First aid for coma

The term coma becomes well understood when getting acquainted with its history. The ancient Greeks wrote it through two “m”, which meant it – a blow. Already in the name of the condition, the definition of the most frequent vascular catastrophe, which caused it, was laid down. The condition is specific, its characteristic features are lack of consciousness, weakening or lack of reactions to external stimuli, extinction of reflexes, violation of the depth of breathing. The patient’s thermoregulation is disturbed, vascular tone changes, the pulse slows down or quickens. From the outside, it seems that a person is fast asleep, but the state of sleep does not end, and it is not possible to wake him up by any external influence. At the same time, his heart works, blood circulation is provided, oxygen exchange processes take place in the lungs, that is, natural life processes are maintained at a minimum level in the body.

Definition and causes of coma

Coma is an extremely serious condition characterized by loss of consciousness, dysfunction of all sense organs, impaired circulation, respiration, and metabolic processes.

Coma, like many other conditions, is not a diagnosis, but the outcome of a large number of painful disorders. Coma is more often caused by vascular accidents in medical practice, but it can develop as a result of general intoxication, metabolic disorders, brain injury, especially destruction of its cortex and trunk. The problem of coma is one of the most acute in modern medicine, since they can manifest themselves due to dozens of different reasons, they do not always have specific warning signs, therefore, it is extremely difficult to manage such patients at the prehospital level due to the rapid development of the condition. Of the common diseases, anoxia or cerebral ischemia (arrhythmia, carbon monoxide poisoning), vasculitis, diffuse connective tissue diseases, brain infections, uremia, diabetic ketoacidosis, liver failure, hypoglycemia, ethyl and methyl alcohols, drugs, as well as status epilepticus can lead to coma. , subarachnoid bleeding, catatonia.

Between the concepts of “coma” and “clear consciousness”, which are diametrically opposed to each other, there is such a category as “stunning” (or “precoma”). Stunning is characterized by some level of reduced wakefulness, which is combined with marked drowsiness.

The onset of coma is preceded by the so-called stupor – a deep stupor while maintaining a reaction to external stimuli. At the same time, motor activity, resistance to danger and harmful influences are partially preserved, for example, a person reacts to pain stimuli.

The most common causes of coma, or a condition requiring its exclusion, are:

• brain damage resulting from stroke, trauma, infectious and viral diseases, epilepsy, tumors or abscesses, epi- or subdural hematomas;
• endocrine diseases and metabolic disorders caused by them;
• the use of certain types of hormonal drugs;
• intoxication in case of poisoning, infectious diseases, damage to the kidneys, liver;
• hypoxia, lack of oxygen in the body.
• acute alcohol intoxication;
• medicines, poisonous plants and mushrooms, drugs.

In adults – 60-70%, in children and adolescents – up to 80-95% of all cases of coma of unknown etiology.

The severity of the pathology

Classifications of degrees of coma, adopted in domestic neurology, are largely similar. According to the dynamic approach developed by Bogolepov, the degrees of coma are stages that replace each other as the state deepens. The staging is based on the gradual shutdown of brain functions in the process of deepening the coma. First of all, phylogenetically young formations suffer, which is accompanied by the “release” of the functions of the underlying structures.

Distinguish:

• moderate coma of the first degree;
• pronounced second degree;
• deep (third degree).

Moderate coma is marked by the absence of obvious signs of impaired vital functions, while the patient retains pupillary reactions to light, corneal reflexes. There may be some increase in muscle tone over time. The victim in a state of coma lies with his eyes closed, and, unlike the stupor, he does not have involuntary motor activity.

A coma of the second degree has a slightly different clinical picture:

• violation of respiratory activity, including the formation of respiratory failure;
• shortness of breath, tachycardia, heart rhythm disturbance;
• unstable hemodynamics;
• sluggish pupillary reactions to light;
• dysphagia;
• decreased muscle tone;
• flaccid tendon reflexes;
• inconsistency of the bilateral Babinski reflex.

Deep coma is also called atonic. In this case, the patient develops respiratory failure, hemodynamic instability and the absence of pupillary reaction to light are noted. A deep type of pathology is dangerous in that it can turn into a transcendent coma, in which a person’s spontaneous breathing function is impaired and the bioelectric activity of the brain stops.

In practice, the clinical division of coma according to degrees is conditional, since they have a certain level of dynamism, because with adequate treatment, the patient may experience a regression of the pathology, and otherwise the coma may progress.

A coma of the fourth degree (outrageous) is equivalent to brain death, in which extensive cell death begins in its tissue. Spontaneous breathing is interrupted, but cardiac activity is preserved.

Also, all comatose lesions are divided into two generalized groups:

• primary;
• secondary.

In turn, primary coma is represented by cerebral and structural pathologies, and secondary – metabolic and dysmetabolic.

Dysmetabolic coma can be:

• endogenous;
• exogenous;
• infectious-toxic;
• toxic.

Reasons for the development of primary and secondary coma

Primary coma can develop due to:

• epidural, subdural, parenchymal hemorrhages;
• extensive hemispheric infarcts;
• abscesses;
• primary tumors;
• metastases;
• hemorrhages and heart attacks in the cerebellum and brain;
• cerebellar tumors;
• encephalitis, encephalomyelitis;
• severe traumatic brain injury;
• hematomas in the posterior cranial fossa.

As for the coma of the secondary type, it is caused by:

• diseases of the endocrine system: hypothyroid disorders, diabetes;
• generalized infections, for example, typhoid fever, staphylococcus aureus;
• various types of intoxication: alcohol, barbituric, opiate.

The development of the lesion can occur according to 4 schemes. In the first case, there is a sharp depression of consciousness along with emerging focal lesions of the brain – a severe form of traumatic brain injury or extensive hemorrhagic stroke. The next type of coma formation occurs in the absence of well-defined focal symptoms, for example, in some types of traumatic brain injury.

Gradual inhibition of brain activity can occur against the background of meningeal syndrome or symptoms of focal organ damage, or without clear meningeal and focal manifestations, but with concomitant convulsive syndrome.

How does a coma develop?

The basis of the clinical syndromes of coma is the depression of consciousness resulting from the mismatch of interneuronal interactions and progressive deep inhibition. The mediator biochemical mechanism is a factor that determines the rate of increase in coma. Its timely correction determines the subsequent possibility of restoring consciousness. Morphological damage to brain cells indicates the irreversibility of the process of oppression of consciousness.

The etiology of comatose lesions is very extensive, however, the pathogenetic algorithm for the development of the disease is universal, and consists in disorders of metabolic processes, on which the satisfaction of the energy needs of the brain directly depends. Normal blood flow in the brain is the basis for an adequate supply of metabolism. In the absence of sufficient oxygen supply to the brain cells, hypoxia develops in them, which further causes a chain of pathological processes based on a violation of the metabolism of nerve cells. As a result, the patient has a decrease in the production of adenosine triphosphate, a substance involved in metabolic processes. The patient develops intracellular acidosis, the permeability of the walls of blood vessels increases, and cerebral edema is formed. These factors negatively affect the state of blood flow in the brain and increase the state of hypoxia.

Due to hypoglycemia, lactate, calcium ions, free fatty acids accumulate inside the cells, as a result of which the cells die.

Acid-base disorders are characterized by metabolic acidosis, while electrolyte imbalance disorders can be based on pathological changes in the concentration of sodium, potassium, calcium, ammonium ions.

Hypoxia and changes in acid-base balance are factors that provoke swelling and edema of the brain, the appearance of intracranial hypertension.

Characterization of various comatose lesions

When it comes to structural coma, the most common are traumatic and apoplexy.

Traumatic coma

The disease is often the result of a severe traumatic brain injury, such as compression of the brain or contusion. It is possible to determine such an origin of the pathology by paying attention to external injuries, subcutaneous hematomas, and abrasions. Clinical manifestations are characterized by a combination of focal and cerebral syndromes, with the latter, most often, predominating. Meningeal syndrome may also develop. In this case, the primary loss of consciousness indicates a contusion of the brain, and its gradual “turning off” indicates a meningeal hematoma and compression of the brain stem.

apoplectic coma

Basically, it is formed in stages, through stunning and stupor (except in cases of extensive subarachnoid hemorrhage, as well as hemorrhage in the trunk and cerebellum). The clinical picture is characterized by pronounced focal symptoms, especially clearly manifested if the process is localized in one of the hemispheres.

If a patient has stem-cerebellar hemorrhage, he develops a stem-type respiratory disorder.

Endogenous coma

Pathology is the result of aggravation of endocrine diseases, as well as diseases of internal organs: these are coma in diabetes mellitus, hepatic or uremic coma.

Coma, or coma in diabetes mellitus, can be:

• ketoacidotic;
• hyperosmolar;
• hyperglycemic;
• hypoglycemic.

Ketoacidotic coma

It develops after severe infections and diseases, starvation, cessation of hypoglycemic therapy. This type of disease is formed gradually, the patient has thirst, polyuria, nausea, vomiting, pain in the abdomen, dehydration with dry skin, deterioration of the turgor of the mucous membrane of the eyeballs. There is a sharp decrease in blood pressure, tachypnea, muscle hypotension appears. There is a characteristic smell of acetone from the oral cavity.

Hyperosmolar coma

Forms slowly, over 5-10 days, usually in patients over 50 with diagnosed insulin-dependent diabetes. Coma can develop after intense vomiting and diarrhea, taking a significant amount of diuretics and glucocorticoids. A person has manifestations of dehydration, shallow breathing, increased body temperature and muscle tone, as well as convulsive seizures.

Hyperglycemic lesion

In hyperglycemic coma, a person experiences an intense increase in blood sugar levels. The victim begins to have convulsions, nausea and vomiting, pupils dilate, and all this against the background of loss of consciousness. The reasons for the formation of such a pathology may be untimely detection of diabetes, skipping an insulin injection or its untimely administration, changing the insulin preparation, a violation of the diabetic diet, surgery, and stressful situations.

Hypoglycemic type

The disease is characterized by acute development, after the introduction of too large a dose of insulin to a patient with diabetes mellitus. This condition can be provoked by exhausting physical work, psychological trauma, diseases of the digestive tract. The patient before the onset of a coma feels severe weakness, increased sweating, nausea and agitation. Coma is accompanied by severe tremor, the presence of tonic-clonic convulsions, blanching of the skin, tachycardia. The patient’s blood pressure is normal.

Eclamptic endogenous coma

It develops after the 20th week of pregnancy, and can last until the end of the first week after childbirth. First, a woman progressively develops a severe headache, visual disturbances, dizziness, nausea, vomiting, diarrhea, a general feeling of weakness, and an increase in blood pressure. Further, the victim develops a generalized convulsive seizure or a series of seizures, after which a coma occurs.

uremic coma

Slowly increases against the background of chronic renal failure. The patient has a smell of urea in the exhaled air, deep, noisy breathing by the type of hyperventilation, dry skin with traces of scratching is noted. Coma may occur after another convulsive seizure.

Chlorhydropenic lesion

It is formed in people who suffer from vomiting for a long time due to various reasons. As a result, the patient develops dehydration, tachycardia, convulsions.

hepatic coma

The result of liver damage in hepatitis, cirrhosis, poisoning with poisons. This condition develops gradually, at first the patient suffers from insomnia, overexcitation and increased muscle tone. In a coma, the patient has dry mucous membranes and moist skin, convulsive syndrome and Cheyne-Stokes breathing are present.

Hypoxic type

Such a coma develops if the patient’s blood circulation slows down, as well as against the background of an infectious lesion with botulism, tetanus, diphtheria, with encephalitis, pneumonia and pulmonary edema. Clinical manifestations look like this – the patient develops skin cyanosis and hyperhidrosis, he has a narrowing of the pupils, and against the background of dyspnea and hyperventilation, auxiliary muscles are included in the respiratory activity.

Exogenous coma

They are also called infectious-toxic, since the formation of such a lesion occurs due to exposure to toxins of microbial origin or the activity of pathogens themselves of a viral or bacterial nature with hypertoxic properties. Infectious diseases in which generalized conditions develop are plague, paratyphoid fever, typhoid fever, salmonellosis, hemorrhagic fevers. Intense intoxication that occurs in severe cases of infections is the main cause of coma. This type of coma can be recognized by the presence of an acute onset of the disease, especially in young patients, the absence of obvious acute pathologies in the functioning of vital systems, for example, the respiratory, endocrine, digestive systems, the absence of meningeal syndrome and high body temperature in the presence of specific signs of the disease.

Exogenous toxic coma

May appear against the background of poisoning with ethyl alcohol, neuroleptics, atropine-containing drugs, narcotic analgesics, organophosphorus compounds.

Ethyl alcohol poisoning

Coma develops with subsequent alternation of periods of drowsiness and arousal, growing gradually. The patient has a purple color of the skin of the face and neck, constriction of the pupils, hyperhidrosis, shallow breathing, vomiting, convulsive seizures.

Poisoning with neuroleptics

Such a lesion is formed abruptly, accompanied by constriction of the pupils, increased sweating, convulsions and spasms of a local or generalized nature.

Poisoning with substances of the atropine series

Before falling into a coma, the patient develops a strong psychomotor agitation. During a coma, the affected person has dry skin, dilated pupils, muscle fibrillation and a decrease in muscle tone, and increased body temperature.

Poisoning with narcotic analgesics

Substances that cause this type of injury are often administered intravenously. In this case, coma occurs abruptly, accompanied by shallow breathing with elements of arrhythmia, increased sweating, bradycardia and a decrease in blood pressure.

Organophosphate poisoning

The pathological condition develops gradually. The patient develops nausea and vomiting, pain in the abdomen, myofibrillation of the neck and face. In a coma, there is a pronounced cyanosis of the mucous membranes and skin, constriction of the pupils, shallow arrhythmic breathing, convulsions.

First aid for coma: what to do

All patients in a coma are subject to immediate hospitalization, therefore, if such a condition is suspected, it is necessary to immediately call an ambulance team. The service dispatcher needs to carefully and in detail describe all signs of the condition, the state of respiration, pupils, pulse, the presence or absence of seizures, the circumstances that preceded the onset of the lesion.

A person who has fallen into a coma, first of all, should be laid on a hard horizontal surface in a position on his back or on his side.

First aid for a coma should begin with determining the type of comatose lesion. In diabetic patients, the occurrence of a condition characterized by loss of consciousness, impaired respiratory function, convulsions, abnormal changes in the size of the pupils can be regarded as a coma.

In diabetic coma, the rules for providing first aid differ depending on the type of lesion.

Hyperglycemic coma is a condition in which a person has a pathologically elevated blood sugar level, therefore, after calling an ambulance, a person must be laid on his side, making sure that vomiting does not enter the respiratory tract. The patient is given an injection of insulin, after which, with a high probability, he will regain consciousness. Next, you need to provide plenty of fluids to replenish the lost fluid. A specialized team determines the need for hospitalization of the patient to provide him with specific medical care.

With a hypoglycemic coma, the health and life of the patient are at risk, so he must be hospitalized. Before the doctors arrive, the patient is laid down with his head turned to one side, and a glucose solution is administered intravenously. If the victim regains consciousness after this, he is given a sweet candy or a spoonful of sugar to eat.

Ketoacidotic coma is considered the most severe complication of diabetes mellitus, and is formed against the background of a sharp insulin deficiency. Prior to hospitalization of the patient, with a ketoacidotic coma, he needs to be kept calm, if possible, to inject insulin, as well as to inject saline sodium chloride solution by infusion. Similarly, first aid is also provided with a hyperosmolar type of lesion.

Traumatic coma usually does not cause difficulties in diagnosis, the patient has pale skin, decreased or no pupillary response to light, vomiting, and muscle weakness. Pre-medical first aid in this case consists in laying the person down and, before the arrival of doctors, monitor his breathing, and prevent vomit from entering the respiratory tract.

Apoplexy coma requires the patient to rest and bed rest before the arrival of doctors. A person is released from clothing, from all elements that can interfere with free breathing. The room must be provided with access to fresh air. The oral cavity is freed from vomit, and the head is turned to one side so that the victim does not choke on vomit. An ice pack is placed on the head. If the patient begins to have convulsions, his head and neck must be gently held.

Endogenous and exogenous comatose lesions also require the transfer of the victim to a horizontal position. In addition, the patient needs a plentiful sweet drink. With convulsions, the head and neck must be carefully held to prevent injury. If the victim begins to vomit, the mouth must be cleaned of vomit, and the head must be turned to one side so that it does not suffocate.

It should be noted that drug therapy before the arrival of doctors can save a person’s life, but it should be carried out only in extreme cases, if the caregiver knows exactly the type of coma and the reasons that caused it.

How dangerous is a coma for a person? It is known that comatose states are characterized not only by damage to the brain, but also by a disruption in the functioning of systems responsible for the functioning of the whole organism. Of course, such a pathology requires urgent hospitalization of the victim, and before the arrival of doctors, he must be provided with peace and, if possible, support for respiratory function.

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