prevent

intoxication with the wastes accumulated in the intestine);

– use extracorporeal detoxification (hemosorbtion,

plasmapheresis, artificial liver);

– provide adequate oxygenation and blood supply of the liver;

– prescribe symptomatic treatment.

Kidneys are very important for the elimination of the poisons

circulating in the blood. So in many cases they are also the “target” of

the toxin. They can be damaged primary (poison affect their tissues

directly) and secondary though the violations of vital functions (for

example hemodynamics in case of exotoxic shock). Their condition

you can control with the help of hourly urine output, which normally

is not less than 0,5 ml/kg.

To prevent the renal failure you should:

– eliminate the poison as soon as possible (gastric lavage and

enemas for gastrointestinal tract; hemodialysis, hemosorbtion,

plasmapheresis for blood);

– give antidotes if they exist (unithiol for heavy metals salts,

sodium bicarbonate for hemolytic poisons, ethylic alcohol for

ethylene glycol and methanol);

– treat disorders of hemodynamics (therapy against exotoxic


– stimulate the urine output with the diuretics on the background

of previous rehydration: this will allow you to eliminate diluted in

the plasma toxins faster and to prevent renal failure; kidney is an

organ which functions normally only if works intensively;

Clinical observations tell us, that incredibly massive infusions

(10_20_30 l/day) with diuresis stimulation really help patient to

dilute and eliminate the toxin without kidneys damage.

In case of acute renal failure you should treat the patient

according to the principles described in chapter 6.

 Ethylic alcohol poisoning

This type of poisoning appears in case of excessive alcohol

consumption. It is one of the most common poisonings, as well as one

of the lightest and prognostically the most favourable (organic

damage is rare). However combined with comorbidities and

complications it becomes one of the first reasons of death in

toxicology, so don’t underestimate it.

Alcohol poisoning, unlike drunkenness, has the characteristic signs

of intoxication: vomiting, inhibition of CNS, disorders of cardiovascular

system and breathing. Patients usually are in comatose condition. Pay

attention to their appearance: clothes are untidy, you can notice sings

of involuntary urination or defecation. There is an alcohol breathing

odour. Skin of the face is hyperaemic and dry. Cyanosis is a sign of

respiratory insufficiency, grey shade of skin is a symptom of cardiac

disorders. Wet skin might be the symptom of hypoglycaemic coma,

hypercapnia or organophosphate poisoning, which are “covered” with

the obvious clinic of alcohol poisoning. In case of moderate coma

vital functions are usually not involved. Pupils are narrowed or dilated,

photoreaction is preserved.

Objective criterion of alcohol poisoning is alcohol

concentration in the blood:

less than 1,5‰ – light inebriation

– 1,5‰_3,5‰ – moderate inebriation

– 3,5‰ and more – severe inebriation

Lethal concentration of alcohol is 5_6‰.

The most common complications of alcohol poisoning are next:

obstruction of the airways with the tongue, soft palate or

biological fluids (vomit, saline, sputum, blood) in supine position;

regurgitation of the gastric contents and development of

aspiration pneumonia; lethality is nearly 70%;

head traumas with brain injuries: patients usually fell and hurt

themselves; the problem with such injuries is the fact that the clinic of

hematoma (subdural, epidural, intracerebtal) is quite often “covered”

with alcohol intoxication. This is why you should always remember

about the differential diagnostics. To make a correct diagnosis in case

of coma you should check the specific symptoms such as anisocoria

(there is no poisoning which causes pupil’s asymmetry!), signs of head

injury (scratches, bruises, skull deformations, oto_liquorrhea and nasal

liquorrhea, nasal and ear bleeding), asymmetric tendon reflexes and

muscle tone, disparity between the amount of alcohol and deepness

of coma, prolonged unconsciousness (alcohol coma even without

proper treatment lasts only 3_4 hours);

other traumatic injuries (rib fractures which violate external

breathing, spleen or liver ruptures with haemorrhagic shock, ruptures

of hollow organs with peritonitis; limb fractures);

compartment syndrome appears when certain enclosed space

within the body for several hours suffers from the decreased blood

flow (for example when patients spends few hours in one inconvenient

position); even when blood supply will be restored necrotic products

will continue pathological process through toxic affection of the life_

important organs (for example free myoglobin can cause renal


There is always a possibility of chronic diseases exacerbations

on the background of alcohol poisoning (stroke, myocardial

infarction). Remember about the necessity of complete examination

(inspection, palpation, percussion and auscultation of an undressed

patient) of such alcohol victims – it is the only way to find all the

diagnostic mysteries” patients hide!

Intensive treatment:

– evaluate CNS condition (deepness of the coma);

– provide airways patency and adequate respiration (described

above; if necessary – intubate the patient and begin artificial


check the cardiovascular system: heart rate, pulse, blood


in case of severe hemodynamic disorders provide infusion


– insert the gastric tube and remove its contents using lavage

with water;

– take blood samples and check blood alcohol level


– prescribe intravenously: 60_80 ml of 40% glucose solution, 60_

80 ml of 4% sodium bicarbonate solution, 5_10 ml of 5% ascorbic

acid, 1_2 ml of vitamin B1 solution;

if there are no comorbidities add analeptic solutions i/m (2_

3 ml of caffeine or 2 ml of cordiamin);

in case of severe intoxication begin forced diuresis.

 Poisonings with alcohol surrogates

Patients can be poisoned with: home_distilled vodka, Cologne

water, denatured alcohol, methyl alcohol, lotion, brake fluid, etc. The

peculiarity of these poisonings is complex effect of the alcohol and

other toxic components of the “drink”.

The most toxic are methyl alcohol and antifreeze (ethylene

glycol) – their lethal dose is 60_100 ml. Lower doses cause neuritis of

optical nerve and thus blindness (methyl alcohol), acute renal and

liver failures (ethylene glycol).

In case of these poisonings detailed anamnesis and blood

identification of the poison (gas chromatography) play the most

significant role in the diagnostics. However for the prognosis volume

of the poisonous fluid, duration of its influence, functional condition

of the liver, effectiveness of the antidote treatment and detoxification

are the most important.

In the body methanol and ethylene glycol are metabolised

according to so called “lethal_synthesis”: during the breakdown of

the poison in the liver substances much more toxic than the parent

compounds are created.

Intensive therapy:

1. Gastric lavage with potassium permanganate (oxidizes methyl


2. Give antidote: 50 ml of 40% ethylic alcohol solution every 3

hours orally or 100 ml of 5% ethanol solution intravenously slowly

combined with glucose solution during 2 days. Antidote will block

the process of poisons biotransformation in the liver until they will

not be eliminated from the body.

3. Actively eliminate the poison from the body through repeated

gastric lavages, forced diarrhoea, extracorporeal methods of

detoxification (hemodialysis, hemosorbtion, plasmapheresis).

4. In order to treat optic neuritis you should perform retrobulbar

injection of steroids.

5. Symptomatic treatment.

. Drug poisonings

In civilized countries these poisoning are the main reason (65_

70% of cases) of hospitalization in toxicology units. Usually patients

overdose sleeping pills, narcotic painkillers, antihistamine drugs,

hypotensive medicines. Among the reasons are suicide tries, drug

abuse, toxicomania and accidental overdose due to hectic pace of

modern life, etc.

Clinical picture is usually connected with CNS affection. There

are phases of somnolence, sleep and coma. Depending on involvement

of other systems coma can be complicated or uncomplicated. Usually

respiratory complications appear: inspiration centre depression,

violations of airways patency due to soft tissues (tongue, soft palate)

or biologic fluids (blood, sputum, saline), pneumonia. In 15_20% of

cases the poisoning development is complicated with the exotoxic

shock. The peculiarities of this shock are next: circulatory disorders

with blood stagnation in the pulmonary circuit, toxic affection of the

myocardium and decrease of orgnism energy metabolism.

To indicate the poison you should ask relatives and witnesses

and check things of the patient (for example you can find medicine

packages). Evaluate the size of the pupils: extremely narrowed pupils

(“poppy seeds”) are the effect of narcotics admission; narrowed pupils

might be the sign of sleeping or sedative medicines overdose; dilated

pupils are the symptom of clofelin, antidepressants or neuroleptics

administration; wide pupils covering the whole iris are usually the

sign of atropine poisoning (or a poisoning with atropine_like

substances: dope, henbane, amanita).

Principles of the intensive treatment in the toxicology unit:

– clean the gastrointestinal tract as soon as possible (gastric and

intestinal lavage, enterosorbtion, cleansing enemas) and as often as


– provide adequate respiration (check airways patency);

in case of comatose patients intubate the trachea and begin

artificial ventilation (sometimes it is necessary for weeks);

– control hemodynamics and treat its violations (infusion

therapy and adrenergic agonists or antagonists if necessary);

– stimulate diuresis: patients with barbiturate poisoning should

be treated with alkaline forced diuresis in order to eliminate the toxin

(add to the infusion 400_600 ml of 4% sodium bicarbonate solution

and prescribe diuretics);

use antidotes: naloxone for opiates, pharmacological

antagonists for anticholinergic and cholinomimetic agents; don’t you

ever prescribe central analeptics for comatose patients with drugs

poisoningcordiamin, caffeine, bemegride , cytiton, lobelinum can

cause “cerebral blood flow steeling effect” and thus they deepen the

hypoxia of brain cells!

– provide extracorporeal detoxification to eliminate toxins

(hemodialysis, hemosorbtion, plasmapheresis);

– prescribe antibiotics for infectious diseases prevention (for

example in case of prolonged artificial ventilation);

symptomatic treatment.

 Alkali and acid poisonings

These poisonings are among the most severe and difficult to treat.

Accidentally or intentionally (suicide) victim can take mineral acids

(hydrochloric, sulphuric, nitric acids), organic acids (acetic or oxalic

acid), alkali (ammonium chloride, battery fluid, etc.).

When corrosive substance gets into the body along its way inside

chemical burn appears: mucous membranes of oral cavity, throat,

oesophagus, stomach are injured. Together they make nearly 14_15%

of the body surface. Patients suffer from unbearable pain, eating and

drinking are impossible. In case of acid burn coagulation necrosis

appears; alkali burn is more severe, because colliquative necrosis

penetrates deeper into the tissues ruining the vessels and causing

bleedings. Organic acids easily get into the blood. Sometimes chemical

substances or their vapours also get into the airways and thus oedema

and risk of asphyxia appear.

Usually part of aggressive substance is spilled over the chin and

you can notice the burn. Systemic disorders are characterized with

exotoxic shock which develops as burn shock (unbearable pain,

dehydration, toxic affection of the heart, decrease of cardiac output,

spasm of arterioles and microcirculation block). Organic acids also

provoke hemolysis of red blood cells: free haemoglobin transforms

into hydrochloric haematin and obturates renal tubules, causing acute

renal failure.

Intensive treatment principles:

– evaluate patient’s condition: external respiration,

consciousness, cardiovascular system;

adequate pain relief with narcotic painkillers and non_steroidal

anti_inflammatory drugs (1_2 ml of 1% morphine solution; 2 ml of

50% analgin solution);

– liquidate the spasm of gastric cardia and oesophagus (1 ml of

0,1% atropine solution i/m, 5 ml of baralgin solution);

– clean the stomach during first 10 hours after poisoning; insert

the gastric tube (cover it thickly with Vaseline and don’t push too

hard); use water for lavage and don’t try to perform chemical

inactivation of the poison, because during the reaction carbon dioxide

can exude and acute expansion of the stomach leads to it rupture;

– provide treatment of shock (sometimes up to 10_12 liters/day

of infusions);

in case of organic acids poisonings (acetic acid, oxalic acid get

into the blood) give 1500_2000 of 4% sodium bicarbonate solution

intravenously slowly with diuretics; these actions will help to remove

hemoglobin (released due to red blood cells hemolysis) and thus to

prevent acute renal failure;

in case of obstructive breathing disorders (mucous membrane

edema) use steroids (90_120 mg of prednisolone), antihistamine drugs

(2 ml of 1% dimedrol solution intravenously), sedative medicines (2

ml of 0,5% diazepam solution); perform tracheostomy or conicotomy

if necessary;

– prescribe antibiotics for infectious diseases prevention (for

example in case of prolonged artificial ventilation);

symptomatic treatment.

During the recovering period patient may need surgeries for

restoration of gastrointestinal tract: the most common practice is

the bouginage of the oesophagus or, if necessary, oesophagus plastic.

 Poisonings with toxic gases

Among the toxic gases are carbon monoxide, car exhausts,

propane and butane, ammoniac gases. The last one is the most toxic:

few inhalations are enough to cause unconsciousness.

The foundation of the pathology lies within the atypical

haemoglobincarboxyhemoglobin – combination of normal

haemoglobin and toxic gas. Oxygen transportation if violated (in case of

severe poisonings there are nearly 70_80% of changed haemoglobin) and

thus haemic hypoxia appears. In addition within the tissues cytochromes

are connected with toxic substances and this leads to tissue hypoxia.

Clinical findings in case of carbon monoxide poisoning depend

on the severity of the poisoning. In case of mild intoxication they are:

headache, nausea, vomiting. Moderate intoxication shows

unconsciousness for 12_16 hours and severe intoxication is

characterized with coma, central disorders of breathing, toxic

affection of heart and other organs, etc.

If intoxication advances changes of central nervous system

become irreversible (brain death is possible).

Intensive treatment.

In case of mild and moderate poisonings you should you should

carry the patient out of the toxic atmosphere as soon as possible. In

hospital conditions you should provide oxygen supply, get an

intravenous line for crystalloids infusion and prescribe vitamins.

In case of severe intoxication begin artificial ventilation with

high oxygen flow. Luckily there is an antidote for carbon monoxide

poisoning: hyperbaric oxygenation. Connection with oxygen is more

natural for haemoglobin and when the pressure of oxygen is higher

than its usual partial pressure carbon monoxide is replaced from the

haemoglobin. Usually in case of comatose patients 40_50 minutes

sessions every 6_12 hours are enough.

To normalize tissue metabolism prescribe antihypoxants: 20%

solution of sodium oxybutirate (20_40 mg/kg i/v) and cytochrome

c (2_3 ml i/v) every 4_6 hours. To improve microcirculation dilute

the blood with crystalloid solutions (check the level of hemodilution

with hematocrit – stop when it will reach 0,3_0,35 l/l).

Prevent the infectious complications and brain oedema with

standard methods.

 Organophosphate poisonings

These are the poisonings with insecticides, acaricides, herbicides,

fungicides, rodenticides, desiccants, defoliants and with chemical

warfare agents such as sorin, soman, V_x.

Organophosphate substances are fats and water soluble and thus

they penetrate easily through the skin and mucous membranes

(gastrointestinal tract, airways, etc.). In the blood they block an

enzyme – cholinesterase – responsible for the breakdown of

acetylcholine. As you remember acetylcholine is a universal synaptic

mediator of nervous impulses and thus its accumulation on the post_

synaptic membranes will cause continuous stimulation of vegetative

nervous system and cross_striated muscles.

Clinically you will see: nausea, vomiting, cramps; unconsciousness

in severe cases. Sometimes in the place of penetration you can see

muscle fasciculation (if the poison was administered orally – tongue

twitching). Stimulated parasympathetic nervous system shows wet

skin, increased salivation and bronchial secretion (sometimes you

can even see white phlegm in the mouth – don’t mistake it with the

pink phlegm of pulmonary oedema), narrowed pupils, bradycardia

(heart rate 40_30 beats per minute). In addition to the obvious clinic

you can always check the environment of the patient for the signs of

organophosphate poisons (specific smell, containers with toxins, etc.).

One third of patients suffer from exotoxic shock, which at first

causes hypertension and then hypotension, unconsciousness and

depression of respiration.

Immediate aid:

– take patient out of the dangerous environment (if you suspect

that the mechanism of poisoning is inhalation);

– clean the stomach with large amounts of cold water; repeat it

several times, because these substances are excreted through the

mucous membranes of gastrointestinal tract;

– give saline laxative;

if the poison affected skin – wash it with alkaline solution, but

make sure it is mild.


a. use peripheral m_anticholinergic drug – atropine: during the

first few hours 2_3 ml of 0,1% atropine solution (up to 30_35 ml during

the whole period of intensive atropinization); pay attention to the

signs of atropine administration as they are the measure of your

antidote treatment effectiveness: termination of excessive bronchial

secretion, dilation of the pupils, tachycardia (90_110/min). During

next 3_5 days continue atropine prescription (from 10_15 mg to 100_

150 mg/day – period of supportive atropinization). Control clinically

the level of atropinization.

b. use cholinesterase reactivators: 1_2 ml of 15% dipiroxim

solution i/m, up to 600 mg; 3 ml of 40% izonotrozin solution i/m up

to 3_4 grams. However remember, that cholinesterase reactivators

can be used only 24 hours after poisoning. Later administered

reactivators will ne not only ineffective, but also toxic for the patient.

You should also provide usual treatment as soon as possible:

infusion therapy, forced diuresis, hemosorbtion, plasmapheresis,

hemodialysis and antibiotics for infection preventions.

In case of ineffective external respiration and coma intubate the

patient and start artificial respiration. Convulsions caused by

organophosphate poisoning are treated with sodium oxybate (75_

100 mg/kg i/v every 4 hours). Cardiac glycosides, calcium chloride,

euphillinum are forbidden in case of organophosphate poisonings,

because they induce toxic heart affection.

Be aware of the possibility of “second poisoning wave”: even 4_8

days after the stabilization of the patient’s condition clinical picture

of the poisoning might return and this time hemodynamics will

decompensate quickly.

 Mushroom poisoning

There are edible, non_edible and relatively edible mushrooms. Non_

edible or poisonous mushrooms can contain toxins harmful for central

nervous system, liver, kidneys and gastrointestinal tract (according


to A. Lokay, 1968). The most dangerous poisoning is caused by deadly

amanita. The poison of this mushroom – amanitotoxin– is not

destroyed during cooking and there is no way to detect it in usual

conditions. In case of severe poisoning the lethality is 80%.

Specific feature of amanita poisoning is prolonged latent period.

Sometimes 6_12 hours pass before the first symptoms of the

poisoning appear. All the other relatively edible mushrooms reveal

clinical signs of the poisoning much earlier – 1_2 hours after


After the latent period is over on the background of complete

health nausea, profuse vomiting and diarrhoea appear. Those

symptoms begin second phase of the poisoning – gastroenterocolitic

phase. Liver enlarges; patients suffer from pain in the right subcostal

area, weakness, and consciousness disorders. Stool becomes watery

and contains mucous. Patients loose up to 4 liters of the fluid during

the day. Unlike bacterial food poisonings, mushroom poisonings are

not characterized with high fever.

Liver failure and acute kidneys injury are the third phase of the

poisoning, which begins on the second or third day of disease. Those failures

are characterized with hepatic encephalopathy, jaundice, gastrointestinal

bleedings, hepatic breath odour and oligoanuria. The level of alanine and

aspartate aminotransferases is very high. When liver returns to its usual

size and consciousness is changed into coma hepatargia is stated and

prognosis for the disease becomes rather unfavourable.

The forth stage is a stage of recovery and it is characterized with

gradual regression of the clinical picture and normalization of the

laboratory results during several weeks. However survival is possible

only for those patients, who ate small amounts of the poisonous


Knowing about the high lethality and severity of the amanita

poisoning, prevention methods become very important.

Mushroomers should know the difference between deadly amanita

and other mushrooms: deadly amanita is a gill_bearing mushroom

with olive or green cap. Its gills are white and not connected with the

stem. Stem has a bulbus with white volva from one side and a white

annulus from another side, under the cap.

Patients should be treated in a special toxicology units or

intensive treatment unit. General principles of intensive therapy are:

gastric and intestinal lavage, enterosorbtion and saline


infusion therapy (necessary to liquidate electrolyte deficiency

and provide forced diuresis);

support of the liver functioning with lipoic or thioctic acid

(1000_2000 mg/day), concentrated glucose solutions, steroids (up

to 40 mg of dexamethasone per day) and silibin (50 mg/day);

extracorporeal detoxification (hemodialysis, hemosorbtion,

plasmapheresis, artificial spleen or liver) as soon as possible;

antibiotics if necessary (penicillin); vitamins (B,C,E);

external drainage of thoracic duct (decreases intoxication

through elimination of toxic lymph).

 Medical operations and manipulations

Gastric lavage

Indications: necessity of poisons and toxins removal from the

stomach, cleaning of the stomachbefore operation or liquidation of

the stagnation during postoperative period.

Equipment required: gastric tube (with two channels if possible),

Janet syringe, water for lavage (15_20 liters of room temperature

water), gloves and watertight apron.

Procedure: gastric lavage of comatose patients is a procedure

for doctors. In our country nurses are not allowed to do this without

control of the doctor: unconscious patients have inhibited reflexes

and thus tube can be easily inserted into the trachea instead of

oesophagus. In this situation neither cyanosis nor cough appear and

everything looks just fine, however feeding or lavage can end with

fatal complications (asphyxia and death).

Put on the gloves, choose the tube of necessary size and oil it with

Vaseline. Patient should lie on the left side (ask nurse to hold patient’s

arms to limit his or her movements during this unpleasant procedure).

If patient is conscious you can previously use lidocaine spray to

anaesthetize mucous membranes. Tubebe can be inserted through

the nose (of course in this case size of the tube is limited) or through

the mouse. Don’t push too hard, especially when you are using nasal

passage: you can cause bleeding. Ask patient to bow his head to the

chest – this will increases chances of correct tube insertion

(oesophagus, not trachea). The length of probe you insert can be

measured in advance as a distance between earlobe, nose and xiphoid.

Confirmations of correct NG tube placement:

auscultate the epigastrium and simultaneously infuse some air

with the syringe– you will hear typical “bubble” noises;

if you made a mistake and probe is in the trachea you can

notice air released from the distant end of the tube according to the

respiratory movements;

pH test of the aspirated contents;


One_time water doe is nearly 200 ml: it will flow out when you

will lower the tube or you will have to evacuate the water with the

syringe. Repeat these actions until the receiving of clean water

(usually it takes nearly 10 liters of water).

Forced diuresis.

Indications: intoxications of different origin (poisonings,

infectious diseases, endogenous intoxications).

Medicines required: normal saline (3_5 liters); detoxification

solutions; polarizing solution (400 ml of 10% glucose solution, 10 ml of

7,5% potassium chloride solution, 12 units of insulin), osmotic diuretics

( mannitol in the dose 1 g/kg), furosemid solution (40_80 mg)

Procedure: get an i/v line (central or peripheral) and insert

urinary catheter. During the first phase of forced diuresis “water”

the patient with crystalloids and detoxification solutions (30_40 ml/

kg). During the second phase infuse osmotic diuretics and furosemide

solution. Excessive urine output brings potassium loss, which you

should treat with polarizing solution. Balance the speed of infusion

with the speed of diuresis: generally per 5_7 liters of infused solutions

you should receive at least 5 liters of urine.