Traumatic brain injuries rank first among all injuries (40%) and most often occur in people aged 15–45 years. The mortality rate among men is 3 times higher than among women. In large cities, every year out of a thousand people, seven receive traumatic brain injuries, while 10% die before reaching the hospital. In the case of a mild injury, 10% of people remain disabled, in the case of a moderate injury - 60%, severe - 100%.

Causes and types of traumatic brain injuries

A complex of injuries to the brain, its membranes, skull bones, soft tissues of the face and head is a traumatic brain injury (TBI).

Most often, participants in road accidents suffer from traumatic brain injuries: drivers, passengers of public transport, pedestrians hit by vehicles. In second place in terms of frequency of occurrence are household injuries: accidental falls, blows. Next come injuries sustained at work and sports.

Young people are most susceptible to injuries in the summer - these are so-called criminal injuries. Elderly people are more likely to get a TBI in the winter, and the leading cause is a fall from a height.

Statistics
Residents of Russia most often suffer a TBI while intoxicated (70% of cases) and as a result of fights (60%).

One of the first to classify traumatic brain injuries was the 18th century French surgeon and anatomist Jean-Louis Petit. Today there are several classifications of injuries.

• by severity: light(concussion, slight bruise), average(serious injury) heavy(severe brain contusion, acute compression of the brain). The Glasgow Coma Scale is used to determine severity. The victim's condition is assessed from 3 to 15 points depending on the level of confusion, ability to open eyes, speech and motor reactions;
• by type: open(there are wounds on the head) and closed(no damage to the scalp);
• by type of damage: isolated(damage affects only the skull), combined(the skull and other organs and systems are damaged), combined(the injury was not only mechanical, the body was also affected by radiation, chemical energy, etc.);
• according to the nature of the damage:
• shake(minor injury with reversible consequences, characterized by a short-term loss of consciousness - up to 15 minutes, most victims do not require hospitalization, after examination the doctor may prescribe a CT or MRI);
• injury(a disruption of brain tissue occurs due to an impact of the brain on the wall of the skull, often accompanied by hemorrhage);
• diffuse axonal brain injury(axons - the processes of nerve cells that conduct impulses - are damaged, the brain stem suffers, microscopic hemorrhages are noted in the corpus callosum of the brain; such damage most often occurs in an accident - at the time of sudden braking or acceleration);
• compression(hematomas form in the cranial cavity, the intracranial space is reduced, crush areas are observed; emergency surgical intervention is required to save a person’s life).

Important to know
Brain injury most often occurs at the site of impact, but often damage occurs on the opposite side of the skull - in the impact zone.

The classification is based on the diagnostic principle; on its basis, a detailed diagnosis is formulated, according to which treatment is prescribed.

Symptoms of TBI

The manifestations of traumatic brain injuries depend on the nature of the injury.

Diagnosis « concussion » diagnosed on the basis of anamnesis. Typically, the victim reports that there was a blow to the head, which was accompanied by a short-term loss of consciousness and a single vomiting. The severity of the concussion is determined by the duration of loss of consciousness - from 1 minute to 20 minutes. At the time of examination, the patient is in a clear state and may complain of a headache. No abnormalities other than pale skin are usually detected. In rare cases, the victim cannot remember the events that preceded the injury. If there was no loss of consciousness, the diagnosis is considered doubtful. Within two weeks after a concussion, weakness, increased fatigue, sweating, irritability, and sleep disturbances may occur. If these symptoms do not disappear for a long time, then it is worth reconsidering the diagnosis.

At mild brain contusion And the victim may lose consciousness for an hour, and then complain of headache, nausea, and vomiting. Eye twitching when looking to the side and asymmetry of reflexes are noted. An X-ray may show a fracture of the bones of the skull vault, and blood in the cerebrospinal fluid.

Dictionary
Liquor - liquid transparent color, which surrounds the brain and spinal cord and also performs protective functions.

Moderate brain contusion severity is accompanied by loss of consciousness for several hours, the patient does not remember the events preceding the injury, the injury itself and what happened after it, complains of headache and repeated vomiting. The following may be observed: disturbances in blood pressure and pulse, fever, chills, soreness of muscles and joints, convulsions, visual disturbances, uneven pupil size, speech disturbances. Instrumental studies show fractures of the vault or base of the skull, subarachnoid hemorrhage.

At severe brain contusion the victim may lose consciousness for 1–2 weeks. At the same time, gross violations of vital functions (pulse rate, pressure level, frequency and rhythm of breathing, temperature) are detected. The movements of the eyeballs are uncoordinated, muscle tone is changed, the swallowing process is impaired, weakness in the arms and legs can reach convulsions or paralysis. As a rule, this condition is a consequence of fractures of the vault and base of the skull and intracranial hemorrhage.

This is important!
If you or your loved ones suspect that you have suffered a traumatic brain injury, you need to see a traumatologist and neurologist within a few hours and carry out the necessary diagnostic procedures. Even if it seems that you are feeling fine. After all, some symptoms (cerebral edema, hematoma) may appear after a day or even more.

At diffuse axonal brain damage a prolonged moderate or deep coma occurs. Its duration ranges from 3 to 13 days. Most victims have a respiratory rhythm disorder, different horizontal positions of the pupils, involuntary movements of the pupils, and arms with hanging hands bent at the elbows.

At compression of the brain Two clinical pictures can be observed. In the first case, there is a “light period”, during which the victim regains consciousness, and then slowly enters a state of stupor, which is generally similar to stupor and numbness. In another case, the patient immediately falls into a coma. Each condition is characterized by uncontrolled eye movements, strabismus, and cross-limb paralysis.

Long-term head compression accompanied by swelling of the soft tissues, reaching a maximum 2–3 days after its release. The victim is in psycho-emotional stress, sometimes in a state of hysteria or amnesia. Swollen eyelids, impaired vision or blindness, asymmetrical swelling of the face, lack of sensitivity in the neck and back of the head. A computed tomography scan shows swelling, hematomas, skull fractures, areas of brain contusion and crush injuries.

Consequences and complications of TBI

After suffering a traumatic brain injury, many become disabled due to mental disorders, movements, speech, memory, post-traumatic epilepsy and other reasons.

Even mild TBI affects cognitive functions- the victim experiences confusion and decreased mental abilities. More severe injuries may result in amnesia, impairment of vision, hearing, speech and swallowing skills. In severe cases, speech becomes slurred or even lost completely.

Disorders of motor skills and functions of the musculoskeletal system are expressed in paresis or paralysis of the limbs, loss of sensitivity of the body, and lack of coordination. In cases of severe and moderate injuries, there is failure to close the larynx, as a result of which food accumulates in the pharynx and enters the respiratory tract.

Some TBI survivors suffer from pain syndrome- acute or chronic. Acute pain syndrome persists for a month after injury and is accompanied by dizziness, nausea, and vomiting. Chronic headache accompanies a person throughout his life after receiving a TBI. The pain can be sharp or dull, throbbing or pressing, localized or radiating, for example, to the eyes. Attacks of pain can last from several hours to several days, intensifying during moments of emotional or physical stress.

Patients have a hard time experiencing the deterioration and loss of body functions, partial or complete loss of performance, and therefore suffer from apathy, irritability, and depression.

Treatment of TBI

A person who has suffered a traumatic brain injury needs medical attention. Before the ambulance arrives, the patient must be placed on his back or on his side (if he is unconscious), and a bandage must be applied to the wounds. If the wound is open, cover the edges of the wound with bandages and then apply a bandage.

The ambulance team takes the victim to the traumatology department or intensive care unit. There the patient is examined, if necessary, X-rays are taken of the skull, neck, thoracic and lumbar spine, chest, pelvis and limbs, an ultrasound of the chest and abdominal cavity is performed, and blood and urine are taken for analysis. An ECG may also be ordered. In the absence of contraindications (state of shock), a CT scan of the brain is performed. Then the patient is examined by a traumatologist, surgeon and neurosurgeon and a diagnosis is made.

The neurologist examines the patient every 4 hours and assesses his condition using the Glasgow scale. If the patient's consciousness is impaired, tracheal intubation is indicated. A patient in a state of stupor or coma is prescribed artificial ventilation. Intracranial pressure is regularly measured in patients with hematomas and cerebral edema.

The victims are prescribed antiseptic and antibacterial therapy. If necessary, anticonvulsants, analgesics, magnesia, glucocorticoids, sedatives.

Patients with a hematoma require surgery. Delaying surgery within the first four hours increases the risk of death by up to 90%.

Prognosis of recovery for TBI of varying severity

In the case of a concussion, the prognosis is favorable provided that the victim follows the recommendations of the attending physician. Full recovery of ability to work is observed in 90% of patients with mild TBI. In 10%, cognitive functions remain impaired and there are sudden changes in mood. But these symptoms usually disappear within 6–12 months.

The prognosis for moderate and severe forms of TBI is based on the number of points on the Glasgow scale. An increase in scores indicates positive dynamics and a favorable outcome of the injury.

In victims with moderate TBI, it is also possible to achieve complete restoration of body functions. But often headaches, hydrocephalus, vegetative-vascular dysfunction, coordination problems and other neurological disorders remain.

With severe TBI, the risk of death increases to 30–40%. Among survivors there is almost one hundred percent disability. Its causes are severe mental and speech disorders, epilepsy, meningitis, encephalitis, brain abscesses, etc.

Of great importance in returning the patient to an active life is the complex of rehabilitation measures provided to him after the acute phase has stopped.

Directions for rehabilitation after traumatic brain injury

World statistics show that 1 dollar invested in rehabilitation today will save 17 dollars to ensure the life of the victim tomorrow. Rehabilitation after TBI is carried out by a neurologist, rehabilitation specialist, physical therapist, occupational therapist, massage therapist, psychologist, neuropsychologist, speech therapist and other specialists. Their activities, as a rule, are aimed at returning the patient to a socially active life. The work to restore the patient’s body is largely determined by the severity of the injury. Thus, in case of severe injury, the efforts of doctors are aimed at restoring the functions of breathing and swallowing, and improving the functioning of the pelvic organs. Specialists are also working to restore higher mental functions (perception, imagination, memory, thinking, speech) that may have been lost.

Physical therapy:

• Bobath therapy involves stimulating the patient's movements by changing the positions of his body: short muscles are stretched, weak muscles are strengthened. People with mobility limitations get the opportunity to learn new movements and hone those they have learned.
• Vojta therapy helps connect brain activity and reflex movements. The physical therapist stimulates various areas of the patient's body, thereby encouraging him to perform certain movements.
• Mulligan therapy helps relieve muscle tension and pain-free movements.
• Installation "Exart" - suspension systems, with the help of which you can relieve pain and return atrophied muscles to work.
• Exercise classes. Classes are shown on cardio simulators, simulators with biofeedback, as well as on a stabilization platform - for training coordination of movements.

Occupational therapy- a direction of rehabilitation that helps a person adapt to environmental conditions. The occupational therapist teaches the patient to take care of himself in everyday life, thereby improving his quality of life, allowing him to return not only to social life, but even to work.

Kinesio taping- applying special adhesive tapes to damaged muscles and joints. Kinesitherapy helps reduce pain and swelling, without limiting movement.

Psychotherapy- an integral component of high-quality recovery after TBI. The psychotherapist carries out neuropsychological correction, helps to cope with apathy and irritability characteristic of patients in the post-traumatic period.

Physiotherapy:

• Drug electrophoresis combines the introduction of drugs into the victim’s body with the influence of direct current. The method allows you to normalize the state of the nervous system, improve blood supply to tissues, and relieve inflammation.
• Laser therapy effectively combats pain, swelling of tissues, and has an anti-inflammatory and reparative effect.
• Acupuncture can help reduce pain. This method is part of a complex of therapeutic measures for the treatment of paresis and has a general psychostimulating effect.

Drug therapy is aimed at preventing brain hypoxia, improving metabolic processes, restoring active mental activity, and normalizing a person’s emotional background.

After moderate and severe traumatic brain injuries, it is difficult for victims to return to their usual way of life or come to terms with forced changes. In order to reduce the risk of developing serious complications after a TBI, you need to follow simple rules: do not refuse hospitalization, even if it seems that you are feeling fine, and do not neglect various types of rehabilitation, which, with an integrated approach, can show significant results.

Traumatic brain injury (TBI) is an injury to the head that affects the skin, skull bones, and brain tissue.

Types of damage

All traumatic brain injuries can be divided into open (when the skin, muscles, tendons and aponeurosis of the skull, bones, hard and soft membranes of the brain, and the brain itself are injured) and closed. Closed skull trauma is divided into the following types:

1. Concussion of the brain (CHM). Occurs as a result of a blow to the head, this is the mildest type of injury. SHM is accompanied by several mandatory signs: loss of consciousness for less than 5 minutes, amnesia, absence of focal neurological symptoms, predominance of general symptoms (headache, dizziness, nausea, vomiting, drowsiness). Such pathological phenomena on the part of the nervous tissue arise as a result of a sharp increase in intracranial pressure in case of injury .
2. Brain contusion. A very serious injury when physical impact is exerted on the very substance of the brain. Either with a traumatic object, or the brain hits the inner wall of the skull hard. The bruise is accompanied by necrosis of a certain area of ​​the brain and hemorrhage. In this case, the same symptoms are observed as with a concussion, but more pronounced, which is combined with focal symptoms (impaired sensitivity, movements in one of the areas of the body or muscle group).
3. Compression of the brain matter. It can occur with increasing swelling of the nervous tissue and membranes against the background of intracranial hematoma (hemorrhage). In this case, signs of injury are first visible, then a period of improvement (hidden well-being) begins. And then the patient’s condition sharply worsens, consciousness is impaired, and severe neurological symptoms appear.

22.03.2014

The basis of these recommendations are international agreement documents. Considering the fact that in these documents most of the principles of surgical and conservative treatment are options, the authors considered it appropriate to additionally offer a Russian version, which is based on the experience of the Research Institute of Neurosurgery named after. N.N. Burdenko and Research Institute of Emergency Medicine named after. N.V. Sklifosovsky and takes into account the peculiarities of the organization of medical care in our country.

1. Management of patients with severe TBI

All regions should have a well-organized neurotrauma care service.

The neurotraumatological care service for victims with severe and moderate TBI should include a neurosurgical department, an on-duty trauma surgeon, an on-duty neurosurgeon, a constantly ready operating room, staffed with equipment and personnel, an intensive care unit and a laboratory service, and all equipment necessary for the treatment of victims with neurotrauma. The ability to conduct a computed tomography examination should be ensured at any time. In hard-to-reach regions where there is no neurosurgeon, the local surgeon must be able to conduct a thorough neurological examination and primary measures of special neurotraumatological care. He is required to perform life-saving operations for meningeal hematomas in victims with a clinical picture of brainstem herniation.

1.2. Examination of victims with severe TBI upon admission to the intensive care unit (options)

1.2.1. Upon admission to the intensive care unit, you must:

• Examination of the entire body of a naked patient, paying attention to bad breath, abrasions, bruises, joint deformities, changes in the shape of the chest and abdomen, leakage of blood and cerebrospinal fluid from the ears and nose, bleeding from the urethra and rectum.
• X-ray examination of the skull in two projections, cervical, thoracic and lumbar spine, chest, pelvic bones and, if necessary, bones of the upper and lower extremities.
• Ultrasound examination of the abdominal cavity, retroperitoneal space and chest (if necessary, laparocentesis)
• Study of hemoglobin concentration, number of erythrocytes and leukocytes, leukocyte formula, hematocrit level, glucose, urea, creatinine, blood bilirubin, acid-base status (ABS), sodium and potassium of the blood. Conduct a general clinical urine test.
• Electrocardiogram in three standard, aVR, aVL, aVF and six chest leads.
• Blood and urine tests for alcohol content. If necessary, after consulting a toxicologist, examine the content of barbiturates, phenothiazines, benzodiazepines, higher alcohols and opiates in biological media.
• Examination by a neurosurgeon, surgeon, traumatologist.
• In the future, at least once a day (more often if indicated), clinical and biochemical blood tests are performed, the CBS, the concentrations of sodium and potassium in the blood plasma are examined. A general urine test is examined once every 2 days, more often if there are anamnestic and clinical indications.

1.2.2. Computed tomography (CT) of the brain

CT is a mandatory method for examining victims with TBI. Relative contraindications to emergency research: unstable hemodynamics (systolic blood pressure below 90 mm Hg, the need for constant infusion of vasopressors); unresolved hemorrhagic or traumatic shock.

Using CT it is necessary to determine:

• The presence of a pathological focus (foci), its topical location.
• The presence of hyperdense and hypodense zones in it, their number, the volume of each type of focus (hyper- and hypodense parts) and their total volume in cubic centimeters.
• The position of the midline structures of the brain and the degree (in millimeters) of their displacement (if any).
• The state of the cerebrospinal fluid-containing system of the brain - the size and position of the ventricles, indicating the cerebroventricular indices, the shape of the ventricles, their deformations, etc.
• Condition of the brain cisterns.
• The condition of the furrows and fissures of the brain.
• The lumen of the sub- and epidural spaces (not normally determined).
• Condition of the bone structures of the vault and base of the skull (presence of cracks, fractures).
• Condition and contents of the paranasal sinuses.
• Condition of the soft tissues of the skull.

In the absence of positive dynamics, a repeat CT scan of the brain is performed after 12-24 hours. If new neurological symptoms increase and appear, an emergency CT scan is performed. All CT examinations must be carried out in two modes: bone and soft tissue. In case of craniofacial damage and suspected liquorrhea, a CT scan of the head in a frontal projection is necessary.

1.2.3. Cerebrospinal fluid examination

To monitor inflammatory changes in the cerebrospinal fluid (suspicion of meningitis), it is necessary to conduct a dynamic study of the composition of the cerebrospinal fluid. Lumbar puncture is performed in the absence of dislocation symptoms and preserved patency of the liquor-conducting pathways in order to avoid the development and increase in the processes of herniation and dislocation of the brain.

1.2.4. Neurological examination

The degree of impairment of consciousness in victims is determined by speech production, reaction to pain and eye opening. Each of these indicators is assessed in points on the Glasgow Coma Scale (GCS) independently of the other two. The sum of points determines the depth of disorders of consciousness - from 3 points (deep coma) to 15 (clear consciousness).

It is possible to assess the degree of impairment of consciousness according to the classification of Konovalov A.N. et al. (1)

According to this classification, 15 points on the GCS correspond to clear consciousness, 13-14 points – moderate stupor, 11-12 points – deep stupor, 9-10 points – stupor, 6-8 points – moderate coma, 4-5 points – deep coma, 3 points – extreme coma (atonic).

In addition, focal, oculomotor, pupillary and bulbar disorders are assessed.

The inspection must be repeated every 4 hours. Patients who are intoxicated should be examined every 2 hours. If depression of consciousness persists in a patient who is intoxicated, it is necessary to urgently perform a CT scan of the brain.

1.3. Primary care for victims with severe TBI (options)

In providing first aid to victims, priority is given to measures aimed at restoring and maintaining vital functions: breathing (restoring airway patency, eliminating hypoventilation disorders - hypoxemia, hypercapnia) and blood circulation (eliminating hypovolemia, hypotension and anemia).

1.3.1. Monitoring

Rational intensive care should be based on monitoring vital functions. Neuromonitoring, circulatory, respiratory and oxygenation monitoring should be sought. Optimal is continuous measurement of intracranial pressure, monitoring of brain oxygenation in one way or another (parainfrared cerebral oximetry or measurement of hemoglobin saturation in the bulb of the jugular vein through a retrogradely inserted cannula), monitoring of blood pressure (preferably by an invasive method), pulse oximetry, monitoring of carbon dioxide content in the end- exhaled air and ECG.

If possible, this diagnostic complex can be expanded by ultrasound examination of cerebral vessels, monitoring central venous pressure and determining the content of gases in arterial and venous blood.

1.3.2. Ensuring airway patency.

In a victim with impaired consciousness according to the GCS of 8 points or less (coma), tracheal intubation should be performed in order to ensure normal oxygenation and eliminate hypercapnia. Any doubts about the need for intubation are interpreted as indications for this manipulation. Intubation must be performed without extension of the cervical spine: either nasotracheally or orotracheally while maintaining the spinal axis. If consciousness is depressed to the point of stupor and coma, auxiliary or controlled artificial ventilation of the lungs is performed with an oxygen-air mixture with an oxygen content of at least 40-50%. When performing mechanical ventilation, episodes of asynchrony between the patient and the respirator, causing a sharp increase in intracranial pressure, should be prevented by selecting ventilation modes or administering short-acting muscle relaxants and sedatives. The main objectives of mechanical ventilation for TBI are to maintain normocapnia (pCO2 art - 36-40 mm Hg) and sufficient cerebral oxygenation (oxygen saturation of hemoglobin in the blood flowing from the brain is at least 60%). To prevent cerebral ischemia and hypoxia, all manipulations associated with opening the ventilator circuit must be accompanied by pre- and post-oxygenation with 100% oxygen.

When performing mechanical ventilation, hyperventilation and associated hypocapnia are avoided. In the absence of signs of intracranial hypertension in patients with severe TBI, prolonged hyperventilation PaCO2 should be avoided

Prophylactic hyperventilation (PaCO2) should also be avoided

Short-term hyperventilation can be used in case of a sharp deterioration in neurological status, or for a longer time if intracranial hypertension persists despite the use of sedation, relaxation, drainage of cerebrospinal fluid from the ventricles of the brain and the use of osmotic diuretics. In case of using hyperventilation with PaCO2< 30 mmHg, следует использовать измерение насыщения крови кислородом в ярёмной вене, измерение артерио-венозной разницы по кислороду (опции).

1.3.3. Correction of arterial hypotension

To correct cerebral perfusion disorders, it is important to maintain cerebral perfusion pressure at a level of at least 70 mmHg. Art. At all stages of care (at the scene, during transportation and in the hospital), arterial hypotension (systolic blood pressure) should be immediately and carefully prevented or eliminated

Monitoring of intracranial pressure (ICP) is indicated in patients with severe TBI (3-8 points on the Glasgow Coma Scale) and pathology on CT (hematoma, contusion, edema, compression of the basal cisterns). ICP monitoring is advisable in patients with severe TBI and CT scan is normal in the presence of at least two of the following features: age over 40 years, presence of unilateral or bilateral decerebration, systolic blood pressure< 90 mm Hg.

ICP monitoring is generally not indicated in patients with mild to moderate TBI.

Currently, measuring ventricular pressure is the most accurate, cheap and reliable way to monitor ICP. This technique also allows you to drain cerebrospinal fluid for therapeutic purposes.

1.3.6. Indications for correction of intracranial pressure

Correction of intracranial pressure should begin when the threshold of 20-25 mm Hg is exceeded. (recommendations).

Interpretation and correction of ICP relative to any threshold should be supported by frequent clinical examination and cerebral perfusion pressure (CPP) data (optional).

1.3.7. Treatment of intracranial hypertension (options)

Common components of intensive care aimed at preventing and managing intracranial hypertension include: head elevation; eliminating the causes that disrupt the venous outflow from the cranial cavity; fight against hyperthermia; elimination of motor agitation, seizures with the help of sedatives and/or muscle relaxants; maintaining adequate oxygenation; elimination of hypercapnia; maintaining a CPP of at least 70 mmHg. When measuring ICP using a ventricular catheter, the simplest method of reducing intracranial pressure is to withdraw ventricular cerebrospinal fluid. If it is not possible to normalize ICP, a repeat CT scan is indicated. If CT does not reveal indications for surgical intervention and intracranial hypertension persists, the use of moderate hyperventilation (PaCO2 = 30–35 mmHg) is indicated, and if it is ineffective, bolus repeated administration of mannitol at a dose of 0.25-1.0 g/kg, if osmolarity does not exceed 320 mOsm/l. If the measures taken do not lead to normalization of ICP, CT or MRI should be repeated. If a surgical situation and persistent intracranial hypertension are excluded, more aggressive methods are used - therapeutic barbituric anesthesia, deep hyperventilation, moderate hypothermia under the control of oxygen saturation in the jugular vein and the arterio-venous oxygen difference.

It should be emphasized that an increase in the aggressiveness of treatment measures is always associated with an increase in the risk of possible complications. When moving to a more aggressive stage of the fight against intracranial hypertension, control CT allows one to diagnose the possible formation of delayed intracranial hematomas, occlusive hydrocephalus, etc., and at the same time undertake the necessary surgical intervention.

1.3.8. Mannitol in the treatment of severe TBI

Mannitol is effective in controlling elevated ICP. The dosage varies between 0.25-1.0 g/kg. (recommendations).

It is advisable to use Mannitol before starting ICP monitoring if there are signs of transtentorial herniation or deterioration in neurological status that are not associated with the influence of extracranial factors. To avoid renal failure, plasma osmolarity should be maintained below 320 mOsm/L. Normovolemia should be maintained by adequate replacement of lost fluid, and it is advisable to catheterize the bladder. Intermittent bolus administration of Mannitol may be more effective than continuous infusion (optional).

1.3.9. The use of barbiturates in the treatment of intracranial hypertension

Therapeutic anesthesia with high doses of barbiturates can be used in victims with severe TBI with stable hemodynamics and the presence of intracranial hypertension resistant to the use of the most aggressive conservative and surgical treatment method (recommendations).

When carrying out therapeutic barbituric anesthesia, it is advisable to control the arteriovenous difference in oxygen, since there is a danger of developing oligemic cerebral hypoxia (options)

Doses taken include an initial dose of 10 mg/kg/hour, followed by 3 doses of 5 mcg/kg/hour, followed by maintaining the achieved concentration by administering a dose of 1 mg/kg/hour using an automatic perfuser.

1.3.10. The role of glucocorticoids in the treatment of severe TBI (standard)

Class I and II studies have shown that the use of glucocorticoids is not recommended to reduce ICP and improve outcomes in patients with severe TBI.

1.3.11. Septic complications and nutrition of patients with severe TBI

Due to disruption of the cough mechanisms and the flow of mucus from the oral cavity into the trachea, pneumonia develops in neurocritical care patients. For the prevention of pulmonary disorders, it is fundamentally important to ensure the patency of the tracheobronchial tree by performing intubation. If mechanical ventilation is continued for more than 5 days, a tracheostomy is necessary. An effective means of preventing pneumonia is the use of special tracheostomy tubes with the possibility of supra-cuff aspiration.

The basis for the treatment of pneumonia is rational antibacterial therapy with mandatory rotation of antibiotics based on the results of microbiological monitoring of a specific intensive care unit. The uncontrolled use of “broad spectrum” antibiotics is unacceptable. The tactics of escalation and de-escalation therapy are chosen based on the initial severity of purulent-septic complications.

Treatment of post-traumatic meningitis is based on intrathecal administration, for health reasons, of modern antimicrobial agents approved for endolumbar administration (for example, vancomycin).

Patients should begin feeding their diet no later than 72 hours after injury, gradually increasing its volume, and by the end of the first week, provide 100% of the caloric requirement based on the assessment of basal metabolism in patients under the influence of muscle relaxants, and 140% in others. Nutrition can be provided either enterally or parenterally, and the nutritional mixture should contain at least 15% protein in terms of calories by 7 days after injury (recommendations).

It is advantageous to install a small intestinal tube through a gastrojejunostomy to prevent gastric congestion and ease of care. The advantages of enteral nutrition over parenteral nutrition are: lower risk of hyperglycemia, lower risk of infection and lower cost (options).

1.3.12. The role of anticonvulsant preventive therapy

There are early (first 7 days) and late (more than 1 week) post-traumatic epilepsy.

In the acute period of TBI, it is recommended to prescribe anticonvulsants (phenytoin and carbamazepine) in victims at high risk of developing early seizures. Risk factors include: the presence of cortical contusion lesions, depressed skull fractures, intracranial hematomas, penetrating head injury, development of a convulsive seizure in the first 24 hours after injury (options).

However, based on class I studies, it has been proven that the prophylactic use of phentoin, carbamazepine, phenobarbital or valproate is not effective in preventing late post-traumatic epilepsy (standard).

Fundamental provisions:

• Muscle relaxants are not classified as anticonvulsants. They stop only the muscle component of seizures and are used temporarily if it is necessary to synchronize the patient with a ventilator.
• Convulsions must be stopped, and the sooner the better. Therefore, if monotherapy is ineffective, it is necessary to use a combination of anticonvulsants.
• Stopping seizures should begin with drugs for intravenous administration. If an intravenous form of the drug is not available, it must be administered through a gastric tube.

Lorazepam (Merlit, Lorafen) is a benzodiazepine. Lorazepam is the best anticonvulsant drug. In Russia there is only an oral form. The drug is used orally at a dose of 0.07 mg/kg 2 times a day. Typically the effect lasts about 12 hours.

Diazepam is the second-line drug of choice (in our country it is the first-line drug for intravenous administration). 0.15-0.4 mg/kg is administered intravenously at a rate of 2.5 mg/min. If necessary, the drug can be reintroduced after 10-20 minutes. It is also possible to administer diazepam by drip - 0.1-0.2 mg/kg-hour.

Midazolam (dormicum) replaces diazepam, as it has almost the same properties and is administered in the same doses (0.2-0.4 mg/kg).

Valproic acid (Depakine) is the third-line drug of choice for oral administration and the second-line drug for intravenous administration. It is administered intravenously over 3-5 minutes at a dose of 6-7 mg/kg, followed by a constant infusion at the rate of 1 mg/kg/hour. The oral dose is equivalent to the intravenous dose.

Phenytoin (diphenin) is the fourth choice drug. Phenytoin is administered through a nasogastric tube at a dose of up to 20 mg/kg.

Carbamazepine (finlepsin, tegretol) is a widely used anticonvulsant of next choice. Usual doses of the drug are 800-1200 mg/day, divided into 3-4 doses.

Thiopental is the third choice drug for intravenous administration in our country after benzodiazepines and depakine. 250-350 mg of the drug is administered intravenously over 20 seconds, then at a rate of 5-8 mg/kg/h.

Phenobarbital (luminal) is used enterally at a dose of 2-10 mg/kg/day.

2. Recommendations for surgical treatment of traumatic brain injury (options)

2.1. Surgical treatment of acute epidural hematomas

– Epidural hematoma more than 30 cm3 requires surgical intervention, regardless of the degree of depression of consciousness according to the Glasgow Coma Scale

– An epidural hematoma with a volume of less than 30 cm3, a thickness of less than 15 mm, with displacement of the median structures of less than 5 mm in patients with a Glasgow Coma Scale of more than 8 points and the absence of focal neurological symptoms may be subject to conservative treatment (with careful neurological monitoring in a neurosurgical hospital).

Timing and methods of operations

– Patients in coma (less than 9 GCS points) with acute epidural hematoma in the presence of anisocoria are indicated for emergency surgery.

– There is no consensus regarding surgical methods, but it is believed that craniotomy provides more complete evacuation of the hematoma

2.2. Surgical treatment of acute subdural hematomas

– In case of acute subdural hematoma with a thickness of >10 mm or displacement of the midline structures >5 mm, surgical removal of the hematoma is necessary, regardless of the patient’s condition on the Glasgow Coma Scale.

– All comatose patients with acute subdural hematoma should have ICP monitored.

– Surgical intervention is also indicated for patients in a coma with a subdural hematoma less than 10 mm thick and a displacement of the midline structures less than 5 mm, if there is: a decrease in GCS by 2 points or more from the moment of injury to admission to the clinic, asymmetry of the pupils or absence of photoreaction and mydriasis, increased ICP> 20 mm.hg

Timing and methods of surgery

– In patients with acute subdural hematoma, if there are indications for surgery, surgery should be performed urgently.

– In comatose patients, acute subdural hematoma is removed by craniotomy with preservation or removal of a bone flap and dura mater plastic surgery.

2.3. Surgical treatment of brain contusions

– For brain contusions that cause progressive deterioration of neurological status, persistent intracranial hypertension refractory to conservative treatment, or signs of mass effect on CT, surgical treatment is required.

– Indications for it are also established for patients in a coma with foci of contusions in the frontal and temporal lobes with a volume of more than 20 cm3, if the displacement of the median structures is >5 mm and/or there are signs of compression of the cisterns on CT, as well as if the volume of the contusion foci exceeds 50 cm3.

Timing and methods of operations

– Craniotomy for the removal of crush lesions causing a threatening mass effect has the same emergency indications as the removal of intracranial hematomas.

– Bifrontal decompressive craniectomy in the first 48 hours after injury is the treatment of choice for patients with diffuse cerebral edema and intracranial hypertension refractory to conservative treatment.

Decompressive operations

– Decompressive surgeries, including infratemporal decompression, temporal lobectomy, hemicraniectomy, may be indicated for persistent intracranial hypertension and diffuse parenchymal damage in patients with clinical and CT signs of tentorial herniation.

2.4. Conservative treatment of brain contusions

– Patients with foci of brain contusions without signs of neurological deterioration, as well as with controlled ICP and a slight mass effect on CT, can be treated conservatively, subject to monitor control and dynamic CT.

2.5. Indications for operations on the posterior cranial fossa

– Absolute indications for surgical treatment for injuries to the posterior cranial fossa are epidural hematomas over 25 cm3, lateral cerebellar injuries over 20 cm3, occlusive hydrocephalus, lateral dislocation of the fourth ventricle.

– Conservative treatment in patients with damage to the structures of the PCF can be carried out with epidural hematomas with a volume of less than 10 cm3, lateral cerebellar injuries of less than 10 cm3, the absence of displacement of the IV ventricle and brainstem symptoms

– Waiting tactics in patients with damage to the structures of the PCF is possible with epidural hematomas with a volume of 10-20 cm3, cerebellar injuries of 10-20 cm3 with a lateral location. When determining treatment tactics, it is necessary to take into account the level of consciousness, the state of the fundus, and data from acoustic brainstem evoked potentials. Such patients require dynamic CT studies, given the risk of delayed hematomas, rapid development of cerebrospinal fluid tract occlusion and decompensation of the patient.

2.6. Surgical treatment of depressed skull fractures

– For open depressed skull fractures greater than the thickness of the bone, surgical intervention is necessary to prevent infection.

– Patients with an open depressed skull fracture can be treated conservatively if there are no signs of damage to the dura mater, significant intracranial hematoma, depression greater than 1 cm, involvement of the air sinuses, cosmetic defect, wound infection, pneumocephalus, severe wound contamination.

– Conservative treatment of a closed depressed fracture is decided individually in each case.

Timing and methods of operations for depressed fractures

– Removal of depression and surgical treatment of the wound are the main elements of the operation.

– In the absence of wound infection, primary bone grafting is possible.

– Treatment for open depressed fractures should include antibiotics.

Damage to the bones of the skull and/or soft tissues (meninges, brain tissue, nerves, blood vessels). Based on the nature of the injury, a distinction is made between closed and open, penetrating and non-penetrating TBI, as well as concussion or contusion of the brain. The clinical picture of traumatic brain injury depends on its nature and severity. The main symptoms are headache, dizziness, nausea and vomiting, loss of consciousness, and memory impairment. Brain contusion and intracerebral hematoma are accompanied by focal symptoms. Diagnosis of traumatic brain injury includes medical history, neurological examination, skull x-ray, CT or MRI of the brain.

General information

Damage to the bones of the skull and/or soft tissues (meninges, brain tissue, nerves, blood vessels). The classification of TBI is based on its biomechanics, type, type, nature, shape, severity of injury, clinical phase, treatment period, and outcome of the injury.

Based on biomechanics, the following types of TBI are distinguished:

• shock-anti-shock (the shock wave propagates from the site of the received blow and passes through the brain to the opposite side with rapid pressure changes);
• acceleration-deceleration (movement and rotation of the cerebral hemispheres in relation to a more fixed brain stem);
• combined (simultaneous impact of both mechanisms).

By type of damage:

• focal (characterized by local macrostructural damage to the brain matter, with the exception of areas of destruction, small and large focal hemorrhages in the area of ​​impact, counter-impact and shock wave);
• diffuse (tension and spread of primary and secondary axonal breaks in the centrum semiovale, corpus callosum, subcortical formations, brain stem);
• combined (a combination of focal and diffuse brain damage).

According to the genesis of the lesion:

• primary lesions: focal contusions and crushes of the brain, diffuse axonal damage, primary intracranial hematomas, brainstem ruptures, multiple intracerebral hemorrhages;
• secondary lesions:

1. due to secondary intracranial factors (delayed hematomas, disturbances in cerebrospinal fluid and hemocirculation due to intraventricular or subarachnoid hemorrhage, cerebral edema, hyperemia, etc.);
2. due to secondary extracranial factors (arterial hypertension, hypercapnia, hypoxemia, anemia, etc.)

According to their type, TBIs are classified into: closed - injuries that do not violate the integrity of the skin of the head; fractures of the bones of the calvarium without damage to the adjacent soft tissues or a fracture of the base of the skull with developed liquorrhea and bleeding (from the ear or nose); open non-penetrating TBI - without damage to the dura mater and open penetrating TBI - with damage to the dura mater. In addition, isolated (absence of any extracranial damage), combined (extracranial damage as a result of mechanical energy) and combined (simultaneous exposure to various energies: mechanical and thermal/radiation/chemical) traumatic brain injury are distinguished.

Based on severity, TBI is divided into 3 degrees: mild, moderate and severe. When correlating this rubric with the Glasgow Coma Scale, mild traumatic brain injury is assessed at 13-15, moderate at 9-12, severe at 8 points or less. A mild traumatic brain injury corresponds to a mild concussion and contusion, a moderate one corresponds to a moderate brain contusion, a severe one corresponds to a severe brain contusion, diffuse axonal damage and acute compression of the brain.

According to the mechanism of occurrence of TBI, there are primary (the impact of traumatic mechanical energy on the brain is not preceded by any cerebral or extracerebral catastrophe) and secondary (the impact of traumatic mechanical energy on the brain is preceded by a cerebral or extracerebral catastrophe). TBI in the same patient can occur for the first time or repeatedly (twice, three times).

The following clinical forms of TBI are distinguished: concussion, mild brain contusion, moderate brain contusion, severe brain contusion, diffuse axonal damage, brain compression. The course of each of them is divided into 3 basic periods: acute, intermediate and long-term. The time duration of the periods of traumatic brain injury varies depending on the clinical form of TBI: acute - 2-10 weeks, intermediate - 2-6 months, long-term with clinical recovery - up to 2 years.

Concussion

The most common injury among possible traumatic brain injuries (up to 80% of all TBIs).

Clinical picture

Depression of consciousness (to the level of stupor) during a concussion can last from several seconds to several minutes, but may be absent altogether. Retrograde, congrade and antegrade amnesia develops for a short period of time. Immediately after a traumatic brain injury, a single vomiting occurs, breathing becomes more frequent, but soon returns to normal. Blood pressure also returns to normal, except in cases where the medical history is aggravated by hypertension. Body temperature during a concussion remains normal. When the victim regains consciousness, there are complaints of dizziness, headache, general weakness, cold sweat, flushing of the face, and tinnitus. The neurological status at this stage is characterized by mild asymmetry of skin and tendon reflexes, small horizontal nystagmus in the extreme abductions of the eyes, and mild meningeal symptoms that disappear during the first week. With a concussion as a result of a traumatic brain injury, after 1.5 - 2 weeks, an improvement in the patient’s general condition is noted. It is possible that some asthenic phenomena may persist.

Diagnosis

Recognizing a concussion is not an easy task for a neurologist or traumatologist, since the main criteria for diagnosing it are the components of subjective symptoms in the absence of any objective data. It is necessary to familiarize yourself with the circumstances of the injury, using the information available to witnesses to the incident. Of great importance is an examination by an otoneurologist, with the help of which the presence of symptoms of irritation of the vestibular analyzer in the absence of signs of prolapse is determined. Due to the mild semiotics of a concussion and the possibility of a similar picture arising as a result of one of many pre-traumatic pathologies, special importance in diagnosis is given to the dynamics of clinical symptoms. The justification for the diagnosis of “concussion” is the disappearance of such symptoms 3-6 days after receiving a traumatic brain injury. With a concussion, there are no fractures of the skull bones. The composition of the cerebrospinal fluid and its pressure remain normal. CT scan of the brain does not detect intracranial spaces.

Treatment

If a victim with a traumatic brain injury has come to his senses, first of all he needs to be given a comfortable horizontal position, his head should be slightly raised. A victim with a traumatic brain injury who is in an unconscious state must be given the so-called. The “saving” position is to lay him on his right side, his face should be turned to the ground, his left arm and leg should be bent at right angles at the elbow and knee joints (if fractures of the spine and limbs are excluded). This position promotes the free passage of air into the lungs, preventing the tongue from retracting and vomit, saliva and blood from entering the respiratory tract. Apply an aseptic bandage to bleeding wounds on the head, if any.

All victims with traumatic brain injury are necessarily transported to a hospital, where, after confirmation of the diagnosis, they are placed on bed rest for a period that depends on the clinical characteristics of the course of the disease. The absence of signs of focal brain lesions on CT and MRI of the brain, as well as the patient’s condition, which allows one to refrain from active drug treatment, allows us to resolve the issue in favor of discharging the patient for outpatient treatment.

For a concussion, overactive drug treatment is not used. Its main goals are to normalize the functional state of the brain, relieve headaches, and normalize sleep. For this purpose, analgesics and sedatives (usually in tablet forms) are used.

Brain contusion

Mild brain contusion is detected in 10-15% of victims with traumatic brain injury. A bruise of moderate severity is diagnosed in 8-10% of victims, a severe bruise - in 5-7% of victims.

Clinical picture

A mild brain contusion is characterized by loss of consciousness after injury of up to several tens of minutes. After consciousness is restored, complaints of headache, dizziness, and nausea appear. Retrograde, congrade, and anterograde amnesia are noted. Vomiting is possible, sometimes with repetitions. Vital functions are usually preserved. Moderate tachycardia or bradycardia and sometimes increased blood pressure are observed. Body temperature and respiration without significant deviations. Mild neurological symptoms regress after 2-3 weeks.

Loss of consciousness with a moderate brain contusion can last from 10-30 minutes to 5-7 hours. Retrograde, congrade and anterograde amnesia are strongly expressed. Repeated vomiting and severe headache are possible. Some vital functions are impaired. Bradycardia or tachycardia, increased blood pressure, tachypnea without respiratory distress, and increased body temperature to subfebrile are detected. The manifestation of meningeal signs, as well as stem symptoms, is possible: bilateral pyramidal signs, nystagmus, dissociation of meningeal symptoms along the body axis. Pronounced focal signs: oculomotor and pupillary disorders, paresis of the limbs, speech and sensitivity disorders. They regress after 4-5 weeks.

Severe brain contusion is accompanied by loss of consciousness from several hours to 1-2 weeks. It is often combined with fractures of the bones of the base and vault of the skull, and profuse subarachnoid hemorrhage. Disorders of vital functions are noted: respiratory rhythm disturbances, sharply increased (sometimes decreased) blood pressure, tachy- or bradyarrhythmia. Possible blockage of the airways, intense hyperthermia. Focal symptoms of hemispheric damage are often masked behind stem symptoms that come to the fore (nystagmus, gaze paresis, dysphagia, ptosis, mydriasis, decerebrate rigidity, changes in tendon reflexes, the appearance of pathological foot reflexes). Symptoms of oral automatism, paresis, focal or generalized seizures can be detected. Restoring lost functions is difficult. In most cases, gross residual motor and mental disorders remain.

Diagnosis

The method of choice for diagnosing a brain contusion is a CT scan of the brain. A CT scan reveals a limited area of ​​low density, possible fractures of the calvarial bones and subarachnoid hemorrhage. With a brain contusion of moderate severity, CT or spiral CT in most cases reveals focal changes (non-compactly located areas of reduced density with small areas of increased density).

In case of severe contusion, CT scan reveals areas of heterogeneous increase in density (alternating areas of increased and decreased density). Perifocal cerebral edema is severe. A hypodense path is formed in the area of ​​the nearest section of the lateral ventricle. Through it, fluid with breakdown products of blood and brain tissue is discharged.

Diffuse axonal brain injury

Diffuse axonal brain damage is typically characterized by a prolonged coma after a traumatic brain injury, as well as pronounced brain stem symptoms. Coma is accompanied by symmetrical or asymmetrical decerebration or decortication, both spontaneous and easily provoked by irritations (for example, painful ones). Changes in muscle tone are very variable (hormetonia or diffuse hypotension). A typical manifestation is pyramidal-extrapyramidal paresis of the limbs, including asymmetric tetraparesis. In addition to gross disturbances in the rhythm and frequency of breathing, autonomic disorders also appear: increased body temperature and blood pressure, hyperhidrosis, etc. A characteristic feature of the clinical course of diffuse axonal brain damage is the transformation of the patient’s condition from a prolonged coma to a transient vegetative state. The onset of this state is indicated by the spontaneous opening of the eyes (with no signs of tracking or fixation of gaze).

Diagnosis

The CT picture of diffuse axonal brain damage is characterized by an increase in brain volume, as a result of which the lateral and third ventricles, subarachnoid convexital spaces, and also the cisterns of the base of the brain are under compression. The presence of small focal hemorrhages in the white matter of the cerebral hemispheres, corpus callosum, subcortical and brain stem structures is often detected.

Brain compression

Brain compression develops in more than 55% of cases of traumatic brain injury. Most often, the cause of compression of the brain is an intracranial hematoma (intracranial, epi- or subdural). Rapidly increasing focal, brainstem and cerebral symptoms pose a danger to the life of the victim. Availability and duration of the so-called “light gap” - expanded or erased - depends on the severity of the victim’s condition.

Diagnosis

A CT scan reveals a biconvex, less often a flat-convex, limited zone of increased density, which is adjacent to the cranial vault and is localized within one or two lobes. However, if there are several sources of bleeding, the area of ​​​​increased density can be significant in size and have a crescent shape.

Treatment of traumatic brain injury

When a patient with a traumatic brain injury is admitted to the intensive care unit, the following measures must be taken:

• Examination of the victim’s body, during which abrasions, bruises, joint deformities, changes in the shape of the abdomen and chest, bleeding and/or liquor leakage from the ears and nose, bleeding from the rectum and/or urethra, and a specific odor from the mouth are detected or excluded.
• Comprehensive x-ray examination: skull in 2 projections, cervical, thoracic and lumbar spine, chest, pelvic bones, upper and lower extremities.
• Ultrasound of the chest, ultrasound of the abdominal cavity and retroperitoneal space.
• Laboratory tests: general clinical analysis of blood and urine, biochemical blood test (creatinine, urea, bilirubin, etc.), blood sugar, electrolytes. These laboratory tests must be carried out in the future, daily.
• ECG (three standard and six chest leads).
• Testing urine and blood for alcohol content. If necessary, consult a toxicologist.
• Consultations with a neurosurgeon, surgeon, traumatologist.

A mandatory method of examining victims with traumatic brain injury is computed tomography. Relative contraindications to its implementation may include hemorrhagic or traumatic shock, as well as unstable hemodynamics. Using CT, the pathological focus and its location, the number and volume of hyper- and hypodense zones, the position and degree of displacement of the midline structures of the brain, the condition and degree of damage to the brain and skull are determined. If meningitis is suspected, a lumbar puncture and dynamic examination of the cerebrospinal fluid are indicated, which allows monitoring changes in the inflammatory nature of its composition.

A neurological examination of a patient with a traumatic brain injury should be performed every 4 hours. To determine the degree of consciousness impairment, the Glasgow Coma Scale is used (state of speech, response to pain and ability to open/close eyes). In addition, the level of focal, oculomotor, pupillary and bulbar disorders is determined.

For a victim with impaired consciousness of 8 points or less on the Glasgow scale, tracheal intubation is indicated, due to which normal oxygenation is maintained. Depression of consciousness to the level of stupor or coma is an indication for auxiliary or controlled mechanical ventilation (at least 50% oxygen). With its help, optimal cerebral oxygenation is maintained. Patients with severe traumatic brain injury (hematomas, cerebral edema, etc. detected on CT) require monitoring of intracranial pressure, which must be maintained below 20 mmHg. For this purpose, mannitol, hyperventilation, and sometimes barbiturates are prescribed. To prevent septic complications, escalation or de-escalation antibacterial therapy is used. For the treatment of post-traumatic meningitis, modern antimicrobial drugs approved for endolumbar administration (vancomycin) are used.

Patients begin feeding no later than 3 days after TBI. Its volume is increased gradually and at the end of the first week following the date of the traumatic brain injury, it should provide 100% of the patient’s caloric needs. The route of nutrition can be enteral or parenteral. To relieve epileptic seizures, anticonvulsants are prescribed with minimal dose titration (levetiracetam, valproate).

The indication for surgery is an epidural hematoma with a volume of over 30 cm³. It has been proven that the method that ensures the most complete evacuation of the hematoma is transcranial removal. Acute subdural hematoma with a thickness of more than 10 mm is also subject to surgical treatment. In comatose patients, acute subdural hematoma is removed by craniotomy, maintaining or removing a bone flap. An epidural hematoma with a volume of more than 25 cm³ is also subject to mandatory surgical treatment.

Prognosis for traumatic brain injury

Concussion is a predominantly reversible clinical form of traumatic brain injury. Therefore, in more than 90% of cases of concussion, the outcome of the disease is the recovery of the victim with full restoration of ability to work. Some patients, after the acute period of concussion, experience certain manifestations of post-concussion syndrome: disturbances in cognitive functions, mood, physical well-being and behavior. 5-12 months after a traumatic brain injury, these symptoms disappear or are significantly smoothed out.

Prognostic assessment in severe traumatic brain injury is carried out using the Glasgow Outcome Scale. A decrease in the total number of points on the Glasgow scale increases the likelihood of an unfavorable outcome of the disease. Analyzing the prognostic significance of the age factor, we can conclude that it has a significant impact on both disability and mortality. The combination of hypoxia and arterial hypertension is an unfavorable prognosis factor.

Clinic. There are closed and open traumatic brain injuries. With a closed craniocerebral injury, there is no violation of the integrity of the scalp or there are soft tissue wounds without damage to the aponeurosis, or a fracture of the bones of the calvarium without damage to the aponeurosis and soft tissues.

Injuries accompanied by injuries to the soft tissues of the head and aponeurosis, fractures of the base of the skull, accompanied by liquor leakage or bleeding (from the ear, nose) are classified as open craniocerebral trauma. Open craniocerebral injuries without damage to the dura mater are considered non-penetrating, and if its integrity is violated, they are considered penetrating.

Based on severity, traumatic brain injury is divided into three degrees: mild - concussion, mild brain contusion; moderate severity - moderate brain contusion; severe - severe brain contusion and compression of the brain.

There are six clinical forms of traumatic brain injury: concussion, mild brain contusion, moderate brain contusion, severe brain contusion (pressure of the brain against the background of a contusion, compression of the brain without accompanying contusion.

Concussion - the impact of mechanical energy during a concussion affects the brain as a whole; in the process of moving the brain, due to anatomical features, the hypothalamic region is the most vulnerable. Hence the variety of autonomic symptoms in concussion. Characteristic is a short-term loss of consciousness, lasting from several seconds to several minutes. There is retrograde amnesia for events preceding the trauma, vomiting. After the patient regains consciousness, typical complaints are general weakness, headache, dizziness, tinnitus, flushing, sweating and other vegetative symptoms. There may be complaints of pain when moving the eyeballs, reading disorder, sleep disturbance, unsteady gait, etc. An objective neurological examination can reveal slight asymmetry of tendon and skin reflexes, small-scale nystagmus, the phenomenon of meningism - all this, as a rule, disappears by the end of the first week. The pressure of the cerebrospinal fluid and its composition are unchanged, the integrity of the skull bones is not compromised.

A cerebral contusion differs from a concussion by changes in the physicochemical properties of brain tissue, the functional state of neuronal membranes and swelling of synapses, leading to disruption of communication between individual groups of neurons. Due to changes in vascular tone, plasma penetrates into the intercellular spaces. This leads to the development of edema-swelling of the brain, and in the case of penetration of erythrocytes (erythrodiapedesis) - extravasation. Numerous small hemorrhages are often the only morphological sign of brain contusion.

Mild brain contusion - characterized by loss of consciousness lasting from several minutes to 1 hour. Upon restoration of consciousness, typical complaints are headaches, nausea, dizziness, etc. Repeated vomiting, retrograde amnesia, sometimes bradycardia or tachycardia, arterial hypertension are observed -zia. Body temperature and breathing are not changed. Nistagmus, mild anisocoria, anisoreflexia, meningeal symptoms that disappear by the end of the 2-3rd week after injury. Cerebrospinal fluid pressure and composition may be altered. Fractures of the bones of the vault and base of the skull are possible.

In case of moderate brain contusion, the duration of loss of consciousness after injury ranges from several tens of minutes to 4-6 hours. Severe headache, retrograde and anterograde amnesia, and repeated vomiting are typical. There are bradycardia (40-50 per minute), tachycardia (up to 120 per minute), arterial hypertension (up to 180 mm Hg), tachypnea, low-grade fever. Nystagmus, meningeal symptoms, pupillary, oculomotor disorders, paresis of the limbs, sensory disorders, speech disorders, etc. Focal neurological symptoms can last for 3-5 weeks or more. The pressure of the cerebrospinal fluid is increased to 250-300 mm of water. Art. Fractures of the bones of the vault and base of the skull and subarachnoid hemorrhage are detected.

Severe brain contusion - the duration of loss of consciousness after injury is from several hours to several weeks, there is motor agitation. Severe disorders of vital functions: bradycardia (up to 40 beats per minute), tachycardia (over 120 beats per minute), arrhythmia, arterial hypertension (over 180 mm Hg), tachypnea, bradypnea, hyperthermia. Focal neurological symptoms: gaze paresis, floating movements of the eyeballs, multiple spontaneous nystagmus, dysphagia, bilateral miosis or mydriasis, divergent strabismus, changes in muscle tone, decerebrate rigidity, areflexia, pathological foot reflexes, symptoms oral automatism, paresis (paralysis) of the limbs, convulsive seizures. Symptoms regress very slowly, and subsequently there are gross residual effects on the motor system and the mental sphere. The cerebrospinal fluid pressure is sharply increased (up to 400 mm of water column). Characterized by fractures of the bones of the vault and base of the skull, massive subarachnoid hemorrhages.

Compression of the brain - observed in the presence of intracranial hematoma (epidural, subdural, intracerebral), severe edema-swelling of the brain, areas of softening, depressed fractures of the skull bones, subdural hydromas, pneumocephalus. Increasing compression of the brain is characterized by a period of imaginary well-being. After an injury in such cases, for some time, calculated in minutes, and more often in hours, the general condition of the patient is satisfactory. Then a headache occurs, increasing in intensity, vomiting, and possibly psychomotor agitation. Pathological drowsiness occurs and bradycardia increases. Tendon and periosteal reflexes become uneven or decrease. An increase in hemiparesis, the appearance of anisocoria, and focal epileptic seizures are possible. With increasing compression of the brain, a soporous, and in more severe cases, a coma state develops. Bradycardia gives way to tachycardia, blood pressure rises. Breathing becomes hoarse, stertorous or Cheya-Stokes type, the face becomes purple-blue, and cardiac activity stops after a short-term increase.

A similar clinical picture develops with supratentorial hematomas, complicated by edema-swelling of the brain, which leads to compression of the oral parts of the brain stem, hippocampus and pinching them in the foramen of the cerebellar tentorium, and then in the magnum occipital. This is the direct cause of death of patients.

The most dangerous are epidural and subdural hematomas, less often - subarachnoid hemorrhages. Epidural hematoma is an accumulation of blood between the dura mater and the bones of the skull. Usually it appears when the meningeal arteries are damaged, less often - when the veins of the outer surface of the dura mater are damaged, as well as the sinuses or veins leading to them. Most often, an epidural hematoma occurs when the integrity of the middle meningeal artery or its branches is damaged. Damage to the artery is often combined with a fracture, crack of the temporal or parietal bone. Such cracks are often not detected on craniograms. As a rule, an epidural hematoma occurs at the site of damage to the skull, less often in the area opposite to it (due to counter-impact).

Bleeding from the damaged artery continues for several hours and leads to the formation of an epidural hematoma, involving the temporal, parietal and frontal regions. Peeling off the dura mater from the bone, it gradually compresses the brain.

The first signs of brain compression appear several hours (3-24) after the injury. Characteristic is the presence of a light gap with the subsequent development of pathological drowsiness, stupor or coma and symptoms of focal brain damage (hemiparesis, dilated pupil on the side of the hematoma).

Typically, the clinical picture of compression occurs against the background of a concussion or bruise of the brain, which often makes its timely recognition difficult.

Subdural hematoma is an accumulation of blood under the dura mater in the subdural space. Most often it is located on the convex surface of the cerebral hemispheres, sometimes occupying a significant area. Its symptoms develop relatively quickly: severe headache, psychomotor agitation, pathological drowsiness, stupor, coma. The skin of the face and visible mucous membranes are hyperemic, the pulse is slow or rapid. Breathing changes. The temperature is rising. Signs of intracranial hypertension, dislocation of brain areas, and secondary stem syndrome appear relatively quickly, which is manifested by a disorder of vital functions. Symptoms of focal brain damage are mild or completely absent. Menopause symptoms may be detected. There is an admixture of blood in the cerebrospinal fluid.

Subarachnoid hemorrhage is an accumulation of blood in the subarachnoid space of the brain. It is characterized by severe headaches, the presence of pronounced membrane symptoms, abundant blood in the cerebrospinal fluid, and increased temperature. Focal symptoms are absent or mild. Possible psychomotor agitation. Consciousness can be preserved. But with massive hemorrhages, an increase in intracranial hypertheisia is observed with the subsequent development of dislocation syndrome.

To objectively assess the severity of a traumatic brain injury in the acute period, it is necessary to take into account the state of consciousness, vital functions and the severity of focal neurological symptoms.

There are five levels of condition of patients with traumatic brain injury: satisfactory, moderate, severe, extremely severe, terminal.

Satisfactory condition: clear consciousness, absence of disturbances in vital functions, absence or low severity of focal neurological symptoms.

Condition of moderate severity: clear consciousness, moderate stupor, absence of disturbances in vital functions (may be bradycardia), presence of focal neurological symptoms (damage to individual cranial nerves, sensory or motor aphasia, spontaneous nystagmus, mono- and hemiparesis, etc.). The severity of the headache is also taken into account.

Severe condition: deep stupor, stupor; disturbance of vital functions, the presence of focal neurological symptoms (anisocoria, sluggish reaction of the pupils to light, limitation of upward gaze, hemiparesis, hemiplegia, epileptic seizures, dissociation of meningeal symptoms along the body axis, etc.).

Extremely severe condition: moderate or deep coma, severe disturbances of vital functions, severe focal neurological symptoms (upward gaze paresis, severe anisocoria, divergent strabismus along the vertical and horizontal axis, tonic spontaneous nystagmus, sharp weakening of pupillary reactions, decerebrate rigidity, hemiparesis, tetraparesis, paralysis, etc.).

Terminal state: extreme coma, critical impairment of vital functions, general cerebral and brainstem symptoms prevail over hemispheric and craniobasal ones.

Providing assistance. First of all, the question should be resolved: does the victim need urgent neurosurgical assistance or can we limit ourselves to conservative treatment.

The need for emergency care arises with a growing intracranial hematoma and a depressed skull fracture, compressing the brain and threatening the development of dislocation phenomena. If there are no indications for urgent surgical treatment, then conservative treatment is performed. In case of a concussion, treatment measures should be aimed at restoring the functional activity of the structures involved. They include: strict bed rest for several days (up to a week), antihistamines (diphenhydramine, pipolfen, fenkarol, suprastin), sedatives (tincture of valerian, peony, motherwort, bromides), tranquilizers (diazepam, oxazepam, rudotel, sibazon, etc.), anticholinergic drugs (bellataminal, belloid, platiphylline, antispasmodic, etc.) in normal doses.

In case of pronounced neurovegetative reactions, aminophylline is administered intravenously to improve microcirculation.

Due to the development of moderate intracranial hypertension during a concussion, dehydrating agents are indicated, mainly saluretics (diacarb, furosemide, dichlorothiazide, ethacrynic acid), which are taken in the morning for 4-5 days while monitoring the potassium content in the blood - if necessary, prescribe Potassium orotate, panangin.

For sleep disturbances, sleeping pills (methaqualone, nitrazepam, noxiron) are prescribed; for asthenia, drugs that stimulate the central nervous system (caffeine 2 ml of a 10% solution intramuscularly 2-3 times a day, acephen 0.1 g, sydnocarb 0.005 g orally 2 times a day - morning and evening). In the future, nootropic drugs (piracetam, pyriditol, aminalon, etc.) are prescribed to prevent traumatic brain disease.

The patient should remain in the hospital for 7-10 days. In case of brain contusion, therapeutic measures should be aimed primarily at restoring cerebral microcirculation, which is achieved by improving the rheological properties of blood (decreasing the aggregation capacity of formed elements, increasing blood fluidity, etc.). To do this, rheopolyglucin, Cavinton, xanthinol nicotinate, trental, 5% albumin solution under the control of hematocrit indicators.

To improve the energy supply to the brain, use glucose as part of a glucose-potassium-insulin mixture (the amount of glucose administered should not exceed 0.5 g/kg), insulin - 10 units for every 200 ml of 20% glucose solution in combination with oxygen therapy. Restoration of the function of the blood-brain barrier is facilitated by purine derivatives (theophylline, aminophylline, xanthinol nicotinate, etc.), isoquinoline (papaverine, nicoshpan). With increased vascular permeability, 10 ml of a 5% ascorbic acid solution is administered intravenously for 1-2 weeks.

Preventive desensitizing therapy is indicated (diphenhydramine, pipolfen, suprastin, etc.). Dehydration therapy is used under the control of blood plasma osmolarity (normal 285-310 mOsm/l). For this purpose, osmotic diuretics and saluretics are used. In severe arterial hypertension and cardiovascular failure, the use of the former is limited - a rebound phenomenon is possible (a secondary increase in intracranial pressure after its decrease).

Saluretics reduce the volume of circulating plasma. From osmotic
Glucocorticoids are used for dehydrating purposes. They help reduce the permeability of the vascular wall. The initial* dose of dexamethasone is 40 mg or more intravenously, the next 4 days - 8 mg every 3 hours and days 5-8 - 8 mg every 4 hours. For dehydration, barbiturates are used: nembulate PS 50-300 mg/g is administered intravenously ( 1.5-4 mg/kg) for 12 hours.

In case of subarachnoid hemorrhage, in the first 8-10 days, amino-caproic acid is administered intravenously - 100 ml of a 5% solution 4-5 times a day (can be in an isotonic sodium chloride solution); in the future, it can be used orally, 1 g every 4 hours. within 10-12 days. Transilol and contrical are prescribed. To stop psychomotor agitation, 2 ml of a 0.5% solution of seduxen or 1-2 ml of a 0.5% solution of haloperidol are injected intramuscularly or intravenously.

In case of fractures of the vault and base of the skull with nasal or auricular liquorrhea, wounds of the soft tissues of the head for the prevention of meningitis, encephalitis, an antibiotic is prescribed - benzylpenicillin sodium salt, 1 million units 4 times a day intramuscularly, in combination with sulfadimethoxine 1-2 g per the first day and 0.5-1 g in the next 7-14 days.

Patients with moderate brain contusions, not complicated by inflammatory processes, stay in the hospital for 3 weeks. At the final stage of inpatient treatment, and then in the clinic, intramuscular injections of lidase are prescribed at 64 units per day (20 injections per course of treatment). Anticonvulsants are indicated. The consumption of alcoholic beverages is strictly prohibited, and sun exposure is contraindicated.

During the recovery period, Cerebrolysin, Aminalrn, Pantogam, Piracetam and others are used, as well as drugs that improve microcirculation (cinnarizine, Cavinton).

Severe brain contusions are accompanied by persistent disturbances of consciousness, severe focal neurological symptoms, often with massive subarachnoid hemorrhages. Foci of crush injury are formed, combined with compression of the brain, which leads to its edema-swelling and dislocation syndromes. Hence the necessity and urgency of surgical intervention