Diagnostic and Diagnostic and emergency assistanceemergency assistance in in

ComaComa

Prepared by:Prepared by: C.m.s., assistant professor C.m.s., assistant professor

of outpatient therapy of outpatient therapy and emergencyand emergency medical medical

emergency KSMUemergency KSMUAA..RR.. Alpyssova Alpyssova

The purpose of the lectureThe purpose of the lecture

After completing the lecture, students After completing the lecture, students should focus on issues of diagnosis should focus on issues of diagnosis and emergency care at koma in the and emergency care at koma in the amount of the first medical care amount of the first medical care (doctor's line crews), and depending on (doctor's line crews), and depending on the patient - in the amount of specialized the patient - in the amount of specialized care (intensive care team, intensive care care (intensive care team, intensive care team).team).

The plan of the lectureThe plan of the lecture

Coma: determination, etiology, pathogenesisComa: determination, etiology, pathogenesis Clinic pictureClinic picture Differential diagnosisDifferential diagnosis Tips caller, mandatory questions in the Tips caller, mandatory questions in the

diagnosis, indications for hospitalizationdiagnosis, indications for hospitalization Undifferentiated therapyUndifferentiated therapy The specific treatment of individual comatose The specific treatment of individual comatose

statesstates

ComaComa

Coma - a state of CNS disease, characterized by a violation Coma - a state of CNS disease, characterized by a violation of its coordination activities, autonomous operation of its coordination activities, autonomous operation of individual systems, graduating at the level of the whole of individual systems, graduating at the level of the whole organism the ability to self-regulate and maintain organism the ability to self-regulate and maintain homeostasis, clinically manifested loss of consciousness, a homeostasis, clinically manifested loss of consciousness, a violation of motor, sensory and somatic functions, violation of motor, sensory and somatic functions, including vital.including vital.

ETIOLOGY AND PATHOGENESISETIOLOGY AND PATHOGENESISTo evaluate the prognosis and treatment selection is very To evaluate the prognosis and treatment selection is very

important to determine the cause of coma:important to determine the cause of coma: Focal lesion hemispheres and / or brain stem with a Focal lesion hemispheres and / or brain stem with a

volume effect and the development of volume effect and the development of dislocation syndrome.dislocation syndrome.

Diffuse lesion of the cortex and brain stem.Diffuse lesion of the cortex and brain stem. The first option is typical for the primary and the latter is The first option is typical for the primary and the latter is

observed almost exclusively in secondary koma.observed almost exclusively in secondary koma.

All All causescauses of whom can be reduced to four of whom can be reduced to four

categories:categories:

Intracranial processes that lead to Intracranial processes that lead to

increased intracranial pressureincreased intracranial pressure (vascular, (vascular,

inflammatory, tumor, brain injury, etc.).inflammatory, tumor, brain injury, etc.).

Hypoxic conditions (respiratory, circulatory, hemiHypoxic conditions (respiratory, circulatory, hemi

c, tissue, etc.).c, tissue, etc.).

Metabolic disorders (primarily in the pathology of Metabolic disorders (primarily in the pathology of

the endocrine system).the endocrine system). Intoxication (both exogenous andIntoxication (both exogenous and endogenous).endogenous).

Despite the diversity of the etiology of comatose Despite the diversity of the etiology of comatose states in the pathogenesis of many things in states in the pathogenesis of many things in common, and the factors that serve as the common, and the factors that serve as the primary causes of some types of components, are primary causes of some types of components, are the pathogenic basis for others.the pathogenic basis for others.

A direct mechanism for cerebral A direct mechanism for cerebral insufficiency are violations of education, distribution insufficiency are violations of education, distribution and transmission of nerve impulses in the brain and transmission of nerve impulses in the brain cells due to inhibition of tissue cells due to inhibition of tissue respiration, metabolism and energy. This is due to respiration, metabolism and energy. This is due to the reduction of oxygen supply and nutrients to the the reduction of oxygen supply and nutrients to the brain (ischemia, venous brain (ischemia, venous congestion, microcirculation, congestion, microcirculation, vascular stasis, perivascular edema), changes vascular stasis, perivascular edema), changes in acid-base and electrolyte balance, increased in acid-base and electrolyte balance, increased intracranial pressure, edema and swelling of the intracranial pressure, edema and swelling of the brain and the meninges, the latter can lead to brain and the meninges, the latter can lead to dislocation of the brain from mechanical damage dislocation of the brain from mechanical damage to the vital centers in the brain stem.to the vital centers in the brain stem.

If any coma at some point it develops tissue hypoxia of If any coma at some point it develops tissue hypoxia of varying severity. Disturbances of acid-base varying severity. Disturbances of acid-base status often have the nature of metabolic acidosis, status often have the nature of metabolic acidosis, although the primary lesion of the respiratory although the primary lesion of the respiratory system develops respiratory acidosis. More rarely, system develops respiratory acidosis. More rarely, such as persistent vomiting, there is metabolic such as persistent vomiting, there is metabolic alkalosis, hyperventilation and alkalosis, hyperventilation and respiratory alkalosis leads to. Characterized by a respiratory alkalosis leads to. Characterized by a combination of various metabolic and combination of various metabolic and respiratory disorders.respiratory disorders.

Among the most significant electrolyte Among the most significant electrolyte disturbances consider changes in the concentration of disturbances consider changes in the concentration of potassium (hypokalemia as well as potassium (hypokalemia as well as hyperkalemia) and hyponatremia. Last played an hyperkalemia) and hyponatremia. Last played an important role in the pathogenesis of brain important role in the pathogenesis of brain edema. Slow metabolism have histotoxic action. With edema. Slow metabolism have histotoxic action. With the deepening coma develop respiratory failure, and the deepening coma develop respiratory failure, and subsequently circulation.subsequently circulation.

CLINIC PICTURECLINIC PICTURE The clinical picture is dominated by the coma of The clinical picture is dominated by the coma of

any disturbance of consciousness with loss of perception any disturbance of consciousness with loss of perception of the environment and oneself, depression of reflexes to of the environment and oneself, depression of reflexes to external stimuli and disturbances of regulation of external stimuli and disturbances of regulation of vital functions. Patients in a coma can not "wake up“ vital functions. Patients in a coma can not "wake up“ any, even the most energetic events. Allocate the any, even the most energetic events. Allocate the following shape changes in the level of following shape changes in the level of consciousness: Stun (shallow and deep),consciousness: Stun (shallow and deep), sopor, who (I-sopor, who (I-III degree). The degree of severity of disorders of III degree). The degree of severity of disorders of consciousness can be assessed by a simple consciousness can be assessed by a simple but informative clinical scale of Glasgow.but informative clinical scale of Glasgow.

Stun (13-14 balls on the scale of Glasgow) is Stun (13-14 balls on the scale of Glasgow) is characterized by drowsiness, disturbances of characterized by drowsiness, disturbances of attention, loss of cohesion of though and attention, loss of cohesion of though and action. With stunning patient is awake, but can action. With stunning patient is awake, but can not perform a task requiring sustained attention. for not perform a task requiring sustained attention. for example, consistently take 7 from 100.example, consistently take 7 from 100.

Stun (13-14 balls on the scale of Glasgow) is Stun (13-14 balls on the scale of Glasgow) is characterized by drowsiness, disturbances of characterized by drowsiness, disturbances of attention, loss of cohesion of thought and attention, loss of cohesion of thought and action. With stunning patient is awake, but can action. With stunning patient is awake, but can not perform a task requiring sustained attention. for not perform a task requiring sustained attention. for example, consistently take 7 from 100.example, consistently take 7 from 100.

Coma surface (I degree, 7-8 on a scale of Coma surface (I degree, 7-8 on a scale of Glasgow): wake up the patient is impossible to pain Glasgow): wake up the patient is impossible to pain stimuli it responds to the simplest, stimuli it responds to the simplest, erratic movements, not localizing pain.erratic movements, not localizing pain.

Deep coma (II degree, 5-6 on a scale of Glasgow): Deep coma (II degree, 5-6 on a scale of Glasgow): The patient is responsible motor responses to pain The patient is responsible motor responses to pain stimuli.stimuli.

Coma atonic (III degree, 3-4 on a scale of Coma atonic (III degree, 3-4 on a scale of Glasgow): complete lack of response of the patient, Glasgow): complete lack of response of the patient, even on very strong pain stimulation. Atony, are even on very strong pain stimulation. Atony, are flexia, impaired flexia, impaired or absent breathing, possibly inhibition of cardiac or absent breathing, possibly inhibition of cardiac activity.activity.

Depression of consciousness and the weakening Depression of consciousness and the weakening of reflexes (corneal, pupillary) tendon, of reflexes (corneal, pupillary) tendon, skin), progressing to full extinction of the skin), progressing to full extinction of the deepening coma. For focal lesions characterized deepening coma. For focal lesions characterized by unilateral neurological symptoms. Meningeal signs by unilateral neurological symptoms. Meningeal signs - stiff neck, Kernig and- stiff neck, Kernig and Brudzinski signs, observed in Brudzinski signs, observed in lesions of the meninges (meningitis, lesions of the meninges (meningitis, meningoencephalitis), can also be caused by brain meningoencephalitis), can also be caused by brain swelling and irritation of the meninges.swelling and irritation of the meninges.

Progression of cerebral insufficiency with the Progression of cerebral insufficiency with the fading of central nervous system leads to fading of central nervous system leads to various respiratory disorders with hypo-or various respiratory disorders with hypo-or hyperventilation and respiratory related shifts the hyperventilation and respiratory related shifts the acid-base status. Gross violations of hemodynamics is acid-base status. Gross violations of hemodynamics is usually attached to a terminal state other usually attached to a terminal state other clinical manifestations, the rate of development of clinical manifestations, the rate of development of coma, clinical history is usually quite specific for coma, clinical history is usually quite specific for different versions of components.different versions of components.

DIFFERENTIAL DIAGNOSISDIFFERENTIAL DIAGNOSISComa differentiated from a pseudocomasyndrome Coma differentiated from a pseudocomasyndrome

(isolated psychogenic are activity, abulic status, (isolated psychogenic are activity, abulic status, inconvulsive status epilepticus)inconvulsive status epilepticus)

Here are the features most frequently observed coma.Here are the features most frequently observed coma. Alcoholic comaAlcoholic coma may develop against the background  may develop against the background

of prolonged alcohol abuse, and the first use of alcohol, of prolonged alcohol abuse, and the first use of alcohol, usually develops gradually, beginning with alcohol usually develops gradually, beginning with alcohol intoxication, ataxia, coma, much less sudden intoxication, ataxia, coma, much less sudden onset of a convulsive seizure. onset of a convulsive seizure. Objectively say congestion and cyanosis of Objectively say congestion and cyanosis of the face, alternating with pallor, pendulum-the face, alternating with pallor, pendulum-like movement of the like movement of the eyeballs, bronhoreia, hyperhidrosis, hypothermia, eyeballs, bronhoreia, hyperhidrosis, hypothermia, decreased skin turgor, muscle atony, hypotension, decreased skin turgor, muscle atony, hypotension, tachycardia, smell of alcohol, according to tachycardia, smell of alcohol, according to which, however, can not reject any other, in which, however, can not reject any other, in particular traumatic or hypoglycemic coma etiology.particular traumatic or hypoglycemic coma etiology.

When hyperthermia coma (heat When hyperthermia coma (heat stroke),stroke), history of present indications of  history of present indications of overheating (the most adverse effects of overheating (the most adverse effects of heat with high humidity). Coma develops heat with high humidity). Coma develops gradually: the gradually: the characters sweating, increasing weakness, headacharacters sweating, increasing weakness, headache, dizziness, tinnitus, nausea, vomiting, che, dizziness, tinnitus, nausea, vomiting, palpitations, shortness of palpitations, shortness of breath, fainting. Objectively say hyperthermia, breath, fainting. Objectively say hyperthermia, flushing of the skin, tachypnea, flushing of the skin, tachypnea, less breathing Cheyne-Stokes or Kussmaul, less breathing Cheyne-Stokes or Kussmaul, tachycardia, tachycardia, hypotension, anuria or oligouriyu, dilated pupils.hypotension, anuria or oligouriyu, dilated pupils.

Hyperglycemic ketoatsidotic coma.Hyperglycemic ketoatsidotic coma. Information  Information about diabetes can not be. Coma may be preceded by about diabetes can not be. Coma may be preceded by fasting, infection or other acute diseases (myocardial fasting, infection or other acute diseases (myocardial infarction, stroke), physical or mental injury, infarction, stroke), physical or mental injury, pregnancy, termination of hypoglycemic pregnancy, termination of hypoglycemic therapy. Coma occurs gradually, against the therapy. Coma occurs gradually, against the background of weight loss increases the overall background of weight loss increases the overall weakness, thirst, polydipsia and polyuria, pruritus. weakness, thirst, polydipsia and polyuria, pruritus. Immediately prior to the development of coma appear Immediately prior to the development of coma appear anorexia, nausea, can be confusing for intense anorexia, nausea, can be confusing for intense abdominal pain until the symptoms of "acute abdominal pain until the symptoms of "acute abdomen", headache, sore throat, and abdomen", headache, sore throat, and esophagus. Against the background of acute interesophagus. Against the background of acute inter current illness coma may develop rapidly with no current illness coma may develop rapidly with no obvious predecessor. Physical examination reveals obvious predecessor. Physical examination reveals signs of dehydration (dry skin and mucous membranes signs of dehydration (dry skin and mucous membranes of the mouth, decreased skin turgor and the eyeballs, of the mouth, decreased skin turgor and the eyeballs, the gradual development of anuria), general pallor and the gradual development of anuria), general pallor and local congestion in the area of the zygomatic arch, local congestion in the area of the zygomatic arch, chin, forehead, cold skin (but low-grade fever is chin, forehead, cold skin (but low-grade fever is possible)possible) muscular hypotonia, hypotension, tachypnea muscular hypotonia, hypotension, tachypnea or Kussmaul breathing, acetone odor from the mouth.or Kussmaul breathing, acetone odor from the mouth.

Unketoatsidotic hyperglycemic hyperosmolar Unketoatsidotic hyperglycemic hyperosmolar coma coma may develop mild diabetes or impaired glucose may develop mild diabetes or impaired glucose tolerance and triggered by factors causing tolerance and triggered by factors causing dehydration and increased osmotic pressure dehydration and increased osmotic pressure of blood vomiting, diarrhea, polyuria, hyperthermia, of blood vomiting, diarrhea, polyuria, hyperthermia, burns, diuretics, and large doses of burns, diuretics, and large doses of glucocorticoids, administration of hypertonic glucocorticoids, administration of hypertonic solutions. This coma develops slowly More than hypersolutions. This coma develops slowly More than hyperglycemic ketoatsidotic coma, possible harbingers glycemic ketoatsidotic coma, possible harbingers of the same (but usually there is no pain in the of the same (but usually there is no pain in the abdomen) may be orthostatic syncope. Typical abdomen) may be orthostatic syncope. Typical signs of dehydration, hypotension up to hypovolemic signs of dehydration, hypotension up to hypovolemic shock, shortness of breath, possible hyperthermia, shock, shortness of breath, possible hyperthermia, muscular hypertonicity, focal or muscular hypertonicity, focal or generalized seizures, bulbar disturbances, generalized seizures, bulbar disturbances, meningeal signs, and aphasia in a shallow depression meningeal signs, and aphasia in a shallow depression of consciousness, the smell of acetone from the of consciousness, the smell of acetone from the mouth is missing.mouth is missing.

Hypoglycemic coma.Hypoglycemic coma. There may  There may be instructions for lowering drugs, although the lack be instructions for lowering drugs, although the lack of information about diabetes and hypoglycemic therapy does of information about diabetes and hypoglycemic therapy does not exclude hypoglycaemia. Note the acute onset (as an not exclude hypoglycaemia. Note the acute onset (as an exception - a gradual), a short period exception - a gradual), a short period of precursors (with atypical course, of precursors (with atypical course, caused dysmetabolic neuropathy, precursors may be caused dysmetabolic neuropathy, precursors may be absent), weakness, sweating, palpitations, trembling all over, a absent), weakness, sweating, palpitations, trembling all over, a keen sense of hunger, fear, excitement (hypoglycemia may keen sense of hunger, fear, excitement (hypoglycemia may be unusual mental disorders, such as euphoria, be unusual mental disorders, such as euphoria, delirium, amentia). On examination reveals hyperhidrosis, delirium, amentia). On examination reveals hyperhidrosis, hypothermia, marked pallor of the skin with an hypothermia, marked pallor of the skin with an unmodified color of mucous membranes, generalized tonic-unmodified color of mucous membranes, generalized tonic-clonic seizures, muscular hypertonicity, clonic seizures, muscular hypertonicity, muscle hypotonia revocable, tachycardia, hypotension (may muscle hypotonia revocable, tachycardia, hypotension (may be uncharacteristic of hypoglycemia autonomic be uncharacteristic of hypoglycemia autonomic dysfunction (hypertension, bradycardia, vomiting)), dysfunction (hypertension, bradycardia, vomiting)), breathing modifications and focal neurological symptoms.breathing modifications and focal neurological symptoms.

Gipokortikoidic coma (adrenal) Gipokortikoidic coma (adrenal) develops or against the develops or against the background of chronic adrenal insufficiency Coy (with background of chronic adrenal insufficiency Coy (with inadequate replaces therapy in a variety of stressful situations) inadequate replaces therapy in a variety of stressful situations) or as a result of various acute pathological conditions or as a result of various acute pathological conditions (haemorrhage in the adrenal glands with meningococcal and (haemorrhage in the adrenal glands with meningococcal and severe viral infections or trauma, acute thrombosis H, DIC, severe viral infections or trauma, acute thrombosis H, DIC, abrupt withdrawal of glucocorticoid therapy), as well as in times abrupt withdrawal of glucocorticoid therapy), as well as in times of stress (infection, trauma and other pathology) on the of stress (infection, trauma and other pathology) on the background or after discontinuation of glucocorticoid background or after discontinuation of glucocorticoid therapy. Coma may develop gradually with the increase obshey therapy. Coma may develop gradually with the increase obshey weakness, fatigue, anorexia, nausea, diarrhea, hypotension, weakness, fatigue, anorexia, nausea, diarrhea, hypotension, orthostatic collapse, fainting, under the influence of adverse orthostatic collapse, fainting, under the influence of adverse factors coma develops rapidly, and in case of hemorrhage in H, factors coma develops rapidly, and in case of hemorrhage in H, such as severe infections - with lightning speed ( syndrome such as severe infections - with lightning speed ( syndrome Waterhouse-Friderihsen). Found note hypotension until Waterhouse-Friderihsen). Found note hypotension until redistributed shock, shortness of breath (perhaps Kussmaul redistributed shock, shortness of breath (perhaps Kussmaul breathing), hyperthermia, dilated pupils, convulsive seizures, breathing), hyperthermia, dilated pupils, convulsive seizures, muscle rigidrit, are flexia. In a number of possible CA-bronze muscle rigidrit, are flexia. In a number of possible CA-bronze color of the skin and giperpigm-Ia (color of the skin and giperpigm-Ia (гиперпигм-ия ) skin folds, ) skin folds, weight loss, hemorrhagic rash.weight loss, hemorrhagic rash.

Alimentary dystrophic coma.Alimentary dystrophic coma. When hungry (alimentary  When hungry (alimentary dystrophic) coma present indications inadequate and dystrophic) coma present indications inadequate and insufficient food for a long time. Characterized by sudden insufficient food for a long time. Characterized by sudden onset of: after a period of excitement growing faint, rapidly onset of: after a period of excitement growing faint, rapidly turning into a coma. On examination reveals hypothermia, turning into a coma. On examination reveals hypothermia, pale peeling skin, it is possible acrocyanosis. Face pale icteric, pale peeling skin, it is possible acrocyanosis. Face pale icteric, and sometimes swollen. Characterized by muscle atrophy, and sometimes swollen. Characterized by muscle atrophy, may tonicity convulsions, hypotension, shallow breathing may tonicity convulsions, hypotension, shallow breathing rare.rare.

Opiate coma.Opiate coma. For opiate coma use of drugs is often hidden  For opiate coma use of drugs is often hidden from medical professionals. Relatively fast growing drug from medical professionals. Relatively fast growing drug intoxication is transformed into a coma. Depressed intoxication is transformed into a coma. Depressed respiration (shallow, irregular, Cheyne-Stokes equations, respiration (shallow, irregular, Cheyne-Stokes equations, sleep apnea), cyanosis noted, hypothermia, sleep apnea), cyanosis noted, hypothermia, bradycardia. Possible hypotension until the collapse, is rare - bradycardia. Possible hypotension until the collapse, is rare - pulmonary edema. Almost always reveal the point pupils pulmonary edema. Almost always reveal the point pupils (except poisoning promedolom or in combination with (except poisoning promedolom or in combination with atropine). Multiple traces from injections and other signs of atropine). Multiple traces from injections and other signs of drug use do not exclude the other (eg, trauma) etiology of the drug use do not exclude the other (eg, trauma) etiology of the coma.coma.

Traumatic coma. Traumatic coma. There are indications There are indications of injury and disease often developsof injury and disease often develops quickly, however, possible, quickly, however, possible, and the presence of a "bright period" during which the and the presence of a "bright period" during which the patient can be confusing for a sharp headache, nausea, patient can be confusing for a sharp headache, nausea, vomiting, psychomotor agitation. Cerebral symptoms may be vomiting, psychomotor agitation. Cerebral symptoms may be associated with meningeal signs andassociated with meningeal signs and symptoms of focal brain symptoms of focal brain lesions. Bradycardia and a rare breath replaced at later stages lesions. Bradycardia and a rare breath replaced at later stages of tachycardia and tachypnea.of tachycardia and tachypnea.

Cerebrovascular comaCerebrovascular coma develops against the background of  develops against the background of hypertension andhypertension and cardiovascular disease, although data cardiovascular disease, although data on hypertension, atherosclerosis, vasculitis,on hypertension, atherosclerosis, vasculitis, aneurysms of the aneurysms of the cerebral arteries can not be. The rate of development and the cerebral arteries can not be. The rate of development and the presence or absence of precursor role in the diagnosis did presence or absence of precursor role in the diagnosis did not play because the pre-hospital differential diagnosis not play because the pre-hospital differential diagnosis of hemorrhagic and ischemic stroke is notof hemorrhagic and ischemic stroke is not carried carried out. Characterized by cerebral and out. Characterized by cerebral and focal neurological, meningealfocal neurological, meningeal symptoms against a symptoms against a background of various disorders of hemodynamics.background of various disorders of hemodynamics.

EEссlampsiclampsic coma occurs between the 20th week of coma occurs between the 20th week of pregnancy and the end of the 1st week after pregnancy and the end of the 1st week after birth. Coma develops after a period of pre-eclampsia, which birth. Coma develops after a period of pre-eclampsia, which lasts from minutes to hours, rarely weeks, accompanied by lasts from minutes to hours, rarely weeks, accompanied by a painfula painful headache, dizziness, visual headache, dizziness, visual disturbances, epigastric pain, nausea, vomiting, diarrhea, mood disturbances, epigastric pain, nausea, vomiting, diarrhea, mood changes, restlessness or adynamia appearing on the changes, restlessness or adynamia appearing on the background of nephropathy. Pre-eclampsia is diagnosed when a background of nephropathy. Pre-eclampsia is diagnosed when a pregnant facial swelling or hands, blood pregnant facial swelling or hands, blood pressure reaches 140/90 mm Hg or systolic blood pressure by pressure reaches 140/90 mm Hg or systolic blood pressure by 30mmHg, and diastolic - by 15 mmHg, 30mmHg, and diastolic - by 15 mmHg, or proteinuria detected. Eor proteinuria detected. Eссlampsiclampsic coma develops after coma develops after a convulsive seizure, which begins fibrillar contractions ofa convulsive seizure, which begins fibrillar contractions of muscles in the face and hands, which are replaced muscles in the face and hands, which are replaced by generalized tonic, and thenby generalized tonic, and then clonic clonic seizures. Possible recurrence of attacks against seizures. Possible recurrence of attacks against the unconscious.the unconscious. Characterized Characterized by hypertension, bradycardia, hyperthermia can be. In some by hypertension, bradycardia, hyperthermia can be. In some cases, coma develops without seizures cases, coma develops without seizures ((inconvulsive form).inconvulsive form).

Epileptic coma. There may be indications Epileptic coma. There may be indications of seizures, head injury, stroke history. of seizures, head injury, stroke history. Coma develops suddenly, often after a Coma develops suddenly, often after a brief aura shutdown of consciousness and brief aura shutdown of consciousness and seizures begin simultaneously. In the first seizures begin simultaneously. In the first period (the period of status epilepticus), period (the period of status epilepticus), tonic seizures, frequent, tonic seizures, frequent, revocable clonic seizures, cyanosis face, foam on revocable clonic seizures, cyanosis face, foam on his lips, his tongue, stridoroz breathing, his lips, his tongue, stridoroz breathing, tachycardia, swollen neck veins, involuntary tachycardia, swollen neck veins, involuntary urination and defecation, and expansion are urination and defecation, and expansion are activity pupils. In the second period (the period of activity pupils. In the second period (the period of  postepilepticus sleep)  postepilepticus sleep) reveals hypotension mouse, are flexia, reveals hypotension mouse, are flexia, abnormal signs iambic, flushing, pallor or cyanosis abnormal signs iambic, flushing, pallor or cyanosis of the face, open mouth, eyes in the direction of the face, open mouth, eyes in the direction of abstraction, mydriasis, tachypnea, tachycardia.of abstraction, mydriasis, tachypnea, tachycardia.

ADVICES FOR CALLERADVICES FOR CALLER You can not transfer the patient to lift his head You can not transfer the patient to lift his head

and put patient; should leave it where he is and put patient; should leave it where he is and not change the position of the body.and not change the position of the body.

You should not undertake activities that affect You should not undertake activities that affect the body temperature (dew patient with the body temperature (dew patient with water, put hot water bottles to the feet, the ice on water, put hot water bottles to the feet, the ice on his head, etc.).his head, etc.).

You can not try to drink and to check whether the You can not try to drink and to check whether the patient swallows. Should not be given to the patient swallows. Should not be given to the patient to smell ammonia.patient to smell ammonia.

Recommended gently turn a head slightly to one Recommended gently turn a head slightly to one side, remove dentures, leftover food from the side, remove dentures, leftover food from the mouth.mouth.

OBLIGATORY QUESTIONSOBLIGATORY QUESTIONS In the diagnosis of coma necessarily should try In the diagnosis of coma necessarily should try

to gather history from relatives and witnesses (the to gather history from relatives and witnesses (the inability to collect a history of the patient significantly inability to collect a history of the patient significantly reduces the value of information obtained). Necessary reduces the value of information obtained). Necessary to clarify the following points.to clarify the following points.

The presence of chronic disease (diabetes, The presence of chronic disease (diabetes, hypertension, liver and kidney disease, thyroid disease, hypertension, liver and kidney disease, thyroid disease, epilepsy, stroke and traumatic brain injury history, epilepsy, stroke and traumatic brain injury history, etc.),intoxications and abuse of alcohol or drugs, as etc.),intoxications and abuse of alcohol or drugs, as well as receiving a present or past well as receiving a present or past drug syndrome "cancellation ", which can occur coma drug syndrome "cancellation ", which can occur coma (glucocorticoids, thyroid hormones).(glucocorticoids, thyroid hormones).

The presence of infection or injury.The presence of infection or injury. The circumstances, leading up to the loss of The circumstances, leading up to the loss of

consciousness (changes in health, thirst, consciousness (changes in health, thirst, polyuria and polydipsia, excessive heat, in polyuria and polydipsia, excessive heat, in coordination, alcohol, seizures).coordination, alcohol, seizures).

The rate of development of a coma.The rate of development of a coma.

INDICATION FOR HOSPITALIZATIONINDICATION FOR HOSPITALIZATION

Mandatory immediate hospitalization in an Mandatory immediate hospitalization in an

intensive care unit, in stroke - in the intensive intensive care unit, in stroke - in the intensive

care unit for patients with acute disorders of care unit for patients with acute disorders of

cerebral circulation, in brain cerebral circulation, in brain

injury or subarachnoid hemorrhage - a injury or subarachnoid hemorrhage - a

specialized neurosurgical department.specialized neurosurgical department.

Recommendations for abandoned homes of Recommendations for abandoned homes of

patients.patients. All patients admitted to the hospital. All patients admitted to the hospital.

Undifferentiated therapyUndifferentiated therapy Restore and maintain adequate breathingRestore and maintain adequate breathing 1. Remediation of the airways to restore their patency, 1. Remediation of the airways to restore their patency,

installing ductwork orinstalling ductwork or documentation of the language, documentation of the language, mechanical ventilation with a mask or a trachealmechanical ventilation with a mask or a tracheal tube, in rare tube, in rare cases - or tracheo-konikotomiya (opening between the cases - or tracheo-konikotomiya (opening between the larynx andlarynx and thyroid cartilage annular).thyroid cartilage annular).

2. Oxygen (4-6 L / min via nasal catheter, or 60% by face 2. Oxygen (4-6 L / min via nasal catheter, or 60% by face mask, tracheal tube).mask, tracheal tube).

3. Before tracheal intubation requires premedication of 3. Before tracheal intubation requires premedication of 0.1% solution of atropine (0.5-1 ml), except in cases of 0.1% solution of atropine (0.5-1 ml), except in cases of poisoning anticholinergic drugs.poisoning anticholinergic drugs.

Relief of hypoglycemia. Relief of hypoglycemia. Regardless of the level Regardless of the level of glucose (a long ill with diabetes,of glucose (a long ill with diabetes, poor compensation hypoglycemic coma may develop against a poor compensation hypoglycemic coma may develop against a normal glucose concentration) required bolus of 20-40 ml 40% normal glucose concentration) required bolus of 20-40 ml 40% glucose solution, in obtaining the effect, but the shortcomings glucose solution, in obtaining the effect, but the shortcomings of its severity, the dose increases. For the prevention of of its severity, the dose increases. For the prevention of acute encephalopathy Wernicke-Gaye before the appointment acute encephalopathy Wernicke-Gaye before the appointment of glucose must enter the thiamine (in the absence of glucose must enter the thiamine (in the absence of his intolerance) at a dose of 100 mg (2 ml of 5% solution).of his intolerance) at a dose of 100 mg (2 ml of 5% solution).

Restoration and maintenance of adequate blood flowRestoration and maintenance of adequate blood flow By reducing blood pressure should start a drip 1000-By reducing blood pressure should start a drip 1000-

2000 ml (less than 1 l/m2/day) 0.9% sodium chloride, 2000 ml (less than 1 l/m2/day) 0.9% sodium chloride, 5% glucose solution and 400-500 ml of dextran of average 5% glucose solution and 400-500 ml of dextran of average molecular weight 50-70 million (poliglyukina ) with the accession molecular weight 50-70 million (poliglyukina ) with the accession of the ineffectiveness of pressor amines infusion of the ineffectiveness of pressor amines infusion therapy - dopamine, norepinephrine.therapy - dopamine, norepinephrine.

In the case of coma, occurred against a background of In the case of coma, occurred against a background of hypertension, correction of a high blood pressure to valueshypertension, correction of a high blood pressure to values , , exceeding the "working" at 10 mm Hg (in the absence of exceeding the "working" at 10 mm Hg (in the absence of anamnestic data - not below 150-160/80-90 mm  Hg) by reducing anamnestic data - not below 150-160/80-90 mm  Hg) by reducing the intracranial pressure (see below) intravenous injection 1250-the intracranial pressure (see below) intravenous injection 1250-2500 mg of magnesium sulfate (5-10 ml 25% 2500 mg of magnesium sulfate (5-10 ml 25% solution ) bolus over 7-10minutes, or drip. In the presence solution ) bolus over 7-10minutes, or drip. In the presence of contraindications to magnesium sulfate, allowed the of contraindications to magnesium sulfate, allowed the introduction of 30-40 mg bendazola (3-4 ml of \% or 6-8 ml of introduction of 30-40 mg bendazola (3-4 ml of \% or 6-8 ml of 0.5% solution intravenous). With a slight increase in blood 0.5% solution intravenous). With a slight increase in blood pressure enough intravenous anpressure enough intravenous an aminophylline (10 ml 2.4% aminophylline (10 ml 2.4% solution).solution).

Restoring adequate heart rate Restoring adequate heart rate in arrhythmiases (mainly by defibrillation).in arrhythmiases (mainly by defibrillation).

Immobilization of the cervical spineImmobilization of the cervical spine in any  in any suspicion of injury.suspicion of injury.

Catheterization of peripheral veins.Catheterization of peripheral veins. If a comatose  If a comatose state, almost all drugs administered state, almost all drugs administered parenterally (preferably - intravenous) through a parenterally (preferably - intravenous) through a peripheral catheter infusion is carried out, peripheral catheter infusion is carried out, with stable hemodynamics and there is no need of with stable hemodynamics and there is no need of detoxification slowly drip detoxification slowly drip administered indifferent solution that provides a administered indifferent solution that provides a constant opportunity for the rapid introduction constant opportunity for the rapid introduction of drugs.of drugs.

Bladder catheterization. Bladder catheterization. Prehospital should be Prehospital should be performed only on strict indications (risk of infection).performed only on strict indications (risk of infection).

Setting the gastric or nasogastric Setting the gastric or nasogastric tubetube (after intubation, which must precede  (after intubation, which must precede premedication with atropine.premedication with atropine.

Therapeutic and diagnostic use of antidotesTherapeutic and diagnostic use of antidotes Antagonist of opiate receptors naloxone is indicated Antagonist of opiate receptors naloxone is indicated

for suspected intoxication drugs, respiratory rate less for suspected intoxication drugs, respiratory rate less than 10 per minute, point pupils. Initial dose - from 0.4-than 10 per minute, point pupils. Initial dose - from 0.4-1.2 to 2 mg (intravenous or endotracheal) may re-1.2 to 2 mg (intravenous or endotracheal) may re-introduction after 20-30 minutes with introduction after 20-30 minutes with repeated deterioration; acceptable combination repeated deterioration; acceptable combination of intravenous and subcutaneous administration to of intravenous and subcutaneous administration to prolong the effect.prolong the effect.

If you suspect If you suspect a poisoning benzodiazepine drugs (diazepam [with a poisoning benzodiazepine drugs (diazepam [with Relanium,seduksenium], oxazepam [tazepamom, nozeRelanium,seduksenium], oxazepam [tazepamom, nozepamom] medazepama [rudotelem,mezapama]) or pamom] medazepama [rudotelem,mezapama]) or suspicion of such, is administered flumazenil (0.2 mg suspicion of such, is administered flumazenil (0.2 mg intravenous for 15 seconds, followed by the intravenous for 15 seconds, followed by the introduction of if necessary to 0.1 mg every minute up introduction of if necessary to 0.1 mg every minute up to a total dose of 1 mg).to a total dose of 1 mg).

Relief of intracranial hypertension, edema and swelling Relief of intracranial hypertension, edema and swelling of the brainof the brain

In the absence of high osmolarity of blood (which occurs, for In the absence of high osmolarity of blood (which occurs, for example,example, hyperglycemia or hyperthermia), and the threat of hyperglycemia or hyperthermia), and the threat of development or strengthening ofdevelopment or strengthening of bleeding (eg, trauma, inability bleeding (eg, trauma, inability to exclude hemorrhagic stroke) for dehydration,to exclude hemorrhagic stroke) for dehydration, mannitol is mannitol is administered at a dose of 1-2 g / kg (in 20 % solution) for 10-20 administered at a dose of 1-2 g / kg (in 20 % solution) for 10-20 minutes, to prevent a subsequent increase in intracranial minutes, to prevent a subsequent increase in intracranial pressure and progressionof cerebral pressure and progressionof cerebral edema after mannitol infusion lead furosemide 40 mg.edema after mannitol infusion lead furosemide 40 mg.

1. Traditionally used glucocorticoids with minimal mineralocortic1. Traditionally used glucocorticoids with minimal mineralocorticoid activity -methylprednisolone or dexamethasone (dose for oid activity -methylprednisolone or dexamethasone (dose for both - 8 mg).both - 8 mg).

2. Limiting the introduction of hypotonic solutions (5% 2. Limiting the introduction of hypotonic solutions (5% Dextrose and 0.9% solution of NaCl - not more than 1 liter / Dextrose and 0.9% solution of NaCl - not more than 1 liter / day), but this does not apply to komah proceedingday), but this does not apply to komah proceeding against haemoconcentration (hyperglycemic, Hyperthermic, against haemoconcentration (hyperglycemic, Hyperthermic, 

gipokortikoidic, alcohol).gipokortikoidic, alcohol). 3. In the presence of appropriate 3. In the presence of appropriate

equipment may conduct mechanical ventilationequipment may conduct mechanical ventilation mode hyperventilation (effective against intracranial mode hyperventilation (effective against intracranial hypertension persists for 1 h).hypertension persists for 1 h).

Neuroprotection and increasing the level of Neuroprotection and increasing the level of consciousnessconsciousness

1. When violations of consciousness to the level of 1. When violations of consciousness to the level of surface glycine sublinguallysurface glycine sublingually shows the coma (or cheek) at shows the coma (or cheek) at a dose of 1 g, Semax 3 drops of 1% solution in each a dose of 1 g, Semax 3 drops of 1% solution in each nostril), an antioxidant etilmetilgidroksipiridina succinate nostril), an antioxidant etilmetilgidroksipiridina succinate (meksidol) at a dose of 30 mg (6 ml of (meksidol) at a dose of 30 mg (6 ml of 5% solution) intravenous, bolus, for 5-7 minutes.5% solution) intravenous, bolus, for 5-7 minutes.

2. With a deep coma spend antioxidant therapy2. With a deep coma spend antioxidant therapy and and injected Semaxinjected Semax

Activities to cease receipt of the toxin in the Activities to cease receipt of the toxin in the body in cases body in cases of suspected poisoning.of suspected poisoning.

1. Gastric lavage through a tube with the introduction of 1. Gastric lavage through a tube with the introduction of the sorbent (after intubation- see above) - when you the sorbent (after intubation- see above) - when you receive the poison from the mouth or during injection of receive the poison from the mouth or during injection of the poison of the gastric mucosa.the poison of the gastric mucosa.

Wash skin and mucous membranes with water - when Wash skin and mucous membranes with water - when you receive the poison through the covering fabric.you receive the poison through the covering fabric.

Symptomatic therapySymptomatic therapy Normalization of body Normalization of body

temperature. When supercooling - warming the temperature. When supercooling - warming the patient patient (without heaters) and warmed intravenous fluids. I(without heaters) and warmed intravenous fluids. In severe hyperthermia - a natural cooling (cold n severe hyperthermia - a natural cooling (cold compresses on his head, and large compresses on his head, and large vessels, wiping with cold water or solutions vessels, wiping with cold water or solutions of ethyl alcohol and vinegar in water) of ethyl alcohol and vinegar in water) and pharmacological methods (metamizol sodium, and pharmacological methods (metamizol sodium, but without the use of lytic mixtures).but without the use of lytic mixtures).

1. Relief of seizures: Diazepam intravenous at 1. Relief of seizures: Diazepam intravenous at a dose of 10 mg.a dose of 10 mg.

2. Relief of vomiting: metoclopramide 10 2. Relief of vomiting: metoclopramide 10 mg intravenous or intramuscularlymg intravenous or intramuscularly

The specific treatment of individual comatose statesThe specific treatment of individual comatose states Hypoglycemic coma.Hypoglycemic coma. Bolus 40% glucose solution at a dose  Bolus 40% glucose solution at a dose

of 20-40-60 ml (not more than 120 ml because of the of 20-40-60 ml (not more than 120 ml because of the danger of cerebral edema), with preliminary administration danger of cerebral edema), with preliminary administration of 100 mg of thiamine. If necessary, further administration of of 100 mg of thiamine. If necessary, further administration of glucose - its infusion solutions in decreasing concentrations glucose - its infusion solutions in decreasing concentrations of 5/10/20% with dexamethasone or methylprednisolone at a of 5/10/20% with dexamethasone or methylprednisolone at a dose of 4-8 mg for the prevention ofdose of 4-8 mg for the prevention of brain edema brain edema and as kontrinsulyar factors. If you need high doses of and as kontrinsulyar factors. If you need high doses of glucose and the absence of glucose and the absence of contraindications acceptable subcutaneous injection of 0.5-contraindications acceptable subcutaneous injection of 0.5-1ml of 0.1% solution of epinephrine, with a duration of a 1ml of 0.1% solution of epinephrine, with a duration of a coma more than a fewcoma more than a few hours is shown intravenous and hours is shown intravenous and 2500 mg of magnesium sulfate.2500 mg of magnesium sulfate.

Hyperglycemic ketoatsidotic and hyperosmolar not Hyperglycemic ketoatsidotic and hyperosmolar not ketoatsidotic coma.ketoatsidotic coma. Infusion of 0.9%  Infusion of 0.9% sodium chloride in sodium chloride in the volumethe volume, respectively, 1,000and 1,500 ml in the first , respectively, 1,000and 1,500 ml in the first hour. When hyperosmolar and prolonged coma hour. When hyperosmolar and prolonged coma ketoatsidotic shown heparin - up to 10 000 units intravenous.ketoatsidotic shown heparin - up to 10 000 units intravenous.

Alimentary dystrophic comaAlimentary dystrophic coma. Rewarming the . Rewarming the patient, infusion of 0.9% sodium chloride patient, infusion of 0.9% sodium chloride solution (with addition of 40% glucose solution at solution (with addition of 40% glucose solution at the rate of 60 ml per 500 ml) with an initial rate of the rate of 60 ml per 500 ml) with an initial rate of 200 ml / 10 min under the control of respiratory 200 ml / 10 min under the control of respiratory rate, heart rate, blood rate, heart rate, blood pressure and lung auscultatory pattern, pressure and lung auscultatory pattern, fractional administration of vitamin - thiamine (100 fractional administration of vitamin - thiamine (100 mg), pyridoxine (100 mg), pyridoxine (100 mg), cyanocobalamin (200 mg), mg), cyanocobalamin (200 mg), ascorbic acid (500 mg);ascorbic acid (500 mg);

Hydrocortisone 125 mg, Hydrocortisone 125 mg, with adequate hemodynamic failurewith adequate hemodynamic failure

infusion therapy and signs infusion therapy and signs of stagnation - pressor amines (dopamine, of stagnation - pressor amines (dopamine, norepinephrine).norepinephrine).

Alcoholic coma. Alcoholic coma. Bolus of 0.5-1 ml of 0.1% solution of Bolus of 0.5-1 ml of 0.1% solution of atropine, and after tracheal intubation through a gastric atropine, and after tracheal intubation through a gastric lavage tube - expedient for 4 h after the last intake of alcohol) lavage tube - expedient for 4 h after the last intake of alcohol) to clean the wash water (10-12 liters of water at to clean the wash water (10-12 liters of water at room temperature) and the introduction room temperature) and the introduction of enterosorbent, warm infusion of 0.9% sodium chloride of enterosorbent, warm infusion of 0.9% sodium chloride solution with an initial rate of 200 ml/10 min under the control solution with an initial rate of 200 ml/10 min under the control of respiratory rate, heart rate,of respiratory rate, heart rate, blood blood pressure and lung auscultatory pattern with a pressure and lung auscultatory pattern with a possible subsequent transition to the Ringer's possible subsequent transition to the Ringer's solution, bolus or drip 120 ml 40% glucose solution, the solution, bolus or drip 120 ml 40% glucose solution, the introduction of fractional vitamins - thiamine (100 introduction of fractional vitamins - thiamine (100 mg), pyridoxine (100 mg), cyanocobalamin(200 mg), mg), pyridoxine (100 mg), cyanocobalamin(200 mg), ascorbic acid (500 mg), with hemodynamic failure of ascorbic acid (500 mg), with hemodynamic failure of adequate fluid therapy - pressor amines (dopamine, adequate fluid therapy - pressor amines (dopamine, norepinephrine).norepinephrine).

Опиатная кома. Опиатная кома. Введение налоксона (см. выше); при необходимости Введение налоксона (см. выше); при необходимости интубации трахеи обязательна премедикация 0,5—1 мл 0,1% р-ра интубации трахеи обязательна премедикация 0,5—1 мл 0,1% р-ра атропина.атропина.

Cerebrovascular coma. Cerebrovascular coma. Since prehospital currently Since prehospital currently assisting impossibleassisting impossible differential diagnosis of ischemic and differential diagnosis of ischemic and hemorrhagic strokes, spend only a generalhemorrhagic strokes, spend only a general treatment.treatment.

When hypertension - blood pressure reduction to a When hypertension - blood pressure reduction to a level higher than the usual valueof 10 mm Hg, and in the level higher than the usual valueof 10 mm Hg, and in the absence of anamnestic data - not below 150-160/80-90mm  absence of anamnestic data - not below 150-160/80-90mm  HgHg

Relief of arterial hypotension is carried out in three stages:Relief of arterial hypotension is carried out in three stages:- intravenous slow introduction of - intravenous slow introduction of methylprednisolone (dexamethasone) in doses of 8-20 mg or methylprednisolone (dexamethasone) in doses of 8-20 mg or prednisolone at a dose of 60-150 mg;prednisolone at a dose of 60-150 mg;- After failure - a dose of 50-- After failure - a dose of 50-100 polyglukin ml intravenous bolus, then infusion of up 100 polyglukin ml intravenous bolus, then infusion of up to 400-500 ml;to 400-500 ml;- With inefficiency - the dopamine drip (5-15- With inefficiency - the dopamine drip (5-15

In severe to reduce the capillary. permeability, improving In severe to reduce the capillary. permeability, improving of μ-the circulation and Haemostasis - bolus of 250 of μ-the circulation and Haemostasis - bolus of 250 mg etamzilata to suppress proteolytic activity - a dripin the mg etamzilata to suppress proteolytic activity - a dripin the vine aprotinin 300 000 KIE (vine aprotinin 300 000 KIE (КИЕКИЕ).).

Neyroprotective therapy: in prevalent symptoms centre of Neyroprotective therapy: in prevalent symptoms centre of defeat crust of big hemisphere (vocal defeats and etc. defeat crust of big hemisphere (vocal defeats and etc.

changes of upper phsyhic functions ) under common brain changes of upper phsyhic functions ) under common brain symptomatic (clear conscious or easy deaf) admitted the symptomatic (clear conscious or easy deaf) admitted the

injection of piracetam (6-12 g. intravenous)injection of piracetam (6-12 g. intravenous)..

Eclampsic coma.Eclampsic coma. 3750 mg bolus of magnesium  3750 mg bolus of magnesium sulfate for 15 min. while maintaining sulfate for 15 min. while maintaining the seizures, diazepam bolus of 5 mg to relieve cramps, a the seizures, diazepam bolus of 5 mg to relieve cramps, a drip of Ringer's solution (INN (drip of Ringer's solution (INN (МНН) - sodium chloride complex pp) at 125 - 150 ml / - sodium chloride complex pp) at 125 - 150 ml / h, dextran [cf. Mol. weight 30 000-h, dextran [cf. Mol. weight 30 000-50 000] (reopoliglyukin) (100 ml / h).50 000] (reopoliglyukin) (100 ml / h).

Hyperthermic coma (heat stroke). Hyperthermic coma (heat stroke). Cooling, the Cooling, the normalization of respiratory, infusion0.9% sodium normalization of respiratory, infusion0.9% sodium chloride solution with an initial speed of 1000-1500 ml / chloride solution with an initial speed of 1000-1500 ml / h to 125 mgh to 125 mg hydrocortisone.hydrocortisone.

Gipokortikoidic (adrenal) coma. Gipokortikoidic (adrenal) coma. Bolus 40% glucose anBolus 40% glucose and thiamine (see above), hydrocortisone 125 d thiamine (see above), hydrocortisone 125 mg, infusion 0.9% sodium chloride solution (with addition mg, infusion 0.9% sodium chloride solution (with addition of40% glucose solution at the rate of 60 ml per 500 ml, of40% glucose solution at the rate of 60 ml per 500 ml, taking into account the number already entered) with an taking into account the number already entered) with an initial velocity 1000-1500 ml / h under the control initial velocity 1000-1500 ml / h under the control of respiratory rate, heart rate, blood of respiratory rate, heart rate, blood pressure and auscultatory pattern in the lungs.pressure and auscultatory pattern in the lungs.

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