Head injury (traumatic brain injury, TBI). Closed craniocerebral injury: classification, clinical picture, diagnosis, emergency care at the stages of medical care

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.

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. Then there are injuries received 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;
• 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).

It is 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 « brain 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 can be observed. 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 performs, among other things, 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. There may be: violations of blood pressure and pulse, fever, chills, sore muscles and joints, convulsions, visual disturbances, uneven pupil size, speech disorders. 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.

It 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 trauma 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.
• Training on simulators. 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, tissue swelling, and has an anti-inflammatory and reparative effect.
• Acupuncture can help reduce pain. This method is part of a complex of therapeutic measures in 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.

Under head injury understand damage to the skull and intracranial contents (brain, meninges, blood vessels, cranial nerves) by mechanical energy.

Traumatic brain injury (TBI) is one of the most common types of injuries in peacetime, accounting for about 40% of all types of injuries. TBI belongs to the category of severe injuries to the human body, accompanied by high mortality: from 5 to 70%. In wartime, the frequency of injuries to the skull and brain is constantly increasing: Great Patriotic War - 11.9%; Vietnam - 15.7%; Afghanistan - 14.4%; Chechnya – 22.7%.

Mechanism of injury

direct and indirect.

Pathogenesis.

In the pathogenesis of TBI, special importance is attached to two main factors of a mechanical nature: 1) temporary changes in the configuration of the skull, such as its general or local deformation, with the occurrence in some cases of a skull fracture; 2) displacement of the brain in the cranial cavity (in relation to the internal walls of the cavity and intracranial fibrous septa) - linear and rotational displacement, change in speed in the linear direction, linear acceleration and deceleration.

Types and classification of skull injuries.

Injuries to the skull and brain are divided into closed And open (wounds) . Distinguish firearms And non-firearms injuries. Closed TBI includes injuries in which there is no disruption of the integrity of the scalp. Open is a head injury with the presence of a wound in the soft tissues of the skull (aponeurosis), as well as a fracture of the base of the skull, accompanied by bleeding or liquorrhea from the ear or nose. When the dura mater is intact, open craniocerebral wounds are classified as non-penetrating , and if its integrity is violated - to penetrating .

Classification.

1. I. Closed head injuries: Brain concussion; 2. Brain contusion: - mild; - moderate severity; - severe degree. 3. Compression of the brain against the background of a bruise and without a bruise: - hematoma: acute, subacute, chronic (epidural, subdural, intracerebral, intraventricular); - hydro wash; - bone fragments; - edema-swelling; - pneumocephalus. 4. Condition of the intrathecal spaces: - subarachnoid hemorrhage; — cerebrospinal fluid pressure: normotension, hypotension, hypertension. 5. Condition of the skull: - no damage to bones; - type and location of the fracture. 6. Condition of the skull: - bruises; - abrasions. 7. Associated injuries and diseases. 8. According to its severity, closed craniocerebral injury is divided into three degrees: – mild (concussion and mild brain contusion), moderate severity (moderate brain contusion) and severe (severe brain contusion with compression).
2. II . Gunshot wounds of the skull and brain: By type of wounding projectile: - bullet, - fragmentation. 2. According to the nature of the injury: - soft tissue, - non-penetrating with bone damage, - penetrating. 3. By type of wound channel: - blind, - tangential, - through, - ricocheting. 4. By localization: - temporal, - occipital, other areas. 5. According to the type of fracture of the skull bones: - linear, - depressed, - crushed, - perforated, - splintered. 6. By the number of wounds: - single, - multiple. 7. By the influence of combinations of various factors: - mechanical, - radiation, - thermal, - chemical. 8. According to the nature of the brain damage: - concussion, - bruise, - crushing, - compression. 9. According to the severity of the injury: - mild, - moderate, - severe. 10. According to the severity of the wounded person’s condition: - satisfactory, - moderate, - severe, - terminal. 11. Blind wounds: - simple, - radial, - segmental, - diametric, - ricocheting, - tangential. 12. Penetrating wounds: - segmental, - diametrical, - tangential.

During TBI, it is customary to distinguish the following periods:

1) acute period - from the moment of injury to stabilization at different levels of functions impaired due to injury (from 2 to 10 weeks, depending on the clinical form and severity of TBI);

2) intermediate period - from the moment of stabilization of functions until their full or partial restoration or stable compensation (for mild TBI - up to two months, for moderate TBI - up to four months, for severe TBI - up to six months);

3) long-term period - clinical recovery or the maximum possible restoration of impaired functions or the emergence and (or) progression of new pathological conditions caused by TBI (up to two years or more). A detailed diagnosis, including all elements of this classification, can only be made in a specialized hospital.

The clinical picture of damage to the skull and brain consists of general cerebral and local (focal) neurological symptoms. General cerebral symptoms include headache, nausea, vomiting, dizziness, etc. Local (focal) symptoms depend on the location of the brain damage and can manifest as hemiparesis, hemiplegia, speech, and visual disturbances.

Closed TBI clinic.

1. Closed brain injury accompanied by symptoms of concussion is a functionally reversible form of brain injury. It is characterized by short-term loss of consciousness from several seconds to several minutes, retro- and anterograde amnesia, vomiting, headache, dizziness and other autonomic disorders. As a rule, only general cerebral neurological symptoms are noted in the neurological status. There are no injuries to the skull bones, the pressure of the cerebrospinal fluid and its composition are without deviations from the norm. The condition of patients, as a rule, improves within the first or second week.
2. Closed brain injury, accompanied by symptoms of brain contusion (degrees - easy, medium, heavy). Brain contusion mild degree It is characterized by turning off consciousness from several minutes to one hour. Then headache, dizziness, nausea, vomiting, retro- and anterograde amnesia are noted. Vital functions are usually not impaired, a moderate increase in heart rate, respiration, and rise in blood pressure is possible. Focal symptoms are mild (nystagmus, pyramidal insufficiency) and disappear after 2-3 weeks. Unlike a concussion, subarachnoid hemorrhages and skull fractures are possible. Brain contusion medium degree characterized by loss of consciousness after injury lasting from several minutes to several hours. Retrograde and anterograde amnesia and other cerebral symptoms are pronounced. Complaints of severe headache, repeated vomiting, possible transient disturbances of vital functions in the form of bradycardia, tachycardia). Nesting symptoms are clearly manifested, determined by the localization of the brain contusion - hemiparesis, speech disorders, visual disturbances, etc. A lumbar puncture usually reveals blood-stained cerebrospinal fluid flowing out under increased pressure. Craniograms often reveal a fracture of the skull bones. Brain contusion severe accompanied by loss of consciousness from several hours to several weeks. Severe disturbances of vital functions are observed: bradycardia or tachycardia, often with arrhythmia, arterial hypertension, respiratory distress. In the neurological status, stem symptoms come to the fore: floating movements of the eyeballs, accommodation paresis, tonic nystagmus, swallowing disorders, decerebrate rigidity (generalized or focal seizures). As a rule, brain contusion is accompanied by fractures of the bones of the vault or base of the skull, massive subarachnoid hemorrhages.
3. Closed brain injury accompanied by symptoms of increasing compression of the brain (with or without bruises of the brain). Brain compression syndrome is characterized by a life-threatening increase at various intervals after injury (the so-called “light period”) of general cerebral, focal and brainstem symptoms. Depending on the background (concussion, brain contusion) against which traumatic compression of the brain develops, the latent period can be pronounced, erased or completely absent. Clinically, pupil dilation appears on the side of compression, and hemiplegia on the opposite side. The appearance of bradycardia is characteristic.

Brain injury clinic.

At the suggestion of E.I. Smirnov (1946) usually divides the course of pathological processes in case of brain injury into five periods.

They are called periods of traumatic brain disease:

– initial period – “chaotic” according to N.N. Burdenko, lasting about three days. Characterized by a predominance of general cerebral symptoms over local ones, disturbances of consciousness, breathing, cardiovascular activity, and the act of swallowing;

II – period of early reactions and complications – (infections and dyscirculation), lasting up to three weeks – 1 month is characterized by an increase in edema-swelling of the brain, its protrusion (benign prolapse). The wounded regain consciousness, focal symptoms are revealed, the course is complicated by the development of meningitis, meningoencephalitis, and suppuration of the wound canal. As a result of the development of infection, malignant protrusions (secondary prolapses) occur;

III – period of elimination of early complications and a tendency to limit the infectious focus, begins in the 2nd month after injury and lasts approximately 3-4 months (depending on the severity of the injury). With a smooth course, the wound heals and recovery occurs.

I V – period of late complications , begins 3-4 months after injury and lasts 2-3 years, characterized by the formation of late brain abscesses, outbreaks of meningitis, meningoencephalitis;

V – period of long-term consequences associated with the presence of a meningeal scar. May last for many years after injury.

Diagnosis of TBI:

1. Identifying a history of injury.

2. Clinical assessment of the severity of the condition.

3. State of vital functions.

4. Condition of the skin - color, moisture, bruises, presence of soft tissue damage.

5. Examination of internal organs, skeletal system, concomitant diseases.

6. Neurological examination: the state of cranial innervation, reflex-motor sphere, the presence of sensory and coordination disorders, the state of the autonomic nervous system.

7. Meningeal symptoms: stiff neck, Kernig’s and Brudzinski’s symptoms.

8. Echoencephaloscopy.

9. X-ray of the skull in two projections.

10. Computer or magnetic resonance imaging of the skull.

11. Ophthalmological examination of the condition of the fundus.

12. Lumbar puncture - in the acute period, it is indicated for almost all victims with TBI (with the exception of patients with signs of compression of the brain) with measurement of cerebrospinal fluid pressure and removal of no more than 2-3 ml of cerebrospinal fluid, followed by laboratory testing.

Providing assistance during the stages of medical evacuation.

First aid

comes down to applying an aseptic bandage to the wound and carefully removing the wounded. The wounded, who are unconscious, are carried out on their sides (in order to prevent aspiration of vomit), they need to unfasten their collar and loosen their belt. If the tongue is retracted and there are signs of asphyxia, insert an air duct (S-shaped tube, breathing tube TD-1). Do not administer drugs (respiratory depression).

First aid

– bandaging the bandage, ventilation of the lungs using a breathing apparatus DP-10, DP-11, oxygen inhalation with a KI-4 apparatus, maintaining cardiovascular and respiratory activity (intramuscular administration of 2 ml of cordiamine, 1 ml of caffeine). Evacuation of the wounded, first of all, on a stretcher.

First aid

– combating asphyxia, carrying out artificial ventilation of the lungs with the DP-9, DP-10 apparatus, oxygen inhalation with the KI-4 apparatus, maintaining cardiovascular and respiratory activity (administration of 2 ml of cordiamine, 1 ml of caffeine, 1 ml of 5% ephedrine).

If necessary, correct the bandage, administer a prophylactic dose of antibiotics (500,000 units of streptomycin, 500,000 units of penicillin), and carry out seroprophylaxis of tetanus by subcutaneous injection of 0.5 ml of tetanus toxoid.

Those wounded in the skull with ongoing bleeding from soft tissue wounds are sent to the dressing room to perform hemostasis using a pressure bandage and applying a clamp to the bleeding vessel. The wounded are not detained at this stage, they are evacuated first of all with ongoing intracranial bleeding and liquorrhea, and secondly those wounded in the soft tissues of the skull. Before transportation, cardiovascular and respiratory devices and an airway are administered according to indications.

It is necessary to transport the wounded to the skull in a prone position and it is better to immediately go to the EMS stage, bypassing the intermediate stages of medical evacuation.

Qualified medical care .

Particular attention should be paid to the wounded, who, as a result of medical triage, are subject to surgical treatment at this stage for life-saving reasons (refusal to surgery can lead to death).

Emergency surgical interventions are performed for the following wounds and injuries: wounds and injuries of the head and neck, accompanied by: - ​​asphyxia (tracheal intubation or tracheostomy); — external bleeding (stopping external bleeding by ligating the vessels of the integumentary tissue or tight tamponade of the wound); — craniotomy and postsurgical surgical treatment of brain wounds are not performed at the stage of providing qualified assistance (including in cases of compression of the brain).

Sorting of skull wounded patients into primary and secondary care during mass admission will often have to be carried out without removing the bandage.

Determination of transportability is made based on an assessment of the general condition, preservation of the reaction of the pupils and corneal reflexes, the state of the pulse, breathing, bandage, etc.

During evacuation, provide for: - wounded with damage to the soft tissues of the skull without focal neurological symptoms - in the emergency room; - wounded with a concussion - in the VPNG. All other wounded people with open skull injuries are sent to a specialized neurosurgical hospital.

Specialized assistance .

The hospital provides comprehensive specialized surgical care to the wounded who have not received qualified surgical care.

1. Questions for self-control.
2. Mechanism of traumatic brain injury.
3. Classification of gunshot injuries of the skull and brain.
4. Classification of non-gunshot injuries of the skull and brain.
5. Clinical picture of a concussion.
6. Clinical picture of brain contusion.
7. Clinical picture of brain compression.
8. Diagnosis of combat trauma to the skull and brain.
9. The volume of medical care at the stages of medical evacuation.
10. Possible complications of traumatic brain injury and their prevention.

Penza State University

medical school

department of technical and electrical engineering

course "Extreme and military medicine"

Traumatic brain injury

Penza 2003

Compiled by: Candidate of Medical Sciences, Associate Professor Melnikov V.L., Art. teacher Matrosov M.G.

Traumatic brain injury is one of the most common injuries and accounts for >40% of the total number; the mortality rate for severe injuries of the skull and brain reaches 70-80%. The mechanism of traumatic brain injury can be direct or indirect. An example of an indirect mechanism would be traumatic brain injury resulting from a fall from a height onto the legs or pelvis. When landing and stopping the movement of the skeleton, the skull, due to inertia, seems to be pushed onto the spine and a fracture of the base of the skull can occur. If this does not happen, the skull stops, and the brain, continuing to move, hits its base and standing bones.

Classification of traumatic brain injuryTable 1.

Closed	Open
1. Concussion	I. Damage to the soft tissues of the head without signs of brain injury
2. Brain contusion (1st, 2nd, 3rd degree)	2. Damage to the soft tissues of the head with impaired brain function (concussion, bruise, compression).
3. Compression of the brain against the background of his injury.	3. Damage to the soft tissues of the head, bones of the cranial vault and brain (bruise, compression) - penetrating and non-penetrating.
4. Compression of the brain without concomitant injury.	4. Fracture of the base of the skull (contusion and compression).
5. Damage to the bones of the cranial vault and brain (bruise, compression).	5.Gunshot wounds.

Syndromes: Hypertensive - cerebrospinal fluid pressure is increased. Hypotensive - cerebrospinal fluid pressure is reduced. Normotensive - cerebrospinal fluid pressure is not changed.

Diagnosis of traumatic brain injury: There are four main groups of clinical symptoms: cerebral, local, meningeal and brainstem.

General cerebral symptoms. Their formation is based on functional (reversible) changes in the substance of the brain. Appearing after injury, these signs gradually regress and, ultimately, disappear without a trace. These include:

1. Loss of consciousness. It proceeds according to the stem type and is characterized by three forms of manifestation: a) stunning - expressed by a short-term disturbance of orientation followed by mild drowsiness. Particular attention should be paid to this form of disorder of consciousness, since victims remain on their feet and do not regard the state of stupor as a loss of consciousness; b) stupor - a more severe degree of impairment of consciousness, in which the reaction to gross stimuli (pain, loud cry) in the form of coordinated defensive movements, opening of the eyes is still preserved; c) coma - prostration with a complete loss of perception of the surrounding world, deepening, characterized by adynamia, atony, areflexia, depression of vital functions.

2. Memory loss (amnesia). It may be: retrograde, when patients do not remember the events immediately preceding the injury; anterograde - loss of memory for events that occurred after the injury; anterograde - a combined form of memory loss for events before and after injury.

Headache. There can be both diffuse and local pain, bursting or squeezing the head.

Dizziness. Instability in the Romberg pose.

Nausea, vomiting. Depending on the type and nature of the injury, nausea can be short-term with one or two vomiting and long-term with frequently repeated vomiting, even indomitable.

Positive Mann-Gurevich sign. The doctor asks the patient to follow with his eyes, without turning his head, any object in his hand, and makes several (3-5) oscillatory movements of the object in the frontal plane. If the patient’s well-being has worsened, cerebral and autonomic manifestations have intensified, and tachycardia has appeared, then the symptom is considered positive.

7. Autonomic symptoms. Weakness, noise or ringing in the ears, pallor or hyperemia of the skin, increased humidity or dryness, lability of the pulse and other vegetative manifestations.

Local(they are also focal) symptoms. The reason for their appearance is organic damage to some part of the brain and loss of function in the zone of its innervation. Clinically defined local signs are nothing more than paresis, paralysis, sensitivity disorders and dysfunction of the sensory organs. For example: motor or sensory aphasia, anisokaria, smoothness of the nasolabial fold, deviation of the tongue, monoparesis of the limbs, hemiparesis, etc.

Meningeal (meningeal) symptoms. They are the result of irritation of the meninges directly by trauma (bruises, ruptures), pressure from bone fragments, foreign bodies, hematomas (the dura mater has baroreceptors), blood, infection and other ingredients. Typical severe meningeal symptoms can be identified during an external examination of the patient. He takes a forced position, lying on his side with his head thrown back and his legs bent at the knees and hip joints (the “trigger” pose). Other characteristic symptoms are photophobia. The victim tries to turn away from the light source or covers his face with a blanket. There is increased excitability, and an extreme reaction to harsh stimuli can be a convulsive seizure.

Patients complain of intense headaches that get worse when moving their heads. Localization of pain is the frontal and occipital areas with irradiation to the neck or eyeballs. Often there is pain in the eyeballs. When the meninges are irritated, nausea and vomiting are observed, the latter being repeated and debilitating.

Pathognomonic meningeal signs are nuchal rigidity and positive Kernig and Brudzinski signs. An increase in body temperature to 39-40°C is typical, especially if an infection occurs.

Stem symptoms. In their genesis they are no different from local ones, but the damage affects only the brain stem and its structures that regulate vital functions. Injury to the brain stem can be primary, or arise as a result of brain dislocation and pinching of the brain stem into the foramen of the cerebellar tentorium or in the occipito-cervical dural infundibulum.

Stem symptoms are divided into non-upper-trunk, lower-trunk and dislocation.

Upper stem(mesodiencephalic syndrome) is characterized by a disorder of consciousness in the form of stupor or stupor. Mild breathing disorders - tachypnea and “orderly breathing”, when the duration of inhalation and exhalation becomes the same. Cardiovascular disorders consist of increased heart rate up to 120 per minute. and an increase in blood pressure to 200/100 mm Hg.

Upper brainstem symptoms include a large number of oculomotor disorders. This is a symptom of “floating gaze”, divergence in the vertical and horizontal planes, convergence, gaze paresis, etc.

Muscle tone is high, reflexes are animated or increased, bilateral pathological reflexes from the feet appear (Babinsky, Gordon, Oppenheim). Swallowing is not impaired. Body temperature is high.

Nizhnestvolova(bulbar) syndrome is characterized by a more severe condition. There is no consciousness - coma. Respiratory disorder reaches an extreme degree, pathological forms of breathing occur. The pulse is weak and frequent. Blood pressure drops to 70/40 mm Hg. and below. The pupils are wide, the reaction to light is subtle. Swallowing is severely impaired. Thermoregulation is reduced.

Dislocation syndrome- this is a rapid transition from the upper brainstem to the lower brainstem syndrome as a result of brain infringement.

Traumatic brain injury can occur with increased, normal or decreased cerebrospinal fluid pressure, depending on which hyper-, normo- and hypotensive syndromes are distinguished. Diagnosis of the syndrome can be carried out on the basis of clinical manifestations and using auxiliary methods.

Hypertension syndrome occurs in 65% of victims with traumatic brain injury. It occurs more often in older people. It occurs with a bursting headache, high blood pressure, and bradycardia. A positive symptom of “raised head” (pillow) is noted - patients take a forced position with the head end raised, since an elevated position reduces headaches.

Traumatic brain injury with hypotension syndrome occurs in 25% of victims. A decrease in cerebrospinal fluid pressure is more often observed in young people, occurring with a compressive headache, with normal or low blood pressure, and tachycardia. Vegetative signs are pronounced, most often manifested by pallor and sweating. Increased fatigue, lethargy, and mental exhaustion are noted. A positive symptom of “lowered head” is that giving the patient a Trandelenburg position reduces headaches.

During a lumbar puncture with the patient in a supine position, cerebrospinal fluid flows out in drops at a frequency of 60 per minute, and the pressure measured by a manometer is 120-180 mm of water column. These numbers are considered the norm. An increase in the frequency of drops and cerebrospinal fluid pressure is regarded as hypertension, and a decrease is considered as hypotension.

Lumbar puncture should be performed in all patients with concussion and more severe TBI.

Additional research methods

Craniography- the most common method. When examining patients with traumatic brain injury, two panoramic craniograms are required: straight and lateral. .

Schemes of craniograms in overview projections with explanations are presented in Fig. 1.

Rice. 1. Scheme of craniograms in direct (A) and lateral (B) projections:

(A) 1. Pyramid. 2. Lesser wing of the main bone. 3. Mastoid process. 4. Atlantooccipital

joint. 5. Atlantoaxial joint. 6. Frontal sinus. 7. Sagittal suture. 8. Lambdoid suture. 9. Coronal suture. 10. Maxillary sinus.

(B) 1. Pyramid. 2. Main bone. 3. Turkish saddle. 4. The anterior part of the large wings of the main bone. 5. Frontal sinus. 6. Coronal suture. 7. Lambdoid suture. 8, 9. Anterior and posterior branches of the meningeal artery, 10. Internal and external auditory canals. 11. Shadow of the auricle cartilage. 12. Nasal bones. 13. Cheek bones. 14. Maxillary sinus

Echoencephalography- this is the registration of the position of the midline structures of the brain (epiphysis, third ventricle, interhemispheric fissure, etc.) by receiving a reflected ultrasound signal from them (M-echo). The method is based on the ability of ultrasound to propagate in various media and give reflection at the border of structural formations with inhomogeneous acoustic resistance. The ultrasonic wave reflected from the object is recorded on the screen of the echoencephalograph in the form of a peak located along the midline. During volumetric processes in the cranial cavity (hematomas, hygromas, traumatic cysts, abscesses, tumors), the midline structures of the brain shift toward the healthy hemisphere. This is revealed on the echoencephalogram in the form of a displacement of the M-echo from the midline by 3 mm or more. With pronounced volumetric processes, for example, with epi- and subdural hematomas, the displacement of the M-echo can reach 8-15 mm (Fig. 2).

Rice.2

Normal echogram (A). Displacement of midline structures and M-echo with intracranial hematoma (B)

Carotid angiography. This research method is based on the introduction into the carotid artery of substances that have the property of absorbing X-rays, which ensures the visibility of blood vessels on an X-ray at different phases of cerebral circulation. By changes in the filling and location of blood vessels, the degree of circulatory disturbance in the brain and its causes are judged.

CT scan- an X-ray method of research using a computer, which allows one to obtain images of the structures of the brain and bones of the skull both in whole form and in sections with a thickness of 3 to 13 mm. The method allows you to see changes and damage to the bones of the skull, structures of the brain, identify intracerebral and intracranial hemorrhages and much more.

Patients with traumatic brain injury should undergo ophthalmological and otorhineurological examination.

Lumbar puncture done to clarify the pressure of the cerebrospinal fluid, determine its composition and the patency of the cerebrospinal fluid pathways.

Manipulation is performed in the position of the patient lying on his side, on a hard table with bent legs brought to the stomach. The back is bent as much as possible. The place for puncture is the space between the III and IV lumbar vertebrae. The skin is treated with iodine tincture, then with alcohol until traces of iodine disappear, the entry of which into the lumbar canal is highly undesirable. The puncture site is anesthetized with a 1% novocaine solution in an amount of 5-10 ml. The puncture is performed with a special needle with a mandrin, directing its course strictly sagittally and at an angle to the frontal plane. The angle corresponds to the inclination of the spinous processes. The feeling of needle failure, as a rule, corresponds to the presence of the needle in the subarachnoid space. When removed from the mandrin needle, cerebrospinal fluid begins to flow out. Pressure is measured with a manometer, and then cerebrospinal fluid is taken in an amount of 2 ml for examination. At high pressure, the cerebrospinal fluid should be slowly, dropwise released until the cerebrospinal fluid pressure normalizes.

Normally, cerebrospinal fluid is clear. In an adult, the subarachnoid space and ventricles contain 100-150 ml of cerebrospinal fluid, which is completely renewed up to 6 times a day. It is absorbed and instead produced mainly by the choroid plexuses of the ventricles.

Laboratory examination: colorless transparent liquid, cytosis in 1 μl - 2-3; pH - 7.35-7.80; protein - 0.15-0.33 g/l; glucose - 0.5-0.8 g/l.

CLINICAL AND DIAGNOSTICS OF INDIVIDUAL

NOSOLOGICAL FORMS OF CRANIOBRAININJURIES

Brain concussion

The cause of a concussion is a mechanical injury of direct or indirect impact, followed by the development of cerebral symptoms. The nature of headaches and position in bed depend on CSF pressure, and the severity of clinical manifestations depends on the severity of the injury.

May appear nystagmus, slight asymmetry of the face due to the smoothing of the nasolabial fold and the drooping of the corner of the mouth, deviation of the tongue. These and other local "microsymptoms" are, as a rule, within 1-2 days. Longer persistence of these signs indicates the presence of a brain contusion.

Additional research methods practically do not provide information that reliably confirms the diagnosis. An exception is lumbar puncture, which can be used to determine changes in cerebrospinal fluid pressure.

With proper treatment, the patient's condition improves by the end of the first week, and complete regression of clinical signs occurs after 2-4 weeks. The most stable are headache and the Mann-Gurevich symptom, the test of which should be used to determine the timing of bed rest. Once it disappears (becomes negative), patients are allowed to sit up in bed and then get up and walk.

Brain contusion

Brain contusion occurs due to direct and indirect mechanisms of impact. An example of an indirect mechanism of injury is a counter-impact, when a wave of “perturbed” brain matter, consisting of 80% water, reaches the opposite wall of the skull and hits its superior parts or is destroyed by tightly stretched areas of the dura mater.

A brain contusion is an organic lesion. As a result of the injury, areas of crushing and necrosis of brain tissue, severe vascular disorders with phenomena of hemorrhagic softening occur. Around the area of ​​brain contusion there is a zone of severe molecular concussion. Subsequent pathomorphological changes are expressed in encephalomalacia and lysis of a portion of the medulla, its resorption. If an infection occurs during this period, a brain abscess is formed. In an aseptic course, the brain tissue defect is replaced by a scar of neuroglia or brain cysts are formed.

The clinical picture of brain contusion is that immediately after the injury, victims experience general and local symptoms, and in severe forms, meningeal and brainstem symptoms are added.

There are three degrees of brain contusions.

/ degree (mild bruise). Loss of consciousness from several minutes to 1 hour. Upon restoration of consciousness, pronounced general cerebral symptoms and local, predominantly microfocal signs are determined. The latter are stored for 12-14 days. Violations of vital functions are not determined.

Grade I brain contusion may be accompanied by moderate subarachnoid hemorrhage and fractures of the bones of the vault and base of the skull, which are detected on craniograms.

// degree (moderate). Switching off consciousness after injury reaches 4-6 hours. During the period of coma, and sometimes in the first days of recovery of consciousness, moderately severe disorders of vital functions (upper brainstem signs) are detected in the form of bradycardia, tachypnea, increased blood pressure, nystagmus, etc. As a rule, these phenomena are transient.

Upon return of consciousness, amnesia, intense headache, and repeated vomiting are noted. In the early post-comatose period, mental disorders may be observed.

When examining the patient, distinct local symptoms are found that last from 3-5 weeks to 6 months.

In addition to the listed signs, with a second degree brain contusion, pronounced meningeal symptoms are always detected, fractures of the vault and base of the skull can be found, and in all cases significant subarachnoid hemorrhage.

Additional research methods: with lumbar puncture, increased cerebrospinal fluid pressure and a significant admixture of blood in it are determined. Craniograms show fractures of the skull bones. Echoencephalography gives a displacement of the M-echo of no more than 3-5 mm.

Illdegree. Loss of consciousness after injury is prolonged - from several hours to several weeks. The condition is extremely serious. Severe disturbances of vital functions come to the fore: changes in heart rate (bradycardia or tachycardia), arterial hypertension, disturbances in the frequency and rhythm of breathing, hyperthermia. Primary brainstem symptoms are clearly expressed: floating movements of the eyeballs, gaze paresis, tonic nystagmus, bilateral mydriasis or miosis, impaired swallowing. If the patient is in stupor or in a state of moderate coma, it is possible to identify local symptoms in the form of paresis or paralysis with impaired muscle tone and reflexes. Meningeal symptoms include stiff neck, positive Kernig and Brudzinski signs.

Grade III brain contusion is usually accompanied by fractures of the vault and base of the skull and massive subarachnoid hemorrhage.

Electroencephalography - with a brain contusion and crushing, high-amplitude delta waves appear in the destruction zone. With extensive convexital lesions, zones of electrical silence are found corresponding to the most severely affected area.

BRAIN COMPRESSION

The causes of compression of the brain can be: intracranial hematomas, bone fragments, foreign bodies, hygromas, pneumocephalus, hydrocephalus, subarachnoid hemorrhage, edema and swelling of the brain. The first four of these causes cause local compression of the brain and are the true root causes of intracranial catastrophes with a fairly typical course and frequent tragic outcome. The remaining nosological forms arise as a consequence of the listed or other severe injuries of the skull and brain, or as a natural subsequent stage of local compression of the brain. They lead to a total increase in brain volume and, as the pathology progresses, can cause dislocation and pinching of the brain in the foramen magnum.

Compression of the brain by bone fragments and foreign bodies

Compression of the brain by bone fragments occurs during fractures of the skull vault with prolapse of fragments deeper than the internal bone plate. Depressed fractures of the calvarium are mainly of two types. The first is when, as a result of mechanical action, the fragments are displaced at an angle, the apex of which “looks” into the cranial cavity, and the peripheral ends of the fragments retain connection with the mother bone. Such fractures are called impression fractures. The second type of fracture (depression) occurs when the injury is inflicted with great force, and the damaging agent has a small contact area. For example, a blow with a hammer, brass knuckles or a similar object. As a result of the injury, a fenestrated fracture occurs, the size and shape of the wounding object. The bone plate that covered the resulting “window” falls into the cranial cavity and leads to compression of the brain (Fig. 3).

Foreign bodies enter the cranial cavity mainly as a result of gunshot (bullet, shrapnel) wounds. However, penetrating injuries to the skull are also possible with cold steel or household objects, parts of which, breaking off, remain in the cranial cavity.

Rice. 3. Depressed fractures of the calvarium: A - impression; B - depressed.

Preliminary data allow us to make a diagnosis of brain contusion (of varying severity), which in fact accompanies depressed fractures and foreign bodies of the skull with compression of the brain. The final diagnosis is made after craniography, computed tomography, echoencephalography, with the help of which depressed skull fractures or foreign bodies in it are identified, and clinical data and the results of additional research methods on the topography of the location of the ingredient causing pressure on the brain tissue must match.

Compression of the brain by intracranial hematomas

Intracranial hematomas occur in 2-9% of the total number of traumatic brain injuries. There are epidural, subdural, subarachnoid, intracerebral, intraventricular hematomas (Fig. 4).

Fig4. Intracranial hematomas: 1 - epidural; 2 - subdural; 3 - intracerebral; 4 - intraventricular

The clinical manifestations of various hematomas are not the same, but in their course a number of patterns can be traced that allow intracranial hematomas to be considered in one group. Schematically, it looks like this: a history of head trauma with loss of consciousness (often for a short period). Upon return of consciousness, general cerebral symptoms are identified, on the basis of which a diagnosis of “concussion” can be made. Optimally, the patient is hospitalized and appropriate treatment is prescribed: rest, sedatives, etc. In some cases, victims may not seek help, since short bed rest, as a rule, relieves general cerebral symptoms. Moderate headaches and amnesia persist. The patient's condition improves significantly. Thus, rupture of an intracranial vessel at the time of injury due to the lack of clinical evidence of brain compression remains unnoticed. As compression increases, meningeal and then local symptoms appear (anisokaria, mono- or hemiparesis, etc.). A disorder of consciousness of the cortical type occurs. Psychomotor and speech agitation occurs, which subsequently turns into depressed consciousness (stupor), often with convulsive seizures and subsequent cerebral coma. The outcome of brain compression if left untreated is usually death. Thus, intracranial hematoma is characterized by a three-phase course: injury with loss of consciousness - improvement of the condition (“bright interval”) - deterioration of the condition with a tragic outcome.

Light interval refers to the time from the return of consciousness after the initial injury to the appearance of signs of brain compression. The duration of the light interval can be from several hours to several days, weeks and even months. Depending on this, hematomas are divided into acute (light interval up to 3 days), subacute (from 4 to 21 days) and chronic (more than three weeks).

What determines the duration of the light interval?

It has now been proven that hematomas are mainly formed during the first three hours, and their volume, significantly exceeding 30-50 ml, does not always interrupt the light interval. The reason is that the brain is not "squeezed" into the skull, but has certain spaces between it and the membranes with a certain intracranial pressure. A formed hematoma at an early stage does not cause pronounced compression of the brain, since it, like any living organ, sacrifices its volume to a certain extent, compensating for its functional state. Gradual vascular disorders, hypoxia, increasing edema, and then swelling of the brain lead to an increase in its volume and a sharp increase in pressure over the area of ​​contact between the hematoma and the brain. A breakdown of the compensatory capabilities of the central nervous system occurs, which is expressed in the end of the light interval. A further increase in brain volume leads to displacement of the midline structures, and then dislocation of the brain stem into the foramen of the cerebellar tentorium and the occipito-cervical dural infundibulum.

An increase in the duration of the clear interval in the acute stage may be due to the absorption of the liquid part of the blood from the hematoma and a decrease in its volume. The duration of imaginary well-being is also facilitated by dehydration carried out in a hospital for patients diagnosed with a concussion or cerebral contusion, which does not allow the development of pronounced swelling of the brain tissue.

With subacute and chronic hematomas, it is possible to increase their volume (on days 16-90) due to the influx of fluid. The decomposition of spilled blood and the increase in the content of high molecular weight proteins increase the oncotic pressure in the hematoma. This causes diffusion of the cerebrospinal fluid until an osmotic equilibrium is created between the liquid contents of the hematoma and the cerebrospinal fluid.

It is possible that the lucid interval may be interrupted by repeated hemorrhages in the epi- or subdural space when a blood clot breaks off from a damaged vessel. This can occur with a sudden sharp change in arterial and intracranial pressure - when sneezing, coughing, straining, etc.

Thus, the duration of the clear interval depends on many factors, and not just on the time and intensity of bleeding.

Epidural hematomas

Epidural hematoma - this is a limited accumulation of blood between the bones of the skull and the hard shell of the brain. Suprapaholic hemorrhages occur as a result of the direct mechanism of injury when exposed to a traumatic agent with a small area of ​​application of force of varying intensity and account for 0.6-5% of all traumatic brain injuries.

The source of the formation of epidural hematomas most often are damage to the branches of the middle meningeal artery, the vein of the same name, or the spongy substance of a broken bone. This explains the fact that epidural hematomas in 73-75% of cases are located in the temporal region. The dura mater is tightly adjacent to the bones of the skull, fused with them along the suture line, so the area of ​​epidural hematomas is limited and most often is 6-8 cm in diameter.

Suprapaholic hematomas usually have a hemispherical shape with a height in the central part up to 4 cm. The amount of blood that has poured into the epidural space is more often in the range of 80-120 ml, although local accumulation of blood in a volume of 30-50 ml leads to compression of the brain.

The clinical picture of acute epidural hematoma is characterized by a predominantly classical course.

From the anamnesis, the presence of a head injury, accompanied by loss of consciousness, is revealed. Upon return of consciousness, only general cerebral symptoms are found in the patient.

In the further clinical course of epidural hematoma, 4 stages can be distinguished: a light gap, the stage of excitation, inhibition and cerebral coma.

The light period is short, from several hours to 1.5-2 days, in most cases it does not exceed 24 hours. This stage begins with the return of consciousness and is characterized by the presence of the already described cerebral symptoms. During the first hours after the injury, the severity of cerebral symptoms fades away. At rest, dizziness and vomiting disappear, nausea and headache decrease. The victim is adequate, oriented in time and space, and critically assesses his condition.

In the next stage, the patient develops unconscious anxiety. He is overly active, strives to change the position of his limbs, sit down, stand up, and leave the room. The face is hyperemic, in the eyes there is alienation or fear. Patients cannot stand bright light, noise. This excitement is caused by increased headaches, which are painful and bursting in nature. The victim covers his head with his hands, takes a forced position, begs or demands immediate help, agrees and insists on surgical treatment.

Persistent nausea, repeated vomiting, terrifying dizziness appear - everything floats before your eyes. The pulse rate slows down, moderate bradycardia occurs (51-59 beats/min), blood pressure increases (from 140/80 to 180/100 mm Hg). Breathing moderately quickens (21-30 breaths per minute). At this stage, focal microsymptoms may appear: mild anisokaria - slight dilation of the pupil on the side of the hematoma, smoothness of the nasolabial fold, moderate deviation of the tongue. Percussion of the skull can reveal areas of increased pain (usually above the hematoma), to which the patient reacts with a pained grimace.

In the stage of inhibition, the behavior of the patient changes radically. He no longer rages and asks for nothing. A secondary disorder of consciousness occurs, beginning with stupor and progressing to stupor. The victim is indifferent to his surroundings, his gaze is pointlessly directed into the distance. Bradycardia (41-50 beats/min.) and tachypnea (31-40 breaths per minute) increase. Asymmetry in blood pressure appears. On the arm opposite to the lesion, blood pressure will be 15-20 mmHg. higher than on the arm on the side of the hematoma. Focal symptoms increase. Among them, the main diagnostic role is played by: dilation of the pupil on the side of the hematoma, smoothness of the nasolabial fold, abnormal grins, deviation of the tongue, spastic hemiparesis with a predominant lesion of the arm on the opposite half of the body. Meningeal signs are identified in the form of stiff neck and positive Kernig and Brudzinski signs.

The final stage of untreated epidural hematoma is the stage of cerebral coma. It is caused by displacement and infringement of the brain. It is characterized by dislocation signs: the transition of bradycardia to tachycardia (120 beats/min. and above), tachypnea to pathological types of breathing, blood pressure begins to steadily decrease, reaching critical numbers (below 60 mm Hg), swallowing disorders, a symptom of floating gaze, gross anisocaria and dissociation of meningeal symptoms, muscle tone and reflexes along the body axis. In the final phase, bilateral mydriasis with lack of pupillary response to light, areflexia, muscle atony, and death occurs.

A favorable outcome for epidural hematoma is possible with early diagnosis and timely adequate treatment. In addition to clinical signs, craniography, computed tomography, echoencephalography and carotid angiography are of diagnostic value, with the help of which they can identify fractures of the cranial vault, most often the scales of the temporal bone, an area of ​​​​increased density of a plano-convex or biconvex shape adjacent to the skull, displacement of the median M-echo by 6-15 mm and displacement of intracerebral vascular structures.

An ophthalmological examination reveals congestion in the fundus.

Subdural hematomas

A subdural hematoma is a limited accumulation of blood between the dura and arachnoid membranes of the brain. The incidence of these hemorrhages ranges from 1 to 13% of all traumatic brain injuries. Subdural hematomas most often occur with an indirect mechanism of injury, such as a counter-strike on the side opposite to the application of force. The area of ​​contact with the traumatic agent is large, so significant destruction occurs in this place: skull fractures, brain contusions, subarachnoid hemorrhages.

The source of the formation of subdural hematomas is most often damage to the transitional veins in the area between the surface of the brain and the sagittal sinuses as a result of displacement of the brain or bone fragments. Another reason is the rupture of the delicate pial vessels during sharp rotation of the head and displacement of the hemispheres around the vertical or horizontal axes. These same vessels are damaged during brain contusions.

Subdural hematomas can reach 250-300 ml, but more often their volume is 80-150 ml. In 60% of cases, hematomas form over the convex surface of the brain in the form of a cloak 1-1.5 cm thick, covering 1-2 lobes over an area of ​​4x6 to 13x15 cm.

Clinical manifestations of subdural hematomas in the classical version are close to the course of epidural hemorrhages, but at the same time they have a large number of distinctive features and signs that allow differential diagnosis of these nosological forms of injury in the acute period. (Table 2).

Thus, there are quite a few signs that make it possible to distinguish the clinical picture of an epidural from a subdural hematoma.

Subdural hygroma

Subdural hygroma - It is a localized collection of cerebrospinal fluid in the space beneath the dura mater resulting from trauma.

Subdural hygromas are much less common than hematomas in a similar situation. The issue of pathogenesis of hygroma has not been completely resolved. The reasons for the limited accumulation of cerebrospinal fluid under the dura mater are considered to be damage to the arachnoid membrane, like a valve that allows the cerebrospinal fluid to move in only one direction - from the subarachnoid to the subdural space. Hygromas can also occur due to changes in the vessels of the dura mater, creating conditions for blood plasma to leak into the subdural space, or as a result of severe brain damage when communications arise between the intrathecal spaces and lateral ventricles.

The clinical manifestations of subdural hygromas are heterogeneous, since they can occur both in isolation and in combination with many nosological forms of traumatic brain injury, most often accompanying severe brain contusion.

If the hygroma occurs in isolation, then its clinical picture is very similar to that of a subdural hematoma, especially in its three-phase course. As a rule, after an injury with a short-term loss of consciousness, a clear interval occurs, usually lasting 1-3 days and with typical cerebral symptoms. Then the headache intensifies, stupor appears and increases, meningeal and local symptoms appear in the form of facial nerve paresis, mono- or hemiparesis, and sensory disturbances.

However, in the classic clinic of intracranial hematoma, you can notice some features typical of subdural hygroma, or signs that are most often found with it. This is a long clear period (1-10 days) - hygromas often have a subacute course. Headaches are paroxysmal, radiating to the eyeballs and cervical-occipital region. Characterized by photophobia and local pain on percussion of the skull. The general condition of patients deteriorates slowly, as do signs of brain compression, which increase relatively more gently and gradually. Mental disorders such as frontal syndrome are often observed (decreased criticism of one’s condition, euphoria, disorientation, apathetic-abulic symptoms), proboscis and grasping reflexes appear. Psychomotor agitation often develops.

Paresis of spastic limbs with hypertonicity and revitalizationreflexes. Quite often, patients with hygromas have convulsive seizures starting from the muscles of the face or on the contralateral side. Subdural hygromas are characterized by a gradual, wave-like deepening of secondary disturbances of consciousness. So, in the early stages, after a convulsive seizure, consciousness is restored and contact can be made with the patient.

Acute hygromas are characterized by the absence of anisocaria, and if it is present, then, unlike hematomas, the reaction of the pupil to light is preserved.

Intracerebral hematomas

Intracerebral hematoma - This is a post-traumatic hemorrhage into the substance of the brain with the formation of a cavity filled with blood. The incidence of intracerebral hemorrhages is approximately 5-7% of all intracranial hematomas. The favorite localization is the frontotemporal lobe. The size of intracerebral hematomas is relatively small and is 1-3 cm in diameter, but can reach 7-8 cm. The volume of spilled blood is most often in the range of 30-50 ml, sometimes more massive hematomas are found - 120-150 ml.

The source of cerebral hemorrhages is damaged vessels of the brain substance due to its contusion or other types of traumatic brain injury

The clinical picture of isolated intracerebral hemorrhages tends to be three-phase and have acute, subacute and chronic stages of the course. The latter depend on the volume of the hematoma and the brain’s response to injury, expressed by edema and swelling.

In the acute course of a hematoma, a clear gap is observed in half of the patients, in the rest it is absent or in an erased form. After the initial loss of consciousness, which can last from several minutes to several days, a period of imaginary well-being begins, which differs from meningeal hematomas in its short duration (no more than 6 hours), the presence, in addition to general cerebral, meningeal and gross focal symptoms in the form of hemiparesis and plegia. It should be emphasized that paresis and paralysis in patients with intracerebral hematomas always develop contralaterally, while pupil dilation in 50% of victims occurs on the side of the hematoma, in the rest - on the opposite side. The light interval, as a rule, ends with a sudden entry into a coma. Vegetative-stem symptoms appear early in the form of respiratory failure, cardiovascular

activities. Hormetonia syndrome often develops, characterized by strong tonic tension in the muscles of the limbs and trunk with a predominance of extensors. Sometimes there are epileptic seizures. All symptoms tend to increase.

Computed tomography, echoEG, angiography and pneumoencephalography can facilitate diagnosis, with the help of which it is possible to respectively identify an area of ​​altered density in the brain substance, a displacement of the M-echo, a displacement of the vascular and median structures of the brain.

Intraventricular hematomas

Intraventricular hematomas - These are post-traumatic hemorrhages in the cavities of the lateral, III and IV ventricles of the brain. This type of hemorrhage occurs only against the background of a severe brain contusion and practically never occurs in isolation.

Intraventricular hematomas account for 1.5 to 4% of all intracerebral hemorrhages. They are caused by rupture of the choroid plexuses of the ventricles as a result of hydrodynamic shock at the time of injury. More often one of the lateral ventricles suffers. 40-60 and even 100 ml of blood can pour into it.

The clinical picture of intraventricular hematoma depends on the rate of bleeding into the ventricle and the severity of the concomitant brain contusion. Blood pressure on the walls of the ventricle and irritation of the reflexogenic zones embedded in them not only aggravate the severity of the injury, but also gives the clinical picture some originality. There is a disorder of consciousness in the form of stupor or coma. Literally following the injury, vegetative-stem disorders appear and rapidly increase. Against the background of progressive intracranial hypertension, combined with arterial hypertension, hyperthermia occurs, reaching 38-41°C. The victim's face and neck are hyperemic with symptoms of hyperhidrosis.

Severe motor agitation with the presence of hormetonia is considered characteristic of intraventricular hematomas. Extensor spasms can be provoked by external stimuli, even by neurological examination techniques. Sometimes they are combined with epileptic seizures.

Neurological symptoms with intraventricular hematomas are usually bilateral.

Dysregulation of breathing appears quite early in the form of tachypnea (30-70 breaths per minute), which persistently progress, reaching pathological forms (Cheyne-Stokes, Biota). Subsequently, signs of brain dislocation appear (transition of bradycardia to tachycardia, reaching 160 or more beats per minute with bilateral mydriasis, the appearance of pathological reflexes from the feet.

In patients with intraventricular hematomas, motor-tonic phenomena are often detected in the form of automated gestures, stereotypical hand movements (“scratching”, “stroking”, “pulling the blanket”), as well as oral and manual hyperkinesis of the subcortical type (sucking and smacking movements of the lips, tremor limbs), which manifest from the initial period and can persist until the agonal state.

Lumbar puncture reveals copious amounts of blood in the cerebrospinal fluid.

Subarachnoid hemorrhage.

Subarachnoid hemorrhage - This is a post-traumatic accumulation of blood in the subarachnoid space, which does not cause local compression of the brain. This intracranial hemorrhage does not occur in isolation, but is a companion to traumatic brain injuries, mainly brain contusion. Subarachnoid hemorrhages occur in 15-42% of all traumatic brain injuries, and in severe forms they reach 79%. Even higher figures are given by forensic doctors, who observed subarachnoid hemorrhages in 84-92% of cases, and some in 100% of all traumatic brain injuries.

The source of subarachnoid hemorrhages is ruptured vessels of the membranes that limit the subarachnoid space, or increased vascular permeability as a result of injury. The spilled blood spreads over large areas (from 50 to 300 cm 2 or more), taking on a lamellar character. Subsequently, most of the blood is absorbed into the subdural space and further into the blood vessels of the dura mater, the remaining red blood cells undergo decay. It has been established that blood and its toxic breakdown products (bilirubin, serotonin) irritate the meninges and cause disturbances in cerebral circulation, liquor dynamics, and sharp fluctuations in intracranial pressure with a disorder of brain functions.

What is pathognomic for subarachnoid hemorrhages is that loss of consciousness after the initial injury is replaced by a state of stupor, disorientation, and often psychomotor agitation. The restoration of consciousness is accompanied by retro- and anterograde amnesia, memory impairment of the asthenic type and Korsakoff traumatic amnestic syndrome.

In victims with subarachnoid hemorrhage, by the end of the first day, meningeal syndrome develops as a response to irritation of the membranes with blood. It is characterized by intense headache in the occipital and frontal regions, pain in the eyeballs and neck, photophobia, nausea and repeated vomiting, stiff neck and positive Kernig syndrome. The syndrome increases, reaching a peak on days 7-8, and then declines and disappears by days 14-18.

As a result of irritation by blood of the recurrent branch of the trigeminal nerve (1st branch), tentorium cerebellum syndrome occurs, manifested by photophobia, injected conjunctival vessels, lacrimation, and rapid blinking. As the flow of fresh blood into the cerebrospinal fluid decreases, the syndrome fades away and completely disappears by 6-7 days.

The breakdown products of blood and brain detritus inhibit the cortical section of the motor analyzer. Because of this, from 2-3 days there is a weakening of the tendon and periosteal reflexes (especially the knee), which disappear completely by 5-6 days. By 8-9, sometimes by 12-14 days, and even later, reflexes are restored and return to normal.

For 7-14 days after the injury, an increase in body temperature remains 1.5-2 degrees above normal.

A reliable sign of subarachnoid hemorrhage is the presence of blood in the cerebrospinal fluid.

SKULL FRACTURES

Fractures of the skull bones account for up to 10% of fractures of all skeletal bones and are classified as severe injuries, because they are unthinkable without damage to the underlying structures - the membranes and substance of the brain. 18-20% of all severe traumatic brain injuries are accompanied by skull fractures. There are fractures of the facial and cerebral skull, and fractures of the vault and base are distinguished among injuries of the cerebral skull.

Fractures of the base of the skull

Fractures of the base of the skull arise predominantly from an indirect mechanism of injury when falling from a height onto the head, pelvis, lower limbs due to impact through the spine, and also as a continuation of fractures of the vault. If the fracture is single, then the fracture line can pass through one of the cranial fossae of the base: the anterior, middle or posterior, which will subsequently determine the clinical picture of the injury. The latter has characteristic manifestations also because a fracture of the base of the skull is accompanied by a rupture of the dura mater, which is intimately fused to it and often forms a connection between the cranial cavity and the external environment. Thus, the picture of a fracture of the base of the skull consists of clinical manifestations of concomitant brain injury (contusion of varying severity) and symptoms that are pathognomonic for a violation of the integrity of the anterior, middle or posterior cranial fossa.

In the first case, hemorrhages occur in the paraorbital tissue (symptom of “glasses”) and leakage of cerebrospinal fluid mixed with blood from the nasal passages. It should be noted that with traumatic brain injuries, multiple bruises of the soft tissues of the head are possible with the formation of a large number of different sizes and localizations of bruises and bleeding from the nose, ear canals, etc. It is necessary to be able to differentiate bruises and bleeding as a result of the direct mechanism of injury from the symptom of “glasses” and liquorrhea.

Traumatic “spectacles” appear 12-24 hours or more after the injury, often symmetrical. The color of the bruise is homogeneous and does not extend beyond the orbit. Palpation is painless. There are no signs of mechanical impact - wounds, abrasions, eye injuries. A fracture of the base of the skull may be accompanied by exophthalmos (hemorrhage into the retrobulbar tissue) and subcutaneous emphysema in case of damage to the air cavities.

With direct trauma, bruising appears immediately after the blow. They are not symmetrical and often go beyond the orbit, painful on palpation. There are signs of direct mechanical impact: skin abrasions, wounds, hemorrhages in the sclera, bruises of non-uniform color, etc.

Blood mixed with cerebrospinal fluid on a white cotton fabric gives a spot in the form of two rings of different colors. In the center, the color is more intense due to the formed elements of the blood, and on the periphery it has a sanious color, formed by an excess of the liquid part.

In case of a fracture of the middle cranial fossa, bruising in the posterior pharyngeal wall and liquorrhea from the auditory canals should be considered as characteristic signs.

A fracture of the posterior cranial fossa is accompanied by severe bulbar disorders (damage to the brain stem) and bruising into the subcutaneous tissue of the mastoid process. It should be noted that all bruises in case of a fracture of the base of the skull appear as a symptom of "points" no earlier than 12-24 hours from the moment of injury. Leading in the diagnosis of fractures of the base of the skull is the clinic, since on primary radiographs in standard laying, bone damage can be detected only in 8-9% of the victims. This is due to the complexity of the anatomical structure of the bones that form the bottom of the cranium, and the no less complex course of the fracture line, which selects holes in the weakest points of the base of the skull. For reliable diagnosis, special styling is required, which cannot always be applied due to the severity of the patient's condition.

Cranial vault fractures

Fractures of the calvarium are the result of a direct mechanism of injury, when the point of application of force and the site of injury coincide. An indirect mechanism is also possible when the spherical cranium is compressed, the fracture occurs at the point of intersection of the lines of force with the transcendental load, and not in the pressure zone.

Fractures of the calvarium are divided into linear (cracks), depressed (impression and depression) and comminuted.

Clinical diagnosis of closed calvarial fractures, which account for about 2/3 of all fractures, is extremely difficult. Subperiosteal and subgaleal hematomas and severe pain complicate palpation, which should already be extremely gentle to avoid

displacement of the comminuted fracture and injury to the underlying formations. The idea of ​​a possible fracture may be suggested by the history of the severity of the mechanical injury and the symptom of axial load - compression of the head in the sagittal and frontal planes. In this case, the pain radiates to the fracture site. To clarify the diagnosis, it is necessary to perform craniography in standard settings, but also according to forensic data In medical autopsies, about 20% of fractures remain unrecognized.

The greatest difficulty in diagnosis is presented by linear fractures, which are often mistaken for a vascular pattern. The latter differs from a linear fracture in that it has a tree-like shape with a wider base and thin apex. In addition, twisted branches extend from the trunk, which in turn have the same branches, but thinner.

Rice. 5. X-ray signs of a calvarial fracture:

A - normal vascular pattern; B - symptom of enlightenment and zigzag;

B - symptom of line doubling (symptom of “ice flake”)

Linear fractures have a number of distinctive features:

1. Symptom of transparency (linear clearing) - is associated with a break in the bone and is often distinct, but sometimes it may be due to the vascular pattern or the contour of the cranial sutures.

Symptom of bifurcation - Along the course of the cracks, in some areas the line bifurcates, and then again goes single. Bifurcation occurs with through cracks, when a beam coming at an angle to the fracture line can separately reflect the edges of the outer and inner vault plates. An illusion is created that islands of bone are gouged out along the fracture line, which is why this sign is called the “ice flake” symptom. The symptom of bifurcation absolutely confirms the diagnosis of a fracture.

Zigzag symptom(lightning) - expressed by a zigzag line of enlightenment. Refers to reliable signs of a fracture that have absolute diagnostic value (Fig. 5).

Sometimes along with cracks there is a divergence of seams.

Treatment of patients with traumatic brain injury

Treatment of patients with traumatic brain injury is a complex and extensive range of medical measures, the choice of which in each specific case depends on the type, severity and progression of the injury, the stage at which therapy was started, age, concomitant diseases and much more.

Assistance to victims with traumatic brain injury can be divided into three periods: assistance at the pre-hospital stage, treatment in a hospital (hospital stage) and “follow-up treatment” in a polyclinic setting (outpatient stage) or under the supervision of a family doctor.

Assistance at the prehospital stage is as follows:

Give the patient a horizontal position. Create peace of mind with improvised means: a pillow, rollers, clothes.

Check and, if necessary, clear the airways from vomit, tongue retraction, etc.

Stop external bleeding by pressing the edges of the wound with your fingers or a pressure bandage.

Cold to the head.

Give oxygen inhalation.

According to indications, the following are used: analeptics (cordiamin, cititon, lobeline), cardiac glycosides (strophanthin K, korglykon).

Transport the patient urgently (necessarily in a supine position) to a medical facility.

All patients with traumatic brain injury are subject to hospitalization! Treatment in a hospital can be conservative or operative. Bloodless treatment methods are used much more often, while surgical interventions are performed according to strict indications.

Patients with concussion, brain contusion, closed calvarial fractures, fractures of the base of the skull, and subarachnoid hemorrhages are treated conservatively.

All patients, regardless of the type of damage, are prescribed:

Strict bed rest. Its duration depends on the severity of the injury. So, with a grade I concussion, strict bed rest lasts 5-7 days, grade II - 7-10 days. For grade I brain contusion - 10-14 days, grade II - 2-3 weeks and grade III - at least 3-4 weeks. To determine the termination of strict bed rest, in addition to the specified periods, the Mann-Gurevich symptom is used. If it is negative, the patient can sit up in bed, and after adaptation, stand up and walk under the supervision of staff.

Cold to the head. Use ice packs wrapped in a towel to prevent frostbite. To cool the head, helmets of various designs were offered (with a system of constantly circulating cold water, with a system of thermoelements, etc.). Unfortunately, our industry does not produce these necessary devices for treating patients. Exposure to head hypothermia depends on the severity of the injury. For mild injuries (concussion and cerebral contusion of the first degree), its exposure is limited to 2-3 hours, and for severe injuries, exposure lasts 7-8 hours or more, up to 1-2 days. But it should be remembered that when using cold for a long time, take a break of 1 hour every 2-3 hours.

The purpose of using cold is to normalize vascular disorders, reduce the production of cerebrospinal fluid, prevent cerebral edema, reduce the need for oxygen in brain tissue, and reduce headaches.

3. Sedatives(sodium bromide, bromocamphor, corvalol), etc. tranquilizers(Elenium, Seduxen, Tazepam).

4. Sleeping pills(phenobarbital, barbamyl, etaminal sodium). Strict bed rest, the prescription of tranquilizers, sedatives and hypnotics are a set of measures aimed at creating rest for the damaged organ, i.e. brain. Medicines weaken external stimuli, prolong physiological sleep, which has a beneficial effect on the functions of the central nervous system.

5. Antihistamines(diphenhydramine, fenkarol, diazolin).

As a result of vascular disorders and hypoxia of the brain, destruction and resorption of intracranial hemorrhages, and disintegration of the destroyed brain matter, a mass of histamine-like substances (serotonin, etc.) is formed, therefore the prescription of antihistamines is mandatory.

The further choice of treatment prescriptions depends on the height of the patient’s cerebrospinal fluid pressure. With increased cerebrospinal fluid pressure (hypertension syndrome), treatment should be as follows: position in bed according to Fowler - with the head end elevated, diet No. 7 with limited salt and liquid.

In order to reduce cerebral edema, dehydration is used. Concentrated hypertonic solutions are administered intravenously to increase the osmotic pressure in the vascular bed and cause the outflow of fluid from the interstitial spaces of the brain. For osmotherapy, use 40% glucose solution, 40% sodium chloride solution, 25% magnesium sulfate solution, 15% mannitol solution at the rate of -1-1.5 per 1 kg of body weight. The last two drugs have pronounced diuretic properties. Of the diuretics, furosemide (Lasix) is most often used for tissue dehydration. Cleansing enemas contribute to the removal of fluid from the body.

Unloading lumbar punctures directly reduce cerebrospinal fluid pressure, when, following a lumbar puncture, 8-12 ml of cerebrospinal fluid are slowly released.

For hypotensive syndrome, the following is prescribed: diet No. 15, position in bed according to Trandelenburg - with the leg end raised. Solutions with low salt concentrations (isotonic Ringer-Locke, 5% glucose solution) are administered intravenously. Subcutaneous injections of caffeine-sodium benzonate 1 ml of 10% solution and vagosympathetic novocaine blockades have a good therapeutic effect.

In some cases, it becomes necessary to prescribe certain groups of drugs and medications. So, for open injuries, when there is a threat of developing infectious complications, antiseptics, antibiotics and sulfonamides are used.

In case of violation of vital functions, analeptic drugs are administered that stimulate the respiratory center and vascular tone (cordiamin, lobeline hydrochloride, cititon); to normalize blood pressure in the entire vascular bed, adrenomimetic substances are used (adrenaline hydrochloride, norepinephrine hydrotartrate, mesatone). Weakness of the heart muscle is treated with cardiac glycosides (strophanthin K, corglycon).

Traumatic brain injury is often part of a polytrauma accompanied by shock and blood loss. In the complex of anti-shock therapy, blood and plasma-substituting solutions (reopolyglucin, gelatinol, Acesol) are transfused, analgesics (morphine hydrochloride, promedol, analgin), hormones (hydrocortisone) and other drugs are administered.

Surgical treatment patients with acute traumatic brain injury is inevitable with open injuries and in the presence of signs of brain compression. For open injuries, primary surgical treatment is performed. The wound is closed with sterile material. The hair around it is shaved off. The skin is washed with soapy water, wiped with napkins and treated twice with a solution of 5% iodine tincture. Local infiltration anesthesia is performed with a 0.25% solution of novocaine with the addition of antibiotics. After anesthesia, the wound is thoroughly washed with an antiseptic solution (furacilin, hydrogen peroxide, rivanol) and examined. If only soft tissue is damaged, nonviable tissue is excised. For compressed wounds with crushed edges, it is better to excise them to a width of 0.3-0.5 cm to the bone. The bleeding is stopped and the wound is sutured.

If a fracture is detected during inspection of the wound, then it is necessary to carefully remove all small loose fragments with tweezers and examine the dura mater. If there is no damage, normal color, or preserved pulsation, the shell is not opened. The edges of the bone wound are resected with pliers to a width of 0.5 cm. Hemostasis is performed and sutures are placed on the wound.

If the dura mater is damaged, i.e. If there is a penetrating wound to the skull, then primary surgical treatment is performed as described above, but with economical excision of the edges of the shell. For better inspection of the subdural space, the wound of the dura mater is expanded. Loose bone fragments, brain detritus, and blood are washed out with hydrogen peroxide and warm isotonic sodium chloride solution. After stopping the bleeding, the dura mater is sutured, if possible, and layer-by-layer sutures are applied to the soft tissues of the skull.

Compression of the brain, regardless of the reasons that caused it, must be eliminated immediately after diagnosis.

For depressed closed fractures of the calvarium, an incision is made into the soft tissue down to the bone with the expectation of exposing the fracture site. A milling hole is placed next to it, through which they try to lift the depressed fragment using a levator. If the fragments were able to be lifted, which happens very rarely, and they do not move, then the operation can be completed, having first made sure that there are no indications for extended surgery. If the fragments cannot be lifted, then the depressed portion of the bone is resected from the side of the burr hole. The further course of the intervention is the same as during primary surgical treatment, but without excision in the dura mater.

If the brain is compressed by hematomas or hygroma, resection or osteoplastic surgery can be performed. The first option of the operation is that a search burr hole is placed in the projection of the suspected hematoma. If a hematoma is detected, the hole is expanded by gradual resection of the bone to the desired size (6x6, 7x7 cm). Through the created window, intervention is performed on the brain and membranes. The operation is completed by suturing the soft tissue, leaving a large defect in the skull bones. This operation creates good decompression of the brain, especially when compression of the brain is combined with severe contusion. But resection trepanation also has negative sides. After this, another intervention is necessary to close the skull defect with synthetic material (steractyl) or autologous bone taken from the rib. If this is not done, post-trepanation syndrome will develop. Changes in intracranial pressure caused by physical stress (straining, coughing, sneezing, etc.) lead to frequent movements of the brain matter into the “window” of the skull defect. Trauma to the brain from the edges of the burr hole causes the development of a fibrotic process in this area. Adhesions are formed between the brain and the membranes, bones and integument of the skull, which cause local pain and headaches, and subsequently epileptic seizures. Osteoplastic trepanation does not leave skull defects requiring subsequent plastic surgery. A semi-oval incision is made from the base downwards in the soft tissue down to the bone. Along the incision line, without separating the soft tissue flap, five milling holes are drilled - two at the base of the flap and three along the arc. Using a guide, a Gigli saw is passed through two milling holes and the bone bridge is sawed off. All holes are gradually connected into a single one, and the bone-soft tissue the flap on the feeding pedicle is turned downwards. The further course of the operation depends on the type of injury. After completion of the intervention in the cranial cavity, the bone flap is put in place and the soft tissue is sutured in layers.

Test task for self-study on the topic"Traumatic brain injury"

Mechanisms of traumatic brain injury.

Classification of traumatic brain injury.

Name the general cerebral symptoms.

Name local symptoms.

Name meningeal symptoms.

Name the stem symptoms.

What is hyper-, hypo- and normotensive syndrome and how to define it?

How is a concussion diagnosed?

On what basis is the diagnosis of “brain contusion” made?

Gradation of injury severity, clinical differences in degrees of severity.

Causes of compression of the brain.

Clinic of compression of the brain by bone fragments and foreign bodies, as distinguished from brain contusion.

Clinic of brain compression by intracerebral and intraventricular hematomas.

Clinic of brain compression by epi- and subdural hematomas, as distinguished from brain contusion.

What is a subdural hygroma?

Difference between the clinic of concussion, bruise and compression by epi- and subdural hematomas.

Clinic of subarachnoid hemorrhage.

Fracture of the base of the skull, diagnosis.

Traumatic glasses and liquorrhea, their diagnosis. Signs of damage to the anterior, middle and posterior cranial fossae.

Fractures of the cranial vault, diagnosis, tactics.

First aid for traumatic brain injuries.

Conservative treatment of acute traumatic brain injury, give a pathogenetic rationale.

Conservative treatment of brain damage during the recovery period.

Surgical treatment of traumatic brain injury (TBI): puncture, trephination, trepanation.

Techniques of various types of trepanations, necessary instruments.

What is post-trepanation syndrome, its treatment.

Outcomes and long-term consequences of TBI.

Traumatic brain injury is damage to the bone (or bones) of the skull, soft tissues, including the meninges, nerves and blood vessels. All traumatic brain injuries are divided into two broad categories: open and closed. According to another classification, they talk about penetrating and not, about concussion and bruises of the brain.

The TBI clinic will be different in each case - it all depends on the severity and nature of the disease. Typical symptoms include:

• headache;
• vomiting;
• nausea;
• dizziness;
• memory impairment;
• loss of consciousness.

For example, an intracerebral hematoma or brain contusion is always expressed by focal symptoms. The disease can be diagnosed based on the anamnestic indicators obtained, as well as during a neurological examination, X-ray, MRI or CT scan.

Principles of classification of traumatic brain injury

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

From a biomechanical point of view, we talk about the following types of traumatic brain injuries:

• shock-anti-shock (when a shock wave passes from the point of collision of the head with an object through the entire brain, right up to the opposite side, and a rapid pressure drop is observed);
• acceleration-deceleration injury (in which the cerebral hemispheres move from a less fixed to a more fixed brain stem);
• combined injury (in which there is a parallel effect of the two above mechanisms).

By type of damage

According to the type of injury, TBIs are of three types:

1. Focal: they are characterized by the so-called local damage to the base of the medulla of a macrostructural nature; usually damage to the medulla occurs throughout its thickness, except for the places of small and large hemorrhage in the area of ​​impact or shock wave.
2. Diffuse: they are characterized by primary or secondary ruptures of axons located in the semioval center or corpus callosum, as well as in the subcortical regions or the brain stem.
3. Injuries that combine focal and diffuse injuries.

According to the genesis of the lesion

Regarding the genesis of the lesion, traumatic brain injuries are divided into:

1. Primary (these include bruises of a focal type, axonal lesions of a diffuse type, intracranial hematomas of the primary type, rupture of the trunk, significant intracerebral hemorrhages);
2. Secondary:

• secondary lesions resulting from intracranial factors of a secondary type: impaired cerebrospinal fluid circulation or hemocirculation due to intraventricular hemorrhage, cerebral edema or hyperemia;
• secondary lesions caused by extracranial factors of a secondary type: hypercapnia, anemia, arterial hypertension, etc.

By type of TBI

Based on type, traumatic brain injuries are usually divided into:

• closed - a type of damage that does not violate the integrity of the skin of the head;
• open non-penetrating TBI, which is not characterized by damage to the hard membranes of the brain;
• open penetrating TBI, which is characterized by damage to the hard membranes of the brain;
• fractures of the bones of the cranial vault (with no damage to the adjacent soft tissues);
• fractures of the base of the skull with the further development of liquorrhea or ear (nose) bleeding.

According to another classification, there are three types of TBI:

1. Isolated appearance - the presence of extracranial injuries is not typical.
2. Combined type - characterized by the presence of damage of the extracranial type, as a result of mechanical influence.
3. Combined type - it is characterized by a combination of different types of damage (mechanical, radiation or chemical, thermal).

The nature

There are three degrees of severity of the disease: mild, moderate and severe. If we assess the severity of the disease using the Glasgow Coma Scale, then a mild TBI falls under 13-15 points, a moderate TBI is 9-12 points, and a severe TBI is 8 points or less.

In terms of its symptoms, a mild degree of TBI is similar to a mild brain contusion, a moderate degree is similar to a moderate brain contusion, while a severe one is similar to a more severe brain contusion.

According to the mechanism of occurrence of TBI

If we classify TBI according to the mechanism of its occurrence, then we distinguish two categories of injuries:

1. Primary: when no cerebral (or extracerebral) catastrophe precedes traumatic energy of a mechanical nature directed at the brain.
2. Secondary: when a cerebral (or extra-cerebral) catastrophe usually precedes traumatic energy of the mechanical type.

It should also be said that traumatic brain injuries with characteristic symptoms can occur either for the first time or repeatedly.

The following clinical forms of TBI are distinguished

In neurology, they talk about several forms of TBI that are striking in their symptoms, including:

• brain contusions (mild, moderate and severe stages);
• concussion;
• compression of the brain;
• diffuse axonal injury.

The course of each of the listed forms of TBI has acute, intermediate and long-term periods. Each period lasts differently, depending on the severity and type of injury. For example, the acute period can last from 2 to 10-12 weeks, while the intermediate period can last up to six months, and the long-term period can last up to several years.

Brain concussion

Concussion is considered the most common injury among TBIs. It accounts for more than 80% of all cases.

Diagnosis

Making an accurate diagnosis of a concussion the first time is not so easy. Usually the traumatologist and the neurologist are engaged in diagnostics. The main indicator in the diagnosis is considered to be a subjectively collected anamnesis. Doctors question the patient in detail about how the injury was sustained, determine its nature, and interview possible witnesses to the injury.

A significant role is given to examination by an otoneurologist, who establishes the presence of symptoms that are an irritation factor for the vestibular analyzer in the absence of signs of the so-called prolapse.

Due to the fact that the nature of the concussion is usually mild, and the cause of its occurrence may be one of the pre-traumatic pathologies, during the diagnosis, great importance is given to changes in clinical symptoms.

This diagnosis can be finally confirmed only after the disappearance of typical symptoms, which usually occurs 3-5 days after the receipt of TBI.

As you know, a concussion does not involve fractures of the skull bones. At the same time, the indicator of cranial pressure, as well as the biochemical composition of the cerebrospinal fluid, remain unchanged. CT or MRI are considered accurate diagnostic methods, but do not reveal intracranial spaces.

Clinical picture

The main indicator of the clinical picture of traumatic brain injury is depression of consciousness, which can last from several seconds to a minute or more. In some cases, depression of consciousness is completely absent.

In addition, the patient may develop amnesia of the retrograde, antegrade, or congrade types. Another characteristic symptom accompanying TBI is vomiting and rapid breathing, which quickly recovers. Blood pressure also quickly normalizes, except in cases where the medical history is complicated by hypertension. The body temperature remains normal.

After the patient regains consciousness, he begins to complain of headache, dizziness and general weakness. Cold sweat appears on the patient's skin, the cheeks become red, and auditory hallucinations may appear.

If we talk specifically about the neurological status, then it is characterized by asymmetry of soft-type tendon reflexes, as well as horizontal nystagmus in the corners of the eyes and mild meningeal symptoms, which may disappear after the first week of the disease.

In the case of a concussion caused by a head injury, after two weeks the patient feels healthy, but some asthenic phenomena may persist.

Treatment

As soon as a person who has received a traumatic brain injury comes to his senses, he must immediately be given first aid. To begin, lay it down, giving it a horizontal position, while raising its head slightly.

The patient with a traumatic brain injury who is not yet conscious should be placed on his side (preferably on the right), with his face turned to the ground, and his arms and legs bent at right angles, but only if the knees or elbows there are no fractures in the joints. It is this position that helps air pass freely, reaching the lungs, and at the same time, preventing the tongue from sinking or choking on one’s own vomit.

If the patient has open wounds on the head, then an aseptic bandage must be applied. It is best to immediately transport a person with a traumatic brain injury to a hospital, where they can diagnose a TBI and prescribe bed rest on an individual basis (it all depends on the clinical characteristics of each patient).

If, after a CT and MRI examination, the examination results do not show any signs of focal brain lesions, then drug treatment is not prescribed and the patient is almost immediately discharged home for outpatient treatment.

In the case of a concussion, active drug treatment is not usually prescribed. The main goal of initial treatment is to normalize the state of the brain, restoring its functionality, as well as relieving headaches and normalizing sleep. For this purpose, various analgesics and sedatives are used.

Forecast

In the event of a concussion and compliance with the doctor’s instructions, the process ends with recovery and return to work. After a while, all signs of a concussion (depression, anxiety, irritability, loss of attention, etc.) completely disappear.

Mild brain contusion

Diagnostics

If we talk about moderate brain contusion, then CT helps to detect and identify various types of focal changes, which include poorly located areas with reduced density and small areas, on the contrary, with increased density. Along with CT, in this case, an additional diagnostic method may be required: lumbar puncture, electroencephalography, and others.

Clinical picture

It should be noted that the main characteristic of a brain contusion of this degree is the duration of loss of consciousness, which manifests itself after the injury. Loss of consciousness with a moderate injury will be longer than with a mild one.

Loss of consciousness may continue for the next 30 minutes. In some cases, the duration of this condition reaches several hours. In this case, congrade, retrograde or anterograde types of amnesia are especially pronounced. The patient may experience severe vomiting and headache. In some cases, disruption of important vital functions may occur.

Moderate brain contusion is manifested primarily by loss of consciousness with varying durations. Vomiting, headache, abnormalities in the cardiovascular and respiratory systems occur.

Other possible symptoms include:

• tachycardia;
• bradycardia;
• tachypnea (without change in breathing);
• increased body temperature;
• the appearance of enveloped signs;
• manifestation of pyramidal signs;
• nystagmus;
• possibility of dissociation of meningeal symptoms.

Among the most pronounced focal signs, a separate category includes: various types of pupillary disorders, speech disorder, sensitivity disorder. All these signs can regress 5 weeks after the onset.

After a bruise, patients often complain of severe headaches and vomiting. In addition, the manifestation of mental disorders, bradycardia, tachycardia, tachypnea and high blood pressure cannot be excluded. Meningeal symptoms are very common. In some cases, doctors note a fracture of the skull bones and subarachnoid hemorrhage.

Moderate brain contusion

Typically, mild brain contusions are detected in 15% of people who have received a traumatic brain injury, while moderate contusions are diagnosed in 8% of victims, and severe contusions in 5% of people.

Diagnosis

The main method for diagnosing a brain contusion is a CT scan. It is this method that helps determine the area of ​​the brain that has low density. In addition, CT can detect a fracture of the skull bones, as well as detect subarachnoid hemorrhage.

In the case of severe contusion, CT can reveal areas of heterogeneously increased density, and, as a rule, perifocal cerebral edema is pronounced with a significant hypodense track extending into the region of the proximal portion of the lateral ventricle. It is through this place that the release of fluid is observed along with various decay products of brain tissue and plasma.

Clinical picture

If we talk about the clinic of a mild brain contusion, then it is characterized by loss of consciousness a couple of minutes after receiving the injury. After the victim regains consciousness, he complains of a severe characteristic headache, nausea and dizziness. Congrade and anterograde amnesia are also very often noted.

Vomiting may occur periodically with repetitions. At the same time, all vital functions are preserved. Tachycardia and bradycardia are very common in victims, and blood pressure may be elevated at times. As for breathing, it remains unchanged, as does body temperature, which is maintained at normal levels. Some symptoms of a neurological nature may regress after 2 weeks.

Severe brain contusion

Regarding severe brain contusion, it is accompanied by loss of consciousness, which can last up to two weeks. Very often, such a bruise can be combined with a fracture of the bones of the base of the skull, as well as with severe subarachnoid hemorrhage.

In this case, the following disorders of human vital functions may be noted:

• respiratory rhythm disturbance;
• increased blood pressure;
• bradyarrhythmia;
• tachyarrhythmia;
• airway obstruction;
• severe hyperthermia.

Interestingly, focal symptoms of the affected hemisphere are often hidden behind other symptoms (gaze paresis, ptosis, nystagmus, dysphagia, mydriasis and decerebrate rigidity). In addition, changes in tendon and foot reflexes may occur.

Among other things, symptoms of oral automatism, as well as paresis and focal seizures may be expressed. It will be extremely difficult to restore damaged functions. Very often, after recovery, patients experience residual disorders in the musculoskeletal system and may have obvious mental disorders.

With a severe brain injury, the patient's condition is considered critical. A person is characterized by a comatose state that lasts from several hours to several days. The patient may be in a state of psychomotor agitation, alternating with a depressed mood.

Regarding the places in which the affected brain tissue will be concentrated, they talk about certain manifestations of symptoms, such as a violation of the swallowing reflex, changes in the functioning of the respiratory and cardiovascular systems.

The duration of loss of consciousness with severe brain contusion is very long and can be up to several weeks. In addition, prolonged excitation of the motor system may be observed. The dominance of neurological symptoms (such as nystagmus, difficulty swallowing, miosis, bilateral mydriasis) is also characteristic of patients with this severity of traumatic brain injury.

Often severe bruises lead to death.

Diagnostics

The diagnosis is made after assessing the following criteria - general condition, condition of vital organs, neurological disorders.

Diagnosis of severe traumatic brain injury is usually carried out using CT and MRI.

Diffuse axonal brain injury

If we talk about the diffuse type of axonal damage to the brain, then it is characterized, first of all, by the manifestation of a coma that occurs after receiving a traumatic brain injury. In addition, stem symptoms are often expressed.

Coma is usually accompanied by symmetrical or asymmetrical decerebration (or decortication). It can also be provoked by ordinary irritations, for example, pain.

Changes in muscle condition are always variable: both diffuse hypotension and hormetonia can be observed. Very often, pyramidal-extrapyramidal paresis of the limb can occur, including asymmetric tetraparesis. In addition to gross changes in the functioning of the respiratory system (disturbances in the rhythm and frequency of habitual breathing), autonomic disorders are also observed, which include increased body temperature, increased blood pressure, and the manifestation of hyperhidrosis.

The most striking sign of diffuse axonal brain damage is considered to be the transformation of the patient’s condition, flowing from a coma into a transient vegetative state. The onset of this condition is indicated by the eyes suddenly opening, but all sorts of signs of eye tracking and gaze fixation may be absent.

Diagnosis

With the help of CT diagnostics, in case of axonal damage to the affected brain, an increase in the volume of the brain can be observed, due to which the lateral ventricles, as well as the subarachnoid convexital areas or the so-called cisterns of the base of the brain, can be compressed. Very often, hemorrhages of a small focal nature can be found, located on the white matter of the cerebral hemispheres and in the corpus callosum, as well as on the subcortical structures of the brain.

Brain compression

In approximately 55% of all cases of TBI, patients experience compression of the brain. It is usually caused by an intracranial hematoma. In this case, the greatest danger to human life is the rapid growth of focal, brain stem and cerebral symptoms.

Diagnosis

CT can reveal a biconvex or plano-convex limited zone, which is characterized by increased density, adjacent to the calvarium or located within the boundaries of one or even two lobes. If several sources of bleeding have been identified, then the area of ​​​​increased density may acquire an even larger size, distinguished by its crescent shape.

Treatment of traumatic brain injury

As soon as a patient with a TBI is admitted to the hospital, doctors carry out the following activities:

• inspection;
• X-ray of the skull;
• Ultrasound of the chest and abdominal cavity;
• laboratory research;
• urine tests and consultations with various specialists.

Examination for TBI

For example, examining the body includes detecting abrasions and bruises, identifying joint deformities, and changes in the shape of the chest or abdomen. In addition, during the initial examination, nosebleeds or ear bleeding may be detected. In special cases, during examination, the specialist also identifies internal bleeding occurring in the rectum or urethra. The patient may have bad breath.

X-ray of the skull

Using an X-ray, the patient's skull is scanned in two projections; doctors look at the condition of the cervical and thoracic spine, the condition of the chest, pelvic bones and limbs.

Laboratory research

Laboratory tests include a general clinical analysis of blood and urine, a biochemical blood test, determination of blood sugar levels and analysis of electrolyte levels. In the future, such laboratory tests should be carried out regularly.

Additional diagnostic measures

If we talk about the ECG, it is prescribed for three standard and six chest leads. Among other things, additional blood and urine tests may be ordered to detect alcohol in them. If necessary, seek advice from a toxicologist, traumatologist and neurosurgeon.

One of the main methods for diagnosing a patient with this diagnosis is CT. There are usually no contraindications for its implementation. However, you should be aware that in cases of obvious hemorrhagic or traumatic shock or poor hemodynamics, CT may not be prescribed. However, it is CT that helps to identify the pathological focus and its location, the number and density of hyperdense areas (or, on the contrary, hypodense), the location and level of displacement of the midline structures of the brain, their condition and the degree of damage.

In case of the slightest suspicion of meningitis, a lumbar puncture and a study of the cerebrospinal fluid are usually prescribed to monitor inflammatory changes.

If we talk about conducting a neurological examination of a person with TBI, then it must be carried out at least every 4-5 hours. To determine the degree of consciousness impairment, the Glasgow Coma Scale is usually used, which allows you to learn about the state of speech and the ability to react with the eyes to light stimuli. Among other things, the level of focal and oculomotor disorders can be determined.

If the patient’s impairment of consciousness on the Glasgow scale is 8 points, then doctors prescribe tracheal intubation, which helps maintain normal oxygenation. If depression of consciousness to the level of coma is detected, then, as a rule, additional mechanical ventilation is indicated, giving the patient up to 50% additional oxygen. With the help of mechanical ventilation, the required level of oxygenation is usually maintained. However, patients who have been found to have a severe TBI with characteristic hematomas and cerebral edema usually require measurement of intracranial pressure, which should be maintained below 20 mm Hg. For this purpose, drugs such as mannitol or barbiturates are prescribed. In order to prevent septic complications, escalation (or, alternatively, de-escalation) antibacterial therapy is used.

Post-treatment therapy

For example, to treat post-traumatic meningitis, various antimicrobial drugs are used, which, as a rule, doctors allow for endolumbar administration.

If we talk about proper nutrition for patients with such a serious injury, it begins 3 days after the injury. The amount of food will increase gradually, and at the end of the very first week, the caloric content of the food should be 100% of the human body’s need for it.

Speaking about feeding methods, we should highlight the two most common: enteral and parenteral. In order to stop epileptic seizures, anticonvulsant drugs are prescribed with a minimum dosage. These drugs include, for example, levetiracetam and valproate.

The main indication for surgical intervention is an epidural hematoma, the volume of which is more than 30 cm³. The most effective method to eliminate it is transcranial removal. If we talk about a subdural type hematoma, the thickness of which is more than 10 mm, then it is also removed surgically. In comatose patients, an acute subdural hematoma can be removed using a craniotomy, and the bone flap can be either removed or preserved. A hematoma larger than 25 cm³ should also be removed as soon as possible.

Prognosis for traumatic brain injury

In more than 90% of all cases of concussion, the patient recovers and his condition is fully restored. A small percentage of recovered people experience post-concussion syndrome, which manifests itself in impaired cognitive functions, changes in the patient’s mood and behavior. A year later, all these residual symptoms disappear completely.

It is possible to give any prognosis for severe TBI based on the Glasgow scale. The lower the level of severity of traumatic brain injury according to the Glasgow scale, the higher the likelihood of an unfavorable outcome of this disease. When analyzing the prognostic significance of the age limit, one can draw conclusions regarding its influence on an individual basis. The most unfavorable symptomatic combination for TBI is considered to be hypoxia and arterial hypertension.