Coma

Coma is a deep loss of consciousness. Coma is not a diagnosis, but, like shock, an indication of a critical condition of the body caused by a certain pathology.

Some types of coma are combined with shock.

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Symptoms comas

The development of a coma can be sudden - within a few minutes, often without precursors, against the background of relative well-being, rapid - within 0.5-1 hour in the presence of precursors; gradual over several hours or more. Rapid and sudden development is possible with any coma, but is more often observed with brain damage, anaphylaxis.

Rapid coma is characterized by sudden loss of consciousness. Respiratory disorder (arrhythmic or stethoric) of the central type of regulation disorder develops. Disturbance of central hemodynamics with development of hypodynamia, tachycardia, arrhythmia, hypervolemic syndrome with polyfunctional insufficiency of the homeostasis system is noted.

Slow development includes a period of pre-comatose states with gradual suppression of consciousness: first stupor, which may have periods of excitement, then a stop, and finally the process progresses to a coma.

With slow development of coma, 3 stages are formed (the first two correspond to precoma), which are clinically manifested:

1. mental anxiety, drowsiness during the day and agitation at night, impaired coordination of conscious movements, ataxia;
2. drowsiness with a sharp inhibition of reactions to external stimuli, including pain and light; an increase and then a decrease in tendon reflexes.
3. patients do not make contact, but pain sensitivity is preserved; muscular dystonia, spastic contractions of some muscles, mainly small ones, are observed; urination and defecation are involuntary, i.e. the above-described three-degree coma develops with a transition to an agonal state.

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Forms

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Apoplectic coma

The main pathogenetic moment is the violation of cerebral circulation, with the development of circulatory hypoxia of the brain. It can be of three types: hemorrhagic stroke with hemorrhage and imbibition of blood in the tissue of the brain or trunk; ischemic thrombotic stroke; ischemic embolic stroke. Hemorrhagic stroke: sudden onset, may be associated with traumatic brain injury (concussion, brain contusion, intracranial or intracerebral hematoma) or diseases (cerebral atherosclerosis, hypertension), in which a vessel ruptures, more often during the day, with physical exertion or stressful situations, mainly develops in elderly people, but can also occur in boys with a ruptured aneurysm of the vessels of the brain, more often during physical education classes. Often preceded by: dizziness, headaches, visual and hearing disorders, tinnitus, high hypertension, orthostatic collapse.

Meningeal syndrome is clearly expressed, with the formation of hemiparesis, disturbance of craniocerebral innervation, and the presence of pathological symptoms. Convulsions are possible.

Laboratory examination of blood and urine does not reveal any specific changes. Cerebrospinal fluid comes in under increased pressure, xanthochromic, with an admixture of blood. According to indications determined by a neurologist or neurosurgeon, instrumental, functional studies of the brain are performed (it all depends on the capabilities of the hospital), while significant changes are revealed on the echoencephalogram, rheogram, Dopplerogram, computer study of the brain.

Ischemic thrombotic stroke develops gradually, more often in the morning, the harbingers are dizziness, fainting, stupor, orthostatic collapse, transient motor or sensory disorders, dysarthria. It is based on the gradual development of atherosclerotic occlusion, less often a tumor.

The main manifestations are: pale face, constriction of pupils, decreased blood pressure, bradycardia up to the development of cardiovascular failure. Meningeal syndrome is manifested by the formation of mono- or hemiparesis, pathological symptoms are smoothed out.

In laboratory studies, the characteristic sign is hypercoagulation of the blood, other tests, including cerebrospinal fluid, have no changes (if there is no other concomitant pathology). Instrumental studies reveal clear signs of thrombosis, especially when performing angiography of the cerebral vessels.

Ischemic embolic stroke develops suddenly with rapid loss of consciousness and deepening coma, more often in young people with chronic cardiovascular diseases, mostly with venous pathology and the presence of varicose veins, thrombophlebitis, phlebothrombosis, in which a thrombus breaks off and blocks the blood vessels of the brain.

The main manifestations are: absence of precursors, paleness of the face, moderate dilation of the pupils, hyperthermia, various signs of cardiac and respiratory failure. Meningeal syndrome is manifested by mono-, less often hemiparesis.

Laboratory changes are not indicative, including cerebrospinal fluid examination. Of the instrumental examinations, the most informative are cerebral angiography and magnetic resonance imaging.

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Hemolytic coma

Occurs during a crisis in patients with hemolytic disease. In the pathogenesis of this coma, the leading moments are hemic hypoxia of the brain due to disruption of oxygen transport and cerebral circulation due to neurocirculatory dystonia and thrombus formation in the microcirculatory bed, which leads to gross metabolic disorders in the brain, up to softening and necrosis with a disorder of the central regulation of body functions.

The development of coma is preceded by progressively increasing hemolytic jaundice, headache, high temperature ("hemoglobinuric fever"), shortness of breath, muscle pain, collapse. Against this background, loss of consciousness develops suddenly, with pronounced meningeal syndrome and convulsions. The differential sign is the presence of hemolytic jaundice, confirmed by laboratory indicators.

Hyperthermic coma

The pathogenesis is based on external overheating of the body or disruption of the body's thermoregulation, leading to water-electrolyte and circulatory disorders, the development of perivascular and pericellular edema with small hemorrhages, including in the brain. It can develop against the background of meningeal pathology.

It develops gradually, with the formation of precursors in the form of lethargy, sweating, headaches, dizziness, tinnitus, a feeling of being stunned, up to fainting, nausea and vomiting, shortness of breath, palpitations. The body temperature rises.

The main clinical manifestations are: hyperthermia, facial hyperemia, mydriasis, total hypo- or areflexia; tachypnea, sometimes with the development of Cheyne-Stokes breathing; tachycardia, hypotension, decreased diuresis, hypo- or areflexia.

Laboratory findings are not characteristic.

Hypocorticoid (adrenal) coma

The causes of this coma are: hypocorticism (crisis) with a sharp decrease in gluco- and mineralocorticoids (more often in young men or boys - they are obese, with a loose body, on the abdomen, have striae); acute adrenal gland damage; Waterhouse-Friderichsen syndrome; Addison's disease; rapid withdrawal of steroid therapy. In the pathogenesis, the main thing is a violation of electrolyte metabolism with loss of water and sodium, leading to secondary disorders of vascular tone and cardiac activity.

Develops: gradually (quickly in Addison's disease), more often after stressful situations, infections, operations, painful manipulations and injuries. Accompanied by: weakness, rapid fatigue, anorexia, nausea, diarrhea, hypotension, orthostatic collapse and fainting;

During external examination, such patients show characteristic signs: in patients with Addison's disease, the skin tone has the appearance of a bronze tan, in other pathologies, hyperpigmentation of the skin folds of the hands and groin area from a bronze shade to black is noted. Hemorrhages may be noted on the skin, hypothermia is characteristic: The pupils are dilated, the turgor of the eyeballs is preserved. The muscles are rigid, areflexia. Breathing is shallow, often of the Kussmaul type. From the cardiovascular system, hypotension, tachycardia, soft pulsation are noted. Vomiting without precursors and relief, involuntary diarrhea are characteristic. When the shock threshold of irritation is reached, and it is very low in these patients, respiratory and cardiac arrest is possible, which requires resuscitation.

Laboratory indicators: hyponatremia, hyperkalemia, hypoglycemia (differentially, it is important not to confuse with acidosis of another genesis); possible - azotemia, lymphocytosis, monocytosis, eosinophilia. In a special study - a decrease in ketosteroids in the blood (17-KS and 17-OKS) and urine. Subsequently - a progressive decrease in potassium ions.

Hypopituitary (pituitary) coma

The pathogenesis is based on: damage to the pituitary gland or compression by tumors, long-term radiation therapy, massive corticosteroid therapy, Sheehan's syndrome with loss of hormonal function. This leads to disruption of the central nervous system and damage to the central regulation of the activity of all organs and systems through the neurohumoral system. Complex functional changes are formed in the systems: central nervous system, respiration, cardiovascular, metabolism and homeostasis, renal and hepatic function. This type of coma is the most difficult for differential diagnosis.

The onset is gradual, most often after injuries, infectious diseases, especially viral etiology. Progressive weakness, drowsiness, and adynamia are noted. Characteristic: swelling of the trunk, dry mouth, dry skin and peeling, bradycardia, decreased blood pressure, and often convulsive syndrome.

In the case of already developed coma, the main differential signs are: hypothermia (below 35 degrees); skin is pale, rough, sometimes with a yellowish tint, dry, cold to the touch. The face is puffy, eyelids are edematous.

Edema of the trunk and extremities is loose and easily pressed through. Breathing is rare, shallow, Kussmaul type. From the cardiovascular system: hypotension, bradycardia, hypovolemia. Oliguria is characteristic. From the central nervous system: hypo- or areflexia.

Laboratory studies reveal: anemia, increased ESR, dysproteinemia, hypercholesterolemia, hyponarthremia, hypochloremia. Due to pathogenesis - signs of respiratory acidosis.

Hunger (alimentary-dystrophic) coma

It is based on insufficient or inadequate nutrition with disruption of energy exchange processes, accompanied by dystrophy and functional insufficiency of all organs and the system, primarily the brain. Clinically and functionally it resembles hypoglycemic coma, often develops in cancer patients or in patients with severe intoxication. But in recent years it has also been found in clinically healthy people (dietary starvation, unbalanced nutrition, etc.).

The onset of coma is rapid. It is accompanied by a feeling of hunger, excitement, a feverish flush on the cheeks; the eyes are shiny, the pupils are dilated. A rapid transition from fainting to coma is noted.

In developed coma, clinical manifestations are different, depending on the etiology. In oncocachexia and prolonged starvation: the skin is dry, pale-gray, cold to the touch, the muscles are atrophic, reflexes in them are reduced. Meningeal syndrome is rarely formed. In alimentary disorders: the skin is pale, cold to the touch, arising due to vegetative-vascular dystonia, pupils are dilated, reaction to light is reduced. Common are: hypotension, weak pulse, tachycardia, hyporeflexia, sometimes painful convulsions.

Laboratory parameters are not typical for differential diagnosis (clinical data and anamnesis play a major role): leukopenia, hypoproteinemia, hypocalcemia, hyperkalemia are revealed, which to a greater extent indicates the development of metabolic acidosis.

Diabetic coma

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Hypoglycemic coma

The main pathogenetic moment is hypoglycemia and decreased utilization of glucose by brain cells. It may be accompanied by cerebrovascular accidents in the form of one of the forms of apoplectic coma. The anamnesis of these patients includes diabetes mellitus with the use of antidiabetic drugs or insulin. If the patient is unconscious, as a rule, there is a note and an "insular kit" in the pockets.

Develops quickly, sometimes develops slowly. Accompanied by: a feeling of hunger, fear, weakness, sweating, palpitations, trembling throughout the body, psychomotor agitation and inadequate behavior, unsteady gait (resembles the behavior of a person in a state of alcoholic intoxication - be careful when conducting differential diagnostics).

In the development of the actual comatose state, the distinctive signs are: paleness and moisture of the skin, the presence of clonic and tonic convulsions, muscle hypertonia, alternating with hypotonia. Sometimes there is a violation of the act of swallowing, but breathing is preserved. The pupils are wide, the turgor of the eyeballs is not disturbed. From the cardiovascular system, the following are characteristic: hypotension, tachycardia, arrhythmia. There is no smell of acetone in the exhaled air.

Laboratory findings: hypoglycemia is detected with a decrease in sugar levels to less than 2.2 mmol/l.

Hyperglycemic comas

Hyperglycemic coma is based on insulin deficiency in diabetes mellitus, which leads to decreased glucose absorption by tissues, its accumulation in the blood with glycemia and plasma hyperosmia, tissue metabolism disorders with ketosis, acidosis, profound depression of the central nervous system due to decreased glucose absorption by brain cells and impaired neurocyte trophism. Hyperglycemic coma is the opposite of hypoglycemic coma. Unlike hypoglycemic coma, there is a lot of sugar in the blood, but it is not absorbed due to a lack of insulin. The causes are: excessive intake of sweet foods with the patient's usual insulin dosage; non-compliance with the insulin administration regimen, dosage error, development of viral and inflammatory diseases in the patient, ineffectiveness of stimulants of natural insulin production by the pancreas (such as bucarban, etc.). There are three types of hyperglycemic coma:

1. hyperketonemic acidotic coma, accompanied by the development of metabolic acidosis due to a decrease in the utilization of ketone bodies with excessive ketogenesis in the liver, a sharp decrease in alkaline reserves in tissues, a violation of the cationic composition of cells with excessive excretion of potassium by the kidneys;
2. hyperosmolar coma caused by severe disturbances in blood supply, hydration and cationic composition of brain cells with high diuresis with loss of salts; accompanied by the development of hypovolemia, hypotension and other microcirculation disorders, which leads to a decrease in renal filtration and secondary retention of highly dispersed proteins and salt osmoids in the blood plasma;
3. hyperlactacidemic coma, develops in patients with diabetes mellitus under conditions of hypoxia caused by severe infection, renal and hepatic failure, and intake of biguanides. In this case, anaerobic glycolysis increases, the lactate/pyruvate system is disrupted, and a powerful metabolic acidosis with damage to the cerebral cortex is formed.

Hyperketonemic coma

The onset is gradual: polydipsia, polyuria, weakness, possible severe abdominal pain, nausea, loss of appetite, drowsiness. Clinical manifestations: the face is hyperemic, the eyeballs are sunken, their tone is reduced, the pupils are constricted. The skin is dry, often pale, its turgor is reduced. The extremities are cold to the touch, the muscles are relaxed, flabby. Rare deep breathing is characteristic, like Kussmaul with the smell of acetone from the mouth. The tongue is dry, often coated with a brown coating. Tachycardia is moderate, blood pressure is reduced, heart sounds are not changed, but there may be a pendulum rhythm.

Laboratory tests: hyperglycemia over 20 mmol/l; plasma hyperosmolarity (normal 285-295 mosmol/kg), hyperketonemia, decreased blood pH to the acidic side, increased residual urea nitrogen, creatinine, increased hematocrit, hemoglobin, neutrophilic leukocytosis. Sugar and acetone in the urine.

Hyperosmolar diabetic coma

Hyperosmolar coma can develop not only with diabetes, but also with other pathologies. In this case, diabetes is an aggravating factor, since the mortality rate for this type of coma is more than 50%. It is caused by massive fluid loss due to: vomiting, diarrhea, taking diuretics, etc.

The onset is gradual. Accompanied by: increasing weakness, polyuria, diarrhea, mental disorders, orthostatic collapse, hemodynamic disorders, up to hypovolemic shock. Clinical manifestations: hyperthermia, dry skin and mucous membranes; tonic abduction of the eyes and their hypotonia, nystagmus; rapid, deep breathing, without the smell of acetone; low blood pressure, tachycardia, arrhythmia, weakening of the pulse. Anuria may be present. Due to impaired cerebral microcirculation, the following are possible: hemiparesis, myoclonic or epileptimorphic seizures, meningeal symptoms.

Laboratory findings: no ketonemia, severe hyperglycemia, increased hematocrit, urea, plasma osmolarity, leukocytosis. Proteinuria is possible, but acetone is never detected in urine.

Hyperlactacidemic diabetic coma

Develops slowly. Characteristic: muscle pain, chest pain, rapid breathing, drowsiness, gradual depression of consciousness. Clinical manifestations: dry/pale skin, amimia, mydriasis, areflexia, meningeal symptoms, changes in the depth and rhythm of breathing, Kussmaul type, tachycardia and hypotension, concomitant clinical picture of purulent intoxication, which provokes the development of this coma.

Coma in meningitis

The basis is meningitis of various etiologies, most often purulent with damage to the meninges, accompanied by cerebrospinal fluid and microcirculatory disorders in the brain substance, venous congestion, edema of perivascular spaces, swelling and dystrophy of nerve cells and fibers, increased intracranial pressure. The main clinical manifestations are accompanied by manifestations of the underlying pathology that caused the infection to penetrate the brain - craniocerebral trauma, mastoiditis and other diseases of the ENT organs, purulent processes of the face, pneumonia.

Develops quickly, against the background of general malaise, hyperthermia, hyperesthesia, headache, vomiting. Clinical manifestations of coma: very high hyperthermia, meningeal syndrome, possible hemorrhagic rashes on the skin, convulsive attacks and convulsive syndrome, more often bradycardia and arrhythmia, rapid and arrhythmic breathing, asymmetry of tendon reflexes and loss of function of the cranial nerves. Liquor pressure is significantly increased, flows in a stream.

Laboratory parameters: blood - typical changes characteristic of purulent inflammation; cerebrospinal fluid with high leukocytosis - neutrophilic in purulent meningitis, moderately elevated lymphocyte protein in serous meningitis.

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Coma in encephalitis

It develops with reactive inflammation of the brain tissue, accompanied by its edema and swelling. Echoencephalography reveals signs of increased intracranial pressure and expansion of the third ventricle of the brain. Cerebrospinal fluid pressure is increased, the cerebrospinal fluid is xanthochromic or hemorrhagic. The development of coma is preceded by: general malaise, hyperthermia, dizziness, vomiting; clinical picture of a viral infection.

Coma develops quickly, accompanied by: high hyperthermia, convulsions, paralysis and paresis, loss of cranial nerve function, strabismus, ptosis, paralysis of the gaze. Laboratory indicators of cerebrospinal fluid - increased protein and sugar 10.

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Coma in acute poisoning

Below are described only the poisonings that are most common in everyday life. It is important to remember that vomit, rinsing water, blood and urine must be sent to a poison control center or a laboratory of the Department of Internal Affairs (by order of the investigator) for analysis of the toxic substance.

Poisoning with barbiturates, drugs, clonidine. They have a uniform picture and are often combined with each other. They develop slowly, with the exception of clonidine poisoning when combined with alcohol. Accompanied by: increasing drowsiness, disorientation, ataxia, vomiting. Muscles are hypotonic, reflexes are reduced, the skin is moist, covered with sticky sweat. Blood pressure is reduced, the pulse is frequent, small in volume. Breathing is rare, intermittent, like Cheyne-Stokes. The eyeballs are floating, the pupils are constricted. Cardiac and respiratory arrest is possible, which requires a resuscitation complex. Laboratory indicators have no specific signs.

Poisoning with ethyl alcohol and alcohol substitutes. When pure methyl alcohol is taken, even in small quantities, a coma develops within a few minutes, its harbinger being acute visual impairment. The smell of formalin from the mouth. Cardiac and respiratory arrest occurs; resuscitation, as a rule, is ineffective. Poisoning with ethyl alcohol (can develop after taking more than 700 ml of vodka) and surrogates develops slowly, from normal alcohol intoxication to coma. Accompanied by vomiting, sometimes with regurgitation that smells of alcohol, the smell of alcohol from the mouth too. The face is cyanotic, the skin is moist, covered with cold sticky sweat. The pupils are wide, the eyeballs are floating. The muscles are atonic, flabby, reflexes are reduced. Breathing is shallow, can be of the Cheyne-Stokes type. Blood pressure is low, the pulse is frequent, small in volume.

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Hepatic coma

It is formed in severe liver failure. Conventionally, since they can be combined, three forms are distinguished:

1. endogenous - caused by a sharp decrease in hepatocytes in cirrhosis, tumors, intoxications, acute disturbances of microcirculation in it - "shock liver";
2. exogenous - caused by external factors, such as purulent intoxication, portal shunting, some types of poisoning, gross violations of diet;
3. electrolyte-hepatic - "false" - associated with a violation of water-electrolyte balance, especially hypokalemia, the use of saluretics, the formation of ascites, hypoxic syndrome.

It develops gradually, rarely quickly, against the background of apparent improvement. The endogenous form is the most severe, accompanied by high mortality. The development of coma is preceded by: increasing weakness, drowsiness, a period of psychomotor agitation, increasing jaundice, dyspeptic and hemorrhagic disorders. The onset of coma is characterized by: an increase in the frequency and depth of breathing, its arrhythmia; muscle twitching (convulsions), clonus of the feet, increasing muscle tone, mydriasis, nystagmus, pathological symptoms are formed. The smell of raw meat from the mouth. Bradycardia and hypotension may be present. Laboratory indicators: bilirubinemia, azotemia, decreased prothrombin index, cholesterol, blood sugar. Liver sediment tests are elevated. In the urine: bilirubin, leucine, tyrosine.

Respiratory coma

It develops with severe respiratory failure, which leads to the development of cerebral hypoxia. There are two forms: peripheral - with lung diseases and chest trauma, and central - with damage to the respiratory center after surgery or with brain trauma. The onset is rapid: headache, shortness of breath, respiratory arrhythmia, convulsions, spasms increase; cardiovascular failure progresses. With the development of coma, the following is revealed: sharp, "cast-iron" cyanosis of the face, as hypercapnia develops, the skin color changes to purple, and then to a cyanotic pink color, the jugular veins are swollen, accessory muscles are involved in breathing, the face is puffy, the extremities are cold, peripheral edema and ascites can be determined. Breathing is shallow, arrhythmic; percussion - boxed or "mosaic" sound; auscultation - cacophony or "silent" lung. Arterial pressure is progressively decreasing, tachycardia, pulse is weak. On the ECG - signs of overload of the right heart:

Laboratory findings: blood - leukocytosis, polycythemia, eosinophilia; acid-base balance study - pronounced and progressive manifestations of metabolic acidosis.

Thyrotoxic coma

It develops with decompensated thyrotoxicosis with its characteristic manifestations: the presence of goiter; exophthalmos. The onset is gradual: severe weakness, sweating, anorexia, nausea, diarrhea, palpitations, severe agitation, insomnia, difficulty swallowing, diasarthria. With the development of coma: hyperthermia, the skin is initially moist, then dry due to dehydration, tachypnea, tachycardia, atrial fibrillation, high blood pressure is replaced by hypotension, exophthalmos, mydriasis are pronounced, muscle tone is increased, bulbar disorders are possible,

Laboratory tests: in the blood - decreased cholesterol, phospholipids, triglycerides, increased levels of thyroid hormones - thyroxine, triiodothyronine, thyrotropin, protein-bound iodine, acid-base balance - development of metabolic acidosis. In urine tests: decreased specific gravity, protein, increased excretion of 17-OCS.

Uremic coma

It develops in the terminal stage of renal failure due to poisoning of the body with blood waste and metabolic products excreted by the kidneys.

The development is gradual, preceded by: headaches, deterioration of vision, skin itching, nausea, vomiting, convulsions, drowsiness with gradual depression of consciousness. With the development of coma: the skin is pale, dry, with a gray coating, often swelling of the face and limbs, pinpoint hemorrhages on the skin; muscle fibrillation, mydriasis, Cheyne-Stokes breathing, less often Kussmaul with an ammonia smell are noted; hypertensive syndrome.

Laboratory findings: anemia, leukocytosis, increased ESR, significant increase in blood toxins, indicanemia, metabolic acidosis, hypocalcemia in urine, if present, high protein, blood.

Chlorhydropenic coma

It develops due to dehydration and loss of acid ions in: vomiting, eclampsia and toxicosis of pregnancy, use of diuretics, toxic infections with profuse diarrhea. The development is gradual, accompanied by progressive weakness, anorexia, thirst, headaches, repeated fainting, apathy with a gradual fading of consciousness. Attention is drawn to sharp exhaustion and dehydration, sunken cheeks, dry skin and mucous membranes, decreased skin turgor. In case of developed coma: hypothermia, wide pupils, shallow breathing, hypotension and tachycardia, decreased reflexes, fine twitching of the facial muscles and limbs, there may be meningeal symptoms.

Laboratory findings: polyglobulinemia, azotemia, hypochloremia, hypocalcemia; acid-base balance analysis reveals metabolic alkalosis.

Diagnostics comas

A full examination of the patient and the implementation of a range of treatment measures is the responsibility of the resuscitator, so in most cases such patients should be hospitalized or transferred to intensive care units.

General clinical examination is carried out according to the general scheme, but the anamnesis is collected from relatives or accompanying persons. When admitted to hospital, such patients are optimally examined by an integrated team of doctors: a resuscitator, a neurosurgeon, a traumatologist, a thoracic surgeon and other specialists of a "narrow" profile. The main thing is the time of diagnosis not of the coma itself, but of the cause that caused it, and the adoption of measures to provide assistance. Be like a "seven spans in the forehead" diagnostician, one cannot cope with the comatose syndrome!

Laboratory examination includes mandatory detailed blood analysis, urine analysis, blood and urine tests for sugar or glucose, determination of blood slags, examination of the coagulation system, electrolytes, plasma osmolarity. Laboratory tests are repeated every 6 hours during the first day, and twice a day in the following days. Vomit, urine, and feces should be sent to a toxicology laboratory.

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Treatment comas

The possibilities of diagnostics and assistance depend on the circumstances: at home or outside a medical institution they are limited to establishing the fact of coma, possibly its type and calling a special ambulance team, in a clinic and a non-specialized department the possibilities are wider - connecting a drip with glucose or saline for hemodilution, administering cardiac glycosides, cordiamine, euphyllin and ganglionic blockers, analgin, despite the unconscious state (narcotics are contraindicated), if possible - steroid hormones.