Poisoning. What should be called poisoning and considered poison? General concepts of poisons and poisonings

What should be called poisoning and considered poison? What science studies the effects of poisons?

Departure called such a disorder of health or death, which is caused by the action of a poisonous substance that has entered the body from the outside. In forensic sciencepoison It is customary to call such a substance that, having penetrated into the body in small doses and acting chemically or physico-chemically, causes poisoning. However, the concept of a poisonous substance is very relative, because under certain conditions the same substance can cause poisoning, be harmless or useful, like a medicine.

The action of toxic substances, their properties, conditions of action, features of poisoning studiestoxicology (from the Greek "toxicos" - poison, the doctrine of poisons), which is separated from forensic medicine into an independent science. It is subdivided in turn into industrial (including pesticides used in agriculture), toxicology of chemical warfare agents and forensic toxicology. In turn, forensic toxicology highlighted forensic chemistry, which was dictated by the need to investigate crimes.

How common is poisoning in forensic practice, and with what poisons?

AT section practice in frequency after mechanical trauma and mechanical asphyxia, death from various poisonings is usually found, in everyday life, at work and in medical practice.

According to professor V.V. ), solvents (1.6%). However, in some regions, these figures may be different. For example, in the Rostov region, poisoning is diagnosed in 10-14% of the number of violent deaths, and carbon monoxide poisoning (39%) is in the first place, ethyl alcohol poisoning (25%), other poisons are in second place, and drug poisoning is much less common (5 %), (especially sleeping pills), poisoning with caustic poisons, including acetic acid, occurred only in 3%. About 1% were poisoned by organophosphorus pesticides, ethyl alcohol substitutes and food products, including mushrooms.

What is the forensic classification of poisons?

AT In forensic medicine, a classification is common that divides poisons into 4 groups depending on the nature of their action on the body as a whole and on individual organs and tissues:

1. Caustic poisons, causing sharp morphological changes at the application site. These include various acids and alkalis.

2. Destructive poisons, causing destructive and necrotic changes in a number of organs and tissues. (Mercury and its compounds: sublimate and granosan, arsenic).

3. Blood poisons, changing the composition of the blood. This is primarily carbon monoxide, as well as methemoglobin-forming poisons: Bertolet salt, aniline, hydroquinone, nitrobenzene, etc.

4. Poisons of functional action, not causing noticeable morphological changes. These include:

a) Poisons that paralyze the central nervous system (CNS). These are organophosphorus compounds (FOS) - chlorophos, thiophos, karbofos, etc., as well as hydrocyanic acid.

b) Poisons that depress the central nervous system. Such common narcotic substances as ethyl alcohol, ether, chloroform, technical liquids (ethylene glycol, methanol, dichloroethane). This also includes narcotic and hypnotic drugs, alkaloids - morphine, etc.

in) Excitatory and convulsive poisons. These are CNS stimulating agents (phena-min, phenatin, etc.), alkaloids (atropine, scopolamine, strychnine).

G) Poisons with a predominant effect on the peripheral nervous system. These are muscle relaxants used in surgery to relax the muscles during anesthesia, as well as pachycarpin, which acts on the muscles of the uterus.

What are the conditions for the action of poison on the body?

Features of the action of poison on the body depend on many external conditions, and before everything from the nature of the substance itself, and internal, flowing and under the influence various functions human body. It is necessary to know these conditions when investigating and conducting a forensic medical examination regarding poisoning.

First of all, thisdose, i.e., the amount of poisonous substance. Small doses that do not cause any health problems are calledindifferent if they have a curative effect -therapeutic. The minimum dose that causes poisoning is calledtoxic leading to deathlethal dose. It is clear that for different chemicals these doses are different. For example, 0.5 g of table salt is indifferent, for aspirin it is therapeutic, for cocaine it is toxic, and for morphine it is lethal. The concentration of the poison in the liquid or air matters. For example, concentrated hydrochloric acid destroys tissues, while diluted hydrochloric acid can have a therapeutic effect. A small concentration of carbon monoxide in the air does not cause poisoning, while in a confined space a high concentration leads to rapid death.

Important as well as the degree of solubility of the substance. Barium sulphate, insoluble in liquids, is swallowed before fluoroscopy of the digestive tract as a contrast agent. And barium carbonate is poisonous because it is easily soluble in water.

The physical state of the poison may be different:

solid, liquid and gaseous. The latter is more quickly absorbed into the blood when it enters the body through the lungs and is therefore more dangerous.

Period and storage conditions of the chemical are of great importance, and the duration of the poison. the longer it lasts, the more dangerous it is.

It should be emphasizedcomplex, overlapping action of different chemical compounds. Especially often this can affect when taking various drugs and alcohol without taking into account the nature of their interaction. In some cases, there is an increase in the action of one substance under the influence of another -synergism (alcohol - barbiturates), in others - a weakening of one substance occurs with the simultaneous action of another -antagonism. A well-known example of the poisoning of Rasputin, when potassium cyanide was added to the cream of the cake, and, despite the lethal dose of poison, it did not lead to death, since glucose contained in sugar and grape wine had an antagonistic effect on it.

Of great importance are the constitutional features and the state of the body at the time of the introduction of the poison. This includes gender, age: in women, children and the elderly, the toxic effect occurs from small doses. The ratio of the amount of substance and body weight also plays a role. A disease has a negative effect on the body, especially of the excretory organs, exhaustion of a person, pregnancy.

It is especially important to emphasize the influence on the occurrence and course of poisoningindividual intolerance, hypersensitivity to certain drugs at usual doses. Such people have an allergic reaction even to widely used drugs.

For some people, long-term use of drugs causesaddictive, which makes it possible to tolerate toxic and even lethal doses. Occasionally, addiction turns into addiction when a person experiences an irresistible the desire to re-induce calm, euphoria, which turns him into a drug addict. In addition to well-known herbal drugs - opium, Indian hemp preparations (hashish, marijuana, marijuana, etc.), as well as morphine, heroin, promedol - these are sleeping pills: barbiturates and non-barbiturate substances. The sudden deprivation of an addict of a habitual drug causes acute severe health disorders, arousal, calledabstinence. In this state, the addict can kill a person.

Finally, the influence of the external environment (temperature and humidity, changes in barometric pressure) can be attributed to the conditions that sometimes affect the course of poisoning.

What is the significance of the conditions and route of entry of the poison from the body? What are the features of the course of poisoning?

For rapid entry into the blood, and this is a prerequisite for the action of poison, the route of its entry is important. Often - this is the introduction of poisonthrough the mouth into the digestive tract, where it is absorbed into the bloodstream through the intestines and partially detoxified in the liver. If the poison penetratesthrough Airways, then it bypasses the liver barrier, entering directly into the bloodstream, and causes poisoning faster. Poison can penetratethrough the skin and then it also quickly enters the bloodstream. It is clear that the most dangerous is the introduction of poisonintravenously, i.e. directly into the blood, it immediately has a toxic effect on all organs. The poison acts quickly, also bypassing the liver, when it is injectedthrough an enema into the woman's rectum or vagina.

The ways in which poison is excreted are also important. These are mainly kidneys, intestines, less often lungs, mammary glands. In such cases, the poison acts at the sites of excretion, affecting these organs (ulcerative colitis, mercurial nephrosis).

Depending on the nature of the poison and the conditions of its action, the course of poisoning in its duration can beacute, subacute and chronic.

Acute is such a poisoning that develops quickly (up to one to two hours), ending in death, and occurs from one dose, which depends primarily on the poison when taking a lethal dose and the influence of other conditions. Acute is usually cyanide poisoning or the more common carbon monoxide poisoning.

Subacute poisoning, like acute poisoning, occurs relatively quickly, within hours or days. It often causes damage to individual organs.

Chronic poisoning occurs when repeated intake of small doses of poison over a long period of time. It develops gradually and is similar to a disease. In forensic medical practice, it is less common than acute and subacute poisonings.

What is the origin of poisoning?

The origin of poisoning can be different. itrandom poisoning at home. The most common: from carbon monoxide, when taking alcohol substitutes, various household and technical means. Medical poisoning when taking strong drugs or medicines with overestimated doses. Children and debilitated patients are especially sensitive to them. This includes substance abuse (alcoholism, morphinism, etc.).

Of particular importance arefood poisoning. Such poisonings usually occur in the same family or among those who ate in the same dining room and more often end happily. However, they can be the subject of investigation and examination, especially in fatal poisonings. Usually, food poisoning occurs when food is contaminated with microbes, substances that are poisonous in themselves can get into it.

Can be distinguished professional poisoning associated with violation of working conditions and safety regulations.

Meet suicide by poisoning. In this case, sleeping pills are often used.

At killings tasteless and odorless poisons are used, which are added to drinks or food. It should be recalled that the evidence and establishment of the type of death is the competence of the investigator.

Examination in case of suspected poisoning is primarily associated with its recognition, i.e., establishing the cause of death or health disorder.

What are the stages of proof of poisoning? What is used for this?

Given that poisoning is one of the most complex types of forensic research, one should never give a conclusion on only one examination of a corpse, it is necessary to take all measures to fully collect the facts of the case and use all the data to draw conclusions. Establishment of poisonings and solution the above questions are carried out in case of poisoning according to the followingstages:

1. Familiarization of the expert with the materials of the investigation, which are important for establishing the poisoning.

2. Participation of an expert in investigative actions, primarily in the inspection of the scene, as well as in searches, interrogations of victims, medical workers and other witnesses.

3. Study and evaluation of the clinical picture of poisoning according to the medical history and other medical documents.

4. Examination of the corpse.

5. Additional laboratory tests. First of all, forensic chemical studies of tissues and organs of the corpse, vomit, gastric lavage, residues of toxic substances; histological examination of internal organs; discussion of the results obtained in laboratory studies.

6. Formulation of expert conclusions (conclusions).

What are the features of a forensic examination of a corpse in case of suspected poisoning?

rules forensic medical examination corpse in cases of poisoning provide some features.

They start by examining the clothes and everything that was delivered with the corpse. Substances suspected of being sources of poisoning are described in particular detail and carefully handled. They are sent to the appropriate laboratory for further testing.

Particular attention is paid to the specific smell, and therefore the room is preliminarily various preparations should be ventilated and removed, the type of cadaveric spots, the color of the blood matters, and therefore the lighting should be natural and sufficient. All tools, glassware only, gloves must be rinsed clean water and dried, and the dissecting table removed from the previous dissection.

Internal examination begins with examination of the chest and abdominal cavity. On the spot, before extracting the organ complex, the pericardium and heart are opened, from which blood is taken, a ligature is applied at the entrance and exit from the stomach, which is opened in a cuvette. Do not wash the organs with water so as not to wash away the poison.

It must be borne in mind that non-compliance with these elementary requirements may adversely affect the results, and the absence of instructions may be used by the parties as an argument against expert opinion in litigation.

What, in addition to the study of the corpse, laboratory research methods are used to diagnose poisoning?

First of all, it should be noted that it is impossible to overestimate laboratory research. At the same time, their use is mandatory even in the presence of other evidence, since it allows obtaining objective evidence of the conclusion about a particular poisoning. Most often, forensic chemical and histological examinations are used, which are carried out in the relevant laboratories of the SME Bureau, less often, depending on the suspicion of poisoning with specific poisons, biochemical, botanical, bacteriological, pharmacological methods of studying various organs and tissues of a human corpse.

What and how should be taken from a corpse for forensic chemical research?

If poisoning is suspected, at least 2 kg is withdrawn from the corpse of an adult for a general forensic chemical analysis. internal organs. Organs are placed in dry, clean glass jars without prior washing. The stomach with the contents is placed in jar No. 1; in jar No. 2 - 1 m of small and large intestine with contents, from the most altered departments; in jar No. 3 - at least 1/3 of full-blooded sections of the liver with a gallbladder; in jar No. 4 - one kidney and all urine; in jar No. 5 - 1/3 of the brain; in jar No. 6 - at least 2 ml of blood; in jar No. 7 - the spleen and 1/4 of the most full-blooded section of the lung.

If you suspect the introduction of poison through the vagina or rectum, you must additionally take them into separate jars, if you suspect subcutaneous or intramuscular injection of poison, remove the area of ​​skin and muscles from the area of ​​​​the proposed injection. In case of fear of rotting, ethyl alcohol is used for preservation - rectified, 300 ml of which is separately sent to the laboratory for control.

These organs are either not fixed, or when the study may be delayed, they are filled with rectified alcohol with the simultaneous sending of about 300 ml of the same alcohol to the laboratory for a control sample.

If poisoning with a specific poison is suspected, another set of organs and tissues is taken, in a smaller amount, as indicated in the rules. For example, if ethyl alcohol poisoning is suspected, it is enough to take 20 ml of blood from large vessels of the extremities or sinus of the dura mater (in its absence - 100 g muscle tissue), as well as all urine. If carbon monoxide (carbon monoxide) poisoning is suspected, blood is taken from the cavities of the heart, dishes with seized tissues are marked and sent to the forensic chemical department.

The jars are hermetically sealed with ground stoppers, and in their absence, with polyethylene, wrapped in clean paper, tied with twine and sealed. A label with the necessary entries is stuck on each jar. The material must be urgently delivered to the forensic laboratory of the Bureau of Forensic Medical Examination. If sent to another city, the banks are packed in such a way as to ensure their safety. An inventory listing the contents is also included here, a copy of which remains with the expert. If the material is seized by the investigator, then together with the banks, a decision is also sent on the appointment of a forensic medical examination, if the expert (at the autopsy) - the direction of a forensic medical expert with summary the circumstances of the death and the data of the study of the corpse, F.I. 0. of the deceased, what kind of poison the poisoning could be, as well as issues to be resolved. When sending for re-analysis - copies of the conclusion of the primary forensic medical examination.

For the study of the exhumed corpse, earth is sent, taken in 500 g from six places (above, under the coffin, near its side surfaces, at the head and foot ends of the coffin), as well as pieces of clothing, upholstery, bedding of the lower board of the coffin, various decorations and objects, found near the corpse.

What are the requirements of the Rules for the withdrawal of material for other research?

As well as chemical, histological examination is often used, for which pieces are taken 0.5 cm thick, 1-1.5 cm long, 1.5-2 cm wide in those places that are most changed with the area of ​​the unchanged part. If the changes are not visible, one should take those places of the organ in which the anatomical structure is better distinguishable. The pieces are placed in a 10-12% formalin solution, which should be 10 times the volume of the material taken. The bank (and sometimes separate pieces) is marked and sent to the forensic-histological department of the Bureau of SME with a separate directional relationship.

The removal of objects (blood, bile and pieces of internal organs) for bacteriological examination, unlike all others, requires sterility. The study is carried out in the bacteriological department of the BureauSME, or (in his absence) in the laboratory of the Center for Sanitary and Epidemiological Surveillance.

As Is the results of a forensic chemical study assessed, taking into account other factors obtained and the circumstances of the case?

At a positive result Forensic chemical research should take into account, taking into account the specific conditions, whether the poison could have got after death or accidentally from environment whether ingested as part of food or medicine. The possibility of deliberate infusion of a poisonous substance after death cannot be ruled out. to simulate suicide or alcohol intoxication, which can be established by examining the stomach and other organs. It is important to analyze the impact of a specific amount of the identified chemical. Finally, one must keep in mind possible technical errors, both in the replacement of material and in the process of chemical research.

At negative As a result, it is necessary to take into account whether the poison was released from the body before death? Did it decompose during life, turning into decay products? Was the poison in very small doses? A negative result can be in the case when a significant time has passed from the opening and removal to the study, but also when, from the moment of death to the opening, the corpse was subjected to decay, which decomposes hormones, accelerates diffusion from the stomach, intestines and changes the distribution of poison. Some poisons can persist for a long time in a corpse. Medications: atropine up to 3 years, morphine up to 13 months, strychnine up to 6 years, barbital up to 1.5 years. Such information exists and must be taken into account. It is also important when the material was taken from the corpse. For example, dichloroethane is detected in 98% of cases on the first day, and later, only in 58% or less. Formalin embalming has a negative effect on cyanides, therefore, if such poisoning is suspected, formalin is not used. The result is affected by unsatisfactory storage of the material, improper implementation of the technique or its absence.

It is important to consider the impact of resuscitation or intensive care, which are used in severe cases of poisoning. These methods change the results of a forensic chemical study, so it is necessary to detail medical history and take into account what was introduced, or, on the contrary, was excreted from the body. Sometimes in such cases, inadequate treatment may arise, that is, associated with the need to establish whether it (and not a toxic factor) affected the deterioration of health or the onset of death.

How important is the analysis of step-by-step data acquisition in cases of suspected poisoning in drawing conclusions?

When discussing the results obtained and drawing conclusions, whatever they may be, positive or negative, it must be remembered that the conditions for the action of the poison, its quality and routes of administration, the sensitivity of the organism and the influence of the external environment are numerous. Their combination in each case affects the occurrence, development and outcome of poisoning. That is why in the process of examination it is necessary to collect information, and at this stage to analyze it. As always, the conclusions must be objectively justified, but this is especially important when the causes of death compete or the results of the autopsy do not correspond to the data of any other stage of the examination, for example, a forensic chemical study. The formulation of expert conclusions in such examinations is especially responsible. This is the final stage, as a result of which it is necessary to make a final judgment about poisoning as a cause of death and to resolve other expert issues.

The results of forensic chemical and other studies must be analyzed by an expert, taking into account the circumstances of the case and the data from the study of the corpse. Neglect or underestimation of forensic chemical analyzes, misunderstanding of the need to use dataall stages leads to obviously erroneous results.

Thus, only after a thorough collection of data and a critical study of the circumstances of the case, the clinical picture, autopsy data and histological examination and discussion of the results, it is possible to draw a scientifically based conclusion about poisoning and answer other questions of the investigator.

If poisoning is suspected, another cause of death must first be ruled out. The clinical picture may be similar in diseases leading to sudden death. For example, a brain contusion was mistaken for alcohol intoxication by clinical manifestations. Only the complex of the above methods, the use of data from all stages of the examination, allows you to avoid errors.

In some cases, if poisoning is suspected, an examination is carried out with a living person in a hospital or outpatient clinic. In this case, after studying the documents, an examination is made with the help of consultants of the relevant specialties in order to prove poisoning and exclude the disease. Conducted laboratory tests of blood, urine, feces, vomit. Moreover, the earlier the material is taken, the more reliable the result. In addition to establishing the substance that caused the poisoning, the expert also establishes the degree of harm to health.

Forensic medical examination of poisoning with certain poisons

What are caustic poisons and how do they work?

caustic poisons, having a pronounced local effect and good absorption, they cause local and general changes associated with metabolic disorders. AT clinical picture the main thing is burning pains immediately after swallowing along the esophagus and stomach, vomiting with blood, spasm of the glottis, coughing, a sharp and rapid deterioration in general condition, death in the first hours from shock, asphyxia or bleeding.

On external examination, this is a chemical burn of the oral mucosa. With the internal - compaction or softening, discoloration and damage to the mucous membrane of the esophagus, stomach, which is perforated in places of prolonged contact, and the poison (acid or alkali) is poured into the abdominal cavity, damaging the organs.

This is the general picture. Acids are characterized by dehydration and thickening of the tissue. Depending on the acid, a scab of a different color (sulfuric - dirty green, nitric - yellow, acetic - brownish). Lethal dose from 5 ml (sulfuric acid) to 10-15 ml (hydrochloric acid).

Alkalis cause proteins to liquefy and tissues become soft, swollen and slippery, a lethal dose is 15-20 ml, for ammonia- 25-30 ml.

What poisons are called destructive and how do they work?

Destructive Poisons characterized by damage, up to necrosis, of various organs, which can be seen at autopsy and examination of the corpse or with the help of histological examination. For example, mercury preparations (mercuric chloride - a lethal dose of 0.2-0.3 g), used in medical practice or granosan, common in agriculture, lead to changes in the places where the poison comes into contact. These are swollen grayish mucous membranes of the mouth, esophagus (mercury stomatitis, gingivitis), stomach, colon (colitis). An increase in the size of the kidney, the cortical layer is thickened, with red stripes and dots (sublimate kidney). Important common features: exhaustion, edema and plethora of the brain, punctate hemorrhages in the membranes, etc. Important (if known) clinic and, of course, the result of a forensic chemical study.

This principle also applies to arsenic, which leads to a health disorder: gastrointestinal or nerve paralytic, as well as peculiar morphological changes. Lethal doses of it - 0.1-0.2 mg; arsenic is found in nails, hair, and therefore a positive result is possible in a century (modern detection of the amount of arsenic in Napoleon's hair).

What kind poisons belong to the blood group and what effect do they have?

blood poisons affect the composition and properties of blood. The most common poisoning is carbon monoxide (which we will dwell on separately), these are methemoglobin-forming poisons (hydroquinone, berthollet salt, aniline - a lethal dose of 10-20 g). The clinical manifestation is characterized by oxygen starvation, because the respiratory center in the brain is paralyzed. When examining a corpse, gray-brown color of blood, cadaveric spots and internal organs, olive color of urine, enlarged kidneys. In a forensic blood test, methemoglobin is found.

What is carbon monoxide? In what cases does poisoning with this gas occur and in what form?

carbon monoxide (CO) refers to blood poisons and is a colorless gas, odorless, although in this pure form practically never occurs. Most often it is included in the composition of carbon monoxide, which is formed during the furnace, exhaust gas - internal combustion engines, lighting - coal gas, powder gas containing up to 50% carbon monoxide.

Compared to oxygen, it has a significant affinity for blood hemoglobin, therefore it very quickly displaces it from hemoglobin, forming instead of the usual compound (oxyhemoglobin) carboxyhemoglobin, which causes oxygen starvation- Hypoxia and giving the blood a bright red color. At the same time, poisoning acts on the central nervous system.

In forensic practice, the most common form of poisoning is acute and even fulminant, although it can also be chronic.

In this case, the person quickly loses consciousness, which does not allow him to take measures to save. If it quickly enters the atmosphere of clean air, then carbon monoxide is excreted through the lungs in a few hours. However, there is still a danger of irreversible changes in the brain, which manifests itself at a later date.

How is carbon monoxide poisoning diagnosed on a corpse? What is its origin?

AT In this case, as always, the data of the examination of the scene of the incident, the clinic, the examination of the corpse and the forensic chemical examination are taken into account. The disease state is characterized by a feeling of heaviness and pain in the head, throbbing in the temples, weakness, dizziness, flickering in the eyes, nausea, vomiting, respiratory distress, loss of consciousness, involuntary excretion of urine, feces, onset of coma, convulsions.

When examining a corpse, attention is paid to the bright red color of cadaveric spots. At autopsy, the same color of blood and the plethora of internal organs are striking. To detect carboxyhemoglobin, blood is taken from the heart, examined by chemical or spectral methods. They are based on the persistence and immutability of carboxyhemoglobin compared to unpoisoned blood containing oxyhemoglobin. In the first samples, in case of poisoning, when a reagent (alkali or tannin) is added to the blood, the color of the blood does not change, while in the control it acquires a brownish-greenish or brown color. In a spectral study, the addition of an oxyhemoglobin reducing agent does not change the two absorption bands in the yellow-green part of the spectrum in the presence of carboxyhemoglobin. In the absence of it, the two bands will merge into one wide band of hemoglobin. However, these samples are used as preliminary at the sectional table. And in order to prove poisoning, it is necessary to send blood to a forensic laboratory, where the amount of carboxyhemoglobin, because when inhaling air in some industries and even smokers, the test may be positive. And death occurs at 60-70% of the content of carboxyhemoglobin. However, when evaluating a negative result, it should be taken into account that the victim could be quickly removed from the scene and the concentration of the poison decreased. At autopsy, signs of acute death are also found, sometimes in protracted cases there are foci of softening in the brain, and dystrophic changes in the internal organs.

Carbon monoxide poisoning in most cases occurs through negligence, non-compliance with safety regulations at home or at work, as well as from the action of exhaust gases when the engine is running in a closed cabin or garage. Occasionally there are suicides with carbon monoxide, isolated cases of murder are described.

What poisons are called functional poisons

actions?

Functional poisons include those substances that in acute poisoning, causing a specific clinical reaction, do not lead to morphological changes in organs. These poisons are difficult to diagnose, since no visible changes can be detected using conventional methods. Functional poisons are divided into three groups: general functional (general cellular) and poisons that act on the peripheral and central nervous system.

What poisons are classified as general functional and how to diagnose them? Do they all cause respiratory failure and death from asphyxia?

This group includes many different subgroups of compounds. These are (organophosphorus compounds):chlorophos - lethal dose -30-60 g,karbofos, thiophos etc., used in agriculture and in everyday life. They cause bronchospasm with mucus secretion, convulsions, loss of consciousness, circulatory disorders, gastrointestinal tract, vision with constriction of the pupils.

hydrocyanic acid (hydrogen cyanide), potassium cyanide (lethal dose 0.15-0.25 g) - the strongest poison contained in apricot kernels(decomposes rapidly in air). It paralyzes the respiratory organs, leads to rapid death, the development of a complex of symptoms. Specific are the smell of bitter almonds from the organs of the corpse and the bright red color (in places with a cherry tint) of blood and cadaveric spots. In addition to a forensic chemical study, if bones are found in the stomach, a botanical study is prescribed.

This group also includes hydrogen sulfide - a colorless gas that is formed during the decay of organic matter, during blasting, in the sewer system, in mines and other industries. It causes severe irritation of the mucous membranes, blurred vision, sore throat, nausea, vomiting, stunning and coma. When opening the cavities, there is a smell of rotten eggs, cherry-colored blood. During the study, blood and internal organs are taken; carbon dioxide - a colorless gas, accumulates in places of decay and fermentation, acts as a narcotic, observed shortness of breath, cyanosis, loss of consciousness, convulsions. At autopsy, there are general signs of asphyxia. It is important to take air from the scene for analysis, because carbon dioxide is not found in the corpse.

What poisons depress the central nervous system?

This large group of poisons does not cause morphological changes or they are insignificant and nonspecific. hope for clinical manifestation is not always justified. Therefore, the diagnosis is based on laboratory data and the exclusion of another cause.

These include:

Poisons that depress the nervous system, ethyl (wine alcohol), which, due to the special significance of poisoning, we will analyze separately).

Methyl alcohol, specific in the diagnosis of which is the expansion of the pupils, the lack of reaction to light, the decrease in visual acuity up to blindness. An autopsy does not reveal characteristic changes, with the exception of prolonged poisoning, when destructive changes in internal organs are found. A forensic chemical examination of blood and internal organs reveals methyl alcohol, the lethal dose of which is 30-50 ml.

ethylene glycol in the form of 50% aqueous solution used as an antifreeze, a liquid that does not freeze at low temperatures. Poisoning occurs in two forms - cerebral and renal-hepatic. In the first case, at autopsy, a change in the meninges is found, a lot of small-point hemorrhages in the internal organs. In the second - plethora, edema, dystrophy, hemorrhages in the kidneys and liver. The lethal dose of ethylene glycol is 100 ml.

Morphine used in medicine as a pain reliever. Acute poisoning develops in three periods: at first - increased heart rate, respiration, redness of the face, then comes apathy, sleep, loss of consciousness, a rare pulse, relaxation of the muscles, constriction of the pupils.

sleeping pills, most often barbiturates (luminal, veronal, barbamil, etc.) cause deep sleep, turning into anesthesia, respiratory paralysis, affect blood vessels, lower the temperature, cause cyanosis. Lethal dose - 1-5 g.

What poisons excite the central nervous system and have a convulsive or relaxing effect on the peripheral nervous system?

These funds are stimulating, increasing physical and mental performance. In toxic doses, they increase blood pressure and are dangerous, especially for patients with cardiovascular diseases. These include alkaloids (atropine, which leads to delirium, hallucinations, and at a dose of more than 0.1 g of death) and convulsive poisons (strychnine, acting on the spinal cord, a lethal dose of 0.03 g). When examining a corpse, a sharp dilation of the pupils is observed with atropine poisoning, with strychnine poisoning - rapidly advancing, pronounced rigor mortis and hemorrhages in the muscles. The peripheral nervous system is affected by muscle relaxants (pahikarpin), used in surgery to relax the muscles.

What food poisoning is most common in forensic practice?

Food poisoning is sometimes the subject of a forensic medical examination. This should be remembered when examining the scene in order to remove suspicious food and drink for chemical and bacteriological examination. This should be remembered by the doctor of the medical institution, collecting an anamnesis.

Food poisoning targets by origin into bacterial and non-bacterial.

The former are caused by microbes, most often by salmonella when eating meat, fish, and canned food. The most severe poisoning is botulism from the strongest botulinum toxin. The clinic is specific: visual impairment occurs, paralysis of the tongue, pharynx, larynx, temperature drops, pulse quickens. Often such poisoning ends in death after 3-4 days. Nothing characteristic is revealed at the autopsy, the post-mortem diagnosis is established mainly by the clinic and biological research on animals.

Non-bacterial food poisoning primarily includes mushroom poisoning (fly agaric, pale grebe, stitches, false mushrooms), poisoning by plants, berries (henbane, belladonna, hemlock, aconite, cockle), as well as plants that are not poisonous at all, but acquiring poisonous properties. Each of them, depending on the mechanism of action, leads to some peculiar clinical and morphological changes. But a feature is the conduct, in addition to other laboratory studies, of a botanical study of the detected particles.

Some types of fish or their caviar (marinka, barbel, pufferfish, khramulya, etc.) can be poisonous. Prevention and investigation of food poisoning is the responsibility of state sanitary and epidemiological surveillance centers in accordance with the Instructions.

Poisonings differ by cause (accidental and intentional) and by the circumstances of occurrence (industrial and domestic). In forensic practice, there are poisons predominantlywith local action (caustic poisons), which include concentrated acids and alkalis, causing sharp morphological changes at the site of application in the form of a chemical burn of varying degrees. When taking caustic substances through the mouth, burns occur in the form of streaks or spots on the skin in the area of ​​​​the mouth, chin, cheeks.

acids have their damaging effect of free hydrogen ions, which dehydrate tissues and coagulate proteins, leading to coagulation (dry) necrosis. The nature of the damaged surface (eschar) often suggests the action of a certain acid. In case of poisoning with sulfuric acid, a dirty gray color and thickening of the mucous membrane of the esophagus and stomach are noted, and the scab becomes brown or almost black. In case of poisoning with nitric acid, a yellow or green-yellow color of the affected tissues is observed; the action of acetic acid is associated with its pronounced hemolytic effect, as a result of which the scab acquires a pinkish-reddish hue.

alkalis have an effect with their hydroxyl ions, causing the liquefaction and melting of proteins with the formation of coliquation (wet) tissue necrosis. The affected areas become soft, swollen, slippery to the touch. On the mucous membrane a scab of a gray-greenish or dark brown color is formed.

The other group includes resorptive poisons, the toxic effect of which is manifested only after their absorption. This group contains the following toxic substances.

destructive poisons, causing dystrophic, necrobiotic and necrotic changes in the internal organs. These include mercury derivatives (mercuric chloride, granosan, etc.) and arsenic compounds (arsenic acid anhydride).

Poisons that change the composition of the blood are blood poisons. These include primarily carbon monoxide ( carbon monoxide), when it enters the organ

nism is the binding of hemoglobin and the formation of carboxyhemoglobin, which gives the blood, muscles, cadaveric spots a bright red color. Other representatives of this group are methemoglobin-forming substances (aniline, Bertolet salt, sodium nitrite, nitrobenzene, hydroquinone, etc.). Like carboxyhemoglobin, methemoglobin is a stable compound, unable to attach oxygen and transport it to tissues.

functional poisons, having a general cellular and neutrotropic effect without pronounced morphological changes. These include poisons: 1) paralyzing or depressing the central nervous system (organophosphorus compounds, hydrocyanic acid compounds (cyanides with the smell of bitter almonds), ethyl and methyl alcohols, ethylene glycol, drugs and sleeping pills); 2) excitatory and convulsive poisons (alkaloids in the form of atropine and strychnine); 3) poisons with a predominant effect on the peripheral nervous system (myo-relaxants, pachycarpine).

Allocate also food poisoning bacterial origin (botulism) and food poisoning of non-bacterial origin (poisonous mushrooms, poisonous plants, poisonous animal products).

Forensic medical examination of poisonings is based on a detailed analysis of the circumstances of the incident, data from medical documents, autopsy results, forensic chemical examination of objects, and the results of other types of laboratory studies (histological, biological, botanical, bacteriological, etc.). It should be remembered that the positive or negative results of a forensic chemical study are not in themselves proof of the presence or absence of poisoning in all cases. False-positive results may be due to the post-mortem ingestion of various toxic substances from the environment into the corpse. Negative results of a forensic chemical study are often associated with the complete elimination of a toxic substance from the body before death or with its various transformations (decomposition, biotransformation).

Scrollquestions, allowedatexpertisepoisoning

1. Could death have occurred from poisoning?

2. What toxic substance caused the poisoning?

3. What could be the dose and concentration of the injected poison?

4. In what way the poison was introduced into the body, in what state of aggregation
yania?

5. Could the substance introduced into the body be destroyed and completely
stand out before death? What is the time required for this
dimo?

6. Could the poisonous substance have entered the body posthumously (from
soil, water, etc.)?

7. What could be the origin of food poisoning (vegetable
animal or animal, bacterial or non-bacterial)?

8. What conditions could contribute to the onset of poisoning (with
concomitant diseases, synergism, addiction, etc.)?

9. Could alcohol intoxication affect the course and outcome of
management?

10. Is the death due to individual re
actions (intolerance) of the organism to the introduced chemical or
drug substance?

Note.

Any substances found at the scene or on the clothes and body of the victim that could allegedly cause poisoning, as well as vomit, urine, feces and other biological secretions, should be sent for examination.

testcontrol

In paragraphs 1-10 below, there are two statements connected by the conjunction “because”. Establish whether each of these statements is true or false separately and whether the connection between them is true. Give the answer marked with a letter according to the following code.

Answer	Statement 1	Statement 2	Connection

1. "Pose of a boxer" is a sign of the lifetime action of a high
what temperature, because under high temperature
shortening and tightening of the muscles.

2. Acids and alkalis are caustic poisons, because in their place
contact with the body causes chemical burns.

3. The moisture content of the skin is conducive to electric shock, because
what Skin resistance increases with moisture.

4. In the initial period of alcohol intoxication, it is noted with
state of euphoria because alcohol first excites
giving effect on the central nervous system.

5. A sign of the lifetime effect of low temperature is
pose "kalachik", because at low temperature man
to reduce the heat transfer surface.

6. The possibility of overheating of the body increases with increasing
air humidity, because with high air humidity
ha reduces the evaporation of moisture from the surface of the skin.

7. Sunstroke is accompanied by a violation of thermoregulation of the head
brain, because while there is a direct and long-term
impact sun rays on the head.

8. Violation of heat transfer processes leads to burns and frostbite
niyam, because disruption of these processes is associated with local
temperature effect on the body.

9. Chemical burns of the skin of the face when caustic substances enter through
mouth usually look like vertical streaks, because degree
chemical burns skin depends mainly on the concentration
tion and exposure to caustic substances.

10. Neurotropic poisons do not cause specific morphological
changes because they belong to the group of functional
poisons, mainly acting on the central nervous system
topic (CNS).

In paragraphs 11-20 below, of the responses indicated by letters,one correct answer must be chosen.

11. Signs of a typical electrical tag are all of the following,
Besides:

A - roller-like elevation of the skin along the edges of the lesion;

B - round or oval shape;

C - crater-shaped depression in the center;

D - detachment of the epidermis;

E - wet surface with purulent overlay.

12. The limit of "safe" electric current voltage is:
A - 12-24 V;

B - 40-60 V; C - 100-110 V; D - 220-240 V; E - 3g0 V.

13. Damaging action electric current depends on:
A - current voltage]

B - current strength;

C - current frequency;

D - resistance;

E - all of the above.

14. Burns of the skin with a hot liquid are characterized by:
A - a significant depth of damage;

B - the presence of singed hair;

C - the form of a burn wound, resembling traces of streaks;

D - the presence of soot on separate parts body;

E - signs of burning clothes.

15. During the examination of poisoning, the expert must answer all questions
sy, except for the following:

A - whether the onset of death is associated with poisoning;

B - what toxic substance caused the poisoning;

C - for what purpose the poisoning was committed (murder, suicide or accident);

D - how the toxic substance got into the body;

E - what diseases the deceased suffered from and whether they contributed to the onset of death.

16. To the factors contributing to the general effect of low temperature
ry, include all of the above, except;

A - low humidity;

B - strong wind;

C - the state of clothing;

D - adynamia;

E - alcohol intoxication.

17. What stage of alcohol intoxication could the subject be in when
life, if 2.8% o ethanol is found in his cadaveric blood:

A - slight intoxication;

B - intoxication medium degree;

C - severe intoxication;

D - severe alcohol intoxication;

E - fatal poisoning.

18. Which of the following substances belongs to the group of destructive
poisons;

A - carbon monoxide;

B - chlorophos;

C - morphine;

D ^ - arsenic anhydride;

E - hydrogen sulfide.

19. In case of poisoning with what substance, the blood becomes bright scarlet
Colour;

A - ethylene glycol;

B - arsenic anhydride;

C - carbon monoxide;

D - acetic acid; E - sublimate.

20. With a significant effect of radiant energy on the body,
occur:

A - acute radiation sickness; B - chronic radiation sickness; C - radiation burns; D - all answers are correct; E - wrong answers.

In paragraphs 21-30 below, indicate the correct answer, indicated by a letter, in accordance with the following code:AND- if 1, 2, 3 is true;AT- if true 1, 3;FROM- if true 2, 4;D - if true 4;E - if everything is correct.

21. What should be attributed to the main mechanism of decompression development?
onnoy disease:

1) nitrogen poisoning;

2) oxygen poisoning;

3) carbon dioxide poisoning;

4) blockage of blood vessels by gas bubbles (gas embo
liya).

22. The most typical signs of a sharp increase in barometric
cal pressure are:

1) barotrauma of the lungs;

2) barotrauma of the hearing organs;

3) barotrauma of the accessory cavities of the nose;

4) barotrauma of the musculoskeletal system.

23. What is the basis for establishing carbon monoxide poisoning:

1) circumstances of the case;

2) cadaveric spots of pinkish-red color;

3) detection of carboxyhemoglobin in the blood with spectral
research;

4) bright red (scarlet) blood.

24. Negative result forensic chemical research mo
can testify to:

1) the absence of poisoning;

2) the destruction of the poison in the body;

3) complete elimination of the poison from the body;

4) deposit toxic substances organs and tissues.

25. In accordance with the forensic classification of poisons under
divided into:

2) destructive;

3) blood;

4) functional,

26. Signs of IV degree frostbite include:

1) local redness and swelling of the skin;

2) the formation of blisters on the skin;

3) necrosis (death) of the entire thickness of the skin;

4) necrosis of the skin and deeper tissues.

27. Factors contributing to overheating of the body are:

1) high ambient temperature;

3) high air humidity;

4) human growth,

28. The conditions for the action of poisons depend on:

1) the amount of the administered substance;

2) concentration and state of aggregation;

3) ways of introduction and removal;

4) the nature of the transformation of the poison in the body.

29. Diagnostic signs of in vivo action on humans
ka high temperatures in a fire are:

1) the presence of soot on the mucous membrane of the respiratory tract;

2) the absence of soot in the depths of the skin folds on the face;

3) a large amount of carboxyhemoglobin in the blood and skeletal
muscles;

4) the pose of the "boxer".

30. Signs of lifetime general effect of low temperature (human hypothermia) are:

1) the presence of frost at the openings of the mouth and nose;

2) pose "kalachik";

3) glaciation of the corpse bed;

4) frostbite in open areas of the body.

For items 31-50 listed below, select the correct answers: the question (phrase) marked with a number must correspond to one correct answer marked with a letter. Each answer can be used once, multiple times, or not used at all.

31. Radiation burns.	A - high action
32. "The figure of lightning."	temperature.
33. Burn shock.	B - action low
34. Rupture of the eardrum.	temperature.
35. "Pose of a boxer."	C - the action of electrics.
36. Acute bullous emphysema (bloating) of the lungs.	Oh - change
37. Pose "knuckle".	barometric
38. Retraction of the testicles into the inguinal canal.	pressure.
39. Violation of thermoregulation of the brain.	E - action
40. Hemorrhage in the paranasal sinuses.	ionizing
41. The presence of small hemorrhages on the mucosa	radiation.
the lining of the stomach (Vishnevsky's spots).
42. Damage on the skin with a crater-like
indentation in the center and roll-like edges.

43. Liquid bright red (scarlet) blood.	A - mercury poisoning.
44. Destruction of internal (parenchymal)	B - carbon monoxide poisoning
45. Dark brown dense scab.	C - acid poisoning.
46. ​​Brown softened scab.	D - alkali poisoning.
47. The smell of bitter almonds from a corpse.	E - cyanide poisoning.
48. Corpse spots of bright pink color.
49. Penetration of poison by air.
50. High concentration of carboxyhemoglobin in

Functional poisons are chemical compounds that do not cause noticeable destructive or non-critical changes on the human body. It is practically impossible to determine the presence of poisonous substances by this group of poisons externally. Special medical and chemical examinations are required.

Functional poisons: types

Functional poisons according to the nature of the impact on the body systems are divided into groups:

• causing paralysis;
• depressant effect on the central nervous system;
• causing convulsions;
• inhibitory to the peripheral nervous system.

Cyanides and organic phosphorus compounds form a group of poisons that cause paralysis of breathing and heartbeat.

Cyanides are generally called chemical derivatives of hydrocyanic acid. Once in the human body, they acquire a specific smell of bitter almonds. By the presence of such a smell, even at the stage of primary investigative actions, cyanide poisoning is assumed, and a decision is made to conduct an examination.

The toxicity of paralytic poisons is manifested in the suppression of cell enzymes that provide cellular respiration. During the examination, the medical examiner ascertains the onset of death from suffocation.

Organic phosphorus compounds are found in almost all common household pesticides. As a rule, these are toxic liquids, but there are also powdered ones: dust, for example. Paralyzing functional poisons are included in the so-called subgroup of blood poisons, that is, they show their toxic properties when they fall into circulatory system person. Phosphorus pesticides have the ability to penetrate even through skin. Toxins enter the bloodstream by dissolving in adipose tissue, or through the lungs.

On autopsy, acute poisoning with phosphorus chemicals is indicated by a specific swelling of the internal organs, overflowing with liquid blood very dark color. chronic poisoning manifests itself as a structural destruction of vital organs, entailing, it would seem, natural causes death - colds, infections, anemia, dystrophy.

Poisoning with functional poisons can occur at any age. Most often this happens during the use of low-quality alcohol.

Poisoning with functional poisons: the reaction of the body

The reaction of the body when cyanide or phosphorus derivatives enter is of two types:

• a lightning-fast reaction occurs when large doses enter the body and manifests itself as a spasm of the throat ligaments, fainting and sudden death in 2-3 minutes;
• delayed reaction manifests itself as a series of sluggish symptoms, such as mild malaise in the heart, unreasonable fear, vomiting, bitterness in the mouth, difficulty breathing. If the antidote is not taken, convulsions occur, and then death.

Ethyl alcohol is considered a toxin that depresses the central nervous system. Surrogates and derivatives of ethyl alcohol are more poisonous and often lead to all sorts of complications. These include barbiturate, chloroform, ether, antifreeze, aldehydes, morphine, luminal, and other sleeping pills. The strength of the toxic effect of alcohol depends on its strength and the amount of fusel oils. The lethal dose is 8 milliliters per 1 kilogram of human body weight.

Functional poisons have an instant negative effect on a person. Most often, poisoning ends with organ failure or death.

A person who has consumed alcohol experiences short period narcotic euphoria, soon changing to paralysis. There is impaired coordination of movements, a feeling of heat. Further impact occurs on the cerebral cortex, aggression appears.

Ethyl alcohol substitutes are distinguished by an unpleasant odor, which is due to the high content of fusel oils. The most common substitutes for ethyl alcohol are methyl and amyl alcohols.

To the general picture of ethanol poisoning, methyl alcohol adds vision loss. The decay products of methyl alcohol are also poisonous. Vapors of formic acid are able to inhibit respiratory enzymes in cells. Depending on the consequences that have occurred, there are three forms of barbiturate poisoning:

• mild, symptoms similar to ethanol intoxication;
• causing damage to the optic nerve - fragmentary vision, blindness;
• generalized - convulsions, coma, death.

Amyl alcohol - a component of moonshine, affects the structures of the medulla oblongata, blocking its centers, which causes respiratory arrest or paralysis of the limbs.

As poisons that cause convulsive syndrome, there are many medicines in case of non-compliance with the dosage of the reception. These are used in medicine and, especially, in surgery, CNS stimulating substances - phenamine, atropine, scopolamine, strychnine.

All of these substances are hard drugs that cause bodily reactions such as confusion, agitation, incoherent speech, hallucinations, paranoid behavior, and delusions. Large doses of drugs lead to a fatal overload of the centers of the brain, which unambiguously entails coma and death.

Poisons with a predominant effect on the peripheral nervous system are also special preparations used in medicine to reduce the tone of smooth muscle muscles, including skeletal muscles.

Most often, muscle relaxants are used in surgery to relax muscles during anesthesia. The method of action of muscle relaxants is to stop the supply of a nerve signal from the brain to the tissues, as a result of which the muscles stop contracting. At high doses, they cause cardiac arrest or a sharp release of histamine.

Unlike the poisons of the previous groups, they do not cause morphological changes, for which they got their name - functional. Representatives of this group are cyanide compounds, hypnotics, ethyl and methyl alcohols, alcohol surrogates. They enter the body through the gastrointestinal tract and are quickly absorbed into the blood.

General action cyanides depends on the dose of poison taken. In doing so, they state:

At high doses - acute loss of consciousness, convulsions, shortness of breath, and rapid death from paralysis of the respiratory and vascular-motor centers;

At low doses - increasing headache, nausea, vomiting, general weakness, excruciating convulsions, loss of consciousness, respiratory arrest and death.

Acute poisoning with ethyl alcohol ranks first among the fatal poisonings studied in forensic medicine.

Alcohol acts on the body as a narcotic substance, while the following phases of its action are distinguished:

a) excitement;

b) anesthesia;

c) paralysis.

Like any drug, alcohol acts primarily on the central nervous system, namely on the cerebral cortex, there is a general inhibition hemispheres and release of the subcortex.

In development alcohol poisoning there are three stages of intoxication - light, medium, heavy.

1) With a mild degree, at first there is an increase in breathing and pulse, expansion of peripheral capillaries (redness), the temperature rises. There is a motor excitation, a feeling of a surge of strength.

2) In an average degree of intoxication, reflexes fade away, movement coordination is disturbed (ataxia). Speech becomes incoherent, signs of paralysis of the inhibitory centers appear. The pupils constrict, the temperature decreases due to increased heat transfer and reduced heat production. There is vomiting.

3) A severe form of intoxication is characterized by the development of diffuse cortical inhibition. Reflexes drop sharply, breathing becomes rare, hoarse, pupils do not react, the temperature drops significantly, muscle and heart weakness progresses, vomiting continues (aspiration of vomit). There is involuntary urination, defecation.

Quite often there is the so-called pathological intoxication, which is characterized by an increased, pathological reaction to alcohol, that is, a very strong reaction occurs from small doses of alcohol. This condition can often occur in congenital epileptics, in persons after a skull injury. Pathological intoxication is a qualitative change in the reaction to alcohol, i.e., illusory representations, deception of feelings, unmotivated anger and fear are observed without the usual signs of intoxication. This condition can come on suddenly and end in sleep after a short time. In most cases, this is followed by amnesia (loss of memory for the past).

Fatal poisoning with sleeping pills is caused by the intake of a derivative of barbituric acid (luminal, veronal, phenobarbital, etc.). The mechanism of action of barbiturates is that when they enter the gastrointestinal tract, they are rapidly absorbed into the blood. After 1-2 hours, the central nervous system is deeply inhibited and a coma develops, hypoxia and death occur.

Psychotropic drugs affect the neuropsychic processes. These include: drugs, antipsychotics, antidepressants, tranquilizers, psychoanaleptics.

Drugs are used in medicine as pain relievers.

Morphine is an alkaloid plant origin, found in opium. On initial stage poisoning, euphoria occurs, which is then replaced by drowsiness, dizziness, dry mouth, nausea, often vomiting, slow breathing, decreased blood pressure. Then a coma develops, the skin becomes pale, the skin feels wet and cold to the touch, and the body temperature drops. Death occurs in a state of deep coma from respiratory paralysis.

Other drugs of plant origin, when introduced into the body, cause a short-term psychosis with hallucinations. These substances (plan, anasha, marijuana, etc.) are capable of causing a short-term mental disorder even in small doses.

Antipsychotic drugs have a calming effect (reduce anxiety, excitement, excessive activity, etc.).

The first signs of poisoning appear a few hours after taking the drugs: pronounced inhibition of the function of the cerebral cortex with loss of consciousness, convulsions, acute respiratory and vascular insufficiency develops.

Tranquilizers (meprobamate, elenium, etc.) are also sedatives. They have low toxicity, but with a significant increase in dose, acute poisoning can occur. The clinic, the autopsy data of the dead and the diagnosis resemble those of neuroleptic poisoning.

Poisoning with pesticides.

Among pesticides, there are: herbicides - substances for the destruction of harmful plants; insecticides - for the destruction of harmful insects; fungicides - means to combat fungal infections.

According to their chemical composition, they are divided into chlorine-containing (disrupt the work of almost all internal organs); containing phosphorus (disrupt the transmission of nerve impulses); containing copper - upon contact with tissues, they have a cauterizing effect. As a result of their impact, dystrophic changes develop in the internal organs.

Food poisoning.

It is customary to call food poisoning caused by poor-quality food, if their poor quality is the result of natural processes. All food poisonings are conditionally reduced to the following groups: true and indirect food poisonings, food poisoning and bacterial intoxications, food mycotoxicoses.

True poisoning causes:

Products that are always poisonous to humans by their nature;

Products that temporarily become poisonous to humans.

In both groups, products can be of plant and animal origin.

herbal products, always poisonous to humans by their nature, are some types of mushrooms (pale grebe, fly agaric, lines, etc.); some plants (aconite, henbane, dope, etc.); kernels of fruit stones and nuts (apricot, peach, cherry).

Products of animal origin that have the same properties include: parts of the body of certain fish species during spawning (marinka, Sevan chromula, lamprey, river eel, puffer fish, barbel, etc.) and some organs of warm-blooded animals (testes, thymus and pancreas, adrenal glands slaughter cattle).

Temporarily poisonous can be old edible mushrooms that have a greenish color, potato tubers with a high content of solanine, honey collected by bees from poisonous plants.

Indirect food poisoning occurs due to food contamination, most often flour, cereals, vegetable impurities (heliotrope, mustard, cockle, etc.) or chemicals, which are part of dishes (copper, lead, zinc), agricultural pest control agents, substances that play the role of chemical food additives to give the product a pleasant smell (vanillin), color (nitrates), storage stability (antioxidants, antimicrobial agents, emulsifiers , stabilizers), flavor enhancers (sweet dulcine). Poisoning occurs when high doses of these substances are present in the product.

Food poisoning infections are caused by foods that are conditionally contaminated. pathogenic flora: Salmonella, Proteus and Escherichia coli. Food poisoning arise with the introduction of toxins with food, which are the waste products of microorganisms: botulinum toxin, staphylococcal toxin.

Food mycotoxicoses develop when eating:

Grain, which was under the snow in a warm winter and affected by poisonous fungi and bacteria;

Rye and wheat infected with a vegetable fungus - ergot.

Forensic medical examination at food poisoning is based on a thorough analysis of the conditions under which the poisoning occurred, determining the number of victims, studying the materials of the sanitary and epidemiological investigation, carefully comparing similar and different clinical symptoms, morphological changes in all victims, evaluating the results of histological, forensic chemical, botanical, bacteriological and zoobiological studies .

Many poisons, depending on their chemical nature and quantity, have relative or predominant selectivity. toxic action. In the clinical picture of poisoning, symptoms of damage to individual systems (cardiovascular, respiratory, etc.) may prevail.
Poisoning by poisons that cause hypoxic conditions (cyanide compounds, hydrogen sulfide, carbon dioxide - carbon dioxide) are of the greatest importance in forensic practice.

cyanide poisoning

Poisoning by cyanide compounds is now rare (potassium cyanide, much less often - sodium cyanide or mercury cyanide). Hydrocyanic acid (hydrocyanic acid) in its pure form is found only in laboratories. The fruits and seeds of some plants (peaches, apricots, cherries, plums, almonds, etc.) contain glucoside, which releases hydrocyanic acid during decomposition, and therefore poisoning can occur if they are consumed excessively.
Cyanide compounds enter the body through the mouth and are quickly absorbed into the blood through the mucous membrane of the mouth, esophagus and stomach. With the penetration of cyanide compounds into tissues, their active cyan groups stabilize the respiratory enzyme - cytochrome oxidase in a stable ferric state, as a result of which the ability of cells to perceive oxygen from the blood is impaired and deep tissue hypoxia develops without anoxemia. First of all, the nerve cells of the brain suffer, which leads to paralysis of the respiratory and vasomotor centers. The lethal dose of pure hydrocyanic acid is 0.005-0.1 g; potassium cyanide - 0.15-0.25 g.
At high doses, death occurs very quickly - within a minute. Loss of consciousness, convulsions, shortness of breath, dilated pupils and death are noted. At lower doses (0.1-0.2 g of potassium cyanide), signs of poisoning are observed after 5-10 minutes, nausea and vomiting appear, increasing weakness, convulsions, loss of consciousness occurs, then respiratory and cardiac arrest. The entire period of poisoning lasts from 15 to 40 minutes.
The section determines the signs of acute death. Cadaverous spots of cherry color, blood is liquid, red.
From the cavities, from the lungs and the brain comes the smell of bitter almonds. Great importance in the diagnosis of poisoning is attached to a forensic chemical study of the stomach with its contents, blood, brain, liver, kidneys and urine.

Hydrogen sulfide poisoning

Hydrogen sulfide - a colorless gas, heavier than air, is one of the components of the so-called cesspool gas. In low concentrations, it has the smell of rotten eggs, in high concentrations it has a cauterizing effect on the nerve endings of the nasal mucosa and is therefore hardly perceptible. It is formed during the decay of organic substances containing sulfur during decomposition rocks and minerals containing hydrogen sulfide compounds. It occurs in mines and workings, during blasting, often formed in sewer networks, cesspools and sewers.
Hydrogen sulfide poisoning is usually the result of an accident. It mainly enters the body through the respiratory tract. It is excreted mainly by the kidneys in the form of oxidized sulfur compounds and partially by the lungs in unchanged form, giving a specific smell to the exhaled air.
Hydrogen sulfide is a highly toxic poison with a pronounced irritant effect on the nervous system, mucous membranes of the eyes and respiratory tract. Its action is similar to the action of cyanide compounds: it inhibits tissue respiration enzymes (binding of iron in cytochromes), causing tissue hypoxia.
The severity of poisoning depends on the concentration of poison in the inhaled air. Severe poisoning proceeds according to the type of convulsive coma - a rapid and deep loss of consciousness occurs, accompanied by convulsions, inhibition of reflexes, hallucinations, damage to cardiovascular activity and respiration, toxic pulmonary edema. A coma can result in death. At very high concentrations, a lightning-fast form of poisoning can develop, leading to almost instant death from paralysis of the respiratory center.
In the section of those who died from acute poisoning with hydrogen sulfide, a picture of an acute onset of death is noted; from the cavities, internal organs, especially the lungs, there is a smell of rotten eggs; blood and internal organs are cherry red. Blood, brain, lungs, liver, kidneys with urine are taken for forensic chemical research. They also analyze the air of the place where the poisoning occurred. The maximum allowable concentration of hydrogen sulfide in the air is 10 mg/m3.

Carbon dioxide (carbon dioxide) poisoning

Carbon dioxide- Odorless, heavier than air. Accumulates (with insufficient ventilation) in places where rotting, fermentation or decay occurs (cesspools, sauerkraut stores, mines, manholes of water pipes, etc.). Under the action of its high concentrations (30% and above), shortness of breath, cyanosis occur, loss of consciousness, convulsions and death occur. At autopsy - signs of acute death. Of decisive importance in the diagnosis is given to the circumstances of the case and the analysis of the air of the place where the poisoning occurred. The maximum permissible concentration in the air is 30 mg/m3.

Acute drug poisoning

Poisoning by sleeping pills is observed in everyday life with an unjustified increase in their dose in cases of self-treatment, with their abuse, and also when they are taken for suicidal reasons. When taking certain sleeping pills (for example, tranquilizers), an intensifying effect of the action of alcohol is noted. The most common poisoning is barbiturates - derivatives of barbituric acid: cyclobarbital, hexabarbital, barbamyl, phenobarbital, etaminal-sodium, barbital-sodium. Of the non-barbituric hypnotics, poisoning with noxiron, oxybutyrate and some other drugs is more common.
The picture of poisoning with sleeping pills in adults largely depends on the dose of the drug and its mechanism of action, the combination of taking these drugs with other drugs that enhance their effect, as well as on the individual reactivity of the body. Already when taking barbiturates in a dose exceeding the therapeutic (hypnotic) by 3-4 times, a mild degree of poisoning occurs. Taking a 15-20-fold dose of the drug causes very severe poisoning, often ending in death. A dose of drugs of 0.1 g per 1 kg of body weight is lethal. Analgesics, neuroleptics and other neurotropic substances enhance the effect of sleeping pills. Most sleeping pills enter the body orally, a number can be administered parenterally (barbital-sodium, barbamil, etaminal).
Barbiturates are very rapidly absorbed from the stomach. Already after 8 hours they are not found there. The mechanism of action of barbiturates is reduced to a deep inhibitory effect on the central nervous system and is accompanied by a coma, inhibition of the function of the respiratory and vasomotor centers, the development of hypoxia and other symptoms. An autopsy showed signs of a rapidly occurring death and certain changes in various parts of the brain. Quantitative determination of barbiturates in the biological media of the body allows you to determine the degree of intoxication and diagnose death from poisoning with them. Blood, urine, cerebrospinal fluid are sent for forensic chemical research. The development of acute intoxication occurs when the concentration of poison in the blood is from 1 to 10 mg%, depending on the nature of the substance. The content of barbiturates in the urine does not depend on the stage of intoxication. In cases of acute lethal poisoning, gastric lavage, urine, blood and cadaveric material should be sent for forensic chemical research. Barbiturates remain in cadaveric material for a long time. So, for example, barbamil is found 6 weeks after death, and in cadaveric material preserved with formalin, after 3 years. Acute poisoning with non-barbituric hypnotics, mainly piperidine derivatives (noxyron, sodium oxybutyrate, etc.), resemble barbiturate poisoning. The toxic dose of noxiron varies over a wide range - from 5 to 20 g (20-80 tablets). Noxiron is slowly absorbed into gastrointestinal tract and therefore the phenomena of intoxication may occur several hours after ingestion. The drug is deposited in adipose tissue, slowly excreted by the kidneys. In toxic doses, it causes a pronounced inhibitory effect on the central nervous system up to the development of severe coma. Pathological changes are the same as in barbiturate poisoning. The diagnosis of acute poisoning is made on the basis of the circumstances of the incident, the clinical picture and the data of a forensic chemical study, in which a quantitative determination of the drug in the blood and urine is made.
Systematic Introduction into the body of sleeping pills, both barbiturates and non-barbiturates, can lead to substance abuse and drug addiction, characterized by similar manifestations physical addiction from drugs. As addictive agents, barbiturates are more dangerous than other sleeping pills. As a result of the growth of tolerance, the maximum doses of barbiturates can reach 4.5-5.0 g.

Acute poisoning with psychotropic drugs

Psychotropic drugs have a directed effect on neuropsychic processes. A number of these substances can have various side effects, in particular, they are addictive (toxicomania). The ever-increasing release of these drugs and their abuse have led to an increase in acute intoxications. Among psychotropic drugs 5 groups are distinguished: drugs (morphine, lysergic acid diethylamide - DLC, cocaine, Indian hemp preparations), neuroleptics or antipsychotics (phenothiazine derivatives, etc.), tranquilizers (meprobamate, amizil, etc.), antidepressants (iprazid, imizin), psychoanaleptics (caffeine, phenamine, etc.).
drugs cause alternating manic and depressive syndromes with aggressive or suicidal overtones, with physical exhaustion and personality disintegration. Intoxication occurs when long-term use drugs due to addiction to them. Many of them are used medicinally as pain relievers. This group includes morphine (a drug derived from opium powder), other opiates, and synthetic drugs with a morphine-like effect.
Lethal single dose morphine when taken orally 0.2-0.4 g, when administered parenterally - 0.1-0.2 g. In parallel with the development of substance abuse, addiction to the drug appears. Cases are described when drug addicts injected 10-14 g of morphine. The action of opium preparations largely coincides with the action of morphine, the main representative of the group of narcotic analgesics. Morphine is rapidly absorbed and exerts its effect 10-15 minutes after subcutaneous administration and 20-30 minutes after oral administration. Morphine is concentrated in various bodies and tissues, most of all in the liver, where it undergoes demethylation. Immediately after absorption, morphine is partially excreted in the bile, and in unchanged form - into the intestinal lumen (with subsequent reabsorption), and is also excreted with feces, urine, saliva, sweat and milk of a nursing mother. The maximum release is noted after 8-12 hours. About 75% of the morphine that has entered the body is released per day.
To the most common reasons Acute opiate poisonings include accidental overdose, intentional overdose in a suicide attempt.
In the picture of poisoning with morphine and its analogues, the leading place is occupied by an acute respiratory failure due to the inhibitory effect of narcotic analgesics on the respiratory center. In the initial stage of poisoning, euphoria, which is replaced by drowsiness, dizziness, dry mouth, nausea, and often vomiting, is marked by constriction of the pupils with a weakening of their reaction to light, slowing of breathing, and a decrease in blood pressure. With the onset of a coma - a sharp narrowing of the pupils, the skin is pale, the skin is wet and cold to the touch, the body temperature is lowered. Death occurs from paralysis of the respiratory center.
Of the other opium alkaloids, noteworthy heroin, the action of which is similar to morphine, but more powerful.
Other drugs of plant origin (lysergic acid diethylamide - DLC, LSD - an ergot derivative, hashish (plan, anasha, marijuana) - a derivative of Indian hemp; cocaine - an alkaloid contained in the leaves of a South African shrub, etc., when introduced into the body, cause short-term psychosis with hallucinations (hence their second name - hallucinogens). These substances are capable of causing a temporary mental disorder even in negligible doses. For example, DLC at a dose of 0.001 mg / kg causes a psychotic disorder lasting 5-10 hours. Lethal doses exceed toxic ones by 100 times and Mental disorder is observed 20-30 minutes after the intake of DLK in the body, reaching a maximum after 1-2 hours and lasts an average of 6-8 hours, sometimes up to 16-20 hours.
Cocaine used in medical practice as a local anesthetic. Overdose of cocaine or accidental use or administration of this substance can cause acute poisoning. The lethal dose when administered subcutaneously is 0.1-0.3 g, when administered through the mouth - 1-1.5 g. Death can occur in a few minutes. Cocaine acts specifically only on the nervous system, it does not affect other organs. Death comes from respiratory paralysis. Displayed for the most part with urine. When taken orally, it is partially destroyed by the liver.
Antipsychotics cause in people a decrease in tension, excitement, anxiety, excessive physical activity, aggressiveness. For this reason, they were called "big tranquilizers." The main group of substances is phenothiazine derivatives, and their main representative is chlorpromazine. A single lethal dose of chlorpromazine is more than 50 mg per 1 kg of body weight, although individual sensitivity to it varies. Deaths from taking 0.5 g of chlorpromazine and cases of recovery when taking 6 g of the drug are described. Children are more sensitive to chlorpromazine, the lethal dose for them averages 0.25 g. chlorpromazine and its analogues are relatively well absorbed in the gastrointestinal tract, almost completely metabolized in the liver and excreted by the kidneys and lungs. Symptoms of intoxication are relatively clearly manifested only a few hours after taking the drugs. Inhibition of the function of the cerebral cortex is noted with the exclusion of consciousness, convulsive reactions, acute respiratory and vascular insufficiency develops. Macroscopic and histological examinations of those who died from acute intoxication with antipsychotic drugs show severe changes - hemorrhages in the meninges, cerebral edema, proteinaceous dystrophy of the liver and kidneys, plethora of internal organs. Diagnosis of poisoning is based on the history, clinical picture and laboratory results. Phenothiazine derivatives can be found in the urine. Quantitative determination of chlorpromazine in the biological media of the body is carried out.
tranquilizers regardless of the chemical structure, they create an overall calming effect. They are of low toxicity, however, if the dosage is significantly exceeded, acute poisoning can occur up to a coma. So, acute poisonings from taking 40-120 tablets of meprobamate (8-48 g), 30-100 tablets of elenium (0.3-1 g) are described. It is believed that a single lethal dose of meprobamate for adults is on average 0.1-0.3 g per 1 kg of body weight. In children, death can occur from taking a much smaller amount.
Pathological changes in poisoning with tranquilizers resemble those in barbiturate poisoning. Diagnosis of poisoning is based on an assessment of the clinical picture: a sharp decline muscle tone, weakness, ataxia, drowsiness, loss of consciousness, respiratory depression, etc., anamnestic data and results of laboratory qualitative and quantitative determination of these drugs in the body.
Convulsive poisons. Strychnine is the main alkaloid of chilibukha seeds containing at least 2.5% strychnine alkaloid. It is used in medical practice in the form of nitrogenous salt of strychnine (colorless crystalline powder) as bitters to improve digestion, stimulate metabolic processes and the functions of the spinal centers. Has a bitter taste. Sparingly soluble in water and alcohol. The drug is also used to control rodents and other wild animals. Cases of murder and suicide are extremely rare. There may be cases of poisoning when taken orally and parenterally. For adults, the lethal dose is 0.1-0.3 g, for children - 0.005 g. The toxic effect of the drug is associated with its effect on interneuronal synapses spinal cord, facilitating the conduct of excitation in them. In the body, strychnine is distributed relatively evenly. About 20% of strychnine is excreted from the body unchanged by the kidneys, about 80% of the drug is destroyed in the liver. Complete release of the drug occurs within 3-4 days, but most of it is released after 10 hours. The severity of poisoning depends on the dose of the administered substance and is manifested in increased reflex excitability of the central nervous system. Doses from 0.01 to 0.02 g cause tremor, fear, the appearance of tonic twitching of the masticatory and occipital muscles. Increased sensitivity to any external stimulus. In the future, tonic convulsions develop up to opisthotonus. At very high doses, paralysis of the respiratory center and rapid death occurs. Death usually occurs either from asphyxia as a result of convulsions, or as a result of central nervous system exhaustion. In the section of those who died from strychnine poisoning, only a picture of an acute onset of death is noted. Strychnine long time remains in the corpse and is found in the organs even several months after death.

Ethyl alcohol poisoning

Ethyl alcohol (ethanol, wine alcohol) is a part of various drinks, has a high toxicity and can lead to severe acute poisoning if it is abused. A lethal dose for humans is 6-8 ml of ethyl alcohol per 1 kg of human body weight, which is approximately 200-300 ml of 95% ethyl alcohol.
A forensic medical examination of alcohol intoxication is carried out during the examination of suspects, victims, as well as during the examination of corpses in case of violent and sudden death.
After a few minutes, 20% of the alcohol that enters the body is absorbed in the stomach, the rest - in the intestines. Concentrated alcoholic beverages are absorbed faster. food products, especially fats and proteins, delay its absorption. When taking ethanol on an empty stomach, its maximum content in the blood is established after 40-90 minutes, when the stomach is filled with food - after 90-180 minutes. The main part of ethyl alcohol (about 90%) undergoes oxidation in the body, the rest is excreted in the urine and exhaled air. In one hour, about 7-9 ml of ethyl alcohol is oxidized in the body. Its absorption (resorption phase) lasts an average of 1 to 3 hours. About an hour after ingestion, its concentration per 1 liter of blood and 1 kg of body weight is compared, which makes it possible to judge the degree of intoxication by the content of ethyl alcohol in the blood. After complete absorption in the stomach and intestines, the content of ethyl alcohol in the blood begins to decrease (elimination phase) and, thus, the amount of ethanol in the urine becomes higher than in the blood. So, with a human body weight of 70-80 kg, the concentration of ethanol in the blood is about 2 g / l or 2 ‰ (corresponding to the intake of 200-300 ml of vodka or 100-150 ml of 96% ethyl alcohol) can cause a pronounced picture of acute intoxication. The presence of 3-4 ‰ in the blood is a severe poisoning, and the concentration of ethanol, equal to 5-5.5 ‰, is considered fatal. These figures are very average. Therefore, it is impossible to judge the severity of poisoning only by the concentration of ethyl alcohol in the blood1.
The severity of acute alcohol poisoning depends on the amount of alcoholic beverages taken, the individual reaction, the age of the poisoned person, and a number of other reasons. Ethyl alcohol acts primarily on the processes of inhibition. Under the influence of its high concentrations in the blood, the process of excitation also weakens. The final effect of ethyl alcohol, especially taken in large doses, is manifested by depression of consciousness, the respiratory center and cardiovascular activity. In the peripheral nervous system, toxic doses of ethyl alcohol inhibit the transmission of impulses. In severe poisoning, acute cardiovascular failure can develop both due to the central paralytic effect of ethanol, and as a result of its direct effect on the heart muscle and blood vessels. Violation of consciousness, disorders of breathing, circulation and autonomic function nervous system are, thus, the result of the action of ethyl alcohol on the cortex, subcortical formations of the brain and the peripheral nervous system.
In forensic practice, it is necessary to establish both the presence and degree of alcohol intoxication (poisoning), and the onset of death from acute ethyl alcohol poisoning. The degree of acute alcohol poisoning varies widely. With regard to forensic medical examination, there are three degrees of alcohol intoxication: mild, moderate and severe. A mild degree of alcohol intoxication is characterized by excitement, swagger, motor excitement, reddening of the face, impaired coordination of movements in a mild degree. With an average degree of intoxication, speech is disturbed, impaired coordination of movements increases, a desire for rudeness, conflicts appears, and then sleep occurs. A severe degree of alcohol intoxication is accompanied by a decrease in reflexes, a decrease in pain sensitivity, loss of consciousness, an alcoholic coma develops with impaired respiratory function and the development of collapse. Vomiting often occurs during this period, while food masses can flow into the respiratory tract and cause mechanical asphyxia.
In forensic practice, the concentration of ethanol is determined using gas chromatography and expressed in ppm (‰).
Definition of the state of alcoholic intoxication
The determination of the state of alcoholic intoxication and its degree in living persons is carried out by psychiatrists and neuropathologists, and in their absence, by doctors of other specialties, including, in some cases, forensic medical experts.
The conclusion about the presence of alcohol intoxication is given on the basis of a clinical examination, qualitative samples (by A. M. Rapoport for the presence of alcohol in the exhaled air, M. A. Mokhov and I. P. Shinkarenko, etc.) and biochemical research blood and urine for the quantitative content of alcohol in them. When assessing the content of ethyl alcohol in the blood and urine, the doctor must take into account the dynamics of its content in these environments from the moment of alcohol intake to its elimination. The greatest difficulties arise when establishing a mild degree of intoxication.
When assessing the state of intoxication, one should adhere to the data given in Table.

Indicative scheme for determining the severity of alcohol intoxication

When examining alcohol intoxication, it may be necessary to determine the amount of alcohol taken in the composition of alcoholic beverages. The calculation is made according to the following formula: A \u003d P (C + βt), where A is the amount of alcohol taken per 100% alcohol, g; C is the concentration of alcohol in the blood for a period of time t; P - body weight, kg; β - drop in blood alcohol concentration for 1 hour, in ‰.
At the beginning of the elimination phase p is equal to 0.10-0.13 ‰, with muscle load- 0.15-0.20 ‰, and with a traumatic brain injury it drops to 0.06-0.08 ‰.
Forensic chemical analysis of blood and urine to determine the concentration of alcohol in them is carried out in the forensic chemical departments of the Bureau of Forensic Medical Examination using the gas chromatography method. When taking blood and urine for a forensic chemical study, one should be guided by the following rules. The blood sample is placed in a small test tube with a capacity of about 5 ml, filling it to the top. In the case of urine sampling, the subject is asked to first release all the urine into a clean glass or cylinder, part of this urine is placed in cleanly washed penicillin bottles. After 30-45 minutes, simultaneously with the second blood sampling, the subject is offered to urinate again, the urine is placed in the second vessel.
At the end of the examination, it is desirable to take a third portion of urine. The dishes in which blood and urine are taken must be absolutely clean, have well-fitted rubber or cork stoppers, previously boiled in water with the addition of alkali, and then washed in distilled water. Samples of blood and urine must be delivered for examination to the forensic chemical department of the Bureau no later than one day after taking.
When evaluating the results of a forensic chemical study, it should be taken into account that in the urine of patients with diabetes mellitus, when stored at room conditions (at a temperature of about 20 ° C), due to the processes of alcoholic fermentation, as a rule, ethyl alcohol is formed, reaching by the 10th day storage 9 ‰ and more. The same applies to the deaths of patients with diabetes mellitus - in the case of long-term storage of their corpses at room conditions in the urine contained in the bladder, in the vast majority of cases, also due to alcoholic fermentation, a steady formation of ethyl alcohol occurs, reaching 7 ‰ or more.
Examination in connection with suspected death from alcohol intoxication
In cases of examination in connection with suspected death from alcohol intoxication, it becomes necessary to prove not only the very fact of taking alcoholic beverages shortly before death and death from ethyl alcohol poisoning, but also to determine the degree of alcohol intoxication in the deceased.
The results of calculations of the amount of alcohol taken in the composition of alcoholic beverages can be of some importance in the examination of corpses only in cases where at the time of the incident the subject was in the stage of alcohol elimination. The main difficulty is to establish the time interval from the intake of alcoholic beverages to the onset of death. If this circumstance is not established, then the expert can only judge the degree of intoxication of the subject at the time of death on the basis of data on the quantitative content of alcohol in the blood of the corpse. The expert cannot establish the amount of alcoholic drinks taken shortly before death. The quantitative content of alcohol in the body of the subject at the time of death can be calculated by the formula; A \u003d P x r x C, where r is the alcohol distribution factor in the body (reduction factor). For more exact definition the dose of alcohol taken to the result should be added to the amount of alcohol that has not had time to be absorbed into the blood and is still in the stomach.
The value of the reduction factor for men is on average 0.68, for women - 0.55. For overweight people, a lower value of the reduction factor (0.55 - 0.65) should be accepted than for subjects of moderate or reduced nutrition (0.70 - 0.75).
There are no morphological changes in the tissues and organs of the corpse specific for death from ethyl alcohol poisoning.
The conclusion about death from alcohol poisoning is given only after a thorough histological examination of the internal organs of the corpse. With such a study, severe diseases of the cardiovascular system can be detected, contributing to the onset of death at relatively low concentrations of ethyl alcohol in the blood. In some cases, on the contrary, the leading cause of death is the disease, and alcohol intoxication is only a contributing factor.
Such cases are very difficult to assess. In cases where an alcohol concentration of 5 ‰ and higher is determined in the blood of the deceased, the forensic expert has the right to conclude that fatal alcohol poisoning, regardless of the nature of the diseases established during the autopsy. At lower blood alcohol concentrations, in order to conclude that death was due to alcohol poisoning, it is necessary to carefully analyze the existing diseases and their possible impact on the onset of death.
Should be considered individual characteristics the personality of the deceased, in particular, those associated with the peculiarities of the genetically determined enzymatic metabolism of alcohol, which depends on the activity of alcohol dehydrogenase (ADH) and acetaldehyde dehydrogenase (ALDH). They break down ethyl alcohol to acetaldehyde, its most toxic metabolite, and acetaldehyde to acetic acid and water. The maximum activity of these enzymes is observed in the liver and kidneys. It has been established that there are two forms of ADH in the human liver - typical and atypical ADH. The atypical form of ADH differs from the usual one in exceptionally high enzymatic activity, exceeding the activity of normal ADH by 8-10 times. The sometimes observed so-called unfavorable metabolic background for the breakdown of ethyl alcohol in the human body largely depends on the presence of an atypical form of hepatic ADH, the exceptionally high activity of which leads to the rapid oxidation of ethyl alcohol to acetaldehyde, and therefore rapid accumulation last in the body.
At the same time, acetaldehyde, being many times more toxic than ethyl alcohol, largely determines the severity of alcohol intoxication. In such persons, insufficient functioning of the ALDH enzyme system, which converts acetaldehyde into water and acetic acid. It also contributes to the rapid accumulation of acetaldehyde in the blood. Persons with such atypical forms of ADH and ALDH can die from ethyl alcohol poisoning with a very low content of the latter in the blood.
When diagnosing alcohol intoxication on the corpse of a victim, significant difficulties also arise in assessing the results of a forensic chemical examination of organs and tissues at various stages of the post-mortem period, when the autopsy is performed a considerable time after the onset of death.
Cases of the formation of ethyl alcohol in a corpse in high concentrations are very rare, since this requires a certain set of conditions: a specific microflora, cadaveric material without pronounced putrefactive changes, and a relatively high ambient temperature. Therefore, the detection of high concentrations of ethyl alcohol in the internal organs of a corpse stored at a relatively low temperature indicates the lifetime intake of alcohol into the body. The same takes place in cases of detection of high concentrations of ethyl alcohol in the study of a decayed corpse. To check the possibility of its formation in a corpse, it is necessary to conduct a bacteriological examination of the internal organs of the corpse.
If it is suspected that death has occurred from alcohol intoxication, the following are taken for a forensic chemical examination: blood from the femoral veins with a syringe into a test tube or into a penicillin vial up to the cork (you can not take blood from the heart, cavities of the corpse); urine; cerebrospinal fluid with a lumbar puncture; the contents of the stomach; blood clots from areas of damage (the presence and a certain concentration of ethyl alcohol in them indicates the degree of intoxication). You can also take intraocular fluid, in which the concentration of alcohol is the same as in the blood. The liquid is taken with a syringe, a needle puncture is made in the corner of the eye (5 ml of liquid can be obtained). At the stage of rotting of a corpse, 500 g of muscles are taken for research, the contents Bladder, stomach with contents. It is also necessary to determine the mass of the corpse. Syringes, pipettes, utensils for taking objects must be chemically clean.

Poisoning by alcohol substitutes and technical liquids

The widespread introduction of chemistry into production and everyday life has led to the emergence of a large number of products called technical liquids, some of which can be used for the purpose of intoxication. Such a peculiar replacement of ethyl alcohol with technical liquids, some of which belong to the class of alcohols, gave rise to a motley picture of all kinds of poisoning, and the technical liquids themselves began to be called "surrogates" of alcohol.
Methyl alcohol(methanol, wood alcohol, carbinol) is widely used in industry as a solvent. It resembles ethyl alcohol in color, smell and taste. Poisoning with it is currently relatively rare, mainly household poisoning, when poison is mistakenly used instead of ethyl alcohol inside. Occasionally there are cases of mass poisoning in industries using methyl alcohol as a technical fluid.
Methyl alcohol is a strong neurovascular poison. Severe poisoning can occur after ingestion of 7-10 ml. The lethal dose ranges from 30 to 100 ml and above. It should be noted the pronounced individual sensitivity of the body to methyl alcohol. Cases of death after taking already 5 ml and recovery after drinking 250-500 ml are described. Persons who have undergone large doses of methyl alcohol are often a source of false information about its "harmlessness", which contributes to its use for the purpose of intoxication.
Methyl alcohol is rapidly absorbed from the gastrointestinal tract. It oxidizes in the body several times slower than ethyl alcohol. The special toxicity of methyl alcohol is associated both with its slow oxidation and with the toxic products of its oxidation (formaldehyde, formic acid). Methyl alcohol in the blood after poisoning is detected within 3-4 days. About 60% of the incoming dose is excreted in the exhaled air, about 10% in the urine. Its excretion by the kidneys occurs within about 3 days, formic acid - in 5-6 days.
The course of poisoning depends on the dose taken and the sensitivity of the body to it. After taking the poison, a kind of euphoria sets in rather quickly, which, unlike alcohol intoxication, is not accompanied by pronounced excitement or high spirits, but rather resembles a hangover state with headache, lethargy, impaired coordination of movements, etc. This state is quickly replaced by heavy sleep. After sleep, the victims feel well. Such a hidden period of imaginary well-being lasts up to 1 day. Then come a sharp general malaise, dizziness, muscle weakness, pain in the lower back and abdomen. Victims during this period may fall into a state of intense excitement or suddenly lose consciousness. There is a sharp decrease in vision, which in severe poisoning ends in blindness. Death usually occurs in a state of deep coma due to paralysis of the respiratory center. Without providing timely medical care death usually occurs on the third day. When recovering, the victims often have persistent visual impairment up to complete blindness, functional inferiority of the liver, etc.
When examining a corpse, a picture is usually determined that is characteristic of a rapidly occurring death. The longest methyl alcohol is in the cerebrospinal fluid - from 3 to 12 and even up to 45 days.
Raw alcohol is a fermentation product of sugar. Rectificate is obtained from it by purification, which is used, in particular, for the preparation of alcoholic beverages. Alcohol surrogates, in addition to ethyl alcohol, contain a large amount of impurities harmful to the human body, in particular fusel oils, consisting of higher alcohols (isoamyl, butyl, isobutyl, isopropyl, etc.). Especially toxic are amyl alcohols, which make up more than a third of fusel oils. Compared to ethyl alcohol, they have greater narcotic power and greater toxicity.
propyl alcohols are also used as solvents for synthetic resins and other substances. By the general nature of the action on the human body, they resemble ethyl alcohol. Cases of fatal poisoning after taking 300 ml or more of poison are known. They are quickly absorbed from the gastrointestinal tract and within a few minutes after ingestion appear in the blood and quickly accumulate in the body, in particular in the brain. Propyl alcohols and their metabolites (propyl and lactic acids, acetone) are excreted from the body with exhaled air, urine, and feces. With a blood content of approximately 15 ‰ isopropyl alcohol, a coma and death can occur.
At autopsy, only signs of a rapidly occurring death are noted. One of the propyl alcohol metabolites, acetone, can be detected in the urine for up to 4 days even after taking a small amount of isopropyl alcohol.
Butyl alcohols- colorless liquids with a characteristic alcohol smell. They are used as solvents in perfumery, the pharmaceutical industry and in a number of other industries, in particular for the manufacture of BSK brake fluid containing 50% butyl alcohol. The lethal dose when taken orally is 200-250 ml, although individual sensitivity fluctuations are quite significant.
Butyl alcohol gives a narcotic effect, while the central nervous system is affected. When ingested, a short-term state of intoxication develops, which after 3-4 hours turns into drowsiness, apathy, later there is a decrease in vision, flickering of "flies" in the eyes. Kidney function is impaired. In the absence of appropriate treatment, a coma usually develops within 2 days and the patient dies.
At autopsy, signs of a rapidly occurring death are revealed; from the internal organs there is a smell of butyl alcohol.
Amyl alcohols- yellowish liquids with a characteristic fusel odor. Poisoning is observed both when taking raw alcohol and when using ASA brake fluid containing 50% amyl alcohol. When taken by mouth, a lethal dose is about 20-30 ml of pure amyl alcohol. Alcohol intoxication when taking ethyl alcohol, even with a small admixture of amyl alcohol, is characterized by a severe course.
By the nature of the impact on the body, amyl alcohols are drugs. First of all, the central nervous system is affected and paralysis of the vital centers of the brain stem occurs. After ingestion, amyl alcohol circulates in the blood for several hours, is excreted through the lungs, with urine. Poisoning is characterized by general weakness, dizziness, nausea, vomiting, burning sensation along the esophagus and abdominal pain. After a few minutes, there is confusion, stupor, cyanosis is growing. Death occurs in a state of severe coma. The picture of poisoning depends to a large extent on the concentration of amyl alcohol in the liquid drunk. The main morphological changes are observed in the gastrointestinal tract. The contents of the stomach have a fuselous odor.
Denatured alcohol used as technical alcohol. It contains a significant amount of impurities, in particular methyl alcohol, which makes it highly toxic.
ethylene glycol- dihydric alcohol, is widely used as one of the main components of antifreeze, brake fluids. To combat icing, it is used in the form of an aqueous 55% solution (B2 antifreeze).
Acute poisoning with ethylene glycol occurs when it is taken orally as a surrogate for alcohol. Mortality in severe poisoning reaches 90-100%. By the nature of the action on the body, ethylene glycol is a neurovascular and protoplasmic poison. In the course of poisoning, several periods are distinguished - latent, brain phenomena and renal and hepatic lesions. After taking ethylene glycol, mild intoxication occurs. Then symptoms of damage to the central nervous system and kidneys, general weakness, headache, nausea, vomiting, abdominal pain, convulsions, and loss of consciousness develop. In severe poisoning, death occurs on the 1-3rd day. The lethal dose is 150 g and above.
The toxicity of ethylene glycol is associated with the rapid formation of intermediate metabolic products (glycolaldehyde, glyoxal, etc.). Death occurs in most cases due to the development of acute kidney failure. In such cases, at the autopsy of the dead, characteristic changes in the kidneys and liver are revealed. An increase in the size and weight of the kidneys (up to 600 g), hydropic degeneration of the epithelium of the convoluted tubules of the kidneys, necrotic nephrosis with focal hemorrhages, bilateral cortical nephrosis and oxalate crystals in the kidneys are noted.
The liver is enlarged, its mass reaches 2200-2400 g, on cuts the liver has a "nutmeg" appearance, centrilobular dystrophy and necrosis are expressed in it.
Tetraethyl lead(TPP) - organic compound lead. It is an oily volatile liquid that evaporates easily. It is included in the amount of 54-58% in the composition of various liquids, which are added as antiknock agents to low-octane gasoline grades. TES easily evaporates even at temperatures below 0 °C. Vapors are much heavier than air, and therefore they accumulate in the lower parts of the premises. It dissolves well in fats, lipids, organic solvents.
Acute TES poisoning occurs when leaded gasoline is mistakenly taken orally; by inhalation of its vapors (when using liquids containing TES as a solvent for paints, for washing hands, cleaning clothes, etc.); as a result of TPP absorption through intact skin. Possible poisoning by the exhaust gases of vehicles running on leaded gasoline, as well as vapors when washing hot parts of the car engine with leaded gasoline in order to clean it. AT recent times in connection with the partial replacement of thermal power plants with other, less toxic antiknock agents, the number of poisonings with them has significantly decreased.
In case of oral poisoning with ethyl liquid, the lethal dose is 10-15 ml. Severe poisoning by inhalation of vapors can occur even in cases of maximum permissible concentrations - MPC (0.005 mg / m3). TES and its metabolic products can remain in the body for a long time (up to 3 months). Excretion occurs in urine and feces.
Poisoning is characterized by a complex lesion of the central nervous system.
At the autopsy of those who died from acute TES poisoning, morphological changes are found mainly in the structural formations of the CNS. Dystrophic and necrobiotic changes are noted nerve cells visual hillock, hypothalamic region, cerebral cortex. When examined under a microscope, the brain and its membranes are plethoric, moderately edematous. In other internal organs, there is a picture of congestive plethora, dystrophic changes, with a prolonged course, catarrhal-hemorrhagic pneumonia develops.
Acetone(dimethyl ketone) is a colorless liquid with a characteristic odor. Mixes well with water; soluble in organic solvents. It is a good solvent for many substances. Acute poisoning is possible by inhalation of high concentration vapors and ingestion. It is taken orally more often by negligence, sometimes while intoxicated. Recently, substance abuse has become widespread by bringing oneself into a state of intoxication with the help of acetone vapors. Most often, alcoholics and drug addicts turn to this remedy in search of euphoria.
The lethal dose for oral poisoning ranges from 60-75 ml. The toxic effect increases significantly when acetone is taken in a mixture with organochlorine and other organic substances due to the possibility of the formation of very toxic substances - chloroacetone and bromoacetone. By the nature of the toxic effect, acetone is classified as a drug. It affects various parts of the central nervous system, actively inhibits oxidative enzymes. Excreted from the body through the lungs, kidneys and skin.
In case of oral poisoning, nausea, vomiting, abdominal pain appear, in severe cases, loss of consciousness occurs within a few minutes. Cyanosis of the skin and mucous membranes is noted, tendon reflexes are absent, the pupils are constricted, do not react to light, the smell of acetone is felt from the mouth. Within 45-60 minutes after taking the liquid, respiratory arrest is possible. In severe cases, death can occur within 6-12 hours after ingestion of the liquid.
Acute severe inhalation poisoning can occur when the content of acetone in the air is 0.003 g / l - loss of consciousness, convulsions, kidney damage, visual disturbances, a sharp increase in blood sugar concentration.
At autopsy, congestive plethora of internal organs, pulmonary edema, membranes and brain matter, dark tarry blood in the cavities of the heart and large vessels are noted.
Dichloroethane used as a solvent and extractant, as an insecticide and fungicide, in everyday life - for cleaning clothes and other purposes. Ingestion of 20 ml of dichloroethane causes a picture of severe poisoning, often ending in death.
The nature of the clinical picture of poisoning depends on the dose of the poison and the routes of entry. Already 10-15 minutes after ingestion of one or more sips of dichloroethane (10-12 ml or more), complaints of headache, sweet taste in the mouth, nausea, vomiting, severe weakness, dizziness, unsteady gait, pain in the epigastric region and right hypochondrium. Subsequently, a coma develops and, in severe forms of poisoning, death occurs (coma often develops after taking 50 ml or more of dichloroethane). Approximately half of those poisoned by dichloroethane die.
Diagnosis of poisoning with dichloroethane is based on the clinical picture of poisoning, the presence of a specific smell of dichloroethane in exhaled air and vomit, a chemical study of washings, vomit, blood, urine, autopsy data and the results of a forensic chemical determination of poison in the organs of a corpse.
To establish poisoning with other chlorinated hydrocarbons, the same research methods are used. For forensic chemical research, it is desirable to take adipose tissue.