Coma types of emergency care. Comatose states: causes of development, clinical symptoms, diagnosis, emergency care

Coma (from the Greek cat, deep sleep)- pathological inhibition of the central nervous system, characterized by complete loss of consciousness, lack of reactions to external stimuli and disorder of vital regulation important functions body.

Coma is a serious complication various diseases. Violations of the vital functions of the body are determined by the nature and severity of the main pathological process, as well as the rate of its development. They form very quickly and are often irreversible (for example, with severe traumatic brain injury) or develop gradually (uremic, hepatic coma).

About 30 species of coma have been described. Conventionally, comas are divided into the following groups:

Coma caused by a primary lesion of the nervous system, or neurological coma (apoplectic coma with stroke, apoplectiform, epileptic, traumatic coma with traumatic brain injuries and coma with meningitis, encephalitis and brain tumors).

Coma due to endocrine diseases caused by metabolic disorders due to insufficient (diabetic, hypocorticoid, hypothyroid, hypopituitary) or excessive synthesis of hormones, or an overdose of hormonal drugs (thyrotoxic hypoglycemic).

Coma, primarily associated with the loss of electrolytes, water and energy substances (chlorhydropenic coma with persistent vomiting, in particular with pyloric stenosis, nutritional-dystrophic, or hungry coma).

Coma caused by impaired gas exchange (hypoxic, respiratory).

Toxic coma developing with toxic infections, various infectious diseases, pancreatitis, liver and kidney damage, as well as coma caused by exposure to exogenous poisons (organophosphorus compounds, alcohol, barbiturates, etc.).

The pathogenesis of comatose states is different. With any type of coma, dysfunctions of the cerebral cortex, subcortical structures and brain stem are observed. Of particular importance is the dysfunction of the reticular formation of the brainstem, its activating effect on the cerebral cortex is “switched off”, disorders of the reflex functions of the brainstem and inhibition of vital autonomic centers are noted. The development of these disorders is facilitated by hypoxemia, anemia, cerebrovascular disorders, blockade of respiratory enzymes, acidosis, microcirculation disorders, electrolyte balance (especially potassium, sodium and magnesium), and the release of mediators. Swelling and edema of the brain and its membranes, leading to increased intracranial pressure, impaired circulation of cerebrospinal fluid and hemodynamic disorders, are of important pathogenetic significance.

A pathological examination reveals swelling of the brain, pockets of hemorrhage and softening against the background of capillary dilation, blood stasis, plasma impregnation and necrobiotic changes in the capillary walls. The originality of the pathomorphological picture in various comas is also due to etiological factors. There are moderate (I degree), deep (II degree) and extreme (III degree) coma.

Moderate coma characterized by complete loss of consciousness, lack of reactions to external stimuli (except for severe pain). In response to painful stimuli, extension and flexion movements of the limbs, tonic convulsions with a tendency to generalize, or hormetonia may appear. Defensive motor reactions are not coordinated and are not aimed at eliminating the stimulus. After painful exposure, the eyes do not open. Pupillary and corneal reflexes are usually preserved. Abdominal reflexes are depressed, tendon reflexes are often increased. Reflexes of oral automatism and pathological foot reflexes appear. Breathing and cardiac activity are relatively stable.

Deep coma characterized by the absence of any reactions to all external stimuli, including severe pain, the complete absence of spontaneous movements, various changes in muscle tone (from decerebrate rigidity to muscle hypotonia), hypo- and areflexia, unilateral mydriasis, severe respiratory and cardiac dysfunction. Kernig's sign may be caused.

Transcendent coma characterized by a severe violation of vital functions - rhythm disorder and change in respiratory rate or apnea, sharp tachycardia, significant decrease blood pressure(or it is not determined), bilateral mydriasis, total areflexia, diffuse muscle atony.

The depth and duration of coma are the most important signs determining the prognosis. Currently in various countries Scales have been developed that allow, based on the assessment of simple clinical symptoms, to fairly accurately determine the prognosis for coma. A.R. Shakhnovich et al (1981) proposed a scale that includes 50 neurological signs, the severity of which is assessed in points. Changes in eye micromovements, clinical and physiological signs, and indicators of evoked brainstem and cortical potentials are taken into account. The following 12 signs turned out to be the most informative:

opening the eyes in response to a sound or painful stimulus - 10 points;

execution of instructions - 8;

absence of mydriasis - 5;

absence of muscle atony - 5;

absence of respiratory dysfunction - 4;

presence of reflexes: corneal - 4;

knee - 4;

pupillary reactions to light - 3;

cough - 3;

absence of Magendie's symptom - 3;

presence of spontaneous movements - 3;

motor reaction in response to a painful stimulus - 3 points.

The total number of points is 55. The first 5 signs are especially informative. The higher the score, the more favorable the prognosis. The authors observed a favorable prognosis for coma assessed at 22 points or more.

Emergency help in case of coma, start immediately. Be sure to take into account the cause of the coma. Below are the basic principles of providing emergency care patients in this condition:

Provide oxygenation.

Support blood circulation.

Add glucose.

Reduce intracranial pressure.

Stop seizures.

Start fighting the infection.

Restore acid-base status and electrolyte balance.

Normalize body temperature.

Enter thiamine bromide.

Select specific antidotes.

Relieve excitement.

Coma III degree often leads to the death of the patient. Very important has a brain death registration. Over the past 20 years, a number of criteria for brain death have been proposed: Harvard (1968), Minnesota (1971) and British (1976), criteria for cooperative studies in the USA (1977), etc. An objective statement of brain death makes it possible to recognize man dead with a beating heart and sufficient gas exchange (using mechanical ventilation). In this case, the following conditions must be met:

The patient must be in a state of extreme coma after completing all prescriptions and therapeutic procedures. The possibility of taking sleeping pills, depressants and other drugs that have a narcotic effect, as well as relaxants and drugs that can cause respiratory failure is excluded. Hypothermia and metabolic endocrine disorders are excluded. Brain damage is irreversible.

Diagnosis of brain death: no spontaneous breathing when switched off ventilator for a period sufficient for an increase in pCO 2 to occur, exceeding the threshold for excitation of the respiratory center (more than 7.98 kPa or 60 mm Hg); there are no reactions of the pupils to the bright light of an electric flashlight, as well as corneal, oculovestibular, oculocephalic and pharyngeal reflexes; there are no motor reactions carried out by the cranial nerves. Isoelectric EEG. According to some experts, it is also necessary to take into account such a test as non-filling of the cerebral vessels during two aortocranial injections of a contrast agent with an interval of 25 minutes. The coma must last at least 12 hours. The decision to turn off the ventilator is made by a competent commission, which includes a resuscitator and a neurologist with at least 5 years of experience in the field of resuscitation, who did not participate in the treatment of this patient before and after the onset of extreme coma and death brain

The nervous system is divided into central and peripheral. The brain (central nervous system and higher autonomic centers, endocrine regulation centers) is located in the cranial cavity. It is reliably protected by bone plates from adverse environmental influences.

• Glasgow scale
• Help with coma

Being the central regulator of all processes occurring in the body, the brain operates in an active metabolic mode. Its weight is only 2% of body weight (about 1500 g). However, for the uninterrupted functioning of the brain, 14-15% of the total volume of circulating blood (700-800 ml) must flow into and out of the cranial cavity every minute. The brain uses 20% of all the oxygen the body consumes. It is metabolized only by glucose (75 mg per minute or 100 g per day).

Other changes in awareness can occur without the unconscious. These are called altered mental status or altered mental status. They include sudden confusion, disorientation, or numbness. Unconsciousness or any other sudden change in mental status should be considered an emergency medical care.

Unconsciousness can be caused by almost any serious illness or injury. It can also be caused by substance use and alcohol use. Suffocating the subject may result in unconsciousness. The information provided here should not be used during any medical emergency or for diagnosing or treating any health condition. Consultation with a licensed healthcare professional is essential for diagnosis and treatment of any and all medical conditions. Call 112 for all medical emergencies.

So, the physiological functioning of brain tissue depends on adequate perfusion with its blood, the content of a sufficient amount of oxygen and glucose, the absence of toxic metabolites and the free outflow of blood from the cranial cavity.

A powerful autoregulation system ensures smooth functioning of the brain. Thus, even with significant blood loss, the perfusion of the central nervous system is not impaired. In these cases, a compensatory reaction of centralization of blood circulation with ischemia of less important organs and tissues is activated, aimed primarily at maintaining adequate blood supply to the brain. The body reacts to another pathological condition - hypoglycemia - by increasing blood flow to the brain and increasing the transport of glucose there. Hyperventilation (hypocapnia) reduces blood flow to the brain; hypoventilation (hypercapnia) and metabolic acidosis, on the contrary, increase blood flow, promoting the removal of “acidic” substances from tissues.

Emergency care for coma

Any duplication or redistribution of the information contained herein is strictly prohibited. All cases of diabetic coma should be evaluated by a qualified medical professional as soon as possible! Failure to obtain an estimate as quickly as possible could result in serious injury or death. Call 112 immediately if you are going through a diabetic coma.

What are the causes of diabetic coma?

Diabetic coma is a condition caused by extremely high blood sugar levels and low insulin production. The condition is a medical emergency and quick treatment. . The cause of diabetic coma may be.

What are the signs and symptoms of diabetic coma

The onset of signs and symptoms of diabetic coma usually spreads over a long period.

With significant damage to brain tissue, insufficient autoregulation or excessive manifestations of the compensatory reaction of the inflow and outflow of blood, the brain cannot voluntarily change its volume. The closed cavity of the skull becomes its trap. Thus, an increase in intracranial volume by only 5% (with hematomas, tumors, hyperhydration, liquor hypertension, etc.) disrupts the activity of the central nervous system with the patient losing consciousness. In another pathology, excessive growth of cerebral blood flow leads to overproduction of cerebrospinal fluid. The brain tissue is compressed between the blood and the cerebrospinal fluid, swelling develops, and functions are impaired.

How is first aid prescribed for a diabetic coma?

Increased thirst Increased frequency of urination Dehydration Drowsiness, confusion, or irritation Increased breathing rate Sweet-smelling breath Loss of consciousness. Assessing the neurological status of unconscious or comatose patients can be a challenge because they may not actively cooperate with your research. But once you master this exam, you can detect early, significant changes in a patient's condition—in some cases, even before they appear in more complex diagnostic tests.

Traumatic destruction of brain tissue, edema and swelling, increased blood pressure, impaired circulation of cerebrospinal fluid, circulatory disorders and other damaging mechanisms lead to hypoxia of CNS cells. It manifests itself primarily as a disturbance of consciousness.

Coma: symptoms, types, diagnosis

Coma is a complete suppression of consciousness with loss of pain sensitivity and reflexes, with general muscle relaxation and dysfunction of vital organs and systems of the body.

Symptoms of impaired consciousness

Subtle changes in results may indicate the need for further testing. Although it is still an integral component of assessment for critically ill patients, it is overlooked or underappreciated by many overnight nurses.

Faster and easier than you think

The Neuro-Exam can be administered quickly and easily integrated into daily assessments. It starts the moment you meet the patient. Doing this early is crucial as it helps you establish a baseline for later comparison.

Classification degrees of impairment of consciousness (Bogolepov, 1982).

• Clear consciousness
• Darkened consciousness
• Stupor
• Sopor
• Coma: moderate, deep, extreme

Symptoms of impaired consciousness

Impaired consciousness	Leading signs	General signs To accurately interpret assessment results, nurses involved in the shift and upcoming shifts should assess the patient's neurological status together during the shift or patient care. Once the initial assessment is completed, subsequent assessments can be either basic or more detailed. The type of neurological exam you perform depends on whether your patient can follow commands. If so, your exam may be more comprehensive and should include an assessment. If your patient is unable to follow commands, you will only be able to assess pupils, eye opening, motor response and a few. However, despite the relative shortness of this type of exam, it can provide a significant amount of information.
Clear consciousness	Cheerfulness, complete orientation in time and space and in one’s face.	Active attention, absolute language contact, thoughtful answers to questions, following all instructions. Free opening of eyes.
Darkened consciousness	Moderate drowsiness or euphoria, partial disorientation in time and space with complete orientation to one’s face. Ask yourself: is there a patent on the airway? If so, can the patient support it? Next, check vital signs: Are respirators adequate? Is her blood pressure high enough to perfuse the brain and other vital organs? Keep in mind that ongoing or progressive damage to the brain and brainstem can make vital signs unstable, but this situation can be complex: although unstable vital signs can reduce the neurological response, brain injury itself can cause unstable vital signs.	The ability for active attention is reduced. Language contact is maintained, but obtaining an answer sometimes requires repeating questions. Commands are executed correctly, but somewhat slowly, especially complex ones.
	Deep drowsiness, disorientation in time and space, upon awakening, follows only simple commands. To properly assess the patient's neurological status, be sure to assess oxygenation and circulation. Ideally, you should perform a neuro-exam when the patient's blood pressure, temperature, heart rate, and heart rate are normal. Keep in mind that temporary decline in neurological status caused by insufficient oxygenation or circulation still constitutes a neurological change - and results in permanent neurological loss if the underlying problem is not corrected. Once you have determined that your patient is stable enough for evaluation, begin the neuro-exam itself. To determine whether the patient is unconscious and unable to follow commands, use the Glasgow Coma Scale to test for eye opening, better motor response, and better verbal response. An unconscious patient is likely to open his eyes only in response to pain, if at all; obviously you can't test your best verbal answer at all.	The state of sleep predominates, sometimes in combination with motor excitement. Language contact is difficult. Unambiguous answers. The defensive reaction to pain is preserved. Control over the function of the pelvic organs is weakened.
	Pathological drowsiness, complete disorientation in time, space and in one’s face. In an unconscious patient, the best response is a localization in which it reaches the midline to the site of the stimulus, as if trying to stop the pain. In a semi-bubble response, she rolls away as if she is trying to escape or escape the pain. The flexor motor response is marked by inward flexion of the elbows, wrists, and arms, accompanied by extension and alignment of the feet. The extension motor response is a straightening or rigid extension of the shoulders, with the wrists externally rotating, the knees and ankles rigidly straight, and the landing leg being the legs. Localization of pathology in the brain The best score is 15, which indicates that the patient is awake, oriented, and following the following commands. The lowest possible score is 3, which means the patient does not open the eyes and has no motor or verbal response to the central stimulus.	Opens eyes to painful stimuli, localizes pain with targeted actions to eliminate it. Reflexes of the cranial nerves and vital functions were preserved.
Coma moderate	There is no consciousness.	There is no reaction to external stimuli. Responds to painful stimuli with uncoordinated defensive movements. Pupillary and corneal reflexes are increased, abdominal reflexes are decreased. Reflexes of oral automatism and pathological reflexes from the feet appear. Sphincter control is impaired. Vital functions are preserved. Student evaluation involves assessing the size, shape, and equality of the student before and after exposure to light. Typically the pupils are equal in size and approximately 2 to 6 mm in diameter, but they can reach 9 mm. In addition, pupils can be pinpoint, small, large or dilated. The shape of a normal pupil is round; variations include irregular, keyhole and ovoid. To assess a patient's pupils, keep both eyelids open and shining a light into the eyes. Students should squeeze immediately and equally bilaterally; after you remove the light, they should immediately unfurl to the baseline. Document the response: Is it brisk, sluggish, non-reactive, or fixed? Report any changes from baseline immediately. In many cases, changes in pupillary response, such as unequal or dilated pupils, are the result of a progressive neurological condition.
Coma deep	There is no consciousness.	The reaction to pronounced painful stimuli in the form of extension of the limbs is preserved. Suppression or absence of skin, tendon, corneal, pupillary reflexes. Rigidity or hypotonia of striated muscles. Respiratory and cardiovascular disorders. Anatomical and functional features of the central nervous system Corrected and extended students are an ominous sign that warrants immediate notification to the physician. The results of a cranial nerve assessment can reveal a lot about a patient's midbrain, pairs, and medullary function. Although some nurses find this assessment intimidating, it is not that difficult. Oculocephalic and vascular tests, which show brain stem function, are performed only by physicians on patients who do not respond to the exam methods described above. These tests help predict the prognosis of patients with severe brain damage.
Coma beyond measure	There is no consciousness.	Areflexia, bilateral fixed mydriasis, muscle atony, significant impairment of breathing and cardiovascular activity. Hypotension (blood pressure below 60 mmHg)

Etiopathogenetic classification of comas

5. Comas that occur under the influence of physical factors (heat, cold, radiation, electric current).

Diagnosing the cause of coma can sometimes be quite difficult, since it is impossible to collect an anamnesis from the patient. Therefore, it is very important to ask the victim’s relatives and witnesses how this coma arose.

Anamnesis. It is necessary to find out the time of loss of consciousness, sudden or gradual deterioration of the condition, ask whether the patient did not fall or hit his head; or there was no high fever, flu or jaundice. It is necessary to establish whether the victim did not have diabetes, hypertension, or epilepsy; Has he had similar cases of loss of consciousness or suicide attempts in the past? If the coma developed gradually, then what the patient complained about, whether he was vomiting, will be judged.

When examining the victim’s belongings, you can sometimes find medical documents, medicine packages, and remains of poisons. These findings may help in making a diagnosis.

In the absence of anamnestic data, it is important to identify individual symptoms on the basis of which the disease can be recognized.

Color

skin. Severe pallor is characteristic of massive blood loss, circulatory collapse, uremic coma, and blood diseases. Severe cyanosis is a sign of hypercapnic coma with insufficient external respiration function, asphyxia during hanging, drowning; after suffering an attack of convulsions. Facial hyperemia suggests poisoning with atropine and its derivatives, carbon monoxide, hyperglycemic coma and an infectious disease.

Head position

. A head thrown back indicates meningitis, tetanus, hysteria; leaning to one side - most likely about a stroke. Hoarse breathing and a distorted mouth are characteristic of a stroke. Pathological types of breathing (Cheyne-Stokes, Biota) are observed with deep damage to the central nervous system. Deep noisy breathing (Kussmaul) indicates the accumulation of acids in the body (metabolic acidosis) of exogenous (in acute poisoning) or endogenous (diabetic ketoacidosis) origin. Hyperthermia and frequent deep breathing are characteristic signs of a coma of infectious origin. With this pathology, an increase in body temperature by 1 0C is accompanied by an increase in respiratory rate by 5-7 per minute.

In order to examine a patient in a coma, a medical professional must approach him from the back of the head. This position is dictated by the following points: firstly, the ability to immediately provide assistance to the victim if necessary (remove the lower jaw, free the tongue from biting, clear the oral cavity of vomit, perform artificial ventilation), and, secondly, the personal safety of the resuscitator, since an unconscious victim can injure him by pushing him with his hand or foot.

Simulation, and sometimes coma of hysterical origin, can be detected when trying to open the patient’s eyes. A person with completely absent consciousness does not strain his eyelids when opening them with his fingers. And vice versa, even barely perceptible resistance when trying to raise them is a sign of preserved consciousness.

By pressing on the eyeballs, you can determine their tone. “Soft” eyeballs indicate hypovolemia (blood loss, hypohydration). They occur in patients with hyperglycemic coma and shock.

Depth

coma Diagnosed by the degree of inhibition of reflexes. Thus, a reaction to eyelash irritation indicates a superficial coma. The reaction to irritation of the sclera is preserved - moderate coma. Lack of pupillary response to light is a sign of deep coma.

The pupils can be of different sizes: constricted - in case of poisoning with sleeping pills, organophosphorus substances; very narrowed (like a poppy seed) - in case of drug poisoning; extended - for hypoxia, poisoning with neuroleptics and antihistamines; very expanded - when consuming atropine-containing substances.

Anisocoria

(pupils of different sizes)- a characteristic sign of focal damage to the central nervous system. Most often, this symptom occurs with traumatic brain injury with the presence. In such patients, a detailed examination of the face and scalp can reveal abrasions, a wound or subcutaneous hemorrhage. Sometimes there is a deviation of the eyeballs to the right or left - in the direction of brain damage.

The absence of knee, Achilles and abdominal wall reflexes indicates deep depression of the central nervous system. The pathological Babinski reflex indicates organic brain damage. Asymmetry of muscle tone is a sign of a space-occupying process in the cranial cavity (stroke, tumor, hemorrhage).

A detailed examination of other organs and systems helps in establishing a diagnosis. Thus, central nervous system failure may be caused by interruptions in the functioning of the heart due to disturbances in its conduction (Morgagni-Edams-Stokes syndrome). In turn, focal brain lesions cause disturbances in the functioning of the cardiovascular system.

Hemodynamic disorders

depending on the location of the pathology in the central nervous system

Localization pathologyin the brain	Manifestations defeatscordially- vascularsystems
Lesions of the fronto-orbital zones	Bradycardia, complete atrioventricular block, atrial extrasystole
Excitation of midbrain structures	Extrasystole, atrioventricular block, ventricular fibrillation
Pathology of the medulla oblongata	turn it on its side; lower the upper part of the body slightly (by 15°), so that the oral opening is lower than the glottis; withdraw lower jaw and support it with your fingers; assess the patient’s breathing efficiency (the color of the mucous membrane and skin, its humidity, depth and frequency of breathing, the presence of pathological noises during breathing, retraction of the jugular notch and intercostal spaces); if there is difficulty in breathing and the presence of gastric contents, blood, and sputum in the oral cavity, it is necessary to ensure patency of the airways (remove foreign bodies and liquids); if breathing is ineffective, use artificial ventilation; palpate the pulse over the main and peripheral arteries; lift the patient’s upper eyelids and evaluate the reaction of the pupils to light; call a medical team. In some patients, against the background of a coma, hyperreflexia is observed, hyperkinesis or convulsions occur. For seizures you must: Lay the patient on a flat surface, preventing injury from surrounding objects; Prevent tongue biting by inserting a mouth retractor (a spatula, a wooden stick, a spoon handle, wrapped in cloth) between the molars; Support the patient’s lower jaw and head, preventing injury and asphyxia; Ensure oxygenation of the body by supplying oxygen through a mask or nasal catheter; During the interictal period, catheterize the peripheral vein using a puncture method, where, as prescribed by the doctor, inject solutions of magnesium sulfate (5-10 ml of 25% solution), sibazon (2 ml of 0.5% solution); Clear the mouth and throat of saliva, blood, and possible gastric contents; In the absence of spontaneous breathing, perform artificial ventilation. A comatose state is a deep disturbance of consciousness with a lack of reflexes and reactions to external influences. Coma can develop suddenly against the background of the patient's relatively favorable condition. Acute development is typical for stroke and hypoglycemic coma. However, in many cases, a coma that complicates the course of the disease develops gradually. This development is typical for diabetic, uremic, hepatic coma and many other comatose conditions. In each specific case of coma, a doctor must be immediately called to the patient. Patients in a coma require constant staff supervision. Diabetic coma (hyperglycemic, acetonemic): there is no consciousness, the face is hyperemic; lips, dry tongue, smell of acetone from the mouth, dry, cold skin, Kussmaul-type breathing, rapid, small pulse, low blood pressure, hypotension of the eyeballs, muscle hypotonia, decreased tendon reflexes, vomiting, sugar in the urine, acetone. Diabetic coma is usually preceded by increasing weakness, itching, increased thirst, nausea, and vomiting. Nurse tactics. Warm the patient. Rinse the stomach with a 5% solution of sodium bicarbonate or isotonic sodium chloride solution (part of the solution is left in the stomach). Give a cleansing enema mu with warm 4% sodium bicarbonate solution. Provide oxygen supply. Immediate hospitalization. In case of delay in hospitalization, intravenous drip administration of isotonic sodium chloride solution. Hypoglycemic coma(insulin): feeling of hunger, weakness, irritability, fear, sweating, trembling of arms, legs, double vision, sometimes headache, bradycardia or tachycardia, pallor of the skin, blood pressure is increased or normal, general muscle hypertension, convulsions, delirium , hallucinations, acute disturbance of the psyche and consciousness. Nurse tactics depends on the severity of the condition: if the patient is conscious, it is necessary to give food rich in carbohydrates (sweet tea, white bread, compote, a spoonful of jam or honey). If the patient is unconscious - intravenous jet injection of 20-50 ml of 20-40% glucose solution. In the absence of consciousness for 10-15 minutes. - intravenous drip administration of 5-10% glucose solution until the patient regains consciousness. Uremic coma(azotemic). Precursors of coma: gradual increase in drowsiness, lethargy, headache, irritability; thirst, dry mouth, nausea, vomiting. The vomit is sometimes streaked with blood or the vomit is the color of coffee grounds; stool is loose, watery; urination is frequent, copious, mainly at night. Visual impairment - unclear outlines of objects before the eyes, narrowing of the field of vision. Observed: anxiety, visual hallucinations, seizures; the skin is sallow in color, there are traces of scratching, itching; bleeding from the nose, gums, ulcerations on the oral mucosa. Breath smells like ammonia. Liver size. Seizures, pupils dilated. Nurse tactics. As prescribed by the doctor, glucose solutions, steroid hormones, and vitamins are administered drip-wise.

Coma is a condition in which a person is unable to interact with the outside world, that is, a person in this state cannot respond to external influences, for example, the patient either does not perceive painful stimulation at all, or perceives it at a reflex level.

Why did the coma occur?

In order to determine what reason led to the development of a coma, it is necessary to conduct a number of general tests:

• determine blood glucose levels using a portable glucometer to determine possible hypoglycemia or elevated sugar levels;
• determine the level of electrolytes and urea. Elevated urea levels may indicate the presence of uremia. Increased osmolarity will indicate the presence of alcohol intoxication. This test can only be performed in a hospital;
• perform a general blood test. In this analysis, you can notice the inflammatory changes that occur in the body. They may result from encephalitis or meningitis;
• measure prothrombin time, an increase in which will indicate liver damage, and accordingly hepatic encephalopathy;
• determination of narcotic and pharmaceutical drugs in the blood.

First aid for coma

If you do not have any knowledge or medication, having knowledge is simply necessary. For this:

What drug therapy is required to bring the patient out of coma? First, it is necessary to establish intravenous administration of glucose, since hypoglycemic coma is immediately stopped when this substance enters the body. In the absence of a glucometer and the impossibility of checking glucose levels, administering 10-20 ml of 40% can be absolutely painless, even if there is not a hypoglycemic coma, but a hyperglycemic one, we will not cause harm. Glucose prevents the transition of hypoglycemic coma from a reversible stage to an irreversible stage. This simple circuit urgent using medications.

In addition to glucose and in parallel with it, vitamin B1 is administered to prevent the development of cerebral edema, which an excess amount of glucose can cause or aggravate the existing one.

If coma occurs due to a drug overdose, the antagonist naloxone is administered. After the drug is administered, the patient in a drug-induced coma comes to his senses.

Metabolic acidosis occurs during poisoning with methanol, salicylates, paraldehyde, isoniazid, phenformin, ethylene glycol, and with the development of uremia. When intoxicated with salicylates, respiratory alkalosis can also develop, that is, alkalization of the body through frequent breathing.

Coma and status epilepticus

When motor activity develops in a patient in a coma, status epilepticus must be assumed. As a treatment, diphenin is used in a dosage of 1-1.5 g intravenously at 50 mg per minute. For children, the dosage is 10-15 mg per kg. If it is impossible to stop status epilepticus in a coma, add 0.75-1 g of phenobarbital to adults and 10-15 mg per kg of the drug for children intravenously at 20 mg per minute.

Coma and brain masses

Help with coma and further tactics for managing the patient are different if the coma arose due to the presence of a diffuse process, for example, encephalitis or meningitis, or the presence of some volumetric, focal process: hemorrhage, tumor, brain abscess. That is why it is necessary to carefully and carefully carry out differential diagnosis in order to determine the real causes of coma and. Incorrect diagnosis and subsequent treatment can lead to a sad outcome for the patient. For example, you cannot perform a lumbar puncture if you have a brain tumor, but if you have meningitis or encephalitis, this procedure is simply necessary.

How to distinguish diffuse pathology from focal pathology?

With diffuse changes in the brain there are:

• preserved reaction of the pupils to light, the pupils are symmetrical and react equally to irritation during neurological examination;
• fever, decreased body temperature;
• stiffness, or extreme tension in the neck muscles;
• constantly changing level of consciousness.

Characteristics of focal pathology:

• the pupils react weakly or not at all to light;
• the pupils are asymmetrical and their motor reaction is not the same during a neurological examination.

Coma and metabolic disorders

Coma may be the result of some metabolic changes in the body. Only a few metabolic conditions often cause coma. For example, an overdose of sedatives can lead to a decrease in the response to a caloric test, while the pupillary response to light is preserved. This condition is accompanied by a decrease in blood pressure, hypothermia, and respiratory depression.

If an overdose occurs with opiates, the pupils become dots and breathing is suppressed. Naloxone restores consciousness to such patients.

Among metabolic disorders, it is worth highlighting hypoglycemic and hyperglycemic conditions. If the patient has a history of diabetes mellitus, hypoglycemic coma is suspected, which is confirmed by improvement in the patient's condition when glucose is administered. Hypoglycemia may be accompanied by seizures and focal symptoms.

Evgeniy Ivanov asks a question:

I have several friends who are sick diabetes mellitus. I read that with this disease there is a high risk of coma. What are the recommendations for emergency care for comatose states?

Expert answer:

Coma is a state of the body that is characterized by loss of consciousness, motor and sensory reflexes, and lack of response to sound, pain, and light stimuli. Since the person cannot be brought back to consciousness, there is a threat to life.

Symptoms

Diabetes mellitus, hepatitis, cerebral hemorrhage, cancer, poisoning, and other diseases can lead to coma. Such patients require constant care and monitoring. In a comatose state, it is important for the doctor to obtain information about the medical history and symptoms that preceded the coma.

A common symptom for all types of coma is loss of consciousness. Most often it is accompanied by pallor of the skin, bites on the tongue, and uneven pupils. In alcoholic coma or cerebral hemorrhage, a red complexion is observed. If the pupils are dilated, the patient has died. With constricted pupils, you need to fight for his life.

Stages

The comatose state occurs in several stages. The first is precoma, lasting from a few minutes to 2 hours. The patient's condition changes dramatically from bouts of fatigue to excitement and activity. Consciousness is confused, the person is stunned, coordination of movements is impaired.

In the first degree of coma, the patient continues to react to external stimuli: bright light, liquid food. In this case, reactions are inhibited, contact with a person is difficult, muscle tone is increased.

In the second degree, there are no reflexes to stimuli, the pupils are constricted, there is no contact with the patient, he has a stupor. Limbs tense or relaxed. Occasionally, chaotic movements may occur. Possible difficulty breathing, involuntary urination or bowel movements.

In the third degree, the patient is unconscious and does not respond to stimuli. Muscle cramps occur, blood pressure and body temperature drop, and breathing becomes difficult. It is important to quickly provide assistance to the victim, otherwise the coma will progress to an extreme stage.

The extreme degree is characterized by the lack of the body’s ability to independently support life. He is connected to a ventilator.

Algorithm of actions

To prevent a comatose state from leading to death, medical assistance must be provided. It is necessary to free the patient's mouth from vomit and turn him on his side to maintain breathing. After this, you need to immediately call an ambulance. Doctors will take measures to restore blood circulation, breathing and vital functions of the body.

Video: First aid for coma

1. Carry out all measures to provide first aid to a patient in a comatose state simultaneously.

2. Mandatory hospitalization

3. Restoration and maintenance of adequate breathing - sanitation respiratory tract to restore their patency, installation of an air duct or fixation of the tongue, mechanical ventilation using a mask or through an endotracheal tube, in rare cases - tracheo- or conicotomy (opening the larynx in the space between the cricoid and thyroid cartilages).

Oxygen therapy (4-6 l/min through a nasal catheter or 60% through a mask, endotracheal tube). Before tracheal intubation, premedication with 0.1% atropine solution (0.5-1 ml) is required, except in cases of poisoning with anticholinergic drugs.

4. Relief of hypoglycemia. Regardless of the level of glycemia (in long-term diabetics with poor compensation, hypoglycemic coma can develop even against the background of normal glucose concentration), a bolus injection of 20-40 ml of 40% glucose solution is required; if an effect is obtained, but its severity is insufficient, dose.

5. Restoring and maintaining adequate blood circulation

When blood pressure decreases, it is necessary to start drip administration of 1000-2000 ml (no more than 1 l/m2/day) of 0.9% sodium chloride solution, 5% glucose solution, and if ineffective - dopamine, norepinephrine.

In case of coma that occurs due to arterial hypertension - not lower than 150-160/80-90 mm Hg, intravenous administration of magnesium sulfate 5-10 ml of 25% solution for 7-10 minutes. If there are contraindications to the administration of magnesium sulfate, it is permissible to administer 30-40 mg of bendazole (3-4 ml of 1% or 6-8 ml of 0.5% IV solution). With a slight increase in blood pressure, intravenous administration of aminophylline (10 ml of 2.4% solution) is sufficient.

6. Restoration of adequate heart rhythm in case of arrhythmias (mainly through defibrillation).

7. Immobilization cervical region spine for any suspicion of injury.

8. Catheterization of a peripheral vein. In a comatose state, almost all drugs are administered parenterally (preferably intravenously); infusions are administered through a peripheral catheter; with stable hemodynamics and no need for detoxification, an indifferent solution is slowly injected dripwise, which provides a constant opportunity for rapid administration of drugs.

9. Installation of a gastric or nasogastric tube.

10. Therapeutic and diagnostic use of antidotes

11. Relief of intracranial hypertension, edema and swelling of the brain. Mannitol at a dose of 1-2 g/kg (in the form of a 20% solution) for 10-20 minutes; to prevent a subsequent increase in intracranial pressure and an increase in cerebral edema after completion of the mannitol infusion, furosemide is administered at a dose of 40 mg.

12. Neuroprotection and increasing the level of wakefulness - In case of disturbances of consciousness to the level of superficial coma, sublingual glycine is indicated in a dose of 1 g. In case of deep coma, antioxidant therapy is carried out Mexidol - 6 ml of 5% solution) intravenously for 5-7 minutes and Semax is administered at 3 drops of 1% solution in each nostril.

13. Measures to stop the entry of the toxin into the body in case of suspected poisoning.

14. Gastric lavage through a tube with the introduction of sorbent

15. Normalization of body temperature.

16. Relief of seizures: diazepam IV at a dose of 10 mg.

17. Relief of vomiting: metoclopramide at a dose of 10 mg IV or IM