Anesthesiology and resuscitation. Acute disturbances of consciousness (lecture notes)

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Anesthesiology and resuscitation. Acute disturbances of consciousness (lecture notes)

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Lecture No. 3. Acute disorders of consciousness

Consciousness is the highest form of reflection of reality, which is a set of mental processes that allow a person to navigate in the world around him, time, his own personality, which ensures his behavior. Impairment of consciousness is the general name for disorders of the integral activity of the brain, expressed in a violation of the ability to adequately perceive, comprehend and respond to the environment, navigate it, remember current events, make speech contact, and perform arbitrary expedient behavioral acts. There are various options for the oppression of consciousness (stupor, stupor, coma of various depths), as well as acute confusion (delirious state or metabolic encephalopathy). The degree of impaired consciousness varies from mild confusion to coma, and there are no clear transitions between these states. In practice, the degree of impaired consciousness is determined by the patient's reaction to stimuli.

Stupefaction is a form of impaired consciousness, characterized by lethargy, slowing down and difficulty in the course of mental processes, rapid exhaustion of attention, an increase in the threshold for the perception of external stimuli, but while maintaining limited verbal contact. Stupefaction is based on a violation of attention, i.e., the ability to select the necessary information and coordinate responses in such a way that the logical sequence of thoughts and actions is not violated. The most common causes of stupor are metabolic and toxic disorders, but sometimes it is also observed with focal lesions of the cortex, especially the right parietal lobe. In such patients, it is possible to achieve a monosyllabic answer or the implementation of the simplest instructions only after persistent appeals to it or additional stimulation. With further oppression of consciousness, the possibility of speech contact is lost and sopor develops.

Sopor is a state of deep depression of consciousness with the loss of the possibility of contact with the patient, but the preservation of coordinated defensive reactions and the opening of the patient's eyes in response to pain, sound or other stimuli. The patient cannot be fully awakened even with the help of painful stimuli, he lies with his eyes closed. The reaction to verbal instructions is weak or completely absent, it is impossible to get a response word or sound from the patient. With further oppression of consciousness, a coma develops.

Coma is an unconscious state characterized by insensitivity to external stimuli. This is a life-threatening state of depression of the functions of the central nervous system and disorders of the regulation of vital functions. Coma can be caused by many different metabolic disorders and structural damage.

Pathophysiology of coma

Most often, coma is due to:

1) intracranial processes with damage to brain tissue (hematoma, abscess, tumor, epilepsy);

2) infectious lesions of the central nervous system (meningitis, encephalitis);

3) toxic damage to the brain (poisoning by alcohol, mushrooms, drugs);

4) failure of cerebral blood flow (consequences of asystole, Morgagni-Adams-Stokes attacks);

5) metabolic causes (impaired water and electrolyte balance, carbohydrate metabolism, acid-base balance, renal and hepatic insufficiency);

6) disorder of temperature balance (heat stroke, hypothermia).

com classification

According to etiology, the following coma is distinguished.

1. Primary, or intracranial: traumatic, vascular, infectious, neoplasms of the brain, epileptic, metabolic and hypoxic.

2. Secondary, or extracranial: severe brain injury.

According to the severity of coma are classified in the following way.

1. Moderate coma, when the patient has a reaction to painful stimuli. In response to them, flexion and extensor movements may appear. But protective motor reactions are uncoordinated. The pain of the patient does not open his eyes. Pupillary and corneal reflexes are usually preserved, abdominal reflexes are depressed, and tendon reflexes are variable. Increased reflexes of oral automatism and pathological foot reflexes.

2. Deep coma. It is characterized by the absence of any reactions to any external stimuli, various changes in muscle tone, a decrease or absence of reflexes without bilateral mydriasis, disorders of spontaneous respiration and cardiovascular activity.

3. Terminal coma is determined by bilateral fixed mydriasis, diffuse muscle atony, severe violations of vital functions, rhythm and respiratory rate disorders, apnea, severe tachycardia; blood pressure is critical or not determined.

Examination of a patient with a coma

The plan of examination of the patient is as follows.

1. Assessment of the functional state of the respiratory and cardiovascular systems.

2. General clinical examinations, taking into account laboratory data, allowing to assess extracranial pathology.

3. Neurological examination.

Laboratory studies: general clinical blood test (signs of a bacterial or viral infection); blood chemistry: glucose, coagulation factors (clotting time, prothrombin, fibrinogen, APTT, antithrombin III, paracoagulation tests, platelet count), urea, creatinine, bilirubin, ALT, AST, osmolarity, electrolytes (K, Na, Mg, Ca ); toxicological screening of blood, urine, gastric contents.

Instrumental studies: radiography of the skull and cervical spine.

Consultation of a neuropathologist (neurosurgeon) determines the further direction of the diagnostic search: computed or magnetic resonance imaging; EEG; ultrasound dopplerography. Lumbar puncture with analysis of cerebrospinal fluid is mandatory after:

1) consultation of an ophthalmologist and exclusion of signs of increased intracranial pressure - edema and elevation of the optic discs;

2) exclusion of signs of herniation of the brain.

The following localizations of the herniation of the brain are distinguished. Diencephalic herniation, which occurs when the medial supratentorial localization is damaged and consists in the displacement of the diencephalon through the notch of the cerebellar tenon. This process calls:

1) Cheyne-Stokes breathing;

2) constriction of the pupils while maintaining their reaction to light;

3) paralysis of gaze up;

4) changes in mental status.

The herniation of the medial parts of the temporal lobe, which occurs when the lateral supratentorial localization is affected, consists in the displacement of the medial parts of the temporal lobe through the notch of the cerebellar tenon. The resulting pressure on the structures of the midbrain is manifested by:

1) impaired consciousness;

2) an enlarged, non-reactive pupil on the side of the herniation, which is associated with compression of the III cranial nerve;

3) hemiparesis on the opposite side.

The movements of the eyeballs are not always disturbed. Herniation of the tonsils of the cerebellum, which is caused by pressure pushing the lower part of the cerebellum through the foramen magnum, which leads to compression of the medulla oblongata. It causes:

1) impaired consciousness;

2) violations of the rhythm of breathing or apnea.

Treatment

Treatment should be as aggressive as possible and primarily aimed at ensuring adequate oxygenation and stabilization of central hemodynamics. If spontaneous breathing is maintained, humidified oxygen insufflation through a mask or nasal catheter is recommended. In the absence of spontaneous respiration or in the presence of pathological respiration, tracheal intubation is performed and the patient is transferred to artificial lung ventilation. With psychomotor agitation and reaction to mechanical ventilation, the use of sedatives (benzodiazepines, butyrophenones) is necessary. Stabilization of central hemodynamics is the normalization of blood pressure. In a hypertensive state, blood pressure must be reduced, but not more than 10% of the original per hour. A good effect is the use of sodium nitroprusside or magnesium sulfate. With hypotension, dopamine, dopamine, dobutrex and hormonal drugs are used.

In the absence of anamnestic data and an unclear diagnosis, ex juvantibus therapy is performed (a positive response to drug exposure, on the one hand, gives the key to the diagnosis, on the other hand, it helps to gain time to avoid irreversible changes):

1) thiamine - 100 mg intravenously, subsequently - 100 mg intramuscularly (especially if there is a history of alcoholism, when determining high concentrations of ethanol in the blood);

2) glucose - a 40% solution of 60 ml intravenously (with an unknown level of glucose in plasma or at a level less than 3 mmol / l);

3) naloxone - 0,4-1,2 mg intravenously, fractionally, repeatedly, especially in the presence of "opiate signs" (traces of intravenous injections, narrow pupils, central respiratory disorders);

4) anexat (flumazenil) - 0,2 mg for 30 seconds, over the next minute, inject another 0,3 mg, over each next minute - 0,5 mg to a total dose of 3 mg. In the absence of an effect, it can be assumed that the coma is unlikely to be caused by benzodiazepine drugs;

5) in case of poisoning or overdose with a known drug or substance, it is necessary to administer the appropriate antidote (if there is a possibility of antidote therapy).

Seizure control. Incoming brain hypoxia can cause status epilepticus. Seizure episodes may also result from anticholinesterase drug toxicity. For treatment, the drug of choice is benzodiazepines: midazolam (Dormikum) 5 mg intravenously in divided doses up to a total dose of 30 mg g, seduxen (Relanium) in divided doses up to 10 mg, intravenously. When status epilepticus develops, following benzodiazepines, it is necessary to administer phenytoin in a total dose of 1-1,5 g at a rate of 50 mg/min. If there is resistance to these drugs, it is necessary to administer phenobarbital (thiopental) in a total dose of up to 1000 mg by slow intravenous infusion (respiration and blood pressure control is necessary). For recurrent seizures, general anesthesia is necessary. In patients with EEG or computed tomography signs of an epileptic focus (hemorrhage, neoplasia, large ischemic infarction, abscess, etc.) and episodic epileptic seizures, maintenance therapy with phenytoin is required - 300 mg once a day per os.

Maintaining normothermia. Control of rectal temperature is necessary: its decrease below 34 °C develops with hypothermia, overdose of sleeping pills and sedatives, hypothyroidism, Wernicke's disease. In these cases, it is necessary to gradually warm the patient to a temperature of 36 °C. Patients with hypothermia and lack of vital functions are subject to CPR, since low temperature reduces the demand for oxygen in the heart and brain and contributes to a better outcome of resuscitation measures (except for cases accompanied by hyperkalemia). The presence of fever in comatose patients requires an active search and treatment of infectious complications. The presence of signs of meningism may indicate the presence of either bacterial meningitis or subarachnoid hemorrhage (although approximately 12 hours must elapse between the onset of bleeding and chemical meningeal irritation). Another cause of fever may be an intracranial abscess or subdural hematoma. If bacterial meningitis is suspected, a lumbar puncture (cerebrospinal fluid analysis) and computed tomography should be performed to determine signs of increased intracranial pressure.

Preventing aspiration of gastric contents. The need for gastric lavage in case of poisoning and drug overdose and, therefore, the installation of a gastric tube increases the risk of regurgitation of gastric contents (due to relaxation of the gastroesophageal sphincter). Therefore, before inserting a gastric tube, it is necessary to perform tracheal intubation with a sealing cuff, which is the best means of protecting the airway.

Urological treatment. To control diuresis, it is necessary to install a Foley catheter, ensuring aseptic conditions and conducting antimicrobial therapy to prevent urogenital sepsis.

Reduced intracranial pressure. An increase in ICP is a clinical emergency that requires the implementation of appropriate measures aimed at reducing it, which avoids secondary damage to the brain due to compression of its tissues or a decrease in cerebral blood flow. Carrying out the above diagnostic measures makes it possible to establish the causes of increased ICP, and, accordingly, the key measures are aimed at its elimination (operative and conservative treatment). Hyperventilation to maintain pCO levels₂ 25-30 mmHg Art. (levels less than 25 mm Hg can cause a significant decrease in cerebral blood flow, leading to cerebral ischemia). Restriction of fluid intake. It is necessary to exclude solutions containing free water (5% glucose). Isotonic NaCl solution, necessary to maintain blood osmolarity, should be administered at half the dose.

Introduction of osmotically active substances. Mannitol is administered at a dose of 1-2 g/kg for 10-20 minutes, and then at a maintenance dose of 0,05-0,3 g/kg every 6 hours. Additionally, furosemide is administered to more effectively reduce ICP. Strict control of the therapy is necessary to prevent complications: a decrease in intravascular volume, hypotension, hypernatremia, hypocalcemia, hypokalemia, as well as a response syndrome and rupture of cortical veins in subdural hematoma.

An important measure to prevent complications is to maintain systolic blood pressure at 100-110 mm Hg. Art. Drugs also lead to a decrease in ICP. The use of muscle relaxants helps to reduce ICP during mechanical ventilation (blockade of increased intrathoracic venous pressure during mechanical ventilation), but they are recommended only for a very short time. The use of corticosteroids is effective in cases of increased intracranial pressure due to neoplasia or focal ischemia (stroke) of the brain. The effectiveness of corticosteroids in the treatment of increased intracranial pressure due to trauma and general cerebral ischemia has not been proven. It is important to remember that glucocorticoids can cause an increase in blood glucose levels and, accordingly, increase cerebral ischemia.

Types of com

Hypoglycemic coma occurs with an overdose of insulin in the treatment of diabetes mellitus or with restriction of carbohydrate intake. The development of coma is preceded by bulimia, irritability, fear. Diplopia, hallucinations, tonic and clonic convulsions are sometimes noted. Excitation is replaced by adynamia and vice versa. The patient quickly loses consciousness and is covered with sweat. The skin is moist and pale, breathing is shallow, rhythmic. Sometimes spontaneous hypoglycemia is observed in athletes and after heavy physical exertion. If the hypoglycemic coma lasts more than 3 hours, the development of gross organic lesions of the central nervous system is possible. It is important to lower the blood sugar level below 3 mmol. There is no sugar or acetone in the urine.

Treatment. Immediately enter 20-40% glucose at a dose of 20-30 ml intravenously as a bolus. After that, blood and urine sugar control is carried out.

Diabetic coma, or hyperglycemic, when the blood glucose level is sharply increased. Coma is preceded by drowsiness, thirst, anorexia, nausea, vomiting, headache. Hyperglycemia, metabolic acidosis are determined in the laboratory, sugar and acetone are present in the urine (not always). The face is pale and hyperemic, the mucous membranes are dry, the skin is also dry, and its turgor is reduced. The eyeballs are sunken, the smell of acetone from the mouth is possible. Breathing is rare pathological. Hemodynamics is disturbed: tachycardia, arterial hypotension, muffled heart sounds.

Treatment. Elimination of hypovolemia with the help of intravenous administration of sodium chloride in a volume of 3-5 liters per day. Insulin therapy consists in the introduction of short-acting insulin 6-10 IU per hour with an infusion pump. With a decrease in blood glucose to 11-13 mmol / l, the dose of insulin is reduced to 4-8 units per hour, and an infusion of 5% glucose begins to avoid a hypoglycemic state.

Thyrotoxic coma is rare, but it should be considered if, with severe tachycardia, there are no typical signs of hemodynamic myocardial insufficiency and there is energy-dynamic heart failure. The presence of struma, eye glare, and tremor usually also draws attention to this possibility. The clinical picture should be supplemented by collecting anamnestic data, since studies confirming the diagnosis (basal metabolism, radioactive iodine) cannot be carried out.

Alcohol intoxication is manifested by the smell of alcohol from the mouth, a delirious state, anxiety, vomiting, and a puffy face. Breathing is slow, pulse is quickened, pupils are dilated. In patients with alcoholism, delirium develops 2-3 days after alcohol withdrawal. The development of delirium is prevented by the use of benzodiazepines when warning signs (fever, tremor, tachycardia, hypertension) appear. With the development of delirium, the drugs of choice are: in young people, diazepam (intravenous administration), and in elderly patients and patients with impaired liver function, lorazepam, but if necessary, a quick effect is preferable to diazepam (5 mg every 5 minutes until the effect is achieved). Cases of the need to administer 2640 mg of diazepam for the treatment of a severe delirious state are described. Additionally, blockers and clonidine are used. Also in these conditions, the use of antipsychotics (haloperidol, droperidol) is useful.

With apoplexy coma (develops with various intracerebral processes), the leading symptom is hemiplegia or paralysis of individual muscle groups. Paralysis appears when the eyes and head are turned in the opposite direction to the paralyzed: "the patient looks at the lesion in the brain." The mouth is skewed to the healthy side: "smoking a pipe on the diseased side." On the hemiplegic side, the elevated limb falls quickly and heavily onto the bed, while the unaffected limb slowly returns to its original position.

Coma with Addison's disease (adrenal coma, often developing with adrenal tuberculosis, trauma, infectious diseases) is rare. The leading symptom is pathologically low, often unmeasurable blood pressure. Along with collapse, this symptom is caused by changes in carbohydrate metabolism (hypoglycemia), electrolyte imbalance and water metabolism. Suddenly there is a sharp pallor, cold sweat. Excitation is quickly replaced by adynamia, then the patient loses consciousness. Acrocyanosis appears, the skin becomes marbled. On the skin of the back and extremities, pigmentation is found in the form of dark spots and a bright red petechial rash. Heart sounds are muffled. Dehydration and oliguria quickly set in. In the blood, metabolic acidosis, hypoglycemia and an increase in residual nitrogen.

Treatment consists in the rapid introduction of glucocorticosteroids at a dose of 1 mg / kg. The dose can be increased by 2-3 times. A similar dose is administered intramuscularly. To combat dehydration, an isotonic solution of sodium chloride is administered, and then glucose.

Author: Kolesnikova M.A.

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