Toadstool poisoning, symptoms. Poisoning in humans with toadstool

Inexperienced mushroom pickers can easily get poisoned by mushrooms, especially toadstool toxins, but dealing with the consequences of such intoxication, which can pose a real danger and threat to human health and life, on the contrary, is quite difficult.

According to statistics, among the available diversity poisonous mushrooms capable of causing food poisoning in humans, namely pale grebe, or rather, its consumption in 90% of cases leads to death.

Therefore, to prevent such a situation, you need to learn to distinguish the described type of poisonous mushrooms from their edible relatives, recognize the symptoms of poisoning with toadstool and, of course, know everything about the rules for providing first aid to a person exposed to such intoxication.

How to distinguish toadstool from champignon or russula

The insidiousness of the described type of mushroom lies in their so-called variability. The cap of the pale grebe can be painted either white or gray-green, and over time it can even take on a stable gray tint. Therefore, people who do not understand mushrooms often mistake this particular type of fly agaric for champignons or russula.

The pale grebe is marked by a characteristic belt, a certain ring on the stem, as well as the presence of a volva in the form of a membranous sac located at the base of the stem, which reaches a width of 3 to 5 cm. The plates on the underside of the cap have a bright white color, which is what distinguishes this poisonous mushroom, for example, from champignon. At the fracture site, the flesh of the toadstool does not change its color, and its taste and smell are weakly expressed and practically do not manifest themselves.

Below are the features by which you can distinguish the described poisonous species of mushroom from its edible relatives:

Russulas lack rings and volvos;
Champignons - have plates on the bottom of the cap brown, these mushrooms also lack a volva;
The float mushroom is indicated by its small size and there is no specific belt on its stem.

How the human body reacts to the venom of the toadstool

Poisoning by the described mushroom occurs immediately after eating it. Moreover, not only the toadstool itself is dangerous, but also its spores, which are carried around by the wind and settle on plants, berries and edible mushrooms.

There are two types of toxins that saturate the pale grebe:

Phalloidins are substances that are not so toxic, but fast-acting and cannot be heat-treated;
Alpha-amanitins are highly toxic substances, but they act with some delay, a day or more after entering the human body.

Even before the appearance of the primary symptoms of poisoning with toadstool, the human body will already be harmed. Studies have shown that 30 milligrams of the described fungus is enough to cause death - this is the dose that is considered lethal for humans.

The above-described toxins present in the described mushroom cannot be digested in the human stomach, so they, almost unchanged, go directly to the liver, it is this organ that bears the first and main blow of these poisons.

Toxins provoke gastroenteritis, have a destructive effect on the cellular structure of the liver, and in addition, the capillaries of all internal organs of the human body lose their integrity. The described poisons act to lower glucose levels in the hematopoietic system, disrupt metabolic processes and have a very negative effect on the human nervous system.

Main symptoms and signs of intoxication

The symptoms of intoxication with the described fungus and the course of the disease itself will depend on the amount of poison received.

The latent period is indicated by the asymptomatic course of the disease, without obvious signs of poisoning by the described fungus. The duration of such a latent period varies from 6 to 40 hours, on average a little more than half a day. By the time the initial symptoms of poisoning occur, the poison of the white toadstool has already entered the bloodstream and begins to carry out its destructive work.

The next period (approximately 6 hours after the poisonous mushroom enters the body) is indicated by acute intoxication with its characteristic symptoms in the form of:

Vomiting reaction to toxins from the body;
Constant greenish or clay-like stools, possibly mixed with blood and with a foul odor (stools may occur as often as once every half hour);
Cutting and pain in the epigastrium, in the abdomen;
Severe dehydration, manifested by dry skin, visible mucous membranes, severe thirst, along with decreased daily norm urine (indicated as saturated - yellow and an unpleasant, pungent odor), weakness;
Severe headaches, visual disturbances, confusion, along with a state of agitation or lethargy.

The period of so-called remission in the victim begins approximately on the third day. The patient demonstrates a clear improvement in health, the symptoms of the above-described intoxication caused by poisoning disappear. And the patient seems to be on the mend. Such an imaginary recovery lasts no more than 24 hours. After this time, intoxication symptoms return again with the addition of new signs of the described disease in the form of:

Kidney and liver failure;
Yellowness of the skin, mucous membranes;
Hepatomegaly - an increased size of the liver is detected by palpation;
Bleeding of various etiologies;
Acute urinary retention;
Tachycardia above 120 beats per minute;
A sharp decrease in pressure.

The severe degree of intoxication with the described fungus is similar to the symptoms of renal, liver and heart failure, due to which the patient’s death occurs approximately on the 10th day.

First aid steps

In case of poisoning with any type of mushroom, including toadstool, especially if the victim is sure of it, it is necessary to call an ambulance medical care.

But before the medical team arrives, a number of mandatory measures need to be taken:

Give the victim a gastric lavage - give him a liter of water at room temperature to drink, and then press with your fingers on the root of the tongue to induce vomiting;
To prevent dehydration, the patient must be constantly given small amounts of fluids;
Give the victim activated carbon at a rate of 1g/kg. weight, some saline laxative or milk (warm).

The above-described methods of providing first aid to a person suffering from poisoning by the described fungus will not be relevant if he has vomiting and diarrhea.

Treatment of poisoning

It is possible to treat intoxication caused by the described fungus, but it is quite difficult, since the poison has already entered the bloodstream, and there is no antidote. In inpatient settings, medical workers are guided by actions aimed at:

For gastric lavage, even with vomiting, to remove possible remnants of the described fungus, which can linger in the stomach for a whole day;
For the use of drug therapy using Benzylpenicillin in dosages from 500 to 1 million units/kg of human weight 6 times a day (such treatment is relevant in the first 3 days after poisoning), as well as Silibinin at a rate of 30 mg/kg daily for 10 days ;
To combat dehydration - using injections in the form of: Acesol, Trisol, Ringer's solution (intravenously). And also using a dropper to administer glucose, which protects the liver tissue and eliminates hypoglycemia;
To quickly rid the body of the toxins of the described fungus through the use of hemosorption and the method of forced diuresis;
To take cardiac medications necessary to tonify the functions of the vasomotor and respiratory centers;
For liver therapy using B vitamins, as well as drugs in the form of Riboxin, Nicotinomide.

The effectiveness of the treatment process will depend on the amount entering the body toxic substances and the general well-being of the patient.

Prevention

In order to prevent and prevent possible poisoning by toadstool, mushroom pickers are advised to collect only those mushrooms that are familiar to them. During the collection process, it is necessary to inspect the mushroom - its shape, color and aroma of the pulp.

It is prohibited to collect mushrooms near highways, near chemical plants and in other similar unfavorable places.

This is due to the fact that mushrooms tend to absorb and accumulate poisons and toxins that are dangerous to human health and life. Therefore, even an edible relative of the described poisonous mushroom can cause serious intoxication in a person when growing in such an area.

Touch any suspicious or unfamiliar mushrooms with your hands, especially for children whose bodies cannot yet fully resist toxins and poisons;
Take mushrooms that are overripe and old due to the process of protein breakdown that has already begun in them;
Eat mushrooms without proper processing, since properly processed and cooked mushrooms are not capable of causing poisoning.

Forecast

Mushroom poisoning has always been considered the most dangerous phenomenon due to its high mortality rate. Therefore, in such a situation, speed of action to provide pre-medical and medical assistance is necessary.

When predicting the outcome of the described intoxication, it is necessary to rely on the patient’s history of information about the condition of his heart and blood vessels. Since a healthy heart and blood vessels increase the likelihood of recovery significantly. Cardiac disorders and pathologies vascular system in case of poisoning with the described fungus, they can worsen the victim’s blood circulation, disrupt the body’s resistance and lead to death due to paralysis of the vasomotor center.

This is especially true for children, who may die by the end of the third day. For most people, the third day is turning point. And if the victim survives it, the chances of his recovery increase significantly.

How to distinguish the poisonous mushroom in the form of toadstool from its edible relatives, as well as the rules for collecting and preparing them, are well outlined in the following video:

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Mushrooms are delicious and useful product, which both adults and children cannot resist. But you need to be very careful when collecting and preparing mushrooms, because sometimes it is difficult to distinguish edible species from inedible, which can lead to serious consequences and even death. An analysis of statistics showed that amateur mushroom pickers most often suffer from poisoning with toadstool - people who decided to go into the forest for their own pleasure, without even knowing the basic rules.

In order to protect yourself from poisoning and the consequences that follow it, you need to understand the distinctive features of the pale grebe:

The body is represented by a shape that looks like an egg.
The mushroom is almost completely covered with a transparent film. You can feel it if you run your palm over the mushroom.
The cap is greenish or light gray in color and does not exceed 15 cm, and the shape differs depending on the location and age of the mushroom and can be represented by either a flat or hemispherical shape.
The fleshy pulp is white in color, which does not change even if damage occurs.
Volva, which reaches approximately 4-5 cm in width. This feature can be considered one of the most important, since it is almost never found in edible mushrooms.

Despite the fact that the pallid grebe has distinctive features, which would seem to help mushroom lovers when picking, mistakes still happen. Confusion occurs for two reasons, namely:

Inattention and simple self-confidence. Many people think that they can easily detect a poisonous mushroom, and therefore do not pay attention to such recommendations.
A coincidence that can be explained by the similarities between different mushrooms.

At the same time, ordinary academic awareness can save the situation and protect consumers from severe poisoning. So, we suggest using an example to look at similar mushrooms and identify the features that will allow you to make a distinction:

Greenfinches and russula, although similar in color, do not have volvo rings. Therefore, no matter how much you would like to quickly complete the task and collect the mushrooms, we advise you to look at the base and leg, at the bottom of which is that very Volva.
occur in champignons age-related changes, which cause the cap plates to turn brown.
floats that not only have no ring, but are also too small to be confused.

REMEMBER! To avoid mistakes, you should not cut off the caps of the mushrooms, because this will not allow you to see the volva and the rings of the toadstool - deadly to humans due to the presence of a toxin such as amanitotoxin.

What happens if you eat toadstool?

Toadstool is a deadly mushroom, and therefore its consumption is strictly prohibited. The result is severe poisoning, which will be accompanied by severe pain, colic and convulsions, causing death.

The consequence of poisoning with toadstool is a rapidly developing and progressive phalloidin syndrome, which manifests itself in the gradual destruction of organs such as the kidneys, liver and gastrointestinal tract. In addition, under the influence of toxins, which are contained in huge quantities in the fungus, necrosis soon develops.

Elderly people and children who have a weakened immune system most often die from such poisoning, which makes them unable to resist poisonous toxins at least for the first time. It is known that even a piece of toadstool, not to mention a whole mushroom, can be enough to cause death. Do not be mistaken that with high-quality heat treatment, all harmful properties will disappear, and the mushroom will become safe for humans, since this is not true.

IMPORTANT TO KNOW! Not only is the body of the mushroom poisonous, but also the spores that are carried by the wind are very dangerous to humans. After all, if contacted, spores, even edible delicious mushroom can turn into a deadly weapon! Therefore, you should not pick mushrooms where you saw a pale toadstool.

Amanitotoxin or why is the venom of the toadstool deadly?

The toadstool contains two completely different groups of toxins, which differ in the strength and speed of their effect on the human body:

alpha amanites (amanitotoxins);
phalloidins.

Amanitotoxins are toxins that, although slower acting than phalloidins, are more dangerous. This is explained by the fact that their lethal dose is several times less than any other poison. They are not weakened or destroyed by drying or heat treatment, are not digested and are certainly not absorbed. After the toxins pass through the intestines, they end up in one of the most vulnerabilities– the liver is the organ to which all the power of the killing poison is directed.

In addition, toxins cause such negative consequences, How:

gradual destruction of cells, which causes liver degeneration;
a drop in glucose levels to a critical point;
destruction of the nervous system, which clearly manifests itself in late stages white toadstool poisoning.

What are the symptoms of toadstool poisoning?

Poisoning occurs unevenly and has several stages, which are accompanied by certain symptoms. Signs may differ depending on the number of toadstools eaten, that is, on the “portion” of poison that entered the body, as well as on the condition of the person himself ( general condition health, age, gender and even the presence of chronic diseases).

There are several stages that have their own specific characteristics:

The first (latent) period, during which a person feels excellent and does not feel even the slightest discomfort. This condition lasts up to 40 hours. If it is somehow possible to discover that the food taken was poisonous, then the chance of saving the person increases. But this happens extremely rarely, which negatively affects the subsequent condition, because toxins penetrate into the blood at great speed and begin to confidently move towards the final goal - the destruction of the body.
The second period does not appear immediately, which can mislead a person and make them think about ordinary food poisoning. Symptoms begin to appear within a day, but sometimes signs of poisoning appear after 5-6 days.

At this time, the condition worsens every minute, and poor health manifests itself in the following symptoms:

severe diarrhea, in which the diarrhea is not only a strange yellowish color, but also has a watery texture. After some time, small blood clots may appear;
vomiting and disturbance of water balance in the body. When you try to drink at least a couple sips of water, vomiting resumes with greater force;
the appearance of cramps and terrible pain in the intestines and abdomen;
dizziness, weakness, and severe headache (sometimes pounding in the temples);
increased heart rate and decreased blood pressure;
deterioration of visual reflexes, which leads to the fact that the picture before the eyes is very blurry;
cramps that cause severe pain in the legs;
minimal or no urination.

The third period, during which there is a significant improvement in the condition, unfortunately, imaginary. Despite the fact that the symptoms disappear, the body continues to deteriorate, which is especially evident in such an analysis as blood biochemistry. Doctors even consider this ten-hour period to be the most dangerous, because drowsiness often occurs, against the background of which death occurs as a result of collapse.
The fourth period, in which all organs are affected. At the last stage, all signs of poisoning resume with renewed vigor. In addition, the eyes and oral cavity acquire an unpleasant yellow color, and pain in the hypochondrium, especially the right one, also appears. In severe poisoning, failure quickly develops: liver and kidney failure, which leads to quick and painful death.

Of course, death does not occur in all cases. A favorable outcome can be influenced by several reasons, including the good health of the victim (strong heart, excellent condition of blood vessels and nervous system), as well as a mild degree of poisoning, in which recovery takes only a few days. In case of serious intoxication, it may take more than one week or even a month, but if all medical recommendations are followed, the organs will fully recover, and the yellow color will disappear in the first few weeks.

First “home” help when signs of poisoning are detected

Despite the fact that in this case it will be practically useless and will not bring any positive effect at all. If you think that the poisoning was caused by toadstool, you should immediately call a doctor or go to the hospital yourself, where all the necessary tests will be carried out. Contacting a specialist within the first 36 hours is a great chance for a complete recovery. By the way, even if signs of poisoning appear in one person, then it is necessary to begin treatment for everyone who could also taste poisonous mushrooms, because slowing down can lead to death.

Therefore, first aid is relevant only until the ambulance arrives. To begin with, it is recommended to rinse the stomach, clearing it of everything, including toadstools. It will be enough to drink up to 2 liters of water, depending on the weight, and “throw out” all the contents. It will not be superfluous to take activated carbon in the usual proportion.

REMEMBER! Self-medication should be kept to a minimum, as it can harm the patient.

Features of treatment for poisoning with toadstool

It is not easy to cope with such poisoning, since it not only affects the gastrointestinal tract, but penetrates the blood almost instantly. The steps that are carried out in the hospital are quite simple, but this does not mean that they should be repeated at home:

gastric lavage, which is carried out regardless of the presence of vomiting, since particles of toadstool may still be inside;
Applications Since there is no special antidote, drugs such as benzene-penicillin, silibinin, and sometimes citric acid. What is important is the quantity and order of application, which doctors calculate based on the stage of poisoning, health and condition of the person;
liquidation important problem– dehydration, which is caused by vomiting. The patient is given a drip, and various devices are introduced intravenously. If necessary, the victim is given salt water, which should replenish the amount of chlorides in the body;
carrying out forced diuresis and hemosorption, which help in removing harmful substances;
prescribing cardiac medications that are necessary for the heart to restore proper functioning;
the use of proteolytic substances that are aimed at preventing disseminated intravascular coagulation;
special therapy (hepatic), which is carried out by replenishing vitamins belonging to group B.

The main thing to remember is that treatment is more effective when treated in the early stages. Poisoning with toadstool is very dangerous and can lead to serious consequences, including death. Therefore, we warn you once again that you should not carry out treatment on your own, because for this there are specialists who know what needs to be done and what actions to take.

How to protect yourself from mushroom poisoning?

Caution is the first and most important rule to remember when you are going into the forest to pick mushrooms. Always remember that if there is any doubt that a mushroom is edible, you should not tempt fate and try it, as this can negatively affect your health and result in severe poisoning.

We offer several rules that will help you save your own life:

poisoning often occurs when a person accidentally mixes or confuses toadstool with an edible mushroom (for example);
a distinctive feature of the disease is the manifestation of symptoms in the form of vomiting and diarrhea over a long period of time;
If one of the group members is poisoned, you should also seek help and undergo all necessary tests.

Toadstool poisoning is one of the most severe, in terms of symptoms and consequences, among all food poisonings. Intoxication with the poison of this mushroom often leads to death.

To protect yourself and your loved ones from misfortune, you need to know the symptoms of toadstool poisoning and the basics of first aid.

Features of the mushroom

If a person is an avid mushroom picker, he needs to clearly know when there is an ordinary edible mushroom in front of him, and when it is its deadly counterpart. There are several signs that allow you to distinguish the pale grebe and avoid it:

the cap is close in shape to an egg, can be either flat or convex, sometimes slimy to the touch, you can see dark hairs grown into its surface, the diameter rarely exceeds 12 cm;
whitish growths resembling warts may be visible on the cap (old mushrooms do not have them, and they may also be absent if it has recently rained);
the cap is endowed with white, thin plates;
the pulp is bright white;
there is a volva - a specific formation near the ground, loosely fitting the leg;
under the cap there is a ring-shaped formation consisting of a thin flexible plate.

If you do not know the characteristics of the mushroom, it can easily be confused with its edible counterparts. A mistake like this can cost a person his life.

For children, the lethal dose of the mushroom is 35-50 g; in adults, a similar dosage causes severe intoxication with the hope of a happy outcome, but a slight excess leads to death.

When medical intervention is needed, basics of therapy

Medical care in a hospital setting is required in 100% of cases, regardless of what dose of poison enters the body.

An antidote that would effectively treat toadstool intoxication has not yet been invented. Treatment of the patient is symptomatic and is aimed at accelerating the removal of toxins from the body. The following measures are being taken:

repeated gastric lavage is performed, regardless of whether this was done during first aid;
some antibiotics can act as a nonspecific antidote to the action of toxins (in the first three days after poisoning, benzyl penicillin at a dosage of 500 thousand - 1 million units per kilogram of weight has a good effect);
thioctic acid in early period poisoning can also be used as a nonspecific antidote;
carry out rehydration therapy adequate to the losses, administer glucose intravenously to compensate for its deficiency; to restore the level of chlorides, it is recommended to use salted water orally;
in cases of toadstool poisoning, methods of forced diuresis and extracorporeal detoxification are widely used to stimulate the removal of poisons from the body;
select therapy that supports the activity of the cardiovascular system;
select drugs that prevent the formation of blood clots due to a decrease in circulating blood volume;
The patient is prescribed vitamin therapy to help the body recover faster.

Have you ever had mushroom poisoning?

Pale grebe (amanita phalloides) belongs to the mushrooms of the fly agaric genus (fly agaric family). The toxic properties of toadstool are due to amanitins. The pale grebe has characteristic external features: a) the presence of a ring on the stalk, in its upper third; b) the stem is tuberously thickened towards the base, covered with a sac-like formation; c) the plates are free, white; d) spores are colorless. The pallid grebe, a green variety, has similar characteristics to edible mushrooms: greenish russula, green, blue-yellow, beautiful volvariella, greenfinch, gray row.
In terms of the composition and amount of toxic substances contained in 1 g of pulp, toadstool is the most dangerous plant poison for humans.

Toxic substances
Pale grebe contains a whole range of different toxicants, of which the largest clinical significance have amanitins - complex chemical compounds protein nature. Toadstool contains 8 hydrophilic amanitins (cyclopeptides), 5 of which have highly toxic properties, which is why they are called amanitotoxins.
The molecular weight of cyclopeptides varies within 1000 daltons. Cyclopeptides block vital intracellular processes. The distribution of amanitotoxins in individual parts of the fungus is uneven. In 1 g of dry mass of the pale grebe, the plates contain on average 2.6 mg of amanitotoxin, the cap - 1.9 mg, the stalk - 1.7 mg, and the volva - 0.6 mg. It should be noted that the total amount of amanitins in the toadstool is not constant and is determined by the place of its growth, weather and environmental conditions. It is estimated that the lethal dose of amanitotoxins for an adult weighing 70 kg is 7 mg. This amount of toxins is contained in 30-50 g of fresh toadstool.
According to experimental studies, amanitotoxins that enter the blood from the intestines circulate freely and do not bind to albumin. The distribution volume of amanitotoxins in the body is predominantly extracellular.

The toxic effect of amanitotoxins occurs due to the inhibition of RNA polymerase type II, an enzyme involved in the synthesis of the messenger RNA precursor responsible for the synthesis of intracellular proteins. Blocking intracellular protein synthesis leads to the loss of a specific cell function. This is most evident among the cells responsible for enzymatic reactions in the body, in particular synthesis and metabolism reactions. Therefore, hepatocytes and enterocytes suffer first and to the greatest extent, which underlies all clinical manifestations of intoxication. To some extent, the selective toxicity of amanitins to the liver is due to the peculiarity of their kinetics in the body: a significant part of amanitotoxins resorbed in the intestine, having gone through the intracellular cycle in the liver, again enters the intestine with bile, followed by repeated toxic effects on hepatocytes.

With a high concentration of amanitotoxins in the intestine, long-term circulation of toxins is observed along the following path: intestine-hepatocytes-bile-intestine. Significant changes occur in the mucous membrane of the gastrointestinal tract. The initial symptom of poisoning is acute gastroenteritis. Damage to the mucosa digestive tract- a consequence of at least two reasons: 1) absorbed fungal toxin (amanitins), disrupting intracellular metabolic processes, destroys enterocytes, which is manifested by widespread necrosis of the intestinal mucosa; 2) the fungal toxin, having a pronounced detrimental effect on the saprophytic intestinal flora, creates conditions for the intensive growth of pathogenic microflora, which, penetrating into the deep layers of the mucosa, destroys it. Damaged intestinal mucosa loses its barrier function against the toxin released by bacteria. The resulting bacterial toxemia in the portal bloodstream has a detrimental effect on the functional state of the liver, which has already been subjected to the destructive effects of the fungal toxin.
The direct toxic effect of amanitotoxins on other organs is very insignificant. Changes in the kidneys are most likely functional in nature and occur at an early stage due to water-electrolyte and hemodynamic disorders, and in more late period as a result of severe changes in the liver and develop according to the type of hepatorenal syndrome.

Changes in the heart and pancreas are secondary, their development is caused by disturbances of homeostasis, the aggregate state of the blood, disseminated intravascular coagulation (DIC) and endogenous intoxication. Manifestations of damage to the central nervous system, such as psychomotor agitation, delirium, hallucinations, euphoria and obnabulation, do not have clear evidence of a direct toxic effect of the fungal toxin on brain cells. The development of asthenia and vascular collapse appear to be directly related to damage to the adrenal cortex by amanitins. Depending on the severity and timing of poisoning, the functional activity of the adrenal glands can fluctuate over a significant range.

Poison Clinic
The clinical picture of poisoning is characterized by the phasic development of pathological symptoms. Based on the well-studied signs of poisoning by toadstool, appearing in a relatively clear chronological sequence, the following 5 periods of disease development have been identified:

I - latent period;
II - period of acute gastroenteritis;
III - period of imaginary well-being;
IV - period of acute hepatic, hepatic-renal failure;
V - recovery period.

I. Latent period. The duration of the period is 6-9 hours, in rare cases 10-15 hours and extremely rarely 16-36 hours. The time period before the first symptoms of poisoning appear is determined not only by the amount of toxic substance entering the body, but also by its concentration in the simultaneously consumed food mass, as well as its constituent components.
The latent period ends with nonspecific, general clinical manifestations - general weakness, malaise, weakness, which is regarded as a harbinger of further development of the poisoning clinic.

II. Period of acute gastroenteritis. In the poisoning clinic, symptoms of damage to the gastrointestinal tract predominate.
This is manifested by sudden profuse, sometimes “gushing” vomiting of food eaten. Vomiting becomes indomitable and becomes painful for the patient. In the absence of food masses, the contents become bile, the secretion of the mucous membrane of the stomach and duodenum. Constant nausea. With increasing spastic pain in the abdomen, diarrhea develops, which in severe cases of poisoning is cholera-like in nature. The frequency of stool reaches 20-25 times a day. The stools are watery, with mucus and blood. Significant disturbances in water balance occur in the body. Loss of fluid and salts causes dry mouth and thirst. Patients report weakness, headache, dizziness. Hematocrit exceeds 50%. Drinking liquid only makes vomiting worse. Electrolyte disturbances are manifested by hyponatremia (115-120 mmol/l), hypokalemia (2.2-3 mmol/l), hypochloremia (65-80 mmol/l). Metabolic acidosis is observed in the blood. Patients become adynamic and note an increase in muscle weakness. Oliguria develops. Functional renal failure is manifested by moderate azotemia: urea 12-16 mmol/l, creatinine 150-175 µmol/l.
Dehydration, electrolyte imbalance, CBS, as well as increasing endotoxemia cause the development of hemodynamic disorders: hypotension (BP 100-60/50-20 mmHg) and tachycardia (pulse 100-130 bpm).
In the case of severe poisoning with toadstool, damage to the gastrointestinal tract leads to profound disorders of homeostasis and life-threatening disruption of cardiovascular activity. These complications are most difficult for children and the elderly, whose compensatory capabilities are largely limited. The duration of the period is 2-6 days.

III. A period of imaginary prosperity. As acute gastroenteritis subsides, a period of imaginary well-being begins, associated with the cessation of painful abdominal pain, tenesmus, nausea and vomiting. The patients feel better. “Improvement in condition” is sometimes regarded as a tendency towards recovery, but after some time (from several hours to 1-2 days) the condition worsens again, which is associated with increasing visceral pathology. It should be noted that in severe cases of poisoning, “improvement of the condition” does not occur, and the disease directly passes into the next stage - the stage of acute liver, hepatorenal failure.

IV. The period of acute liver, hepatic-renal failure. The degree of dysfunction of the liver and kidneys varies: from the absence of any clinical manifestations to the development of life-threatening symptoms. According to numerous studies, toxic hepatopathy develops already on the 1st day of poisoning, which is confirmed in the laboratory within 8-10 hours after ingestion of toadstool. Clinical manifestations in the form of hepatomegaly, jaundice, DIC syndrome, etc. are observed only on days 3-5. In this regard, to assess the severity of hepato-nephropathy, all clinical, laboratory and instrumental data obtained during the examination of patients are considered in aggregate.
According to the course of hepatopathy and nephropathy, there are 4 degrees of severity of poisoning: mild (hepatopathy stage I and nephropathy stage I), moderate (hepatopathy stage II and nephropathy stages I-II), severe (hepatopathy stage III and nephropathy I-II Art.) and extremely severe (hepatopathy stage III and nephropathy stage III)
Analysis of the dynamics of biochemical parameters depending on the severity of poisoning revealed the following: 1) predicting the outcome of poisoning is extremely difficult, and in 1 day it is almost impossible; 2) starting from day 2, it is possible to assess the severity of poisoning by biochemical indicators and, above all, reflecting the condition of the liver and kidneys; 3) when assessing the severity of poisoning, it is necessary to take into account the premorbid state of the victim, since the pathology is multiorgan in nature.

Studies of the long-term results of poisoning with toadstool are worthy of attention. The tendency towards chronicity of the pathological process in the liver is largely determined by the timing of the effect of the fungal toxin on internal organs (the duration of the toxicogenic phase) and the individual reactivity of the victim’s body. Thus, as a result of the effect of the fungal toxin on the cellular structures of internal organs in the body, deep disorders of homeostasis, hemostasis, and condition occur. cell membranes, immune and hormonal status. The resulting changes in the body are clinically manifested in the form of severe polyvisceropathy and, above all, the development of acute gastroenterocolitis and hepatic-renal failure.

At autopsy, jaundice is noted in those who died from poisoning with toadstool. skin and mucous membranes, multiple petechial, pinpoint and focal hemorrhages in the skin, sclera, connective membranes of the eyes, hemorrhages in the mucous membranes. Pathological changes found in all internal organs. The macroscopic picture in the liver corresponds to acute yellow atrophy. Histological examination reveals gross lesions - massive centro-lobular necrosis. Most of the hepatocytes in the border zone are in a state of degeneration (protein, hydropic or fatty). The structural basis of acute liver failure is massive diffuse centrilobular necrosis. In the kidneys, the tissue is swollen; when cut, the cortex is expanded, protruding beyond the capsule; it contrasts with the full-blooded pyramids. Histological examination reveals diffuse hydropic degeneration of nephrocytes.

The structural basis of acute renal failure is cholemic nephrosis. Enteritis is found in the intestines. Histological examination reveals blood clots in the mucous and submucous membrane of the large intestines, which is accompanied by an ulcerative-necrotic process. Microbial invasion into the deep layers of the intestinal wall is noted.

For early diagnosis of toadstool poisoning, the following data can be used:
Presence of characteristic external signs poisonous mushrooms.
Latent period over 6 hours.
Profuse diarrhea in the presence of blood streaks in the stool.
Exotoxic shock (in severe and extremely severe poisoning).
Hyperfermentemia 10-12 hours after the development of clinical poisoning.
Increasing hepatic, hepatic-renal failure.
Coagulopathy (from 2 days).
Increasing encephalopathy (from 3-4 days).
Decrease in PTI.

Treatment
There is no specific treatment for poisoning with toadstool. Over the years, scientists have tried to create a serum by immunizing horses and rabbits that are insensitive to amanitotoxins. However, all studies were inconclusive; it was not possible to obtain a therapeutic serum. Such attempts were abandoned after it became clear that antibodies to amanitotoxin were not formed.
To date, there is no unified treatment regimen for patients with poisoning. poisonous mushrooms. Modern treatment of patients with toadstool poisoning consists of several areas and, in addition to emergency care measures, includes a set of conservative and active methods to remove poison from the body, correction of homeostasis, prevention and treatment of multiple organ failure.

Treatment aimed at removing fungal toxin from the body and preventing multiple organ failure
To remove fungal toxin (the period of exogenous intoxication), clinical toxicology uses a complex of conservative and active methods of detoxification of the body.
Conservative methods
1. Gastric lavage.
2. Intestinal lavage.
3. Gastrointestinal sorption.
4. Forced diuresis.

Gastric lavage is an essential part of the treatment of patients with phalloidin syndrome. The procedure is carried out as emergency care at the prehospital stage and upon admission of the patient to the hospital, especially in cases where the patient continues to experience nausea and vomiting.
Intestinal lavage allows you to remove the fungal mass containing the toxin and the fungal toxin that enters the intestines with bile. Amanitins are contained in significant quantities in the intestinal contents within 24-94 hours. Thus, the concentration of osamanitin can reach 6986 μg/l, (3-amanitin 14,900 μg/l.

Gastrointestinal sorption is carried out to remove unabsorbed fungal toxin from the intestine and to interrupt the enterohepatic circulation of toxic substances. For patients in a comatose state, the sorbent is administered through a probe. A contraindication to the use of gastrointestinal sorption is intestinal paresis.

Forced diuresis is an extremely effective method for detoxifying the blood. The concentration of amanitins in urine is 28-75 times higher than in blood. In the first 24 hours after poisoning, amanitins are detected in 100% of cases; in the next 24 hours, a positive result is noted in 80% of patients. In severe cases of poisoning, amanitins can be detected in fairly high concentrations up to 3 days after poisoning. By day 5, amanitins, as a rule, are not detected. Based on these data, reflecting the toxicodynamics of amanitins in the victim’s body, the procedure of forced diuresis should be carried out within a period of up to 4 days.

Active methods
1. Hemosorption. Taking into account the life-threatening nature of poisoning, early detoxification treatment is carried out as emergency care.
Of the active detoxification methods aimed at removing amanitins from the body, hemosorption is indicated during the first 36 hours from the moment of poisoning. The procedure is used to reduce endotoxemia in the development of grade II-III hepatopathy. When hemosorption is performed in patients with grade II hepatopathy, a clear positive dynamics of the clinical condition is observed: there is a decrease in hepatocerebral insufficiency, patients emerge from a state of lethargy, become more active, and are better oriented. With grade III hepatopathy, after 16-20 hours, intoxication increases again, which is an indication for repeating the procedure. As studies show, in patients with severe hepatocerebral insufficiency, the positive effect is short-term and is clinically expressed only by the revival of reflexes.
Hemosorption is carried out for 30-45 minutes. This time is considered optimal, since with a longer duration there is a risk of developing thrombocytopenia and hypoproteinemia. Due to the danger of bleeding, hemosorption is carried out using regional heparinization: heparin is administered in the extracorporeal circuit before the column, protamine sulfate after the column in a ratio of 1:3. The dose of heparin is calculated based on the blood clotting time, 15-18 minutes is considered optimal. In patients with severe coagulopathy and unstable hemodynamics, hemosorption is not performed.
In severe hepatopathy, occurring against the background of multiple organ failure and severe homeostasis disorders, the effectiveness of hemosorption is very problematic.

2. Pasmapheresis, plasma exchange and plasma sorption
The methods are carried out with the aim of removing protein-bound toxic metabolites of various molecular weights from the body. The volume of plasma replacement during plasmapheresis is 800-1200 ml. The removed toxic plasma is replenished with protein solutions. During plasmasorption, 1.5-2 volumes of circulating plasma are perfused. Pasmapheresis and plasma sorption are carried out 1-3 days from the moment of poisoning, and at a later date - in the event of the development of toxic hepatopathy. Each patient undergoes 2-5 procedures. To prevent hypoproteinemia, patients are administered intravenously protein preparations during the methods - plasma (250-500 ml), albumin (100 ml), protein (150-200 ml).

3. Dialysis and filtration methods
To remove hydrophilic fungal toxin from the body, the use of hemodiafiltration, prolonged veno-venous hemodiafiltration and hemofiltration is fully justified. Carrying out procedures, especially extended ones (for 6-10 or more hours), as well as any extracorporeal methods of treatment, represents high risk development of bleeding. In these cases, instead of heparin as an anticoagulant, the use of sodium citrate is more justified. Carrying out a peritoneal dialysis procedure that does not require the administration of heparin encounters certain difficulties associated with acute gastroenteritis.

4. Physio- and chemohemotherapy. In the toxicogenic phase of poisoning, the use of photo- and chemohemotherapy, which has a destructive effect on the fungal toxin, is fully justified. First of all, this concerns the method of electrochemical oxidation of blood using sodium hypochlorite.

Prevention and treatment of visceral pathology
When poisoned by toadstool under the influence of a fungal toxin, the intestine loses its protective function against pathogenic microflora. The liver is exposed to the destructive effects of fungal and bacterial toxins. Uncompensated losses of fluid and electrolytes cause microcirculatory disorders in the internal organs. Ultimately, with increasing symptoms of intoxication, multiple organ failure develops. In this regard, the effectiveness of treatment is determined not only by the amount of fungal toxin that has entered the body, but also by the time of providing first aid to detoxify the body, as well as the initiation of measures for the prevention and treatment of multiple organ failure.

Mandatory drug therapy during the first 3 days from the moment of poisoning includes intravenous administration of penicillin-G sodium salt at a dose of 300,000-500,000 IU/kg per day (hepatoprotective effect relative to amanitins) and the herbal preparation silibinin (Legalon), which have a protective effect in case of poisoning with toadstool. . If the water-electrolyte balance and CBS are disturbed as a result of acute gastroenteritis, patients undergo intravenous administration of electrolyte solutions, 5-10% glucose solution, asparkam, panangin, 4% sodium bicarbonate solution under the control of hematocrit in order to normalize the parameters under the control of hematocrit.
In order to treat enteritis, combat dysbiosis, restore intestinal barrier function and parietal digestion, enterosorbents, intestinal antibiotics and eubiotics are prescribed. Treatment also includes oral administration of enterosan, normase, diflucan (or nystatin).

During infusion therapy, patients gradually restore the function of the gastrointestinal tract, improve intestinal motility, and normalize stool. From the moment the intestinal absorption function is restored, the enteral route of administration medicines and nutritional mixtures becomes the main one.
In order to decontaminate the intestines and reduce enterohepatic intoxication, antibiotics and probiotics are prescribed orally: chloramphenicol (0.5 g 4 times), neomycin (1 g 4 times), panfu-rex (1 capsule 4 times), ercefuril (1 capsule 4 times ), glutamine, pectin, bifidumbacterin, lactobacterin, linex, bificol, colibacterin, bactisubtil.
Patients with increased bleeding are prescribed intravenously aminocaproic acid (100 ml per day), Vicasol (3-5 ml), 10% calcium chloride solution (10-20 ml), and if bleeding develops, dicynon, fresh donor blood (100- 150 ml).

Protective liver therapy includes daily intravenous and intramuscular administration of vitamins B-) (1 ml of 5% solution 2 times a day), B6 (1 ml of 5% solution 2 times), B12 (200 grams 2 times), essentiale intravenously or intraportally (10 ml 2 times) or orally (2 capsules 3 times), Hepatosan (2 capsules 3 times), Heptral intravenously (10 ml or 800 mg), legal (2 capsules 3 times, which corresponds to 840 mg of silymarin). In order to regulate lipid and carbohydrate metabolism, as well as to achieve a lipotropic effect, lipoic acid is prescribed in 5-8 ml of 0.5% solution or 2 capsules 4 times.

In the case of the development of toxic encephalopathy, cytoflavin, hepamerz (10-20 ml) are prescribed intravenously. For patients with severe toxic brain damage, the dose of the drug is increased to 40-60 ml (20-30 g ornithine aspartate). The active inclusion of ornithine aspartate in metabolic processes is accompanied by a decrease in ammonia intoxication, which is clinically manifested by clearing consciousness, and in some comatose patients - restoration of consciousness.

Due to dysfunction of the adrenal cortex, treatment includes the administration of corticosteroids: prednisolone, dexazone or hydrocortisone. For comatose patients, the dose of prednisolone is up to 4 mg/kg per day.

Treatment includes the administration of antioxidant drugs: atocopherol solution (2 ml 4 times a day) intramuscularly or orally (2 capsules 4 times), vitamin C intravenously (up to 1-1.5 g), Mexidol.
When toxic encephalopathy is relieved and hemodynamic parameters are stabilized, treatment is supplemented with a course of hyperbaric oxygenation. According to CBS data, 02 tension in arterial and venous blood increases. Hyperbaric oxygenation has an effect on central hemodynamics positive influence(systolic pressure before the session 169.3 ± 7.1 mm Hg, at the end of the session 158.4 ± 6 mm Hg). After 3-6 sessions in patients with acute hepatic-renal failure in the oliguria stage, a stimulating effect of the method on diuresis is noted.

Active methods
Hemodialysis with xenogeneic hepatocytes The procedure helps restore reduced liver function. Biological dialysis is included in the complex treatment of patients with moderate, severe and extremely severe poisoning with toadstool. A day after the procedure, the content of bilirubin in the blood decreases by an average of 28.2% and enzymes by 14.5%. Dialysis helps to correct the amino acid composition of the blood and leads to an improvement in the absorption and excretion function of hepatocytes. After 3 days, the prothrombin level increases by 19.5%. The results of a study of the effect of biological cellular dialysis on the state of lipid peroxidation show that the method does not influence the level of diene conjugates in the blood serum of patients, but at the same time there is a 1.5-fold decrease in the content of the secondary product of lipid peroxidation - malondialdehyde. The total assessment of the imbalance in the LPO-AOS system by coefficient K indicates a tendency towards normalization of the studied indicator.
Application of the method in early dates diseases has a pronounced healing effect. In patients in extremely critical condition, dialysis 6-8 days after poisoning is ineffective: only during the operation is there a slight decrease in toxic encephalopathy, and in patients in a coma, reflexes are quickened.

Hemodiafiltration
The phenomena of acute gastroenteritis cause the development of pronounced water-electrolyte disorders and CBS, the effective correction of which by conservative methods sometimes fails. In these cases, prolonged venovenous hemodiafiltration and hemofiltration using special filters with a sorption effect are completely justified.
In patients with multiple organ failure, the optimal procedures for detoxification and correction of homeostasis are low-flow venovenous hemodiafiltration, venovenous hemodialysis or venovenous hemofiltration.
The combination of dialysis-filtration methods with hemosorption, plasmapheresis, and plasmasorption promotes significant removal of large-molecular and protein-related toxic substances from the bloodstream.

Lymph detoxification
In patients with severe and extremely severe poisoning by toadstool (hepatopathy II-III degree and nephropathy II-III degree), the complex detoxification of the body includes the operation of external drainage of the thoracic lymphatic duct. External drainage of lymph containing high concentrations of metabolites leads to effective detoxification of the body.
The method of replacement therapy for lymphorrhea is intravenous reinfusion of lymph purified from toxic substances using a sorbent (lymphosorption method). The detoxified lymph is reinfused intravenously into the patient.
The operation of external drainage of the thoracic lymphatic duct with lymphosorption leads to the removal of a significant amount of toxic metabolites from the lymph and blood. The content of bilirubin in the lymph decreases by 2-2.8 times, in the blood by 1.9-2.3 times; nitrogenous wastes - in the lymph by 2.1-3.8 times, in the blood by 1.7-1.9 times; MSM - in lymph 2-2.4 times, in blood 1.7-2.2 times. Transumbilical therapy
For an earlier restoration of the detoxification and synthetic function of the liver, to increase the effectiveness of conservative therapy and to improve intrahepatic blood circulation, medications are administered to patients through a bougie and catheterized umbilical vein. The method is used to treat patients with severe and extremely severe poisoning and, as a rule, in combination with other methods of active detoxification - hemosorption, plasmapheresis, plasmasorption, cellular dialysis, lymphosorption, hemodiafiltration, continuous venovenous hemofiltration. Intraportal therapy includes the administration of hepatotropic drugs (glucose solution, vitamins B and C, Essentiale, glutamic acid) and hormones (prednisolone). The daily volume of transumbilical therapy was 400-800 ml.
Against the background of this treatment method, normalization of pressure in the umbilical vein is noted (from 120-210 mm water column to 40-60 mm water column), and biochemical parameters improve. According to Doppler ultrasound, intrahepatic blood flow is restored: the initially increased resistance index in the arterial vessels of the liver decreases by 15-20%.

Liver transplantation
With the development of grade III hepatopathy, even in the conditions of a complex of active and conservative treatment methods, mortality associated with acute liver failure can reach 55-80%. In this regard, poisoning that occurs with the development of severe hepatopathy should always be considered as a variant of severe widespread damage to the liver parenchyma, which does not exclude the possibility of irreversibility of the pathological process in hepatocytes. A similar conclusion can be reached already 3-4 days from the moment of poisoning, when, despite the complex treatment being carried out, clinical and laboratory data indicate negative dynamics. In this case, liver transplantation should be considered as perhaps the only way to save the patient's life.
When choosing the timing of surgery, the kinetics of the fungal toxin in the human body should be taken into account. In case of poisoning with toadstool, amanitotoxins can be detected in the blood within 3 days. On the 4th day, amanitotoxins are detected only in rare cases, and then in trace concentrations. In this regard, if the operation is performed in the early stages, the transplanted liver will be exposed to amanitotoxins, and widespread necrosis will also develop in it. Since poisoning with toadstool occurs with the development of acute gastroenterocolitis, leading to disruption of homeostasis, a necessary condition in the preoperative period is to achieve maximum correction of the identified changes. The condition of the intestine, whose barrier function against infection is reduced, should also be taken into account. Enteral infection through the portal vein system can have a detrimental effect on the transplanted donor liver. This fact becomes special meaning in conditions of immunosuppressive therapy.
Thus, liver transplantation can be performed no earlier than 4 days from the moment of poisoning with corrected homeostasis and effective preoperative intestinal decontamination.

The indication for liver transplantation is the absence of a positive effect from intensive therapy within 48-72 hours. The negative dynamics of the patient’s condition are as follows:
Increasing encephalopathy.
Development of coagulopathy: prothrombin index below 20%.
High hyperbilirubinemia, hyperfermentemia and hyper-ammonemia (tens of the norm).
Increasing renal failure: decreased renal concentration function, hyperazotemia, oliguria and anuria.
Metabolic acidosis, hypoglycemia, hypofibrinogenemia, hypophosphatemia, thrombocytopenia, lymphopenia.
Presence of widespread necrosis during liver puncture biopsy.
Surgery is indicated before the development of cerebral edema. Acute gastroenteritis with signs of bleeding is not a contraindication to liver transplantation.

Thus, in case of poisoning with toadstool, in order to obtain a positive result in the treatment of patients, it is necessary to use methods aimed at removing the fungal toxin from the intestine, intra- and extravascular sectors as early as possible. This is achieved by gastric and intestinal lavage, gastrointestinal sorption, forcing diuresis, and the use of sorption, apheretic and dialysis-filtration methods through blood, plasma and lymph. Intestinal antibiotics and drugs that restore the natural intestinal microflora are prescribed orally. Taking into account the hepatotropism of the fungal toxin, intensive protective liver therapy is carried out by administering hepatoprotectors intravenously, orally and intraportally. Intravenous administration of penicillin 1-3 days after poisoning has a hepatoprotective effect.

In order to prevent and treat multiple organ failure, conservative therapy and active methods are used aimed at correcting homeostasis, water-electrolyte composition, CBS, the aggregate state of the blood and reducing endotoxicosis. Cell therapy is carried out: biological dialysis, oral administration of lyophilized xenogeneic hepatocytes (Hepatosan) and enterocytes (Enterosan). The complex of therapeutic measures is determined by the period of development of phalloidin syndrome and the main pathological symptoms.