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
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
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
volume – exotoxic 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
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 >
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
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
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!
– 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
– 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
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.
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).
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
poisoning – cordiamin, 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
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
– 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
– 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
haemoglobin – carboxyhemoglobin – 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).
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
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.
– 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
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
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
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
– 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
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