Who is called a life-threatening condition of a person when he is, as it were, between life and death. The condition is specific, its characteristic signs are lack of consciousness, weakening or absence of reactions to external stimuli, fading of reflexes, violation of the depth of breathing. The patient's temperature regulation is violated, the tone of the vessels changes, the pulse slows down or quickens. From the outside it seems that the person is sleeping soundly, but the state of sleep does not end, and it is not possible to wake the affected person by any external influence. At the same time, his heart works, blood moves through the body, oxygen exchange processes take place in the lungs, that is, the body supports the natural processes of life, but at a minimum level.
The concept and causes of coma formation
In medicine, coma denotes an acute developing condition associated with inhibition of the central nervous system, impaired respiratory and cardiovascular systems. The affected person has a loss of consciousness.
In some cases, the state of coma may be accompanied by such a decrease in the functioning of vital systems of the body, after which brain death occurs, that is, coma precedes brain death and subsequent death of the patient. A brain death is characterized not only by a lack of consciousness, but also by a complete lack of reflex activity, disruption of the cardiovascular and respiratory systems, metabolism, and the absorption of nutrients.
Why can a person develop a coma? The problem of coma is one of the most acute in modern medicine, since they can occur due to dozens of different reasons, they do not always have specific signs of precursors, and at the prehospital level, it is extremely difficult for doctors to treat such patients because of the coma can develop in a very short time. The attending physician simply does not have time to study the features of the functioning of the body of a particular person and understand how and why he had a coma.
Between the concepts of “coma” and “clear consciousness”, which are diametrically opposed to each other, there is still such a category as “stunning”. Stun is characterized by a certain level of wakefulness reduction, which is combined with severe drowsiness.
The onset of coma is preceded by the so-called stupor - deep stunning with the preservation of the reaction to external stimuli. At the same time, motor activity, resistance to danger and harmful effects are partially preserved, for example, a person tries to avoid exposure to the body of high temperature or dangerous acids on the skin.
Why can a person develop a coma? Doctors refer to the following factors determining the development of coma conditions:
- brain damage resulting from a stroke, trauma, infectious and viral diseases, epilepsy;
- endocrine diseases and metabolic disorders caused by them;
- the use of certain types of hormonal drugs;
- intoxication with poisoning, infectious diseases, damage to the kidneys, liver;
- hypoxia, lack of oxygen in the body.
Degrees and varieties of pathology
Coma refers to types of impaired consciousness, so deep that a person completely disappears from contact with the outside world, as well as mental activity is inhibited, and it is impossible to remove the affected person from it even through intense stimulation.
It should be noted that one of the criteria for differentiating coma types is precisely the so-called depth of damage, that is, the level of “disconnection” of the body from the surrounding world.
- moderate coma of the first degree;
- pronounced second degree;
- deep (third degree).
A moderate coma is noted by the absence of obvious signs of a violation of vital functions, while the patient retains pupil reactions to light, corneal reflexes. There may be some increase in muscle tone over time. The victim in a coma lies with his eyes closed, and, unlike the stupor, he does not have involuntary motor activity.
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;
- stable hemodynamics;
- sluggish pupillary reactions to light;
- decreased muscle tone;
- flaccid tendon reflexes;
- the inconstancy of the bilateral Babinsky reflex.
A deep coma is also called atonic. In this case, the patient has respiratory failure, hemodynamic instability, and the lack of pupil response is not light. A deep type of pathology is dangerous because it can go to a beyond coma, in which the person's spontaneous breathing function is impaired and the bioelectric activity of the brain ceases.
In practice, the clinical division of coma into 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 fourth-degree coma (beyond) is equivalent to brain death, in which an extensive death of the cells of its tissue begins. Spontaneous breathing is interrupted, but cardiac activity persists.
Also, all coma lesions are divided into two generalized groups:
In turn, the primary coma is represented by cerebral and structural pathologies, and the secondary ones are metabolic and dysmetabolic.
Dysmetabolic coma can be:
- infectious toxic;
Causes and patterns of primary and secondary coma
The primary coma may develop due to the presence of:
- epidural, subdural, parenchymal hemorrhages;
- extensive hemispheric heart attacks;
- primary tumors;
- hemorrhages and heart attacks in the cerebellum and brain;
- cerebellar tumors;
- encephalitis, encephalomyelitis;
- severe head injuries;
- hematoma in the posterior cranial fossa.
As for the coma of the secondary type, it is caused by:
- endocrine system diseases: hypothyroid disorders, diabetes;
- generalized infections, such as typhoid fever, staphylococcus aureus;
- various types of intoxications: alcoholic, 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 brain lesions - a severe form of traumatic brain injury or an extensive hemorrhagic stroke. The next type of coma formation occurs in the absence of clearly defined focal symptoms, for example, with some types of craniocerebral injuries.
Gradual inhibition of brain activity can occur against the background of meningeal syndrome or symptoms of focal organ damage, or without clear shell and focal manifestations, but with the accompanying convulsive syndrome.
How does a coma develop in a patient
The basis of clinical coma syndromes is depression of consciousness resulting from a mismatch in interneuronal interactions and progressive deep inhibition. The mediator biochemical mechanism is a factor that determines the rate of growth of a coma. Its timely correction determines the possibility of recovery of consciousness later. Morphological damage to brain cells indicates the irreversibility of the process of oppression of consciousness.
The etiology of comatose lesions is very extensive, but the pathogenetic algorithm for the development of the disease is universal, and consists in metabolic disorders, on which the satisfaction of the brain's energy needs directly depends. Normal blood flow in the brain is the basis for adequate metabolic support. 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 impaired metabolism of nerve cells. As a result, the patient has a decrease in the production of adenosine trinphosphate - a substance involved in metabolic processes. The affected person 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, worsen 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.
Disorders of the acid-base state are characterized by metabolic acidosis, while disturbances in the electrolyte balance can be based on a pathological change in the concentration of sodium, potassium, calcium, ammonium ions.
Hypoxia and a change in the acid-base balance are factors that provoke swelling and swelling of the brain, the appearance of intracranial hypertension.
Characterization of coma lesions of various types
When it comes to structural coma, the most common are traumatic and apoplexy.
The disease is often the result of a severe traumatic brain injury, such as compression of the brain or contusion. You can determine this origin of the pathology by paying attention to external injuries, subcutaneous hematomas, abrasions. Clinical manifestations are characterized by a combination of focal and cerebral syndromes, with the latter most often prevailing. Meningeal syndrome may also develop. In this case, the initial loss of consciousness indicates a shell-shocked state of the brain, and its gradual “shutdown” indicates a hematoma and squeezing of the brain stem.
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 the clarity of focal symptoms, which is especially evident if the process is localized in one of the hemispheres.
If the patient has cerebellar hemorrhage, he develops a stem-type breathing disorder.
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 sugar coma, in diabetes can be:
Appears after severe infections and diseases, starvation, termination of hypoglycemic therapy. This type of disease is formed gradually, the patient has thirst, polyuria, nausea, vomiting, abdominal pain, dehydration with dry skin, worsening turgor of the mucous membranes of the eyeballs. A sharp decrease in blood pressure occurs, tachypnea, muscle hypotension appears. The characteristic smell of acetone from the oral cavity is felt.
It is formed slowly, within 5-10 days, usually in patients older than 50 years with diagnosed insulin-dependent diabetes. It can appear after vomiting, intense diarrhea, taking a significant amount of diuretics and glucocorticoids. A person has signs of dehydration, shallow breathing, fever and muscle tone, as well as seizures.
With hyperglycemic coma, a person experiences an intense increase in blood sugar. The patient begins cramps, nausea and vomiting, the 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 an insulin-containing drug, violation of a diabetic diet, surgical intervention, as well as stressful situations.
The disease is characterized by acute development after administering too much insulin to a patient with diabetes. Exhausting physical work, psychological trauma, and diseases of the digestive tract can provoke this condition. The patient before the onset of coma feels severe weakness, increased sweating, nausea and agitation. Coma is accompanied by severe tremor, the presence of tonic-clonic seizures, blanching of the skin, tachycardia. In this case, the patient's blood pressure is normal.
Eclampic endogenous coma
It develops after the 20th week of pregnancy, and can last until the end of the first week after childbirth. At first, the woman develops on the rise a severe headache, visual impairment, dizziness, nausea, vomiting, diarrhea, a general feeling of weakness, increased blood pressure. Further, the victim develops a generalized convulsive seizure, or a series of seizures, after which a coma occurs.
Slowly growing against a background of chronic renal failure. The patient smells urea from the oral cavity, deep, noisy breathing as a hyperventilation, dehydration of the skin is noted, traces of scratching appear on it. A coma may occur after another seizure.
It is formed in people who for a long time suffer from vomiting due to various reasons. As a result, the patient appears dehydration, tachycardia, convulsions.
The result of liver damage with hepatitis, cirrhosis, poisoning by poisons. This condition develops gradually, at first the affected one suffers from insomnia, overexcitation and increased muscle tone. In a coma, the patient has dry mucous membranes and wet skin, there is a convulsive syndrome and periodically deepening Cheyne-Stokes breathing.
Such a coma develops if the patient's blood circulation stops, and is absent for 3-5 minutes, as well as against the background of an infectious lesion with botulism, tetanus, diphtheria, with encephalitis, pneumonia and pulmonary edema. The clinical manifestations look like this - the patient develops skin cyanosis and hyperhidrosis, he has narrowing of the pupils, and against the background of dyspnea and hyperventilation, auxiliary muscles are included in the respiratory activity.
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, for example, of a viral nature with toxic properties. Infectious diseases in which generalized conditions are present in the pathogenesis are plague, paratyphoid fever, typhoid fever, salmonellosis. Intensive intoxication, which occurs in severe cases of infection, is the main cause of the onset of coma.This type of coma can be recognized by the acute onset of the disease in young patients and high body temperature, the absence of obvious acute pathologies in the operation of vital systems, for example, respiratory, endocrine, digestive, and the absence of meningeal syndrome.
Exogenous Toxic Coma
May appear against the background of poisoning with ethyl alcohol, antipsychotics, atropine-containing drugs, narcotic analgesics, organophosphorus compounds.
Coma develops, followed by alternating periods of drowsiness and arousal, increasing gradually. The patient has a crimson skin of the face and neck, narrowing of the pupils, hyperhidrosis, shallow breathing, vomiting, convulsive seizures.
Such a lesion forms sharply, accompanied by a narrowing of the pupils, increased sweating, convulsions and spasms of a local or generalized nature.
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 decreased muscle tone, increased body temperature.
Substances causing this type of damage are often administered intravenously. In this case, a coma occurs abruptly, accompanied by shallow breathing with elements of arrhythmia, increased sweating, bradycardia and a decrease in blood pressure.
Organophosphate poisoning and compounds
The pathological condition develops gradually. The patient develops nausea and vomiting, pain in the abdomen, myofibrillation of the neck and face. In a coma, marked cyanosis of the mucous membranes and skin, narrowing of the pupils, superficial arrhythmic breathing, bronchorrhea, and convulsions are noted.
First aid for coma: what to do
All patients in a coma are subject to immediate hospitalization, so if you suspect the presence of such a condition, you must immediately call the ambulance team. The service dispatcher needs to carefully and thoroughly describe all the signs of the condition, state of breathing, pupils, heart rate, the presence or absence of seizures, the circumstances that preceded the appearance of the lesion.
A person who has fallen into a coma, first of all, needs to be laid on a solid horizontal surface in a position on his back or side.
First aid for coma should begin with a determination of the type of coma. If the affected person has diabetes, the onset of a condition characterized by loss of consciousness, impaired respiratory function, convulsions, an abnormal change in the size of the pupils can be regarded as falling into a coma.
In a 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, so after calling an ambulance, you need to lay on your side, monitor the release of vomiting so that it does not get into the respiratory tract. The injured person is given an injection of insulin, after which, with a high probability, he will regain consciousness. Next, he needs to be given a plentiful drink to make up for the lost fluid. Arriving doctors will determine whether it is necessary to transport the victim to the hospital to provide him with specific medical care.
With a hypoglycemic coma, the patient’s health and life are at risk, therefore he will be hospitalized. Before the arrival of the doctors, the patient is laid by turning his head to the side, and a glucose solution is administered intravenously. If the victim returns to consciousness after this, they give him a sweet candy or a spoonful of sugar.
Ketoacidotic coma is considered the most serious complication of diabetes mellitus, and is formed against a background of severe insulin deficiency. Before the patient is hospitalized, with a ketoacidotic coma, he needs to rest, if possible, inject an insulin, and also infuse a solution of sodium chloride in a concentration of 0.9% as an infusion method. Similarly, first aid is provided with the hyperosmolar type of lesion.
Traumatic coma usually does not cause difficulties in diagnosis, since the main reason that causes it is brain injury. The patient affected by fainting has pale skin, a decrease or absence of the reaction of the pupils to light, vomiting, muscle weakness. First-aid first aid in this case is to lay the person and before the arrival of the doctors to monitor his breathing, to prevent the entry of vomit into the respiratory tract.
Apoplexy coma requires the patient to have rest and bed rest before the doctors arrive. A person is freed from clothing, from all elements that may interfere with free breathing. The room must be provided with access to fresh air. The oral cavity is freed from vomiting, and the head is turned to one side so that the victim is not choked with vomiting. An ice pack is placed on the head. If the patient begins to cramp, his head and neck must be carefully held.
Endogenous and exogenous coma lesions also require the transfer of the victim to a horizontal state. In addition, the patient needs a plentiful sweet drink. In case of convulsions, the head and neck must be carefully held to prevent injury. If the patient begins vomiting, the oral cavity should be cleaned of masses, and the head should 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, however, it should be carried out only in extreme cases, if the carer knows exactly the type of coma and the reasons that caused it.
How dangerous is coma for humans? It is known that coma is characterized not only by brain damage, but also by a malfunction of the 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 the doctors he needs to ensure peace and, if possible, maintain respiratory function.