If you hit a hard object or surface, or if you hit the head, you can get a brain contusion. With a slight bruise, soft tissue injury occurs, so there are no special consequences. During the impact, a rupture occurs blood vessels, which causes the formation of a hematoma.
When you receive a slight bruise, pain appears in the area of injury, and subsequently the formation of a lump. However, with a serious blow to the head area, serious damage to the brain can occur, while manifestations of a bruise may not be observed.
Brain contusions can be divided into 3 degrees of severity:
- Mild bruise;
- Moderate bruise;
- Severe bruise.
For mild to moderate treatment, it is necessary to take a course intensive care, and also take medications for brain contusions. And when seriously injured, patients are in intensive care under the supervision of specialists.
When a brain injury occurs, breathing and the circulatory system are restored. To restore respiratory function, prevent asphyxia, use oxygen inhalers. If necessary, connect to an artificial respiration apparatus.
Necessary actions
When you get a head injury, the first thing you should do is apply ice, a so-called compress, to the injured area. Apply ice for 15-20 minutes, then repeat periodically throughout the day. Ice promotes the outflow of blood from the site of the bruise, which helps reduce the resulting hematoma.
You can also apply hot salt, wrapped in a bag or freshly boiled salt, to the bruise site. egg. A compress with vegetable oil helps very well.
You can also use it for bruises:
- Bodyagu;
- Heparin ointment;
- Alcohol solution Yoda.
Please read the attached instructions carefully before use.
Drugs for treatment
When treating brain contusions, you can resort to using medicines. Each of them affects specific areas. To strengthen the walls of blood vessels, as well as to prevent pain and swelling, you can use pain-relieving ointments:
- Troxevasin;
- Dolobene-Gel;
- Fastum-gel;
- Rescuer and others.
When treating brain contusions, a solution of manganese, furatsilin, brilliant green, iodine and other agents are used for physiotherapy purposes. In addition to tonic preparations for the treatment of bruises, tincture of ginseng and Eleutherococcus is used.
When eliminating pain, all medications for brain contusion are prescribed taking into account the patient’s condition. Such drugs include:
- Sedalgin;
- Analgin;
- Pentalgin;
- Baralgin.
When treating brain injuries, they try to avoid aggressive medications, since the main goal is to restore the functioning of the gray matter. Also, the primary objectives are: eliminating pain, symptoms of dizziness and other unfavorable conditions. Doctors try to prescribe medications in the form of capsules or injections.
If dizziness occurs, the following medications are prescribed for brain contusions:
- Papaverine;
- Tanakan;
- Belloid;
- Bellaspon.
To improve sleep, Phenobarbital or Reladorm are prescribed; you can also use regular Diphenhydramine.
If necessary, admission sedatives resort to reception:
- Valoserdin;
- Corvalol;
- Valerian or motherwort tincture.
When a brain injury occurs, brain tissue is damaged, so medications should be used to provide nutrition to the brain cells. The following means are used:
- Semax;
- Actovegin;
- Ceraxon;
- Cerebrolysin;
- Mildronate;
- Somazin.
You should also simultaneously use medications that will improve microcirculation: Cavinton, Sermion, do not forget about taking vitamins E and B. If an open injury occurs, you should use antibiotics: Azithromycin or Cefotaxime to prevent infection.
While taking medications for a brain contusion, it is also necessary to carry out procedures to treat metabolic and vascular system to prevent post-concussion disorders.
It is also worth ensuring the victim’s rest, and if complications arise in the form of persistent headaches, bleeding, or the appearance of new symptoms, it is worth calling for medical help.
Sergey Anatolyevich Derevshchikov.
659700. Altai Republic, Gorno-Altaisk. Kommunistichesky Ave., 130, Republican Hospital, Department of Anesthesiology and Reanimatology.
Tel. 2-58-89, E-mail: [email protected]
1. GENERAL PRINCIPLES OF MANAGEMENT OF PATIENTS WITH TBI.
1.1. If the functions of vital organs are impaired, the examination should be preceded by urgent measures - tracheal intubation, mechanical ventilation, administration of vasopressors.
Collect information according to the following scheme: Who? Where? When? What happened? Because of what, after what? What happened before?
1.2. Determine the depth of consciousness impairment using the Glasgow scale.
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Nature of activity |
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Opening your eyes |
Independent |
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to a verbal command |
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absent |
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Motor reaction |
execution of a verbal command |
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localization of pain |
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withdrawal of limb |
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flexion of a limb for pain |
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extension of a limb for pain |
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absent |
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Verbal response |
definite |
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confused |
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inadequate |
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incomprehensible |
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absent |
Total 3 - 15 points.
CONFORMITY of characteristics according to the Glasgow scale with traditional methods.
15 - clear consciousness
13 - 14 - stun.
9 - 12 - support.
4 - 8 - coma.
3 - brain death.
1.4 Patients diagnosed with TBI should undergo dynamic neurological monitoring and instrumental methods examinations.
upon admission to the department.
in 3 hours.
every other day and then every day.
1.4 Scope of examination for the diagnosis of TBI:
Neurological examination (neurologist).
X-ray of the chest and skull in two projections.
Echoencephaloscopy.
Computed tomography - if the diagnosis is unclear.
Lumbar puncture if other methods do not provide sufficient information.
Laboratory examination according to the standard scheme.
Surgeon consultation.
2. ANESTHETIC GUIDE
USE:
semi-open circuit.
mode of moderate hyperventilation.
sodium thiopental, midazolam, fluorothan up to 1 vol.%, narcotic analgesics, benzodiazepines.
sodium hydroxybutyrate for unstable hemodynamics.
DO NOT USE:
Calypsol, ether, nitrous oxide, glucose solutions, dextrans (if there is no shock, hypovolemia).
ATTENTION!
avoid hypotension.
After the end of the intervention, do not transfer the patient to spontaneous breathing until consciousness is restored. Transfer to the intensive care unit with controlled breathing!
3. TREATMENT OF ACUTE PERIOD OF TBI (1st PERIOD) GENERAL MEASURES.
GENERAL EVENTS. Performed to the maximum short time. Their execution must be completed within 2 hours from the moment of receipt.
3.1 ENSURING PATESTITY OF THE UPPER AIRWAY.
If there are signs of aspiration syndrome, disturbance of consciousness such as coma, deep stupor, immediate tracheal intubation.
If there are solid food particles in the aspirated liquid and the progression of acute respiratory failure, emergency therapeutic and diagnostic bronchoscopy is indicated.
3.2 STABILIZATION OF HEMODYNAMICS.
Strive for a normodynamic or moderately hyperdynamic state of hemodynamics. If the patient has traumatic shock, infusion and other anti-shock therapy should be carried out in full.
3.3 ARTIFICIAL VENTILATION.
Indications for mechanical ventilation for TBI:
Comatose state (3 - 8 points on the Glasgow scale).
Hyper and hypo ventilation syndrome.
Breathing rhythm disturbance.
The need for therapeutic anesthesia.
With signs of increasing intracranial hypertension.
With concomitant chest injuries.
For traumatic shock 2 - 3 tbsp.
With signs of decompensated respiratory failure of any origin.
IF ANY DOUBT ABOUT THE PATIENT'S CONDITION, THE ISSUE SHOULD BE DECIDED IN FAVOR OF VENTILATION!
If long-term mechanical ventilation is expected, nasotracheal intubation is desirable.
The endotracheal tube is additionally secured with adhesive tape.
ATTENTION!
If the patient’s synchronization with the ventilator is disturbed in the early period, it is advisable to use muscle relaxants.
If it is not possible to perform mechanical ventilation, refuse to administer sedatives and narcotics to the patient.
3.4 BASIC THERAPY IN PATIENTS WITH TBI.
Goal: strive to maintain parameters within the specified limits until the patient recovers from a serious condition.
Place the patient in a position with the head end elevated (30-40 degrees).
PaO2 > 70 mmHg.
SpO2 > 92%.< 160 мм.рт.ст.
PaCO2 35 - 40 mmHg.
BP syst. > 100
Water balance ±500 ml.
Blood sodium 135 - 145 mmol/l.
Osmolarity 280 - 295 mOsm/l.< 37,50 С градусов.
Hb > 100 g/l.
Hematocrit - 30 - 35 percent. Body temperature Central perfusion pressure > 60 mmHg.
Attention!. Measurement cuff
blood pressure
Do not apply to the limb on the side of the paresis.
3.5 ANTIBACTERIAL THERAPY. Start no later than three hours from the moment of admission. Closed injury - penicillin 2.0 after 4 hours IV, IM. or ampicillin 1.0 * 6 r/day i.v., i.m. Penetrating, open TBI
, state after
Consider the feasibility of prophylactic subarachnoid injection antibacterial agents(kanamycin 1 mg/kg or gentamicin 0.1 mg/kg or dioxidine 0.5 mg/kg).
3.6. SYMPTOMATIC TREATMENT.
Used for TBI of varying severity.
With tachycardia; 110 beats per minute - anaprilin (obzidan) 20 - 40 mg * 1 - 4 times / day in a tube or other blockers.
Attention! If the patient receives Nimotop, blockers should not be prescribed.
If the body temperature rises above 37.50 C, use non-steroidal analgesics in normal doses (for example, analgin 50% 2.0 - 4.0 IV * 3 - 4 times / day). If ineffective, physical cooling of the patient is carried out (for example, wet wrapping and blowing air flow, lining the limbs with ice packs, etc.) against the background of neurovegetative blockade (seduxen, aminazine).
4.1 TREATMENT IN THE ACUTE PERIOD OF SEVERE TBI (first period).
Criteria: 3 - 8 points on the Glasgow scale. The upper and lower parts of the brain and the medulla oblongata are affected.
Clinic: coma, less often stupor, normothermia or hyperthermia, decreased or increased blood pressure, heart rate, respiratory rhythm disturbance. Neurodystrophic changes internal organs, skin, blood pressure asymmetry. The approximate duration of this period is 7 - 14 days.
4.1.1 Sodium thiopental
2 - 4 mg/kg IV bolus. Then 0.5 - 3 mg/kg per hour continuously by dispenser or bolus. Select the dose of sodium thiopental, focusing on the clinic: normalization of body temperature, reduction of tachycardia, normalization of blood pressure, relief of motor agitation, synchronization of the patient with a ventilator. Maintain superficial anesthesia (so that the patient’s voluntary moderate motor activity, reaction to painful stimuli, and cough reflex are maintained. From day 2, reduce the dose by approximately 50%. On the fourth day, stop administering the drug and prescribe barbiturates long acting
, for example, benzonal 0.2 * 1 - 2 rubles / day.
In case of unstable hemodynamics, ataractics are used instead of sodium thiopental (for example, Seduxen 10 mg/i.v. 3-5 times/day).
If there is a combined injury, then narcotic analgesics are additionally used.
Magnesium sulfate: 20 ml of a 25% solution (5 g) is administered intravenously over 15 - 20 minutes, then intravenous infusion at a rate of 1 - 2 g/hour for 48 hours. The use of magnesium sulfate is contraindicated if the patient has renal failure.
4.1.3 Glucocorticoids.
Attention! - Appoint at the most early dates. 8 hours after injury, the therapy below is less effective!
When prescribing, consider contraindications: the presence of purulent infection, gunshot wounds, peptic ulcer in exacerbation, etc.
The drug of choice is methylprednisolone sodium succinate. Other glucocorticoid drugs may be less effective.
Methylprednisolone 30 mg/kg bolus over 10 to 15 minutes. Then 5 mg/kg/hour by dispenser or bolus throughout the day. In the next 48 hours - 2.5 mg/kg per hour.
Other glucocorticoid drugs - in equivalent doses.
In the absence of a sufficient amount of the drug, use in smaller dosages.
4.1.4 Tirilazad mesylate
(Fridox) 1.5 mg/kg IV drip. every 6 hours for 8 days.
Note: the cost of a course of treatment with this drug is several thousand dollars. If there is no specified drug, then Vit."E" 30% - 2.0 IM * 1 r.
days for 8 days.
4.1.5 Infusion therapy.
Physical solution 0.9% i.v.
Evenly throughout the day - 2.0 -2.5 liters (30 - 35 ml/kg/day) 2 days. saline solution 0.9% w/w
Evenly throughout the day - 1.5 -2.0 liters (25 - 30 ml/kg/day) From the end of the second or at the beginning of the third day, switch to tube feeding with caloric content 1 -1.5 KCAL/day in
total volume
up to 1.5 - 2.5 l/day.
In the following days, the caloric intake is gradually adjusted to the actual metabolic needs of the patient.
4.2 TREATMENT IN THE ACUTE PERIOD OF MODERATE SEVERITY TBI (first period).<38,5, АД, ЧСС нормальные или умеренно повышены, асимметрия рефлексов.
Criteria: 9 - 12 points on the Glasgow scale. The cerebral hemispheres and extrapyramidal system are affected
Clinic: stupor, hypokinesia, hypomimia, increased muscle tone of the limbs, cataleptic state, hyperthermia>37< 100мм.рт.ст!
4.2.1 Sedative therapy.
Long-acting barbiturates, for example benzonal 0.2 * 1 - 2 r/day.
If there are episodes of psychomotor agitation, take antipsychotics. Approximate doses: aminazine 12 - 50 mg * 2 - 3 times / day. or haloperidol 12 - 25 mg * 2 - 3 r/day. i.v. or i.m.
4.2.2 Tirilazad mesylate
(Fridox) 1.5 mg/kg IV drip. every 6 hours for 5 days. If there is no specified drug, then Vit."E" 30% - 2.0 IM * 1 r. days for 5 - 8 days.
(Brain contusion, combination of brain contusion and hematoma, condition after surgery for acute hematomas, fracture of the vault and base of the skull in adults).
4.2.3 Infusion therapy
Physical solution 0.9% i.v. Evenly throughout the day - 2.0 -2.5 liters (30 - 35 ml/kg/day) 2nd day and subsequent days.
Intake of fluids and food
PER OS in a volume of 1.5 - 2.5 liters with a calorie content of 2 - 3 KCAL/day.
4.3 TREATMENT IN THE ACUTE PERIOD OF SEVERE AND MODERATE TBI IN CONDITIONS
NON-SPECIALIZED DEPARTMENT (no specialists, equipment for ventilation and monitoring, no possibility of intensive treatment).
Therapy is symptomatic. In patients with severe TBI, early tracheostomy is recommended. Do not prescribe narcotic analgesics, and use sedatives very carefully, in minimal dosages. The patient should not be deeply sedated. Most patients from the second to third days need to be prescribed osmotic diuretics to reduce intracranial pressure (see section 6.1). In treatment, you can use the recommendations given in sections 3.6 and 4.2.
5.SECOND PERIOD (early compensation)
5.1.
"ACTIVATING THERAPY"
ATTENTION! This therapy should be used when the patient’s consciousness is restored or when the patient’s level of consciousness is stabilized at the same level.
It is contraindicated in the acute period of TBI, with increased intracranial pressure.
In the period of early compensation, it is indicated in patients with symptoms of “loss” of neurological functions and is contraindicated in patients with symptoms of “irritation”.
It is usually prescribed from 4 to 5 days for moderate TBI, and from 8 to 14 days in patients with severe TBI.
Instenon 2.0 * 3 rubles/day.
Cavinton 20 mg* 3 times a day.
Eufillin 2.4% - 10.0 * 3 rubles/day.
Piracetam 20% - 5.0 * 4r/day
Instenon 4 mg * 3 r/day.
Nimodipine 30 mcg/kg/hour for 5 days.*
Cerebrolysin 10.0 1 r/day intravenous administration, but if the patient is conscious, the enteral route of administration is also possible. As a rule, two drugs with different mechanisms of action are prescribed simultaneously depending on the patient’s condition (age, blood pressure, etc.).
If necessary, change medications after 7-10 days. *Note: In the absence of high intracranial pressure, nimodipine can apparently be used in acute period
TBI.
When prescribing it, careful hemodynamic monitoring should be carried out.
In case of developed akinetic state
(functional decortication, akinetic mutism), vegetative state, additionally selegeline hydrochloride (Yumex) 5 mg * 2 times a day.
From the second to third days (from the start of treatment), the dose of the drug is increased to 20 mg/day. If there is no effect within 4 - 5 days, then additionally calypsol (ketalar) 1 mg/kg IM 1 time per day. If necessary, the administration of calypsol is repeated once every three days.
In the absence of selegelin hydrochloride (Yumex), levodopa preparations (Nakom, Sinemet, etc.) are used - 1.0 - 4.0 per day, however, the clinical effectiveness of drugs in this group is noticeably lower, and the frequency of side effects is higher.
In the presence of symptoms of “irritation”
(convulsive syndrome, vegetative crises) predominantly use sedative therapy: benzonal 0.1 - 0.2 * 1 - 2 times / day, aminazine 12 - 50 mg * 3 times / day IM (for psychomotor agitation), Relanium 10 mg * 2 - 3 r/day IM.
etc. The dose of the drug and their combination must be selected individually.
For movement disorders, galantamine 5 - 10 mg 2 r/day, i.v., i.m., if not, then proserin 0.5 - 1 mg i.v., i.m., * 3 r/day. if not, then proserin 0.5 - 1 mg IV, IM, * 3 times a day. 6. INCREASED INTRACRANIAL PRESSURE. THERAPY.
Manifestations
A. Nonspecific signs:
2. Herniation of the medial parts of the temporal lobe occurs with damage to the lateral supratentorial localization and consists of displacement of the medial parts of the temporal lobe through the notch of the cerebellar tentorium. The resulting pressure on the structures of the midbrain is manifested by: (1) impaired consciousness;
(2) a dilated pupil that does not respond to light on the side of the herniation, which is associated with compressed III cranial nerve;
(3) hemiparesis on the opposite side. The movements of the eyeballs are not always impaired.
3. Herniation of the cerebellar tonsils is caused by pressure pushing the inferior portion of the cerebellum through the foramen magnum, resulting in compression of the medulla oblongata.
It causes:
(1) disturbances of consciousness and (2) disturbances in breathing rhythm or apnea.
INDICATIONS FOR ANTI-EDEMEEDIC THERAPY:
with the development of dislocation syndromes.
on the operating table at the request of the surgeon.
with an increase in intracranial pressure more than 200 mm. rt.
Art.
with rapid (within several hours) deterioration of neurological symptoms.
6.1 Mannitol (mannitol) is administered quickly (in 15 - 20 minutes) at the rate of 1 g/kg body weight. After this, it is administered 3 - 4 times a day at the rate of 0.25 - 0.3 mg/kg.
If the effect is insufficient or hydrocephalus, Lasix 1 mg/kg is additionally used, if necessary, 2-3 times a day. If osmolarity is >320 mOsm/L, do not use osmodiuretics.
6.2 If there is no effect from this therapy, transfer of the patient to mechanical ventilation and administration of sodium thiopental is indicated, as indicated in section 4.1. But in this case, the first (loading dose) of sodium thiopental is increased to 8 - 10 mg/kg.
6.3 CSF drainage through a ventricular catheter is indicated for hydrocephalus. But it is not always feasible and increases the risk of purulent complications.
6.4 Moderate hypothermia (31 - 330 C), performed over several hours, is quite effective, but requires special equipment and is not yet available.
6.5 In the most severe cases: with rapid deterioration of neurological symptoms (hours and minutes) and the absence of effect from therapy with other methods, if it is impossible to use other methods (for example, low systemic blood pressure), hypertonic sodium chloride solution can be used.
Sanitation and diagnostic fibrobronchoscopy. Inspection of the trachea is mandatory - bronchial tree in the first hours after injury. The frequency of bronchoscopy during mechanical ventilation is determined individually; they are re-assigned as the broncho-obstructive syndrome progresses.
2. Turn in bed every two hours.
3.Toilet oral cavity every six hours.
4. If there is purulent discharge from the endotracheal tube or tracheostomy, introduce antibiotics and antiseptics into it.
5. A tracheostomy is indicated if, a week after intubation, the patient cannot independently and voluntarily cough up sputum. Tracheostomy is indicated early if the expected duration of impaired consciousness exceeds 2 weeks.
8. TRAUMATIC MENINGITIS,
Occurs more often on days 2 and 6 from the moment of injury. For diagnosis, subarachnoid puncture and cerebrospinal fluid bacterioscopy are indicated. Start treatment immediately after diagnosis!
For traumatic meningitis, if you have not previously received treatment:
Penicillin 3.0 * 12 r/day i.v. + cephalosporins third generation, for example, cefotaxime (claforan) 2.0 * 6 r/day or ceftriaxone 2.0 * 2 r/day i.v. + gentamicin 0.2 mg/kg or kanamycin 2 mg/kg subarachnoidally.
If there is no effect from the indicated therapy within two days, consider the possibility of using one or more of the following drugs: meronem or tienam 4 - 6 g / day, dioxidine 1.0 - 1.2 g / day, ciproflosacin 1.2 - 1 .8 g/day. For penicillin-resistant coccal microflora - rifampicin 0.9 - 1.2 g / day or vancomycin 3 - 4 g intravenously. The daily dose of all these drugs is administered intravenously in 3 to 4 injections.
Amikacin 1 mg/kg or brulamycin 0.2 mg/kg is administered subarachnoidally.
Additionally: Metrogyl 500 mg * 4 times a day IV - if an anaerobic infection is suspected, if there is a brain abscess.
ATTENTION!
do not inject penicillin subarachnoidally (severe convulsive syndrome very often develops).
perform subarachnoid punctures daily (for severe meningitis), or every other day (for stable positive dynamics), until the cerebrospinal fluid is sanitized.
9. FEATURES OF PATIENT MANAGEMENT FOR SOME NEUROSURGICAL INTERVENTIONS
after operations associated with craniotomy for TBI with preserved consciousness (in patients without signs of severe brain contusion, cerebral hypertension) - depressed fracture, vault fracture, epi and subdural hematomas in early stage small volume, etc.
Extubate the patient against the background of fully restored consciousness, usually no earlier than 2 hours after the end of the intervention.
IN postoperative period do not use narcotic analgesics.
If necessary (combined injury), it is allowed to use them in reduced doses, organizing continuous monitoring of the patient. Use 0.9% solution sodium chloride
to replenish daily fluid losses.
The patient should be in bed with the head end elevated.
Please enable JavaScript to view the One of the most common and severe forms of damage nervous system
is . Victims often become temporarily disabled or disabled for life. Therefore, in addition to treatment, rehabilitation after a traumatic brain injury is very important. IN complex treatment each method performs its own tasks. The goals of treatment are to eliminate the consequences of injury and prevent complications. Restoration tasks include: strengthening general condition
, elimination of muscle weakness, adaptation to physical activity.
Treatment of the head after TBI Before treating a traumatic brain injury, the severity of the patient’s condition and tissue damage are determined. There are open and closed damage skulls In turn, open injuries can be penetrating or non-penetrating. TO closed injuries
include bruises and concussions. In each individual case, patients are prescribed treatment. Patients are given rest and bed rest for up to three days. If there are no complications, the patient is observed in an outpatient hospital for up to 6 days. Drug treatment
head after injury comes down to prescribing painkillers, sedatives and sleeping pills, multivitamins, and antihistamines. Patients are given a glucose solution with ascorbic acid , calcium chloride, diphenhydramine. At stressful situations The patient is prescribed tranquilizers. Even with mild degree
In case of brain contusion, before treatment, the localization of focal lesions is determined using MRI and CT. Patients are prescribed the same as for a concussion. Therapy includes decongestants and medications that improve blood flow.
If small focal hemorrhages are detected in a patient, the goals of therapy include:
- elimination of edema;
- improved blood circulation;
- increasing energy supply to the brain;
- improvement metabolic processes in brain tissue.
Patients are prescribed medications for traumatic brain injury that effectively cope with the assigned tasks. Severe bruises with destruction of brain tissue are treated according to the same principles as moderate bruises, but with the inclusion of intensive care. In severe condition of the patient, artificial ventilation is indicated. If a patient experiences compression of the brain due to injury, the following treatment measures are carried out:
- surgical intervention for increasing compression;
- restoration of patency respiratory tract(intubation, ventilation on a ventilator);
- prevention of intracranial pressure (Manitol, Lasix);
- analgesia();
- fight against fever (Amidopyrine);
- intense infusion therapy(intravenously up to 3-4 liters of solutions);
- prescription of nootropic drugs;
- carrying out spinal taps for the purpose of sanitizing the cerebrospinal fluid.
When treating a brain injury, if the patient is in serious condition, great importance has the prevention of pneumonia. For patients on mechanical ventilation, tracheal sanitation using proteolytic enzymes (Trypsin) is indicated. Patients are in the hospital until doctors restore acute disorders of the nervous system. In severe cases, patients are given disability.
Patient recovery methods
Rehabilitation after a head injury is divided into periods. At the early stage, which lasts up to 5 days, everything is limited physical exercise. For seriously ill patients, exercises are recommended with the help of a massage therapist or rehabilitator. The subsequent period lasts about a month. The complex includes breathing exercises, massage and independent movements.
Advice! The main place is occupied by independent exercises to restore muscle endurance and breathing exercises.
During the recovery phase, patients are taught to stand and walk. Patients learn again to correctly distribute body weight on both legs and move their legs. Rehabilitation specialists focus on recovery vestibular apparatus. Patients bend and turn their heads.
In residual rehabilitation period patients perform a course of exercises on simulators. To restore everyday skills, occupational therapy and massage are indicated. The goal of rehabilitation measures is to restore blood supply to paretic muscles.
Thanks to adequate treatment and rehabilitation, recovery from a head injury is much more efficient and faster. Patients with disabilities return to everyday or work processes and recover faster personality traits after severe injuries and adapt to new living conditions.
Attention!
A specialist from an Israeli clinic can advise you -
Mild injuries (according to GCS) are observed in 80% of patients with TBI brought to the department emergency care. If the loss of consciousness was short or did not occur, if vital functions are stable, normal on CT, normal cognitive and neurological status, then such patients can be discharged home with recommendations for relatives about the need for home monitoring of the condition of the victims for 24 hours. Relatives are warned about the need to return the patient to the hospital if: disturbances of consciousness appear; focal neurological symptoms; increased headache; vomiting or deterioration of cognitive function.
Patients with minimal or no neurological changes but minor changes on CT should be admitted to the hospital and observation and repeat CT are indicated.
Treatment of moderate to severe traumatic brain injury
Moderate injuries occur in an average of 10% of patients with traumatic brain injury presenting to the emergency department. They often do not require intubation and mechanical ventilation (in the absence of other injuries) or monitoring of intracranial pressure. However, due to the possibility of deterioration, these patients should be hospitalized and monitored, even in the absence of changes on CT.
Severe injuries occur in 10% of patients with traumatic brain injury presenting to the emergency department. They are hospitalized in the intensive care unit. Because airway protective reflexes are typically depressed and intracranial pressure is elevated, such patients are intubated while measures are taken to reduce intracranial pressure. Dynamic observation using GCS and determining the reaction of the pupils, repeated CT is necessary.
Increased intracranial pressure
Patients with traumatic brain injury who require airway management or mechanical ventilation are intubated orally because nasal intubation is more likely to increase intracranial pressure. To minimize the increase in intracranial pressure during intubation using this method, appropriate medications should be used, for example, some experts recommend intravenous lidocaine at a dose of 1.5 mg/kg 1-2 minutes before the administration of muscle relaxants. Suxamethonium chloride is usually used as a muscle relaxant at a dose of 1 mg/kg intravenously. Good choice Etomidate is considered for induction anesthesia, since its effect on blood pressure is minimal (the dose for adults is 0.3 mg/kg or 20 mg for an average-sized adult; for children - 0.2-0.3 mg/kg). Alternatively, if hypotension is not present and hypotension is unlikely, propofol is available at a dose of 0.2 to 1.5 mg/kg during intubation.
The adequacy of oxygenation and ventilation is assessed by blood gas composition and pulse oximetry (if possible, also the end-tidal CO2 concentration). The goal is to maintain normal p (38-42 mmHg). In the past, prophylactic hyperventilation (p 25 to 35 mm Hg) was recommended. However, although low p reduces intracranial pressure by narrowing cerebral vessels, this in turn reduces intracerebral blood supply and can cause ischemia. In this regard, hyperventilation is used only in the first hours to combat increased intracranial pressure, which cannot be corrected by other methods, only up to p from 30 to 35 mm Hg. and within a short time.
For patients with severe traumatic brain injury who do not follow simple commands, especially those with CT abnormalities, dynamic monitoring and monitoring of intracranial pressure and IVD are recommended. The main goal is to maintain intracranial pressure
Preventing agitation, excessive muscle activity (eg, delirium), and pain will also help prevent increased intracranial pressure. For sedation of adults, propofol is more often used, due to the rapid development and rapid cessation of its action (dose 0.3 mg/kg per hour continuously intravenously, titrated to 3 mg/kg per hour), a loading bolus is not necessary. Possible by-effect- arterial hypotension. Benzodiazepines (eg, midazolam, lorazepam) are also used for sedation. Antipsychotic drugs slow down awakening and should be avoided if possible. For delirium, haloperidol can be used for several days. If delirium persists, trazodone, gabapentin, valproic acid, or quetiapine can be used, although it is not clear why these drugs are better than haloperidol. Occasionally, muscle relaxants may be required; in such cases, adequate sedation must be provided, since it will not be possible to assess excitability clinically in these conditions. Opioid analgesics are often required for adequate analgesia.
It is necessary to maintain normal circulating blood volume and osmolarity, although a slight increase in the latter is acceptable (target plasma osmolarity ranges from 295 to 320 mOsm/kg). To reduce intracranial pressure and maintain plasma osmolarity, intravenous osmotic diuretics (for example, mannitol) are prescribed. However, this measure should be reserved for patients whose condition worsens, as well as in the preoperative period for victims with hematomas. A 20% solution of mannitol is administered at a dose of 0.5-1.0 g/kg over 15-30 minutes, repeating the administration at a dose of 0.25-0.5 g/kg as often as required by the clinical situation (usually up to 6 times within 8 hours). This reduces intracranial pressure for several hours. Mannitol should be used with great caution in patients with severe coronary artery disease, cardiac and renal failure or venous stagnation in the lungs, since mannitol can very quickly increase intravascular volume. Because osmotic diuretics increase fluid excretion relative to Na + ions, long-term use of mannitol may lead to fluid depletion and hypernatremia. Furosemide at a dose of 1 mg/kg intravenously also helps reduce general content fluids in the body, especially if it is necessary to avoid temporary hypervolemia associated with the use of mannitol. Water and electrolyte balance should be monitored, primarily when using osmotic diuretics. As alternative remedy 3% saline solution is being studied to control intracranial pressure.
Hyperventilation (i.e., CO2 30 to 35 mm Hg) may be necessary for very short periods of time when increased intracranial pressure does not respond to standard treatment. Alternative method For the treatment of traumatic brain injury, which is accompanied by intractable high intracranial pressure, decompression craniotomy remains. During this intervention, a bone flap of the calvarium is removed (which is subsequently returned) and dura plastic surgery is performed. meninges, allowing swelling to spread beyond the skull.
Another treatment for traumatic brain injury is pentobarbital coma. Coma is induced by administering pentobarbital at a dose of 10 mg/kg over 30 minutes, then 5 mg/kg per hour for up to 3 doses, then 1 mg/kg per hour. The dose can be adjusted to slow the burst of EEG activity, which must be continuously monitored. Hypotension occurs frequently and is treated with fluids or, if necessary, vasopressors.
The effectiveness of therapeutic systemic hypothermia has not been proven. Glucocorticoids are useless for controlling intracranial pressure. In recent international research worsening outcomes were found with their use.
Treatment of traumatic brain injury and seizures
Prolonged seizures, which can worsen brain damage and increase intracranial pressure, should be prevented and stopped as soon as possible when they occur. Patients with significant structural injuries (eg, major contusions or hematomas, brain injuries, depressed skull fractures), or
Treatment of traumatic brain injury due to skull fracture
Closed skull fractures without displacement do not require specific treatment. For depressed fractures, surgery is sometimes indicated to remove bone fragments, ligation of damaged vessels of the cerebral cortex, restoration of the dura mater, processing of brain tissue. At open fractures surgical treatment is indicated. The use of antibiotic prophylaxis is controversial due to the limited amount of data on its effectiveness and due to the problem of the emergence of antibiotic-resistant strains of microorganisms.
Surgical treatment of traumatic brain injury
For intracranial hematomas, the spilled blood is surgically evacuated. Rapid evacuation of the hematoma can prevent or eliminate displacement and compression of the brain. However, many hematomas do not require surgical intervention, including small intracerebral hematomas. Patients with small subdural hematomas can also often be treated without surgery. Indications for surgical treatment serve:
- displacement of the brain from the midline by more than 5 mm;
- compression of the basal cisterns;
- progression of neurological symptoms.
Chronic subdural hematoma may require surgical drainage, but its urgency is significantly lower than in acute cases. Large or arterial hematomas are treated surgically, but small venous epidural hematomas can be monitored dynamically using CT.
First aid to a victim with a traumatic brain injury consists of making him comfortable. horizontal position with his head slightly raised.
If the person who has received a TBI continues to be unconscious, the so-called rescue position is preferable - on the right side, with the head thrown back or turned to the ground, left hand and the leg is bent at a right angle at the elbow and knee joints(you must first exclude fractures of the limbs and spine).
This position, ensuring the free passage of air into the lungs and the unhindered flow of liquid from the mouth to the outside, prevents breathing problems due to the retraction of the tongue, the flow of saliva, blood, and vomit into the respiratory tract.
All victims with a traumatic brain injury, even if it seems mild from the very beginning, must be transported to an emergency hospital, where the diagnosis is clarified.
The basis of treatment tactics in patients with traumatic brain injury should be, first of all, the data of an objective examination, and not the very fact of a traumatic brain injury suffered by the patient.
Conservative symptomatic treatment is carried out when the patient has:
Brain concussion;
Mild brain contusion;
Moderate to severe brain contusion without signs of brain compression;
Diffuse axonal damage to the brain substance.
In the case of minor injuries that occur with a picture of a concussion, treatment is purely individual.
Drug treatment for concussion should not be aggressive.
It is aimed mainly at normalizing the functional state of the brain, relieving headaches, dizziness, anxiety, insomnia and other complaints.
Conservative treatment severe forms Traumatic brain injuries (severe brain contusion, diffuse axonal brain damage) has its own characteristics and should be carried out in specialized neurosurgical hospitals, in intensive care units.
Principles of conservative treatment of mild traumatic brain injuries:
Bed rest depending on the course of the disease;
Symptomatic treatment of headaches;
Prescription of tranquilizers;
Normalization of cerebrospinal fluid pressure;
Vagosympathetic blockade or blockade of the vertebral artery;
Appointment for 5-7 days nootropic drugs, vitamins, vascular drugs.
The impact of a traumatic agent is the trigger for a complex of pathogenetic mechanisms, which mainly boil down to disturbances in neurodynamic processes, disorders of tissue respiration and energy metabolism, changes in cerebral circulation in combination with hemodynamic restructuring, homeostatic reactions of the immune system and the subsequent development of autoimmune syndrome. The complexity and diversity of TBIs resulting from pathological processes, which are closely intertwined with the processes of adaptation and compensation of impaired functions, force conservative treatment of TBI to be carried out differentiatedly, taking into account the clinical form of the lesion, age and individual characteristics of each victim.
For concussion(SHM), the pathogenesis is based on temporary functional disorders of the central nervous system, in particular its autonomic centers, which leads to the development of asthenovegetative syndrome. This determines treatment tactics aimed at reducing the dysfunction of individual groups of neurons and restoring their functional synergy. In the treatment of concussion as the most light form traumatic brain injury doctors medical institutions the seriousness of its consequences is often underestimated, which leads to a persistent asthenovegetative state and impaired liquor dynamics.
The complex of therapy for patients with concussion includes mandatory for 7-10 days in combination with sedative treatment, which consists of prescribing drugs that prolong physiological sleep (andante, etc. ) in the afternoon and at night. Dosage regimen The duration of therapy should not exceed 2 weeks. The drug should be taken orally immediately before going to bed, 2 hours after eating, or after the patient feels that he cannot fall asleep. Recommended dose for adults- 10 mg. Maximum daily dose 10 mg (the patient must be warned about the dangers of taking a repeated dose within one night). For elderly people, the drug is prescribed at a dose of 5 mg (due to greater sensitivity to sleeping pills).
A hypnotic drug of the pyrazole-pyrimidine type, its chemical structure differs from benzodiazepines and other hypnotics. Significantly reduces the latent time of falling asleep, prolongs sleep time (in the first half of the night), does not cause changes in the ratio of different phases of sleep. When used at a dose of 5 mg and 10 mg for 2-4 weeks, it does not cause pharmacological tolerance. Except
In addition, it has a sedative, slightly expressed anxiolytic, anticonvulsant and central muscle relaxant effect. Excites benzodiazepine receptors (ω) of GABA type A receptor complexes. Interaction with ω receptors leads to the opening of neuronal ionoform channels for chlorine ions, the development of hyperpolarization and increased inhibition processes in the central nervous system.
The main clinical symptom of traumatic brain injury is headache. A large number of medications are used to relieve headaches. The prescription of painkillers should be made taking into account the cerebrospinal fluid pressure. For example, with increased cerebrospinal fluid pressure, the administration of citramone containing caffeine is inappropriate.
In the treatment of concussion, the use of glutamic acid, picamilon (0.5 g orally 3 times a day), which is an amino acid that is oxidized directly in the brain and takes part in the regulation of oxidative metabolism. It promotes the release of mediators (adrenaline) and exhibits pronounced depolarizing properties. The drug has proven itself to be effective in the treatment of concussions. Mexidol. The mechanism of action of the drug is determined primarily by its antioxidant properties, the ability to stabilize cell biomembranes, activate the energy-synthesizing functions of mitochondria, modulate the functioning of receptor complexes and the passage of ionic currents, enhance the binding of endogenous substances, improve synaptic transmission and the interconnection of brain structures.
Thanks to this mechanism of action, the drug has cerebroprotective, nootropic, antihypoxic, tranquilizing, anticonvulsant, anti-alcohol, anti-stress and vegetotropic effects. In addition, it has the ability to improve cerebral circulation and inhibit platelet aggregation. Mexidol increases the body's resistance to the action of various extreme damaging factors, such as hypoxia, ischemia, and various intoxications. Mexidol has a clear antihypoxic and anti-ischemic effect. For concussion, it is used in the dosage: 100-250 mg (2-5 ml) IV or IM 2-3 times a day for 10-15 days, then 125-250 mg (1-2 tablets) 3 times a day 2-4 weeks.
The criteria for expanding the regime should be the stabilization of autonomic reactions, the disappearance of headaches, dizziness (Betaver - orally, 8–16 mg 3 times a day. ) normalization of sleep and appetite.
Considering the fact that cerebrospinal fluid pressure during a concussion is increased in 19-20% of cases, decreased in 25% and normal in 55%, upon admission to the hospital the patient must undergo a lumbar puncture, which makes it possible to determine the level of intracranial pressure and choose the right therapy. In this case, manometric measurement of cerebrospinal fluid pressure is required and its result recorded in the medical history.
For hypertension, prescribed orally lasix (furosemide) 40 mg 1 time per day or veroshpriron 1 tablet. 1 time per day.
With low blood pressure, intravenous administration of isotonic solutions (saline solution 0.9%, glucose solution 5%) 500 - 600 ml is necessary once a day for three to four days. The duration of inpatient treatment for a concussion is 1-2 weeks, followed by outpatient observation for 7-10 days.
In case of a concussion, the complex of treatment measures should include the so-called reflex-drug therapy - carrying out novocaine blockades - vagosympathetic node, sympathetic plexus of vertebral arteries via posterior access, etc.). This is especially important when patients receive craniocervical brain injury. The cause of this type of combined traumatic brain injury is the extensor-flexion mechanism in cervical spine upon receipt of a traumatic brain injury. This mechanism of injury is most typical in road traffic accidents.
Mild to moderate brain contusions in contrast to a concussion, they are accompanied by morphological damage to blood vessels and (or) the substance of the brain, which is manifested by focal neurological symptoms of varying intensity, subarachnoid and intracerebral hemorrhage, as well as fractures of the bones of the vault and (or) the base of the skull. Subarachnoid hemorrhage, even the slightest, leads to vascular spasm, which, in turn, contributes to brain hypoxia with metabolic disorders and edema-swelling of brain tissue. General cerebral symptoms of mild traumatic brain injury are more intense and persist longer than with a concussion, which determines the timing of drug therapy.
The complex of therapy for patients with brain contusion also includes mandatory bed rest for 10-12 days in combination with sedative treatment, which consists of prescribing drugs that prolong physiological sleep (andante, (zaleplon) etc.). The recommended dose for adults is 10 mg. Elderly people – 5 mg. Take orally just before bedtime, preferably in bed. Duration of treatment: no more than 2 weeks.
Upon admission to the hospital, the patient must undergo echoencephaloscony before diagnostic procedures, and after that a lumbar puncture to determine cerebrospinal fluid pressure and the presence of subarachnoid hemorrhage. Lumbar punctures must be performed every three to four days before sanitizing the cerebrospinal fluid.
To relieve vascular spasm, which in mild traumatic brain injury causes transient neurological focal symptoms, it is used stugerone (cinnarizine), papaverine, aminophylline in therapeutic doses along with. The rapid elimination of vascular spasm and the removal of spilled blood reduce the exposure of brain antigens to immunocompetent blood cells, which reduces the influence of the antigenic stimulus and reduces the intensity of the immune response. The autoimmune process either does not develop or is less intense. This is also facilitated by the administration of antihistamines and desensitizing agents in therapeutic dosages for 1-1.5 weeks.
IN Lately For the treatment of brain contusions of varying severity, especially those accompanied by subarachnoid hemorrhage, the drug Cerebrolysin is widely used.
Cerebrolysin contains low molecular weight biologically active neuropeptides that penetrate the blood-brain barrier and directly enter nerve cells. The drug has an organ-specific multimodal effect on the brain, i.e. provides metabolic regulation, neuroprotection, functional neuromodulation and neurotrophic activity.
Cerebrolysin protects neurons from the damaging effects of lactic acidosis, prevents the formation of free radicals, increases survival and prevents neuronal death under conditions of hypoxia and ischemia, and reduces the damaging neurotoxic effect of excitatory amino acids (glutamate).
In acute conditions (ischemic stroke, traumatic brain injury, complications of neurosurgical operations), Cerebrolysin is recommended to be administered as drip infusions in a daily dose of 10-60 ml in 100-250 ml of saline solution for 60-90 minutes. Course duration is 10-25 days. According to the study Koenig et al , 2000 the greatest effect of treatment is achieved when using Cerebrolysin 50 ml IV in 50 ml NaCl 6 hours after injury. The duration of treatment should be up to 21 days
Dehydration for traumatic brain injury is carried out depending on the magnitude of intracranial pressure and consists of using lasix(0.5-0.75 mg/kg) parenterally or orally, glycerin(70-75 ml) orally. The criterion for effectiveness is diuresis of 1.5-2 liters caused by taking this saluretic. Glycerol at a dose of 1-1.5 g/kg reduces intracranial pressure by 50-120 mmH2O. Art. for a period of 3-3.5 hours. By alternating the use of this drug with Lasix, you should achieve a uniform hypotensive effect throughout the day. When carrying out dehydration, it is necessary to remember that in elderly patients, in 20-30% of cases in the acute period, liquor hypotension is noted. This point emphasizes the importance of lumbar puncture for determining treatment tactics.
According to the combination of pathogenetic factors, a moderate brain contusion does not differ from a mild brain contusion, however, persistent focal disorders, more pronounced cerebral symptoms and autonomic disorders indicate a very significant intensity of pathogenetic disorders, which strongly dictates the need for careful monitoring of the patient’s condition and more active therapy . Characteristic feature moderate brain contusion is the instability of compensation in the acute period and the possibility of worsening disorders if therapy is not started in a timely manner or is inadequate. In case of moderate brain contusion, morphological damage to the structure of the latter and massive subarachnoid hemorrhage leads to the penetration of proteolytic enzymes through the blood-brain barrier, which leads to worsening of neurological symptoms and the condition of patients. Therefore, even with this form of damage, the use of protease inhibitors is indicated ( kontrikal, gordoks, trasylol), which help reduce permeability vascular wall and brain capillaries. Currently most widely used for this purpose kontrikal 10,000 units 3 times a day per 150 ml of 5% glucose solution intravenously for 4-6 days. For moderate brain contusion, it is more advisable to use glutamic acid in the form of a 1% solution, administered 400 ml intravenously once a day. If consciousness is preserved, instead of aminalon, nootropil is prescribed in capsules of 0.4 g 3-4 times a day, and if consciousness is impaired, piracetam (5 ml of a 20% solution 2 times a day intravenously).
Dehydration therapy is enhanced by administering 10 ml of a 2.4% solution of aminophylline in combination with Lasix (20-40 mg) intravenously up to two times a day. Such stimulation of diuresis creates a favorable gradient in the system: tissue - interstitial space - blood.
Currently, approaches to prescribing physiotherapeutic procedures for traumatic brain injury have also changed.
The difficulties of a targeted and systematic search for specific effects of therapeutic factors of physiotherapeutic procedures led to an exaggeration of the principles of the universality of the use of any physical factors used in physiotherapy for various diseases, the unity of the mechanisms of therapeutic and preventive action of natural and artificial physical factors that dominated in physiotherapy of the 20th century. Meanwhile, doctors are well aware that physical factors in various diseases have unequal physiotherapeutic effectiveness. The unequal nature of diseases suggests a combination of different pathogenetic variants (syndromes).
Based on this, the body’s reactions to the physical factor of a physiotherapeutic procedure are specific to a certain state of the body, although medicinal effects sometimes develop on the basis of general (nonspecific) reactions of the body.
Such specificity requires a targeted selection of a physiotherapy factor and a method of its application, which constitutes the essence of the pathogenetic effect of therapeutic physical factors. Under these conditions, following the principles of “universality” and the imaginary “unity” of the mechanisms of the therapeutic effects of physiotherapy practically deprives the doctor of the opportunity to optimally select therapeutic physical factors. It is difficult to draw the line between the specific and nonspecific effects of many therapeutic factors in physiotherapy. Many of them have several effects, expressed to varying degrees, so it is better to focus on the dominant therapeutic effect.
Physical treatment methods are aimed at improving cerebral hemodynamics (vasodilating, hypocoagulating methods), activating the metabolism of nervous tissue and its functional properties (enzymatic stimulating methods), correcting the consequences of injuries (psychostimulating methods), increasing body tone (tonic methods) and reducing high blood pressure cerebrospinal fluid (diuretic methods).
Vasodilator methods: galvanization And drug electrophoresis vasodilators and stimulators of cerebral circulation. (actovegin, instenon, potassium hydroxide, aminophylline, aminazine, etc.)
Enzyme-stimulating methods: drug electrophoresis metabolism stimulants, air baths, transcerebral UHF therapy, IR laser therapy.
Diuretic methods: low intensity DMV therapy, sodium chloride baths.
Hypocoagulating method.LOC.
Psychostimulating method: oxygen baths.
Sedatives: Darsonval currents, Faraday currents on the head, electrosleep, massage of the collar area, cervical region.
Clinical picture of severe brain contusion is caused by the involvement of subcortical formations and the brain stem in the pathological process, which is manifested by the predominance of diencephalic and mesencephalobulbar syndrome. In this regard, the scope of therapeutic measures is expanding significantly and should be aimed primarily at eliminating pathological factors that are crucial in the chain of pathogenesis. In this case, pathogenetic therapy should be carried out simultaneously with symptomatic correction of systemic hemodynamics and respiration. In the complex of therapeutic measures for brain contusion, the prescription of Mexidol. Studies have shown that Mexidol has a cerebral vasodilatory effect, reduces cerebral vascular resistance, significantly increases pulse fluctuations of cerebral vessels and promotes hemodynamic changes that improve blood outflow into the brain. venous system without having a significant effect on systemic blood pressure. In patients with TBI who received Mexidol, there was a significant regression of consciousness disorders when assessed by GCS. The functions of the motor sphere were restored much faster and more clearly, at an earlier time, and positive dynamics were observed in the restoration of coordination, mnestic and cognitive functions. Mexidol had a positive effect on patients with vestibular disorders, reducing uncertainty when walking, non-systemic dizziness, and reflexes of oral automatism regressed faster. For brain contusion, the therapeutic dosage is usually as follows: 200-500 mg (4-10 ml) intravenously in a stream or drip 1-2 times a day for 10-15 days. Subjective and objective positive effects during treatment with Mexidol are usually observed by the end of the week after the start of therapy.
If peripheral breathing is impaired, the airway is restored and the trachea is intubated with an endotracheal tube for up to 3 days. In the future, if adequate breathing is not possible, a tracheostomy should be performed. Violation of the central regulation of breathing in most cases requires transfer to artificial ventilation until the normal rhythm of respiratory movements is restored. Considering the development of the so-called “shock lung” syndrome in victims with TBI, special importance must be given to measures aimed at preventing aspiration pneumonia, the development of which is very likely against the background of this syndrome. Most effective in these cases percussion massage chest, vibration massage followed by aspiration of the contents of the tracheobronchial tree, soda inhalation to alkalize the acidic contents entering the lungs from the stomach and oropharynx, as well as inhalation of proteolytic enzymes and phytoncides at least 4-6 times a day. In cases of massive aspiration with atelectasis, sanitation bronchoscopy is indicated. In specialized institutions, in the presence of an experienced anesthesiologist, a high (at the level of II-VI thoracic segments of the spinal cord) long-term epidural blockade (5 ml of 2% lidocaine solution) is advisable 4-6 hours after the admission of the patient with TBI within 24-48 hours (not more!). This method is effective in preventing shock lung syndrome, but its implementation requires certain experience of doctors and nurses. Treatment of systemic hemodynamic disorders should be carried out according to the principle “from simple to complex”, since iatrogenic errors in the treatment of victims with severe brain contusion are fraught with serious consequences.
Elimination of hypovolemia by intravenous administration of large molecular dextrans (400 ml polyglucin), reogluman and hemodez, As a rule, it helps stabilize blood pressure. For the same purpose, a solution of mannitol on polyglucin has proven itself well: 30 g of mannitol and 400 ml of polyglucin (Uvarov B.S. et al., 1983). Instability of blood pressure with a full plasma volume of the bcc indicates a decrease in vascular tone, with dysfunction of the vasomotor center as a result of reversible hypoxic changes or morphological damage. This condition is relieved by administering 50 mg of a 5% solution of ephedrine, as the most mildly acting vasopressor (15 mg intravenously per 10 ml of 5% glucose solution and 35 mg intramuscularly). The absence or short-term effect of the above measures may indirectly indicate the development of acute adrenal insufficiency, and only then does the need for the use of corticosteroids arise. Fundamental in this sense is the use of a suspension of hydrocortisone, since only it contains a fraction of mineralocorticoids that determine the vascular effect of hormones. A more rare cause of disturbances in systemic hemodynamics is hypocapnia, which occurs as a result of hyperventilation when this technique is used to relieve cerebral edema. With severe intracranial hypertension, the increase in blood pressure is compensatory in nature - it is aimed at maintaining cerebral blood flow . Therefore, measures to lower blood pressure should be carried out with caution, since relative arterial hypotension can lead to an uncompensated decrease in cerebral blood flow, even to its cessation. The use of antihypertensive drugs should be accompanied by an adequate reduction in intracranial pressure, which in severe brain contusion reaches critical values (more than 350 mm H2O). In such cases, it is necessary to observe the principle of uniformity of dehydration therapy. In practice, this is carried out as follows: in the morning, during a lumbar puncture, 10-15 ml of liquid is withdrawn slowly (under a mandrin) for 10-15 minutes; after 2-3 hours, 10 ml of a 2.4% solution of aminophylline with Lasix (20 mg) is administered; after another 3-4 hours, an infusion of a 5-10% solution of mannitol (30-60 g) follows, after which, after 4-5 hours, the intravenous administration of Lasix and aminophylline is repeated, and at night 50-70 g of glycerin are given orally. If necessary, at 6-7 am, an additional 20 mg of Lasix is administered intravenously. The above dehydration scheme in most cases provides a sustainable decrease in intracranial pressure, which contributes to a spontaneous decrease in blood pressure to normal values. High arterial hypertension at a safe level of intracranial pressure can prevent the restoration of autoregulation of cerebral circulation. Therefore, it must be corrected by intramuscular injection of 0.5-1 ml of a 5% pentamine solution or 4-6 ml of a 0.5% dibazole solution. It should always be remembered that it is advisable to always precede the infusion of mannitol or another osmodiuretic with the administration of Lasix. This will avoid overload of the pulmonary circulation (pulmonary edema) as a result of transient hypervolemia and will promote unimpeded venous outflow from the cranial cavity. Intensive diuretic therapy leads to the rapid development of potassium deficiency in the patient's body, which must be compensated with a glucose-potassium-insulin mixture from Labori. This mixture consists of 400 ml of a 10% glucose solution with the addition of 10 units of insulin and a 5% potassium chloride solution so that the patient receives at least 3-4 g of potassium per day. In the absence of renal failure and abundant diuresis, there is no need to worry about hyperkalemia. Potassium ions, penetrating into brain cells, compete with sodium ions, which reduces the hydrophilicity of tissues. Reducing the spasmogenic effect of the sympathetic nervous system is achieved by blocking the stellate ganglion or sinocarotid zone with a 1% solution of novocaine up to 4 times a day. Reopolyglucin (400 ml) has a good therapeutic effect in the treatment of microcirculation disorders in the brain, the administration of which can be repeated twice a day. In case of diencephalic syndrome with a tendency to hyperergic reactions (high blood pressure, tachycardia, tachypnea, persistent hyperthermia), a neurovegetative blockade is necessary, the depth and duration of which depend on the severity of diencephalic-catabolic manifestations that occur on the 2-3rd day after a severe brain contusion and lasting for 4-6 days. For neurovegetative blockade, droperidol (5-10 mg), seduxen (10 mg), diphenhydramine (40 mg) and pyrroxan (10-20 mg), which are administered simultaneously intramuscularly or (less often) intravenously, are preferable. It is advisable to alternate the administration of this lytic mixture with the use of sodium thiopental (300 mg of a 10% solution intramuscularly up to 3 times a day). Without preventing the spread of excitation along the axons of neurons, they reduce the excitability of the cerebral cortex, reduce the brain's need for oxygen and at the same time increase the excretion of CO 2. Like other barbiturates, these drugs reduce lactate levels and restore the metabolism of buffer bases in the brain. If drug neurovegetative blockade is insufficient and hyperthermia persists, physical cooling is resorted to (drying wet tissues on the patient with a fan, applying ice packs) until body temperature decreases to a normal or subnormal level (36.5-37.5 C). Before starting physical cooling, it is advisable for the patient to intravenously administer 20 ml of a 20% solution of sodium hydroxybutyrate, 5 mg of droperidol and 50-100 mg of a 5% solution of nicotinamide. The use of prostaglandin inhibitors (acetylsalicylic acid, less commonly indomethacin), which help improve microcirculation in the brain and normalize thermoregulation, is also indicated. In case of hyperthermia of infectious origin, broad-spectrum antibiotics should be used, the route of administration of which (intramuscular, intravenous, endolumbar, intracarotid) depends on the type and severity of the inflammatory complication. Indications for surgical treatment for severe brain contusion arise in cases of intracranial hematomas, areas of crushing of the brain, pneumocephalus, depressed skull fractures, swelling and dislocation of the brain caused by the growth of an unremoved contusion focus. An effective method for the treatment and prevention of hypoxic conditions in severe brain contusion with areas of crushing of the cerebral hemispheres is hyperbaric oxygenation. It is most effective in patients with lesions of the diencephalic and mesencephalic parts of the brain stem of secondary origin. The optimal regime is a pressure of 1.5-1.8 atm for 25-60 minutes (for mesencephalic lesions 1.1-1.5 atm for 25-40 minutes). Contraindications to hyperbaric oxygenation in case of severe brain contusion are: unremoved intracranial hematoma, unresolved upper respiratory tract obstructions, bilateral pneumonia, severe epileptic syndrome, primary damage to the brain stem at the bulbar level and other individual contraindications established by a specialist (Kasumov R.D. et al., 1982). The period of inpatient treatment depends on the intensity of the recovery processes, the activity of rehabilitation measures and averages 1.5-2 months.
