What is asphyxia in medicine? Types, symptoms and consequences. Asphyxia. What it is? Asphyxia time
Description:
The state of increasing suffocation, leading to a lack of oxygen in the blood and tissues (hypoxia) and to the accumulation of carbon dioxide in them (hypercapnia).
Symptoms:
The clinical picture of asphyxia depends on its cause. In acute strangulation and obturation asphyxia, respiratory movements acquire a convulsive character, but there is no breathing as such. A sharp cyanosis of the face develops rapidly, consciousness is lost, general ones appear. Involuntary urination and defecation are possible. comes in 2-3 minutes.
With gradually increasing obstructive asphyxia, breathing becomes rare, deep, hoarse or wheezing at first. Respiratory noises are heard at a distance, while inhaling, auxiliary muscles tense. Then breathing becomes frequent, superficial, arrhythmic. First, the pulse quickens, arterial and venous pressure rises, darkening in the eyes is observed. Then the pulse slows down, consciousness is lost, arterial and venous pressure decreases, convulsions appear. Later, respiratory arrest occurs. As a result of a decrease in the oxygen content and the accumulation of carbon dioxide in the body, the blood acquires a dark red color, ventricular fibrillation may occur.
If asphyxia is based on compression of the lung, breathing immediately becomes frequent and shallow. The affected half of the chest lags behind or even sinks during inhalation (with multiple fracture of the ribs). In traumatic asphyxia, unconsciousness is preserved, but excitation, pronounced cyanosis and swelling of the face, multiple hemorrhages in the skin, conjunctiva and sclera of the eyes are noted.
Causes of occurrence:
The main causes of asphyxia:
1) compression of the upper respiratory tract from the outside during hanging, strangulation (strangulation asphyxia), neck injuries;
2) ingress of foreign solid or liquid bodies into the upper respiratory tract and trachea, which leads to their partial or complete obstruction (mechanical obstructive asphyxia);
3) retraction of the tongue in a patient lying on his back or affected, who is in a coma;
4) pathological processes in the larynx and trachea (edema, burn, tumor,);
5) accumulation in the pleural cavity of air (tense), blood (hemothorax), fluid (hydrothorax); rupture of the diaphragm with movement of the abdominal organs into the pleural cavity;
6) traumatic compression of the chest, abdomen, and sometimes the entire body with solid or loose bodies (traumatic asphyxia). The causes of asphyxia can also be acute violations of the function of the respiratory muscles in case of trauma to the upper spinal cord, some intoxications (residual effect of muscle relaxants, poisoning, etc.), convulsive syndromes (tetanus,) and other diseases (myasthenic crisis, ascending polyradiculoneuritis, etc.).
Treatment:
For treatment appoint:
With asphyxia, immediate intensive resuscitation, therapeutic and surgical measures are necessary. First of all, it is necessary to restore the patency of the airways when they are compressed or obturated (removing the loop or removing the object that squeezes the neck of the victim, removing foreign bodies from the airways). To maintain airway patency and to combat rapidly increasing hypoxemia, retraction of the root of the tongue should be eliminated. To do this, the patient's head is given a position of maximum occipital extension, or an air duct is inserted into the oral cavity, or the lower jaw is pushed forward beyond its corners, or the tongue is removed from the oral cavity by placing a tongue holder on it. The effectiveness of the manipulation is evidenced by the restoration of breathing, which becomes even and silent. It is also necessary to remove vomit and blood from the mouth and oropharynx, foreign bodies from the upper respiratory tract using techniques that increase pressure in the chest and airways below the site of their obstruction (applying jerky palm strikes to the interscapular region and jerky pressure on the epigastric region - reception Heimlich) or with special tools during a straight line; with pneumothorax - apply an occlusive bandage.
After restoring the patency of the respiratory tract, they start first by the mouth-to-mouth method, then with the help of portable and stationary respirators. If cardiac arrest occurs, heart massage is started simultaneously with artificial respiration. Artificial ventilation of the lungs is continued until the patient's consciousness is fully restored, sometimes for several hours or even days. This is especially important after strangulation and traumatic asphyxia. The convulsions and sudden motor excitation arising in these cases are eliminated by repeated administration of short-acting muscle relaxants (myorelaxin, dithylin) against the background of artificial respiration, and in the most severe cases, long-acting muscle relaxants (tubarin).
A nurse or paramedic, especially those who work independently, are sometimes forced to carry out manipulations that are normally performed only by doctors, such as tracheal intubation, drainage of the pleural cavity, conduction novocaine blockades, etc. In some emergency situations (laryngeal edema, compression of it by a tumor, hematoma) asphyxia can be effectively eliminated only with the help of a tracheostomy, which is performed only by a doctor. In desperate situations, the paramedic may resort to percutaneous puncture of the trachea with a thick needle with the introduction of a catheter into it and subsequent intermittent jet ventilation of the lungs with an air-oxygen mixture or oxygen. The midwife may be faced with the need to treat newborn asphyxia, which is manifested by a state of prolonged apnea at birth.
Treatment of asphyxia in diseases such as botulism,
Asphyxia is a pathological condition that develops acutely, disrupts the functions of vital body systems. It occurs due to a sharp decrease in the supply of oxygen to the organs. Lack of gas exchange between the external environment and the body leads to the accumulation of carbon dioxide in the tissues. Oxygen starvation and the impossibility of normal breathing ends in loss of consciousness, death. Death as a result of asphyxia can also occur due to reflex arrest of the heart muscle. A similar condition is diagnosed with irritation of the superior laryngeal nerve from compression of the neck.
Signs of asphyxia
Numerous post-mortem signs are determined by the rate of onset of death, the characteristics of the organism and the lifetime course of suffocation. They are also present in other variants of quick death. Among them there is not a single constant and absolutely true. External and internal signs of death from asphyxia are determined.
Internal signs
Choking is diagnosed by a number of clinical symptoms. The color and coagulability of blood matters. After death, the blood darkens, which is associated with its transformation from arterial to venous due to the rapid absorption of red blood cells by tissues.
Liquid blood is a common sign of rapid death. It is explained by saturation with carbon dioxide, autolysis. Blood clots are rarely observed, with a slow course of asphyxia. Coagulation is associated with leukocytosis, and with a rapid lethal outcome, it is not.
Point hemorrhages, or Tardieu spots under the membrane of organs, are considered an indicator of the onset of death. Arise as a result of increased permeability of the walls of blood vessels, rupture of capillaries. Other internal signs include plethora of organs, respiratory mucosa, overflow of blood in the right atrium and ventricle, anemia of the spleen. These symptoms can be observed not only with suffocation.
External signs
External signs of death from oxygen deficiency include. They have an intense blue-purple color. They appear due to the movement of a large amount of blood to the lower parts of the body. The color is due to oxygen-poor and carbon-dioxide-rich blood.
Death from asphyxia is indicated by cyanosis of the face and nails. It is observed in the first stage of suffocation. The reason is stagnation of blood, expansion and overflow of the vessels of the head. The blueness disappears within a few hours after death. The pathological process is accompanied by involuntary urination and.
Causes of asphyxia
The reasons are reduced to two groups. The first is characterized by a disorder of external respiration, the second - interstitial. Suffocation can occur in the absolute absence of oxygen while in an enclosed space. Common causes of suffocation include:
- mechanical compression of the neck, chest, abdomen;
- damage to the respiratory tract;
- their closure by a liquid or a foreign body;
- accumulation of air or blood in the pleural cavity due to injury;
- cooling;
- poisoning.
Asphyxia is the cause of death from electric shock. It is also observed in infectious processes, epilepsy, accompanied by spasm of the respiratory muscles. To suffocation lead to violations of the functions of the respiratory center, which occur due to organic damage. This outcome is observed when
Attention! The oxygen reserve in the body is 2-2.5 liters. The mentioned volume is only enough to save life for several minutes.
Suffocation occurs during high-altitude hypoxia. Poisoning with strychnine and other substances can also be aggravated by asphyxia, convulsions, and death.
Clinic of asphyxia
The main sign of suffocation is respiratory failure. It develops gradually, paroxysmal or suddenly. In acute asphyxia, breathing becomes frequent, deep and noisy. Inhales are longer than exhalations. The reason is irritation of the respiratory center with carbon dioxide. Auxiliary muscles are included in the respiratory act, the intercostal spaces and the epigastric region sink down.
The skin acquires a blue-purple color of the face and neck,. The period of excitation is replaced by increasing muscle weakness, slowing of the heartbeat. In the first minute there is a loss of consciousness. After respiratory arrest and cardiac activity, death occurs.
Types of asphyxia
Strangulation is intrauterine, primary and secondary. The first two types include asphyxia of the fetus and newborn. The composition of secondary asphyxia includes:
- mechanical asphyxia;
- reflex asphyxia;
- suffocation from lack of oxygen in the air;
- asphyxia with damage to the nervous system;
- asphyxia, which develops with spasticity.
Death from mechanical asphyxia is more often diagnosed. This type of strangulation occurs due to compression of the neck with hard objects and through hanging, strangulation with hands or a noose. Occurs when squeezing the chest and abdomen (compression asphyxia). Varieties include drowning, blocking the airways with foreign bodies, suffocation with vomit. Hanging and drowning account for the largest percentage.
When examining the corpse, general signs of death from mechanical asphyxia are found. These include cyanosis of the skin of the face, slow cooling of the body, involuntary defecation, urination, ejaculation, moderate. A sign is small-point hemorrhages in the conjunctiva of the eyelids.
Stages of suffocation
Regardless of the specifics of the factors initiating suffocation, there are preasphyxic and asphyxic periods of its development. The first period lasts from 10 seconds to 1 minute, the second is conditionally divided into successive stages.
|
Stage |
Clinical course |
| Stage of inspiratory dyspnoea |
|
| Stage of expiratory dyspnea |
|
| The stage of short-term respiratory arrest |
|
| Stage of terminal respiration |
|
| Persistent respiratory arrest |
|
The duration of the pathological process is 5-6 minutes. After the expiration of this time, irreversible changes occur in the cerebral cortex. The duration of the stages is affected by age, human health, type of suffocation.
The task in case of suffocation is the rapid restoration of the normal functioning of the respiratory tract. The preservation of the life and health of the victim depends on the speed of action. You should call and call a doctor.
Algorithm for emergency care:
- If the person is conscious but unable to breathe due to a foreign body in the airway, stand behind and wrap your arms around your waist.
- Clench one hand into a fist. Grab your fist with your other hand.
- With a sharp movement, press the stomach below the ribs above the navel.
- Repeat the steps until the object is out of the respiratory tract.
The provision of assistance in each case has its own specifics and depends on the reasons that led to strangulation. Thus, the supply of oxygen contained in the human body is negligible. Acute oxygen starvation of tissues leads to disruption of metabolic processes at the cellular level and death of the organism.
Video
Mechanical asphyxia is a state of oxygen deficiency caused by a physical blockage of the air flow path or the inability to make respiratory movements due to external restrictions.
Situations in which the human body is squeezed by external objects, or when external objects have caused injury to the face, neck or chest, are usually referred to as traumatic asphyxia.
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Classmates
Mechanical asphyxia - what is it?
For the diagnostic classification of diseases associated with strangulation, the International Classification of Diseases of the Tenth Revision is used. Mechanical asphyxia microbial 10 has the code T71 if strangulation occurred during squeezing (strangulation). Suffocation due to obturation - T17. Compression asphyxia due to crushing with earth or other rocks - W77. Other causes of mechanical suffocation - W75-W76, W78-W84 - include suffocation with a plastic bag, inhalation and ingestion of food, foreign body, accidental suffocation. 
Mechanical asphyxia develops rapidly, begins with a reflex breath holding, often accompanied by loss of consciousness during the first 20 s. Vital indicators during classical strangulation pass through 4 stages in succession:
- 60 s - the onset of respiratory failure, an increase in heart rate (up to 180 beats / min) and pressure (up to 200 mm Hg), an attempt to inhale prevails over an attempt to exhale;
- 60 s - convulsions, blueness, decrease in heart rate and pressure, an attempt to exhale prevails over an attempt to inhale;
- 60 s - short-term cessation of breathing;
- up to 5 minutes - intermittent irregular breathing persists, vital signs fade, the pupil dilates, respiratory paralysis sets in.
In most cases, death with complete respiratory arrest occurs within 3 minutes.
Sometimes the cause of this can be sudden cardiac arrest. In other cases, episodic palpitations may persist for up to 20 minutes from the onset of suffocation.
Types of mechanical asphyxia
Mechanical suffocation is usually divided into:
- Suffocation-strangulation;
- suffocation-obturation;
- suffocation due to compression.
strangulation asphyxia
Strangulation - mechanical overlap of something, in the context of asphyxia - the airways.
Hanging
When hanging, the airways are blocked with a rope, cord or any other long elastic object that can be tied on one side to a fixed base, and the other - fixed in the form of a loop around the person's neck. Under the influence of gravity, the rope pinches the neck, blocking the air flow. However, more often death by hanging does not occur from a lack of oxygen, but due to the following reasons:
- Fracture and fragmentation of the I and / or II cervical vertebra with displacement of the spinal cord relative to the oblong - provides 99% mortality almost instantly;
- increased intracranial pressure and extensive cerebral hemorrhage.
In rare cases, hanging can take place without the use of elastic objects, for example, from squeezing the neck with a fork of a tree, a stool, a chair, or other rigid elements that are geometrically located in such a way that they suggest the possibility of clamping.
Of all strangulation suffocations, death during asphyxia by hanging occurs most quickly - often within the first 10-15 seconds. Reasons may include:
- Localization of compression in the upper part of the neck poses the greatest threat to life;
- high degree of trauma due to a sharp significant load on the neck;
- minimal possibility of self-rescue.
Loop choke
Injuries and traces characteristic of mechanical asphyxia
The strangulation furrow (trace) from hanging is characterized by clarity, unevenness, openness (the free end of the loop is not pressed against the neck); shifted to the top of the neck.
The furrow from violent strangulation with a noose runs along the entire neck without a break (if there were no interfering objects between the noose and the neck, for example, fingers), it is uniform, often non-horizontal, accompanied by visible hemorrhages in the larynx, as well as in the places where knots, rope overlaps, is located closer to the center of the neck. 
Traces of pressure by hands are scattered all over the neck in the form of hematomas in places of maximum compression of the neck with fingers and / or in places of wrinkling and pinching of the skin. Nails leave additional traces in the form of scratches.
When strangling with a knee, as well as pinching the neck between the shoulder and forearm, visual damage to the neck often does not occur. But criminologists easily differentiate these types of strangulation from all others.
With compression asphyxia, due to large-scale disturbances in the movement of blood, the strongest blue of the face, upper chest, and limbs of the victim is observed.
White and blue asphyxiation
Strangulation signs of white and blue asphyxia
Cyanosis or bluish discoloration of the skin and mucous membranes is a standard feature of most asphyxia. This is due to factors such as:
- Change in hemodynamics;
- increase in pressure;
- accumulation of venous blood in the head and limbs;
- supersaturation of the blood with carbon dioxide.
Those affected by mechanical compression of the body body have the sharpest bluish tint.
White asphyxia accompanies strangulation, in which the main symptom is rapidly increasing heart failure. This happens when drowning by choking (I type). In the presence of cardiovascular pathologies, white asphyxia is possible with other mechanical asphyxiation.
Traumatic asphyxia
Traumatic asphyxia is understood as compression asphyxia resulting from an injury in an accident, at work, during man-made and natural disasters, as well as any other injuries that lead to the impossibility or limitation of breathing.
The reasons
Traumatic asphyxia occurs for the following reasons:
- the presence of external mechanical obstacles that prevent the performance of respiratory movements;
- jaw injuries;
- neck injuries;
- gunshot, knife and other wounds.
Symptoms
Depending on the degree of compression of the body, the symptoms develop with varying intensity. The key symptom is a total violation of blood circulation, outwardly expressed in severe edema and a bluish tinge of parts of the body not subjected to compression (head, neck, limbs).
Among other symptoms: fractures of the ribs, collarbones, cough.
Signs of external wounds and injuries:
- bleeding;
- displacement of the jaws relative to each other;
- other traces of external mechanical impact.
Treatment
Hospitalization required. The main attention is paid to the normalization of blood circulation. Carry out infusion therapy. Prescribe bronchodilators. Organs damaged by trauma often require surgery.
Forensic science of mechanical asphyxia
Modern forensic science has accumulated a large amount of information that allows, by direct and indirect signs, to establish the time and duration of asphyxia, the participation of other persons in suffocation / drowning, and, in some cases, to accurately determine the perpetrators.
Mechanical strangulation is often violent. For this reason, the external signs of asphyxia are of decisive importance when the court decides on the causes of death.
The video discusses the rules for artificial respiration and chest compressions
Conclusion
Mechanical asphyxia is traditionally the most criminalized of all types of suffocation. Moreover, strangulation has been used for centuries as a punishment for crimes committed. Thanks to such a "wide" practice, today we have knowledge about the symptoms, course, duration of mechanical suffocation. It is not difficult to define violent strangulation for modern forensics.
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asphyxia ( Greek- asphyxia; a - negative prefix, sphyxis - pulse) - a pathological condition caused by insufficient oxygen supply to the body or individual organs or tissues.
The concept of “asphyxia”, which is rooted in forensic medicine, in contrast to “hypoxia”, owes its origin to an old misconception. In Greek, “sphygmos” means only a rapid pulse, and in the literal translation asphyxia, therefore, means the absence of a pulse, which, of course, does not reflect the essence of this pathological process.
As follows from the definition, hypoxia is the basis of the asphyxial state - oxygen starvation of organs and tissues up to the complete cessation of oxygen supply to the body. In the broad sense of the word, asphyxia is suffocation (cessation of external respiration), which has various causes and mechanisms.
Various definitions of asphyxia
Asphyxia (suffocation) is an acute violation of gas exchange in the body. Most often, it occurs due to the cessation of air access or the accumulation of carbon dioxide harmful to the body. In both cases, oxygen starvation of the body develops, ultimately leading to death.
Asphyxia (asphyxia; Greek negative prefix a- + sphyxis pulse; synonymous with suffocation) is an acute or subacute developing and life-threatening pathological condition caused by insufficient gas exchange in the lungs, a sharp decrease in the oxygen content in the body and the accumulation of carbon dioxide.
Asphyxia (from the Greek a - without and sphyxis - pulse, heartbeat) is a condition in which there is a lack of oxygen supply to tissues, which occurs due to the impossibility of normal breathing. Asphyxia causes widespread hypoxia, which primarily affects organs and tissues most sensitive to lack of oxygen, such as the brain.
Asphyxia literally translates from Greek as "lack of pulse", but usually this term refers to death under conditions of hypoxia and anoxia.
The term "asphyxia" is recognized by many forensic doctors as vague and confusing. In the broad sense of the word, this term describes the state when the body does not receive enough oxygen with a developing excess of carbon dioxide (hypoxia and hypercapnia). This results in loss of consciousness and/or death.
However, before any death comes a state characterized by a lack of oxygen and an excess of carbon dioxide, so that asphyxial death is when a decrease in oxygen supply is not caused by natural causes.
Asphyxia is a deficiency of oxygen and an excess of carbon dioxide in the blood and tissues. Asphyxia often associated with suffocation is usually the result of respiratory failure due to mechanical blockage of the airway, paralysis of the respiratory muscles due to electrical shock, etc.
Dorland's Illustrated Medical Dictionary
Asphyxia is a pathological change caused by a lack of oxygen in the inhaled air, which leads to hypoxia and hypercapnia.
Asphyxia - the Greek word (a - a negative particle, sphygmos - zhelobienie, pulse) translated into Russian means the absence of a pulse, therefore, a condition in which the cessation of the activity of the heart is expected. At present, the concept of asphyxia has significantly deviated from the original meaning of this word, and means suffocation - an acute pathological process that occurs due to a lack of oxygen in the blood and tissues and the accumulation of carbon dioxide in the tissues. The reasons for the development of asphyxic conditions can be painful conditions of the body (endotoxic asphyxia) and mechanical obstacles to the entry of air into the body (mechanical asphyxia). This manual discusses the types of mechanical asphyxia.
Asphyxia is an acute pathological process that occurs due to a lack of oxygen in the blood and tissues and the accumulation of carbon dioxide and is characterized by a severe symptom complex of disorders of the central nervous system, cardiovascular system and respiratory organs.
Asphyxia classification
Following the principle of classification of death, there are:
- Violent asphyxia, which can occur under the influence of a number of reasons. For example, from mechanical obstructions to breathing, in case of poisoning, in case of electric shock, etc. A variety of violent asphyxia is mechanical asphyxia, which is defined as a violation of external respiration under the influence of mechanical factors.
- Non-violent (pathological) asphyxia, which develops with various kinds of diseases. This also includes neonatal asphyxia.
Classification of asphyxia depending on the method of obstructing breathing
- Mechanical asphyxia from compression
- a) strangulation asphyxia
- hanging
- loop choke
- hand strangulation
- strangulation with other objects or other parts of the body
- b) Compression asphyxia
- chest compression
- compression of the abdomen
- compression of the chest and abdomen with hard and loose objects
- a) strangulation asphyxia
- Mechanical asphyxia from closing
- a) Obstructive asphyxia (closing of the openings of the mouth and nose with soft bodies and objects)
ASPHYXIA (asphyxia; Greek a - negative + sphyxis pulse) - suffocation; a life-threatening pathological condition caused by an acute or subacute lack of oxygen in the blood and the accumulation of carbon dioxide in the body and is manifested by a severe symptom complex of disorders of the vital functions of the body, mainly the activity of the nervous system, respiration and blood circulation.
Types of Asphyxia
Asphyxia as a result of respiratory disorders occurs most frequently. The cause of asphyxia may be mechanical obstruction of air access to the respiratory tract when they are squeezed from the outside (for example, suffocation) or their significant narrowing. The latter can be caused by an inflammatory process (for example, diphtheria), laryngeal edema, retraction of the tongue (with injuries of the lower jaw; during anesthesia and other unconscious states), a tumor, spasm of the glottis or small bronchi (for example, with bronchial asthma). Often the cause of asphyxia can be the closure of the airway lumen as a result of aspiration of food and vomit, blood, water (during drowning), the ingress of various foreign bodies, etc. In the fetus, asphyxia of this kind can occur in cases of premature spontaneous respiratory movements and admission amniotic fluid into the respiratory tract, as well as with complete or partial obstruction of the respiratory tract caused by the accumulation of mucus. Wounds and closed injuries of the chest that disrupt its respiratory excursions, as well as collapse of the lungs when significant amounts of air enter the pleural cavities (pneumothorax) or accumulation of fluid in them (exudative pleurisy, hemothorax) can also lead to asphyxia.
Asphyxia from lack of oxygen in the inhaled air can be observed with altitude sickness (see), in specific production conditions associated with breathing in closed systems with a forced supply of a gas mixture in cases where the supply of oxygen and the absorption of carbon dioxide are disturbed; asphyxia occurs when staying in an isolated closed space, when there is a gradual drop in the oxygen content in the air and a progressive increase in the concentration of carbon dioxide. Vital disorders characteristic of asphyxia develop in such cases at first against the background of normal or even increased pulmonary ventilation. In the future, the activity of the respiratory center is disturbed, the volume of ventilation decreases, and asphyxia acquires its usual course.
Asphyxia as a result of damage to the nervous system also due to ventilation disorders. This includes cases of paralysis of the respiratory muscles resulting from conduction disorders of neuromuscular synapses (poisoning with curare-like drugs, the action of bacterial toxins, poisonous substances), paralysis of the respiratory nerves (multiple neuritis) or widespread damage to the motor neurons of the spinal cord in the cervical and thoracic segments during injuries, poliomyelitis and other infectious and non-communicable diseases.
Asphyxia can also occur during prolonged spastic conditions, for example, with tetanus, poisoning with strychnine and other poisons that cause convulsions.
One of the common causes of asphyxia is severe disorders of the respiratory center, resulting from its organic lesions of a different nature, as well as intoxication, an overdose of hypnotics and narcotic drugs, and hypoxia of the bulbar structures, accompanied by energy depletion of the neurons of the respiratory center and the weakening or complete cessation of their function. .
Disorders of external respiration, leading to asphyxia, may be of a reflex nature. This is observed when the receptors of the trachea and bronchi are irritated by various gas and vaporous chemicals. compounds, smoke, dust particles, a pathological process (inflammation, tumor) localized in the lung tissue or respiratory tract. The resulting reflex influences on the respiratory center disorganize the act of breathing.
Asphyxia also occurs in cases where respiratory excursions cause persistent pain (with fractures of the ribs, pathological processes in the pleural cavity, intercostal neuralgia).
Asphyxia as a result of impaired oxygen transport occurs with acute blood loss and other cases of acute circulatory failure, with difficulty in the outflow of venous blood from the cranial cavity (congestive asphyxia), in case of poisoning with "blood poisons" (carbon monoxide, methemoglobin formers). In the experiment, this form of asphyxia occurs when both carotid and vertebral arteries are ligated (the so-called acute ischemic asphyxia).
Asphyxia as a result of interstitial respiration disorder characterized by impaired oxygen utilization by tissues. These disorders may be different; for example, cyanide compounds, hydrogen sulfide paralyze cytochrome oxidase, preventing the oxidation of reduced cytochrome, and thereby cause tissue hypoxia in the brain and other tissues, which leads to tissue asphyxia. Some bacterial toxins and viruses also cause asphyxia by blocking various links of oxidative processes in tissues. Tissue asphyxia is characterized by a normal oxygen content in the blood.
Fetal asphyxia occupies a special place; it can be a consequence of maternal asphyxia, accompanied by a decrease in oxygen and an increase in carbon dioxide in the blood supplying the fetus, as well as a consequence of disorders of the uteroplacental or umbilical circulation. Gross violations of the function of the respiratory center of the newborn also lead to asphyxia. In some cases, their action can be mediated through the mother's body (hypoxia, drug overdose, infectious intoxication, etc.), in others it is directed directly to the fetus (birth trauma to the head, circulatory disorders). In some cases, in the absence of apparent causes, asphyxia is associated with reduced excitability of the respiratory center of the newborn in relation to carbon dioxide (see Asphyxia of the fetus and newborn).
Thus, it is obvious that asphyxia can occur at a certain stage of any form of hypoxia, if the latter leads to severe disorders of gas exchange and the accumulation of carbon dioxide in the body.
Biophysical mechanisms of asphyxia
As a result of oxygen starvation of tissues in the blood, a large amount of intermediate metabolic products accumulates, metabolic acidosis progresses. The products of incomplete oxidation circulating in the blood, affecting the biochemical processes in cells, cause a sharp inhibition of their function; tissue hypoxia occurs. The cells of the body lose their ability to absorb oxygen, and a number of irreversible chemical, physicochemical, and other changes occur in them, which are apparently a direct or indirect consequence of a violation of the cell membrane structures and intracellular organelles. The most vulnerable elements of the cell are the phospholipid components of the membranes. With a decrease in the oxygen concentration in cells, ATP decreases or disappears completely, the function of redox enzymes is disrupted, the amount of acidic metabolic products, in particular lactic acid, increases, and the pH decreases. The membranes react to these changed conditions by dropping the membrane potential and a sharp increase in permeability (due to lack of ATP) or complete rupture (due to a decrease in pH), which leads to cell death. A temporary decrease in the oxygen content creates the preconditions for lipid peroxidation, mainly unsaturated fatty acids, which later, with sufficient access to oxygen, leads to chain radical lipid oxidation and the associated sharp increase in the permeability of cell membranes and inactivation of vital enzymes and processes ( Yu. A. Vladimirov, 1972). One of the reasons for the violation of membrane structures is the action of hydrolytic enzymes of lysosomes. As a result of an increase in the permeability of cell membranes or their rupture, lysosomal hydrolases are released: cathepsins, phospholipases and others, activated by Ca 2+ ions, fatty acids and low pH. The action of lysosomal hydrolases on cellular components leads to autolysis and cell death. The labilization of lysosomes and the release of hydrolytic enzymes do not occur immediately, but only after diffuse changes in the ultrastructure of the cell membrane, endoplasmic reticulum, and mitochondria, which develop during the first hour of ischemia, earlier than changes in lysosomes.
Violation of all types of metabolism and the development of proteolytic processes during asphyxia most rapidly occurs in brain cells. With the localization of these irreversible processes in the respiratory and vasomotor centers, death occurs. In the heart, asphyxia affects muscle fibers and interstitial tissue. In muscle fibers, dystrophic changes, edema, vacuolization and often necrosis of individual groups of fibers are revealed; in the interstitium - edema, hemorrhage and increased development of connective tissue. In the walls of the blood vessels of the heart and in the aorta, edema, disintegration of collagen and elastic fibers, and accumulation of acid mucopolysaccharides are observed. These phenomena are based on profound disturbances of metabolic processes in the cells of tissues and organs.
The pathophysiological changes characteristic of asphyxia are determined by oxygen starvation of tissues, the specific effect of excess carbon dioxide and acidosis, which occurs both as a result of hypercapnia and the accumulation of underoxidized metabolic products. Each of these factors plays a significant role in the development of asphyxia, but hypoxia is of decisive importance. In the initial stages of asphyxia, these factors act as irritants of the corresponding receptor structures (chemoreceptors of the sinocarotid and cardiaortal zones, receptor structures of the reticular formation of the medulla oblongata) and cause a number of reactions in the body that are protective and adaptive in nature. As the asphyxia deepens, manifestations of various disorders due to hypoxia (see), hypercapnia (see) and acidosis (see) increase.
Pathological anatomy of asphyxia
Morphological changes in asphyxia depend on the causes that caused it. There are, however, a number of common features, which are divided into external and internal. The external ones include: 1) cyanosis of the face, which appears in the first minutes of asphyxia during life and remains on the corpse; 2) the rapid appearance of diffuse bluish-purple cadaveric spots, which depends on the liquid state of the blood, characteristic of asphyxia; against the background of cadaveric spots, multiple ecchymosis can be observed; 3) petechial hemorrhages in the connective membranes of the eyelids; 4) traces of involuntary urination, defecation, eruptions of sperm; 5) expansion, less often narrowing of the pupils. Of greater importance are internal signs: 1) the liquid state of the blood due to hypercapnia; 2) overflow of the right heart with blood when its left half is empty as a result of stagnation and hypertension in the pulmonary circulation and rigor mortis of the heart muscle; 3) plethora of internal organs; 4) small-spotted hemorrhages in the serous membranes (more often in the pericardium and pleura - Tardieu spots, Fig. 1); 5) acute (alveolar, rarely interstitial) pulmonary emphysema that occurs during shortness of breath; 6) pulmonary edema.
The most vulnerable in asphyxia is the central nervous system. In all its departments, circulatory disorders are observed [vascular dystonia, perivascular edema (Fig. 2) and hemorrhages], they are more pronounced in the brain stem. In nerve cells, hydropic dystrophy, pericellular, perinuclear edema, a “severe disease” of nerve cells (a large number of vacuoles, dispersion of a basophilic substance, karyopyknosis, acidophilia), and lipoid dystrophy occur. In astrocytic glia, there is swelling of the bodies, as well as processes of astrocytes, fragmentation of the latter, coagulation of protoplasm, disappearance of the contour of the bodies of astrocytes. In microglia, dystrophic changes are less pronounced. In oligodendroglia, the appearance of a large number of edematous (drainage) cell forms is observed. To a greater extent, changes are expressed in phylogenetically younger parts of the brain; the medulla oblongata and spinal cord change to a lesser extent.
All of the listed morphological features are not specific and permanent. In different combinations, they are also found in other cases of rapidly occurring death.
Clinical picture
It is customary to distinguish between several phases of asphyxia. The first phase is characterized by increased activity of the respiratory center in the form of an increase and an increase in the power of its rhythmic excitation cycles, an increase in blood pressure, an increase in heart rate, and mobilization of deposited blood. Often in the first phase, inhalation is lengthened and intensified, and therefore this stage of asphyxia is called the phase of inspiratory dyspnea. In general, it is characterized by a picture of increased excitation of the respiratory and vasomotor centers and the predominance of sympathetic effects in the field of autonomic regulation. The second phase is characterized by a decrease in breathing, often accompanied by increased exhalation (expiratory dyspnea) and a significant slowing of the heartbeat (vagus pulse); arterial pressure at the beginning of the second phase is usually still elevated, but then gradually decreases. At this stage of asphyxia, the effects of excitation of the parasympathetic nervous system predominate, in the occurrence of which great importance is attached to the direct action of carbon dioxide on the nuclei of the vagus nerves.
A sharp excitation of the parasympathetic nuclei, which are normally responsible for the implementation of inhibitory effects on the respiratory center, underlies the next - third stage of asphyxia. It is characterized by a temporary (from several seconds to several minutes) cessation of the rhythmic activity of the respiratory center - the so-called preterminal pause. At this time, blood pressure usually decreases significantly, spinal, ocular and other reflexes fade, loss of consciousness occurs.
The fourth phase is manifested by rare deep convulsive "sighs" - the so-called terminal, or agonal, breathing, usually lasting several minutes, but sometimes much longer. At this time, severe convulsions develop, often there is an involuntary eruption of feces and urine, the release of sperm, which depends on the sharp excitation of the centrum anospinale and centrum vesicospinale. With acute asphyxia in pregnant women, spontaneous abortion may occur.
Death from asphyxia occurs due to respiratory paralysis; heart contractions, as a rule, continue for some time after the cessation of breathing.
Electrocardiographic studies show, in addition to tachycardia alternating with bradycardia, a variety of cardiac arrhythmias, conduction disturbances, changes in R and T waves; when breathing stops, monocomplex changes occur.
In the initial stage of asphyxia, desynchronization of the electrical activity of the cerebral cortex is usually observed; as breathing slows down, the main rhythm is suppressed, slow theta and delta waves begin to predominate. Biocurrents usually completely disappear when terminal respiration appears or somewhat earlier.
On the part of the biochemical composition of the blood, asphyxia is characterized by a decrease in pH, an increase in the alkaline reserve, a decrease in the content of chlorine in the plasma and its increase in erythrocytes. The sugar level rises, which is associated mainly with the action of carbon dioxide on the vegetative centers and the breakdown of liver glycogen. Blood clotting is usually reduced.
The clinical picture of asphyxia and the rate of its development significantly depend on the characteristics of the etiological factor that caused the asphyxia. So, if the cause of asphyxia was the primary inhibition of the respiratory center, there is no excitation phase. With asphyxia from drowning, the first phase is holding the breath when immersed in water and the absence of an increase in respiratory movements when staying under water; breathing resumed after primary apnea immediately becomes slower compared to the original and remains so until the terminal pause. When hanging and strangling, the nature and sequence of changes in breathing depend on the level of strangulation (above or below the larynx), etc.
The total duration of asphyxia (from its onset to death) can also vary within fairly wide limits. With a sudden complete cessation of pulmonary ventilation, the duration of asphyxia is no more than 5-7 minutes. In cases of gradually developing asphyxia (for example, when breathing in a confined space or with neurological diseases), the duration of asphyxia can be much longer.
There are significant age differences in sensitivity to asphyxia. The younger the animal, the easier it tolerates asphyxia. So, a rat at the age of 12-15 hours lives without access to air for up to 30 minutes, a six-day one - about 15 minutes, a twenty-day one - about 2 minutes; an adult - 3-6 minutes, while a newborn - 10-15 minutes.
Features of resuscitation
Resuscitation in asphyxia consists in eliminating the causes that caused it, maintaining the function of vital organs in the fight against the consequences of hypoxia and hypercapnia. The basis of resuscitation directly at the scene is the restoration of airway patency (removal of foreign bodies, fluid, mucus, vomit, the introduction of an air duct when the tongue is retracted, the release of the neck from the compressive loop, etc.), artificial respiration (see) and in clinical death external heart massage (see). These measures should be carried out immediately after the victim has been evacuated from the danger zone (premises filled with natural gas, engulfed in fire, from water or moving traffic, etc.), and not only by a health worker, but also by any adult who finds himself on scene.
The most effective method of artificial ventilation in the absence of any apparatus or devices is mouth-to-mouth or mouth-to-nose breathing. Patients unconscious to prevent aspiration are transported with the head turned to the right and placed on the right forearm in the position on the right side. If there is a danger of regurgitation, the introduction of a gastric tube is indicated. In cases of acute violation of the patency of the larynx, trachea or bronchi (foreign bodies, aspiration of blood or food masses, trauma, stenosis or tumor), tracheal intubation is necessary (see Intubation), tracheotomy (see) or bronchoscopy (see). In an out-of-hospital setting, a tracheotomy can be replaced by a cryo- or conicotomy (see Laryngectomy). With laryngospasm, the introduction of muscle relaxants, tracheal intubation and artificial ventilation of the lungs are indicated.
Certain features are resuscitation with bronchospasm (see).
The first measures for asphyxia resulting from bilateral pneumothorax include puncture of the pleural cavities with thick needles and suction of air from the pleural cavities. After the elimination of acute disorders, the main attention should be paid to maintaining adequate respiration and circulation, as well as correcting violations of the acid-base state and water-electrolyte balance. The desire to compensate for the inefficiency of ventilation by increasing the concentration of oxygen in the inhaled gas mixture is erroneous: this does not prevent hypercapnia and respiratory failure. Therefore, if spontaneous breathing is ineffective, as well as with convulsions and sudden motor excitation, after tracheal intubation or tracheotomy, long-term artificial ventilation of the lungs with a respirator should be carried out until spontaneous breathing and consciousness are fully restored. These measures do not completely eliminate the risk of airway obstruction due to bronchospasm, accidental endobronchial obstruction, compression, bending or blockage of the endotracheal tube, etc. Therefore, constant monitoring of the effectiveness of artificial ventilation is necessary. Important in the system of resuscitation in asphyxia is the prevention of pulmonary and cerebral edema (rational artificial ventilation, hormonal and dehydration therapy, hypothermia, etc.). In connection with the increase in venous pressure in asphyxia, it is advisable to bleed from a vein. With toxic asphyxia, along with other resuscitation measures, complete or partial blood replacement is indicated. At asphyxia as a result of defeat by toxic agents (see) application of antidotes plays an important role. When drowning in fresh water, as well as under the influence of certain toxic substances, drugs, hypoxia and hypercapnia, after a sharp hyperventilation, ventricular fibrillation may occur, which must be immediately eliminated by electrical defibrillation (see).
Mental disorders
Acute asphyxia (for example, during self-hanging) is accompanied by an almost instantaneous loss of consciousness. After removal from this state, anterograde, retroanterograde amnesia, amnesia for current events, more often of a transient nature, is observed. Intellectual impairments, up to complete dementia, are determined by the severity and duration of asphyxia, and may be irreversible (mnestic-intellectual dementia).
With asphyxia arising from a lack of oxygen (“altitude sickness” of pilots), anxiety, a decrease in the acuity of sensations and perceptions, estimates of time and spatial relationships, euphoria, and obnubilation are observed (see Stunning). Loss of consciousness occurs without warning. There are cases when there are no violations of well-being or, if they are present, the critical attitude towards them sharply decreases. In some cases, lethargy, hypobulia, changes in the emotional state are observed: indifference or anger. Differences in manifestations are associated with individual characteristics: congenital resistance to oxygen starvation, fitness, etc. Vegetatively labile faces (after a traumatic brain injury, neuropaths) are more sensitive to hypoxia. Euphoria, impaired consciousness is a subjective factor in accidents and disasters where the performance of duties is associated with the possible occurrence of hypoxia.
In asphyxia from acute carbon monoxide poisoning, elementary visual and auditory deceptions were noted with preserved consciousness. Coma follows. And after helping the victim, he is in a stunned, disoriented state, his actions are uncoordinated, reminiscent of a state of intoxication. Retrograde amnesia, fixation dysmnesia are observed. In chronic carbon monoxide poisoning - dizziness, as in intoxication, asthenia, anxiety, indecision, delusional episodes; in severe cases - a picture of pseudoparalysis.
Forecast
With timely resuscitation in victims with asphyxia, it is possible to restore vital functions. However, people who have undergone asphyxia often have mental and neurological disorders, in particular retrograde amnesia, paresis of the vocal cords; Pulmonary edema and pneumonia are the most common cause of death in people who are taken out of asphyxia.
Asphyxia in forensic terms
In connection with the development of the doctrine of hypoxia, the definition of asphyxia in forensic terms has lost its former meaning and is currently conditional. Previously, under the term "asphyxia" in forensic medicine, various types of death from acute oxygen starvation, which arose as a result of various external influences, mainly from violations of external respiration, were combined. However, asphyxia does not always occur and cannot always be proven. Therefore, there is every reason to define such types of death as death from hypoxia.
In the thanatogenesis of death from respiratory disorders, not only oxygen starvation itself can be leading, but reflex cardiac arrest due to irritation of the vagus nerve endings, for example, when the airways are closed with a foreign body, when drowning and death in water, when hanging, strangling with a noose or hands.
The concept of "hypoxia" includes asphyxia. Therefore, asphyxia in forensic medicine is understood in the broad sense of the word asphyxiation due to oxygen starvation. There are asphyxia caused by mechanical obstructions to breathing (mechanical asphyxia), and asphyxia due to the damaging effect of various substances on the physiological mechanisms that ensure gas exchange (toxic asphyxia).
The most common in forensic practice are the following types of mechanical asphyxia: hanging, strangulation with a noose, hands; closing the openings of the nose and mouth with soft objects; closure of the lumen of the respiratory tract with various foreign bodies, food masses, etc.; compression of the chest and abdomen by any objects, for example, a car, earth during landslides; drowning. Each of these types of death as a result of mechanical asphyxia has its own pathophysiological and morphological features, which makes it possible to establish these types on a dissecting table.
Toxic asphyxia occurs when a damaging agent acts directly on the respiratory center (morphine), on the respiratory muscles (strychnine, curare), on the blood (carbon monoxide, aniline, nitrites), on the respiratory enzymes of cell protoplasm (cyanides); the same types of asphyxia include asphyxia from pulmonary edema occurring from exposure to suffocating OB, etc. Cases of toxic asphyxia are diagnosed on the basis of the characteristics of the clinical course (poisoning with morphine, strychnine) or the morphological picture (poisoning with carbon monoxide - carboxyhemoglobinemia, aniline, nitrites - methemoglobinemia) , as well as forensic chemical examination of internal organs, spectral analysis of body fluids.
Cadaveric phenomena in asphyxia are represented by a complex of non-permanent changes observed in general with a rapidly occurring death of various origins. These signs include: well-marked cadaveric spots, cyanosis of the skin of the face, ecchymosis in the conjunctiva, skin of the face, dark liquid blood in the heart, vessels, sinuses of the dura mater, plethora of internal organs, subpleural and subepicardial ecchymosis, etc. Previously, a complex of these signs considered pathognomonic for asphyxia. In fact, each of these signs individually and all together do not give grounds for diagnosing asphyxia, since they are also observed in other types of death and can occur even after death. For example, with a low location of the head of a corpse, cyanosis of the skin of the face and ecchymosis in the skin, in the conjunctiva may also occur posthumously. With rapid death from acute cardiovascular insufficiency, electrical trauma, etc., the blood is always liquid and dark. There may also be ecchymosis in the conjunctiva, under the pleura and epicardium. On the other hand, in subjects with cachexia, secondary anemia, with certain death from asphyxia, all these signs may be absent. The main diagnostic value are signs characterizing certain types of mechanical disturbance of external respiration: strangulation furrow, damage in the neck (see Hanging, Strangulation), diatom plankton in the internal organs (see Drowning).
Traumatic asphyxia
Traumatic asphyxia is a kind of symptom complex caused by a temporary cessation of breathing during a sharp compression of the chest, abdomen or the entire body by car wheels, fragments of destroyed buildings, soil during collapses in mines, heavy objects, etc. The name of the symptom complex comes from the similarity of the color of the victim’s face with the color skin in severe asphyxia.
The symptoms of traumatic asphyxia were described by Ollivier in 1837. A more complete description of its clinic and pathogenesis was given by G. Perthes and Braun in 1899.
Traumatic asphyxia during the Great Patriotic War was observed in 0.2% of closed chest injuries. In peacetime, traumatic asphyxia occurs in 0.2% of all patients with injuries, and with closed injuries of the chest and trunk, from 1.1 to 11.6% of cases.
Etiology and pathogenesis
Traumatic asphyxia occurs with a sharp compression of the chest in the anterior-posterior direction. Traumatic asphyxia in children is very rare, but it is extremely difficult. In young people, the chest skeleton is quite elastic and can be compressed with a force of up to 1.2-1.7 kg / cm 2 without breaking the ribs. In persons of mature and elderly age, compression of the chest with a force exceeding 0.3-0.6 kg / cm 2 is accompanied by a fracture of the ribs (G. S. Bachu). Strong compression of the lungs, with their extensive vascular system, is accompanied by a delay and a sharp restriction of breathing, compression of the superior vena cava and a violation of the outflow of blood from it. This causes a sharp increase in pressure in the system of the superior vena cava and a reverse flow of blood in the veins. Milner (P. Milner) believes that convulsive closure of the glottis and a sharp tension in the abdominal press are of great importance. Due to the absence of valves in the brachiocephalic veins (vv. brachiocephalica dextra et sinistra) and acute insufficiency of valves in the venous trunks flowing into these veins, which is associated with an increase in the lumen of the veins under the influence of a sharp, sudden increase in pressure in them, the blood rushes to the periphery in areas of the upper half of the body free from compression; in this case, there is a sharp overstretching of the venous walls, small veins, paresis of capillaries and venous stasis of blood in them. In severe cases, in addition, there is a rupture of capillaries and venules and, as a result, petechial hemorrhages.
Beach and Cobb (Beach, Cobb) at microscopic examination of the skin of the victims did not find hemorrhages around the vessels, while Aschoff (L. Aschoff) observed them. This is apparently explained by the varying severity of patients with traumatic asphyxia observed by the authors. G. S. Bachu observed the appearance of petechial hemorrhages in the skin of the upper part of the body with compression of the entire surface of the chest, even on fresh corpses (up to 6 hours).
The violet-blue or purple-blue color of the skin of the upper half of the body is mainly due to persistent capillary venous stasis, since in the process of recovery, the skin color changes to greenish, brown and yellow, as happens with resorption of subcutaneous hemorrhages.
Clinical picture
The face of the victim is puffy, the skin is painted in purple, purple-red, dark purple, and in severe cases almost black (masque ecchymotique). This coloration ends abruptly on the upper half of the chest. It does not disappear, but only slightly decreases when pressed with a glass spatula. Against this background, small hemorrhages are often visible. In the place where parts of clothing (collar, suspenders, bra straps, etc.) fit snugly against the skin, strips of normally colored skin remain. Often found subconjunctival hemorrhages, exophthalmos, and in severe cases visual impairment due to hemorrhage in the retrobulbar tissue and the vitreous body of the eye.
Visual acuity may be weakened, sometimes there is no perception of color, especially red. In severe cases, complete blindness is possible due to damage to the optic nerve. The pupils are dilated, sluggishly react to light. Sometimes there is a loss of consciousness.
Hemorrhages are also noted on the mucous membrane of the nose, tongue, mouth, larynx and are sometimes accompanied by hoarseness, nasal tone of speech, less often complete aphonia. Hearing is often reduced due to paresis n. vestibulocochlearis, caused by the stagnation of venous blood in the capillaries of the cochlea and the organ of Corti.
Often there are pains in the inguinal and axillary areas, making it difficult to move. Pain is caused by overstretching, possibly by a violation of the integrity of the valves of the veins by the reverse flow of blood that occurs at the time of chest compression. The veins of the upper extremities are dilated, filled with blood, and bulge distinctly through the skin.
Although the appearance of the patient resembles severe asphyxia, the condition of patients, in the absence of severe concomitant injuries (fractures, damage to internal organs), remains satisfactory. Shock, loss of consciousness usually indicate the presence of severe concomitant injuries or prolonged crushing of the chest muscles. Body temperature is normal or low. Diuresis is usually lowered, protein, cylinders, erythrocytes are found in the urine. In severe cases, acute renal failure, uterine bleeding, and flaccid lower paraplegia develop due to circulatory disorders in the spinal cord.
Associated injuries and complications are diverse: multiple fractures of the ribs, damage to the lung tissue and bronchi, hemo-pneumothorax, violation of the integrity of the abdominal organs, extensive crushing of the muscles, accompanied by a kind of long-term crushing syndrome (crush syndrome), or the so-called. traumatic toxicosis (see), characteristic for to-rogo is acute renal failure (see). Sometimes there is damage to the spine, spinal cord and other organs.
Forecast favorable for uncomplicated pure forms of traumatic asphyxia. The cyanotic coloration of the skin begins to decrease from the 3-8th day and disappears after 2-3 weeks. Hemorrhages on the mucous membranes and sclera resolve after 4-6 weeks. Severe course and death are possible only in the presence of concomitant injuries.
Treatment symptomatic: semi-sitting position in bed, oxygen, cardiac agents and analgesics; carrying out special measures for the treatment of associated injuries and their complications - see Hemothorax, Bleeding, Traumatic toxicosis, Shock.
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