Head injury (craniocerebral injury, TBI). Closed craniocerebral injury: classification, clinic, diagnosis, emergency care at the stages of medical care

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

Varieties 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, the brain itself are injured) and closed. Closed trauma of the skull is divided into the following varieties:

1. Concussion of the brain (CCM). It occurs as a result of a blow to the head, this is the easiest type of injury. CGM is accompanied by several obligatory signs: loss of consciousness for less than 5 minutes, amnesia, absence of focal neurological symptoms, the 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 intracranial pressure in case of injury .
2. Brain injury. A very serious injury, when the physical impact is already on the very substance of the brain. Either a traumatic object, or the brain hits hard on the inner wall of the skull. A bruise is accompanied by necrosis of a certain area of ​​the brain, hemorrhage. In this case, the same symptoms are observed as with concussion, but more pronounced, which is combined with focal symptoms (impaired sensitivity, movement in one of the areas of the body or muscle group).
3. Compression of the substance of the brain. It can occur with an increase in edema of the nervous tissue, membranes against the background of intracranial hematoma (hemorrhage). At the same time, signs of a bruise are first visible, then a period of improvement (latent well-being) begins. And then - the patient's condition deteriorates sharply, consciousness is disturbed, severe neurological symptoms appear.

Traumatic brain injuries rank first among all injuries (40%) and most often occur in people aged 15–45 years. Mortality among men is 3 times higher than among women. Every year in large cities, out of a thousand people, seven receive head 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%, and a severe one - 100%.

Causes and types of traumatic brain injury

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

Most often, participants in road accidents suffer from craniocerebral injuries: drivers, passengers of public transport, pedestrians hit by vehicles. In second place in terms of frequency of occurrence are domestic injuries: accidental falls, bumps. Then there are injuries received at work, and sports.

Young people are most susceptible to injuries during the summer period - these are the so-called criminal injuries. The elderly are more likely to get TBI in the winter, with falling from height becoming the leading cause.

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

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

• by severity: light(concussion, slight bruising) average(serious injury) heavy(severe brain contusion, acute compression of the brain). The Glasgow Coma Scale is used to determine severity. The condition of the victim is estimated from 3 to 15 points depending on the level of confusion, the ability to open the eyes, speech and motor reactions;
• type: open(there are wounds on the head) and closed(there are no violations of the skin of the head);
• by type of damage: isolated(damages affect only the skull), combined(the skull and other organs and systems are damaged), combined(the injury was received not only mechanically, 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 scan or MRI);
• injury(there is a violation of the brain tissue due to the impact of the brain on the wall of the skull, often accompanied by hemorrhage);
• diffuse axonal brain injury(axons are damaged - processes of nerve cells that conduct impulses, the brain stem suffers, microscopic hemorrhages are noted in the corpus callosum of the brain; such damage most often occurs during an accident - at the time of sudden braking or acceleration);
• compression(hematomas are formed in the cranial cavity, the intracranial space is reduced, foci of crushing are observed; emergency surgical intervention is required to save a person's life).

It's 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 zone of impact.

The classification is based on the diagnostic principle, on its basis a detailed diagnosis is formulated, in accordance with which treatment is prescribed.

Symptoms of TBI

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

Diagnosis « brain concussion » based on history. Usually the victim reports that there was a blow to the head, which was accompanied by a short loss of consciousness and a single vomiting. The severity of the concussion is determined by the duration of the loss of consciousness - from 1 minute to 20 minutes. At the time of examination, the patient is in a clear state, may complain of headache. No abnormalities, except for the pallor of the skin, are usually not detected. In rare cases, the victim cannot remember the events that preceded the injury. If there was no loss of consciousness, the diagnosis is made as 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 injury and the victim may lose consciousness for an hour, and then complain of headache, nausea, vomiting. There is twitching of the eyes when looking to the side, asymmetry of reflexes. X-ray can show a fracture of the bones of the cranial vault, in the cerebrospinal fluid - an admixture of blood.

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

Moderate brain injury 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, soreness of 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 injury 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 in him. The movements of the eyeballs are uncoordinated, the muscle tone is changed, the process of swallowing is disturbed, weakness in the arms and legs can reach convulsions or paralysis. As a rule, such a 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 assume that you have received a traumatic brain injury, it is necessary to see a traumatologist and neurologist within a few hours and carry out the necessary diagnostic procedures. Even if it seems that health is in order. After all, some symptoms (cerebral edema, hematoma) may appear after a day or even more.

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

At brain compression two clinical pictures can be observed. In the first case, a “light period” is noted, during which the victim regains consciousness, and then slowly enters a state of stupor, which is generally similar to stunning and stupor. In another case, the patient immediately falls into a coma. Each of the conditions is characterized by uncontrolled eye movement, strabismus, and crossed paralysis of the limbs.

long head compression accompanied by soft tissue edema, 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, asymmetric swelling of the face, lack of sensation in the neck and back of the head. Computed tomography shows edema, hematomas, fractures of the bones of the skull, foci of brain contusion and crushing.

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 a mild TBI affects cognitive functions- the victim experiences confusion and decreased mental abilities. In more severe injuries, amnesia, impairment of vision and hearing, speech and swallowing skills can be diagnosed. In severe cases, speech becomes slurred or even completely lost.

Disturbances of motility and functions of the musculoskeletal system expressed in paresis or paralysis of the limbs, loss of sensation of the body, lack of coordination. In the case 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 the injury and is accompanied by dizziness, nausea, and vomiting. Chronic headache accompanies a person throughout life after receiving TBI. The pain can be sharp or dull, pulsating or pressing, localized or radiating, for example, to the eyes. Attacks of pain can last from several hours to several days, intensify at moments of emotional or physical exertion.

Patients have a hard time with the deterioration and loss of body functions, partial or complete loss of working capacity, therefore they suffer from apathy, irritability, and depression.

TBI treatment

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

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

The neurologist examines the patient every 4 hours and assesses his condition on the Glasgow scale. If consciousness is disturbed, the patient is shown tracheal intubation. A patient in a state of stupor or coma is prescribed artificial ventilation of the lungs. Patients with hematomas and cerebral edema regularly measure intracranial pressure.

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

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

Recovery prognosis for TBI of varying severity

In the case of a concussion, the prognosis is favorable, provided that the victims follow the recommendations of the attending physician. Complete recovery of working capacity is noted in 90% of patients with mild TBI. In 10%, cognitive functions remain impaired, a sharp change 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 patients with TBI of moderate severity, it is also possible to achieve a complete restoration of body functions. But often there are headaches, hydrocephalus, vegetative vascular dysfunction, coordination disorders and other neurological disorders.

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

Of great importance in the return of the patient to an active life is the complex of rehabilitation measures rendered to him after the relief of the acute phase.

Directions of 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 a head injury is carried out by a neurologist, a rehabilitation doctor, a physical therapist, an ergotherapist, a massage therapist, a psychologist, a neuropsychologist, a 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. So, in case of a severe injury, the efforts of doctors are aimed at restoring the functions of breathing and swallowing, at improving the functioning of the pelvic organs. Also, specialists are working on the restoration of higher mental functions (perception, imagination, memory, thinking, speech), which could be lost.

Physical therapy:

• Bobath therapy involves stimulating the patient's movements by changing the positions of his body: short muscles are stretched, weak ones are strengthened. People with movement limitations get the opportunity to learn new movements and hone the ones they have learned.
• Vojta therapy helps to connect brain activity and reflex movements. The physical therapist irritates various parts of the patient's body, thereby inducing him to make certain movements.
• Mulligan therapy helps to relieve muscle tension and pain relief.
• Installation "Exarta" - suspension systems with 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 stabiloplatform - for training coordination of movements.

Ergotherapy- the direction of rehabilitation, which helps a person to adapt to the conditions of the environment. The ergotherapist teaches the patient to take care of himself in everyday life, thereby improving the quality of his life, allowing him to return not only to social life, but even to work.

Kinesiology taping- the imposition of special adhesive tapes on damaged muscles and joints. Kinesitherapy helps to reduce pain and relieve swelling, while not restricting movement.

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

Physiotherapy:

• Medicinal electrophoresis combines the introduction of drugs into the body of the victim with exposure to 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 fights pain, swelling of tissues, has anti-inflammatory and reparative effects.
• Acupuncture can reduce pain. This method is included in the complex of therapeutic measures in the treatment of paresis and has a general psychostimulating effect.

Medical therapy It is aimed at preventing brain hypoxia, improving metabolic processes, restoring active mental activity, and normalizing the emotional background of a person.

After craniocerebral injuries of moderate and severe degree, it is difficult for the 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 TBI, it is necessary to follow simple rules: do not refuse hospitalization, even if it seems that you feel 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 damage 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: the 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, two main factors of a mechanical nature are of particular importance: 1) temporary changes in the configuration of the skull according to the type of 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 velocity in a 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 wounds. Closed TBI includes injuries in which there are no violations of the integrity of the head cover. An open TBI is called with the presence of a wound of 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. With the integrity of the dura mater, open craniocerebral injuries are classified as non-penetrating , and in case of violation of its integrity - to penetrating .

Classification.

1. I. Closed head injuries: Brain concussion; 2. Brain contusion: - mild; - moderate severity; - severe degree. 3. Compression of the brain on the background of a bruise and without a bruise: - hematoma: acute, subacute, chronic (epidural, subdural, intracerebral, intraventricular); - hydrowash; - bone fragments; - edema-swelling; - pneumocephalus. 4. State of the subshell spaces: - subarachnoid hemorrhage; CSF pressure: normotension, hypotension, hypertension. 5. Condition of the skull: - without damage to the bones; type and location of the fracture. 6. Condition of the integument of the skull: - bruises; - abrasions. 7. Associated injuries and diseases. 8. According to its severity, a closed craniocerebral injury is divided into three degrees: - mild (concussion and mild brain contusion), moderate (medium 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. By the nature of the wound: - soft tissues, - non-penetrating with bone damage, - penetrating. 3. According to the type of wound channel: - blind, - tangent, - through, - ricocheting. 4. By localization: - temporal, - occipital, other areas. 5. According to the type of fracture of the skull bones: - linear, - depressed, - crushed, - perforated, - comminuted. 6. By the number of wounds: - single, - multiple. 7. According to the influence of combinations of various factors: - mechanical, - radiation, - thermal, - chemical. 8. According to the nature of brain damage: - concussion, - bruise, - crush, - compression. 9. According to the severity of the injury: - light, - moderate, - severe. 10. According to the severity of the condition of the wounded: - satisfactory, - moderate, - severe, - terminal. 11. Blind wounds: - simple, - radial, - segmental, - diametrical, - rebounding, - tangential. 12. Through 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 various 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 to their full or partial recovery or stable compensation (with mild TBI - up to two months, with moderate TBI - up to four months, with 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 the elements of this classification, can only be made in a specialized hospital.

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

Clinic of closed TBI.

1. Closed brain injury with concussion symptoms is a functionally reversible form of brain injury. It is characterized by short-term loss of consciousness from a few seconds to several minutes, retro- and anterograde amnesia, vomiting, headache, dizziness, and other autonomic disorders. In the neurological status, as a rule, only cerebral neurological symptoms are noted. There are no injuries to the bones of the skull, 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 there is a headache, dizziness, nausea, vomiting, retro- and anterograde amnesia. Vital functions are usually not impaired, a moderate increase in heart rate, respiration, and an increase in blood pressure are possible. Focal symptoms are mild (nystagmus, pyramidal insufficiency) and disappear after 2-3 weeks. Unlike concussion, subarachnoid hemorrhages and skull fractures are possible. brain contusion medium degree It is characterized by a loss of consciousness after an injury lasting from several minutes to several hours. Expressed retrograde and anterograde amnesia and other cerebral symptoms. Complaints of severe headache, repeated vomiting, transient disturbances of vital functions in the form of bradycardia, tachycardia are possible). Nested symptoms are clearly manifested, determined by the localization of the brain contusion - hemiparesis, speech disorders, visual disorders, etc. With a lumbar puncture, blood-colored cerebrospinal fluid is usually detected, flowing under high pressure. Craniograms often show skull fractures. brain contusion severe accompanied by a loss of consciousness from several hours to several weeks. Severe violations 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, paresis of accommodation, tonic nystagmus, swallowing disorders, decerebrate rigidity (generalized or focal seizures). As a rule, a brain contusion is accompanied by fractures of the bones of the vault or base of the skull, massive subarachnoid hemorrhages.
3. Closed trauma of the brain, accompanied by symptoms of increasing compression of the brain (against the background of bruises or without bruises of the brain). The brain compression syndrome is characterized by a life-threatening increase at various intervals after the injury (the so-called "light period") of cerebral, focal and stem symptoms. Depending on the background (concussion, brain contusion), on which traumatic compression of the brain develops, the latent period may be pronounced, erased, or absent altogether. Clinically, in this case, pupil dilation appears on the side of compression, and hemiplegia on the opposite side. The appearance of bradycardia is characteristic.

Clinical brain injury.

At the suggestion of E.I. Smirnov (1946) it is customary to divide the course of pathological processes in 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. It is characterized by a predominance of cerebral symptoms over local ones, impaired consciousness, respiration, cardiovascular activity, and the act of swallowing;

II - the period of early reactions and complications - (infection and discirculation), 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 detected, the course is complicated by the development of meningitis, meningoencephalitis, suppuration of the wound channel. As a result of the development of infection, malignant protrusions (secondary prolapses) occur;

III - the period of elimination of early complications and a tendency to limit the infectious focus, begins on the 2nd month after the injury and lasts about 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 the injury and lasts 2-3 years, is 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. Identification of an anamnesis of trauma.

2. Clinical assessment of the severity of the condition.

3. The state of vital functions.

4. The condition of the skin - color, moisture, bruising, the presence of soft tissue damage.

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

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

7. Shell symptoms: stiff neck, symptoms of Kernig, - Brudzinsky.

8. Echoencephaloscopy.

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

10. Computed 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 brain compression) with the measurement of cerebrospinal fluid pressure and the removal of no more than 2-3 ml of cerebrospinal fluid, followed by laboratory testing.

Providing assistance at the stages of medical evacuation.

First aid

is reduced to the imposition of an aseptic dressing on the wound, the careful removal of the wounded. The wounded, who are unconscious, are taken out on their side (in order to prevent aspiration of vomit), they need to unfasten the collar, loosen the belt. In case of retraction of the tongue and signs of asphyxia, introduce an air duct (S-shaped tube, breathing tube TD-1). Do not inject drugs (respiratory depression).

First aid

– Bandaging of the bandage, ventilation of the lungs with the help of the DP-10, DP-11 breathing apparatus, oxygen inhalation with the KI-4 apparatus, maintenance of cardiovascular and respiratory activity (intramuscular injection of 2 ml of cordiamine, 1 ml of caffeine). Evacuation of the wounded in the first place on a stretcher.

First aid

- fight against asphyxia, artificial ventilation of the lungs with the DP-9, DP-10 apparatus, oxygen inhalation with the KI-4 apparatus, maintenance of cardiovascular and respiratory activity (introduction of 2 ml of cordiamine, 1 ml of caffeine, 1 ml of 5% ephedrine).

If necessary, the bandage is corrected, a prophylactic dose of antibiotics is administered (500,000 units of streptomycin, 500,000 units of penicillin), tetanus seroprophylaxis is carried out by subcutaneous injection of 0.5 ml of tetanus toxoid.

The wounded are directed to the dressing MPP in the skull with ongoing bleeding from soft tissue wounds for hemostasis with a pressure bandage, 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 secondarily those wounded in the soft tissues of the skull. Before transportation, according to indications, cardiovascular and respiratory means, an air duct are introduced.

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

Qualified medical care .

The wounded deserve special attention, who, as a result of medical triage, are subject to surgical treatment at this stage for health reasons (refusal to operate can lead to death).

Urgent 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 ligation of the vessels of the integumentary tissues or tight tamponade of the wound); - trepanation of the skull and PST of a brain wound at the stage of rendering qualified assistance (including with compression of the brain).

Sorting of the wounded in the skull on OMedB and OMO in case of mass admission will often have to be carried out without removing the bandage.

Determination of transportability is made on the basis of an assessment of the general condition, preservation of the reaction of the pupils and corneal reflexes, the state of the pulse, respiration, dressing, etc.

When evacuating, provide for: - wounded with damage to the soft tissues of the skull without focal neurological symptoms - in the GLR; - wounded with concussion - in VPNG. All other wounded 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 concussion.
6. Clinical picture of brain injury.
7. Clinical picture of brain compression.
8. Diagnosis of combat trauma of the skull and brain.
9. The volume of medical care at the stages of medical evacuation.
10. Possible complications in traumatic brain injury and their prevention.

Penza State University

medical institute

department of TO and VEM

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 belongs to the category of the most common injuries and accounts for > 40% of their total number, mortality in severe injuries of the skull and brain reaches 70-80%. The mechanism of traumatic brain injury can be direct and indirect. An example of an indirect mechanism is a traumatic brain injury as a result of a fall from a height onto the legs or pelvis. When landing and stopping the movement of the skeleton, the skull, due to inertia, is, as it were, placed on the spine and a fracture of the base of the skull may 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 (1, 2, 3 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 (contusion, compression).	5. Gunshot wounds.

Syndromes: Hypertensive - the pressure of the cerebrospinal fluid is increased. Hypotensive - the pressure of the cerebrospinal fluid is lowered. Normotension - the pressure of the cerebrospinal fluid is not changed.

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

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

1. Loss of consciousness. It proceeds along the stem type and is characterized by three forms of manifestation: a) stunning - is expressed by a short-term disorientation followed by mild drowsiness. Special attention should be paid to this form of consciousness disorder, since the 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 impaired consciousness, in which the reaction to gross stimuli (pain, loud cry) is still preserved in the form of coordinated protective movements, opening the eyes; c) coma - prostration with a complete loss of perception of the surrounding world, deepening, characterized by adynamia, atony, areflexia, depression of vital functions.

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

Headache. There is both diffuse and local nature of pain, bursting or squeezing the head.

Dizziness. Instability in the Romberg position.

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

Positive symptom of Mann-Gurevich. 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 health worsened, cerebral and vegetative manifestations intensified, tachycardia appeared, then the symptom is considered positive.

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

Local(they are focal) symptoms. The reason for their appearance lies in the organic lesion of any part of the brain and the loss of function in the zone of its innervation. Clinically determined local signs are nothing more than paresis, paralysis, sensory disorders and dysfunction of the sense organs. For example: motor or sensory aphasia, anisocaria, smoothness of the nasolabial fold, deviation of the tongue, monoparesis of the limbs, hemiparesis, etc.

Meningeal (shell) 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 pronounced meningeal symptoms can be detected already with 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 knee and hip joints (the “trigger” position). Another characteristic feature is photophobia. The victim tries to turn away from the light source or covers his face with a blanket. Increased excitability is noted, and a convulsive seizure can become an extreme reaction to gross stimuli.

Patients complain of intense headache, aggravated by head movement. Localization of pain - frontal and occipital regions with irradiation to the neck or eyeballs. Often disturbed by pain in the eyeballs. With irritation of the meninges, nausea and vomiting are observed, the latter being repeated and debilitating.

Pathognomonic meningeal features are neck stiffness and positive Kernig and Brudzinsky signs. An increase in body temperature to 39-40 ° C is characteristic, especially if an infection joins.

Stem symptoms. According to their genesis, they are no different from local ones, but the damage concerns only the brain stem and its vital functions regulating structures. Trauma to the brainstem can be primary, or it occurs as a result of dislocation of the brain and infringement of the brainstem in the opening of the cerebellar tenon or in the occipitocervical dural funnel.

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

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

Upper stem 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 disturbed. Body temperature is high.

Lower stem(bulbar) syndrome is characterized by a more severe condition. Consciousness is absent - coma. Respiratory distress reaches an extreme degree, pathological forms of respiration 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 barely perceptible. Swallowing is severely impaired. Thermoregulation is reduced.

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

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

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

Traumatic brain injury with hypotension syndrome occurs in 25% of patients. A decrease in cerebrospinal fluid pressure is more often observed in young people, it occurs with a compressive headache, with normal or low blood pressure, and tachycardia. Expressed vegetative signs, often manifested by pallor, sweating. Increased fatigue, lethargy, mental exhaustion are noted. A positive symptom of "head down" - giving the patient the position of Trendelenburg reduces headache.

With a lumbar puncture in the supine position of the patient, the cerebrospinal fluid flows out in drops at a frequency of 60 per minute, and the pressure measured by the manometer is 120-180 mm of water column. These numbers are considered normal. An increase in the frequency of drops and cerebrospinal fluid pressure is regarded as hypertension, a decrease 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 review craniograms are required: straight and lateral. .

Schemes of craniograms in survey projections with explanation are presented in fig. one.

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

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

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

(B) 1. Pyramid. 2. Main bone. 3. Turkish saddle. 4. Anterior part of the large wings of the main bone. 5. Frontal sinus. 6. Coronal seam. 7. Lambdoid seam. 8, 9. Anterior and posterior branches of the sheath artery, 10. Internal and external auditory canals. 11. Shadow of the cartilage of the auricle. 12. Bones of the nose. 13. Cheekbones. 14. Maxillary sinus

Echoencephalography- this is a registration of the position of the middle structures of the brain (pineal gland, III ventricle, interhemispheric fissure, etc.) by receiving a reflected ultrasonic signal (M-echo) from them. The method is based on the ability of ultrasound to propagate in various media and give reflection at the boundary 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. With volumetric processes in the cranial cavity (hematomas, hygromas, traumatic cysts, abscesses, tumors), the median structures of the brain are shifted towards the healthy hemisphere. This is revealed on the echoencephalogram as 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 median structures and M-echo in intracranial hematoma (B)

Carotid angiography. This research method is based on the introduction into the carotid artery of substances that have the ability to absorb x-rays, which provides visibility on the x-ray of the vessels at different phases of cerebral circulation. By changing the filling and location of the vessels, the degree of circulatory disorders of the brain and its causes are judged.

CT scan- X-ray method of research using a computer, which allows to obtain images of the structures of the brain and bones of the skull both in its entirety 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 head substance, to identify intracerebral and intracranial hemorrhages, and much more.

Patients with traumatic brain injury should undergo ophthalmological and otorhinoneurological survey.

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

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 maximally bent. The puncture site is the gap 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 1% solution of novocaine in the 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 the mandrin is removed from the needle, cerebrospinal fluid begins to flow. 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 research: 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.

CLINIC AND DIAGNOSIS OF INDIVIDUAL

NOSOLOGICAL FORMS OF CRANIO-BRAININJURIES

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. A longer persistence of these signs indicates the presence of a brain contusion.

Additional methods of research of information, reliably confirming the diagnosis, practically do not give. An exception is a lumbar puncture, which can be used to establish changes in cerebrospinal fluid pressure.

With proper treatment, the patient's condition improves by the end of the first week, and a complete regression of clinical signs occurs after 2-4 weeks. The most stable are headache and Mann-Gurevich symptom, 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 around.

brain contusion

Brain contusion occurs due to the direct and indirect mechanism of action. An example of an indirect mechanism of injury is a counter-strike, when a wave of “perturbed” medulla, consisting of 80% water, reaches the opposite wall of the skull and hits its protruding parts or collapses against tightly stretched areas of the dura mater.

A brain contusion is an organic lesion. As a result of trauma, there are areas of crushing and necrosis of the brain tissue, gross vascular disorders with phenomena of hemorrhagic softening. Around the site of brain injury 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 joins in this period, then an abscess of the brain is formed. In an aseptic course, a brain tissue defect is replaced by a neuroglia scar or brain cysts are formed.

The clinic of a brain contusion is that immediately after the injury, the victims develop cerebral and local symptoms, and in severe forms, meningeal and stem symptoms join.

There are three degrees of brain injury.

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

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

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

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

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

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

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

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

III degree brain contusion, as a rule, is accompanied by fractures of the vault and base of the skull and massive subarachnoid hemorrhage.

Electroencephalography - when the brain is bruised and crushed, delta waves of high amplitude appear in the destruction zone. With an extensive convexital lesion, zones of electrical silence are found, corresponding to the most severely affected area.

COMPRESSION OF THE BRAIN

The causes of brain compression 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 a frequent tragic outcome. The rest of the nosological forms arise as a result 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 the volume of the brain and, with the progression of the pathology, can cause dislocation and infringement 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 with fractures of the cranial vault with prolapse of the fragments deeper than the internal bone plate. Depressed fractures of the cranial vault are mainly of two types. The first is when, as a result of mechanical action, the fragments are displaced at an angle, the top of which “looks” into the cranial cavity, and the peripheral ends of the fragments remain connected with the maternal 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 an injury, a fenestrated fracture occurs, the size and shape of which repeats the injuring object. The bone plate, which closed 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 damage to the skull is also possible with cold weapons or household items, parts of which, breaking off, remain in the cranial cavity.

Rice. 3. Depressed fractures of the cranial vault: A - impression; B - depression.

Preliminary data make it possible to diagnose brain contusion (of varying severity), which actually accompanies depressed fractures and foreign bodies of the skull with brain compression. The final diagnosis is made after craniography, computed tomography, echoencephalography, which reveal depressed skull fractures or foreign bodies in it, and the clinical data and the results of additional research methods on the topography of the location of the ingredient that causes 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 a number of patterns can be traced in their course, which allow us to consider intracranial hematomas in one group. Schematically, it looks like this: a history of head trauma with loss of consciousness (often for a short period). Upon the return of consciousness, cerebral symptoms are revealed, on the basis of which a diagnosis of "Concussion of the brain" can be made. In the best case, the patient is hospitalized and appropriate treatment is prescribed: rest, sedatives, etc. In some cases, victims may not seek help, since a short bed rest, as a rule, relieves cerebral symptoms. Moderate headaches and amnesia persist. The patient's condition improves significantly. Thus, the rupture of an intracranial vessel at the time of injury due to the absence of a clinical picture of brain compression remains unnoticed. As compression increases, meningeal and then local symptoms appear (anisocaria, mono- or hemiparesis, etc.). There comes a disorder of consciousness according to the cortical type. There is psychomotor and speech excitement, which later turns into depressed consciousness (stupor), often with convulsive seizures and subsequent cerebral coma. The outcome of compression of the brain in the absence of treatment, as a rule, is death. Thus, an intracranial hematoma is characterized by a three-phase course: trauma with loss of consciousness - improvement of the condition (“light gap”) - deterioration of the condition with a tragic outcome.

light gap called the time from the return of consciousness after the primary injury to the appearance of signs of compression of the brain. 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 gap?

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 gap. 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. The formed hematoma at an early stage does not cause a pronounced compression of the brain, since it, like any living organ, is given up to a certain limit by its volume, while compensating for the 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. There comes a breakdown of the compensatory capabilities of the central nervous system, which is expressed in the end of the light interval. A further increase in the volume of the brain leads to a shift in the median structures, and then the dislocation of the brain stem into the opening of the cerebellar tenon and the occipitocervical dural funnel.

An increase in the period of the light 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 the imaginary well-being is also facilitated by dehydration performed in a hospital for patients diagnosed with a concussion or contusion of the brain, which does not allow the development of pronounced edema 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 the outflowing blood and the increase in the content of high-molecular proteins increase the oncotic pressure in the hematoma. This causes CSF diffusion until an osmotic equilibrium is created between the liquid content of the hematoma and the cerebrospinal fluid.

Interruption of the light gap and repeated hemorrhages in the epi- or subdural space are not excluded when a blood clot breaks off from a damaged vessel. This can occur with a sudden sharp drop in arterial and intracranial pressure - when sneezing, coughing, straining, etc.

Thus, the duration of the luminous interval depends on many factors, and not only 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 of 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 the return of consciousness, only 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 interval is short, from several hours to 1.5-2 days, in most cases 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, vomiting disappear, nausea and headache decrease. The victim is adequate, oriented in time and space, critically assesses his condition.

In the next stage, the patient develops unconscious anxiety. He is overly active, tends to change the position of the limbs, sit down, stand up, leave the ward. The face is hyperemic, in the eyes there is alienation or fear. Patients cannot stand bright light, noise. Such arousal is due to an increase in headache, which is excruciating, bursting in nature. The victim covers his head with his hands, assumes a forced position, begs or demands immediate assistance, agrees and insists on surgical treatment.

There is persistent nausea, repeated vomiting, frightening dizziness - everything floats before my eyes. The pulse rate slows down, moderate bradycardia sets in (51-59 bpm), 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 anisocaria - a 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. There comes a secondary disorder of consciousness, starting with stunning and turning into a stupor. The victim is indifferent to the environment, his gaze is pointlessly directed into the distance. There is an increase in bradycardia (41-50 bpm) and tachypnea (31-40 breaths per minute). There is an asymmetry in blood pressure. On the opposite hand from the lesion, the blood pressure will be 15-20 mm Hg. higher than on the arm from the side of the hematoma. Increasing focal symptoms. Among them, the main diagnostic role is played by: pupil dilation on the side of the hematoma, smoothness of the nasolabial fold, grin disturbances, tongue deviation, spastic hemiparesis with a predominant lesion of the arm on the opposite half of the body. Reveal meningeal signs in the form of stiff neck and positive symptoms of Kernig and Brudzinski.

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 into tachycardia (120 bpm and above), tachypnea into pathological types of breathing, blood pressure begins to steadily decrease, reaching critical numbers (below 60 mm Hg), swallowing disorder, a symptom of floating gaze, gross anisocaria and dissociation of meningeal symptoms, muscle tone and reflexes along the axis of the body. In the final phase, bilateral mydriasis with no pupillary response to light, areflexia, muscle atony, and death occur.

A favorable outcome in 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 it is possible to detect fractures of the bones of the cranial vault, most often the scales of the temporal bone, a zone of increased density of a plano-convex or biconvex shape adjacent to the skull, a 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 frequency of these hemorrhages ranges from 1 to 13% of all traumatic brain injuries. Subdural hematomas often occur with an indirect mechanism of injury such as a counterattack 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 delicate pial vessels with a sharp rotation of the head and displacement of the hemispheres around the vertical or horizontal axes. These same vessels are damaged by bruising of the brain.

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 in an area from 4x6 to 13x15 cm.

The clinical manifestations of subdural hematomas in the classic 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 - this is a limited accumulation of cerebrospinal fluid in the space under the dura mater resulting from trauma.

Subdural hygromas are much less common than hematomas of a similar situation. The question of the pathogenesis of hygromas has not been finally resolved. The reasons for the limited accumulation of cerebrospinal fluid under the dura mater are considered damage to the arachnoid by the type of 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, which create conditions for blood plasma to leak into the subdural space, or as a result of severe brain damage, when there are messages between the intrathecal spaces, the lateral ventricles.

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 accompanied by severe brain contusion.

If the hygroma arose in isolation, then its clinic is very similar to that of a subdural hematoma, especially the three-phase flow. As a rule, after an injury with a short-term loss of consciousness, a lucid interval occurs, more often 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 paresis of the facial nerve, mono- or hemiparesis, and sensitivity disorders.

However, in the classical clinic of intracranial hematoma, one can notice some features typical of subdural hygroma, or signs that are most common with it. This is a large light interval (1-10 days) - hygromas often have a subacute course. Headaches are paroxysmal, radiating to the eyeballs, the cervical-occipital region. Characterized by photophobia and local pain on percussion of the skull. The general condition of patients worsens slowly, as do signs of brain compression, which grow relatively milder and gradually. Often there are mental disorders according to the type of frontal syndrome (decrease in 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 that begin with the muscles of the face or on the contralateral side. Subdural hygromas are characterized by a gradual, undulating deepening of secondary disturbances of consciousness. So, in the early stages, after a convulsive seizure, consciousness is restored and you can make contact with the patient.

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

Intracerebral hematomas

Intracerebral hematoma - This is a post-traumatic hemorrhage in the substance of the brain with the formation of a cavity in it filled with blood. The frequency of formation 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 blood flowed out is most often in the range of 30-50 ml, sometimes there are more massive hematomas - 120-150 ml.

The source of cerebral hemorrhages are damaged vessels of the substance of the brain in case of a bruise or other types of craniocerebral injury.

The clinic of isolated intracerebral hemorrhages has a tendency to three-phase and acute, subacute and chronic stages of the course. The latter depend on the volume of the hematoma and the reaction of the brain to injury, expressed by edema and swelling.

In the acute course of a hematoma, a light gap is observed in half of the patients, in the rest it is absent or is 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 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 the victims occurs on the side of the hematoma, while in the rest it occurs on the opposite side. The light interval, as a rule, breaks off 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, M-echo displacement, displacement of the vascular and median structures of the brain.

Intraventricular hematomas

Intraventricular hematomas - These are post-traumatic hemorrhages in the cavity 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 does not happen in isolation.

Intraventricular hematomas account for 1.5 to 4% of all intracerebral hemorrhages. The cause of their occurrence is the rupture of the choroid plexuses of the ventricles as a result of hydrodynamic impact 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.

Clinic intraventricular hematoma depends on the rate of bleeding into the ventricle and the severity of concomitant brain injury. Blood pressure on the walls of the ventricle, irritation of the reflexogenic zones embedded in them not only exacerbates 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 after 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 face and neck of the victim are hyperemic with symptoms of hyperhidrosis.

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

Neurological symptoms in intraventricular hematomas are usually bilateral.

Quite early, violations of the regulation of breathing appear in the form of tachypnea (30-70 breaths per minute), which stubbornly progress, reaching pathological forms (Cheyne-Stokes, Biota). Subsequently, there are signs of brain dislocation (transition of bradycardia into tachycardia, reaching up to 160 or more beats per minute with bilateral mydriasis, the occurrence 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 an abundant admixture 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 give local compression of the brain. This intracranial hemorrhage does not occur in isolation, but is a companion of craniocerebral injuries, mainly brain contusion. Subarachnoid hemorrhages occur in 15-42% of all traumatic brain injuries, and in severe forms 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 hemorrhage is torn vessels of the membranes that limit the subarachnoid space, or an increase in vascular permeability as a result of injury. The outflowing 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 erythrocytes undergo decay. It has been established that blood and its toxic decay products (bilirubin, serotonin) irritate the meninges and cause impaired cerebral circulation, liquor dynamics, a sharp fluctuation in intracranial pressure with a disorder of brain functions.

It is pathognomic for subarachnoid hemorrhages that the loss of consciousness after the primary injury is replaced by a state of stupor, disorientation, and often - psychomotor agitation. Restoration of consciousness is accompanied by retro - and anterograde amnesia of memory impairment in the asthenic type and Korsakov's traumatic amnestic syndrome.

In victims with subarachnoid hemorrhage, meningeal syndrome develops by the end of the first day 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's syndrome. The syndrome increases, reaching a peak at 7-8 days, and then subsides and disappears by 14-18 days.

As a result of blood irritation of the recurrent branch of the trigeminal nerve (1 branch), a syndrome of cerebellar numbing occurs, manifested by photophobia, injection of 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 decay 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 tendon and periosteal reflexes (especially the knee), which disappear completely by 5-6 days. By 8-9, sometimes by 12-14 days and even at a later date, the reflexes are restored and come to normal.

For 7-14 days after the injury, the body temperature rises by 1.5-2 degrees above normal.

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

FRACTURES OF THE SKULL BONES

Skull fractures account for up to 10% of fractures of all bones of the skeleton and belong to the category of 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. Distinguish between fractures of the facial and cerebral skull, and in the damage to the brain skull, fractures of the arch and base are distinguished.

Fractures of the base of the skull

Fractures of the base of the skull arise mainly from the 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: middle or back, 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 intimately soldered to it and often forms a communication between the cranial cavity and the external environment. Thus, the picture of a skull base fracture consists of clinical manifestations of concomitant brain injury (contusion of varying severity) and symptoms that are pathognomonic for violations of the integrity of the anterior, middle, or posterior cranial fossae.

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

Traumatic "glasses" appear after 12-24 hours or more from the moment of injury, often symmetrical. The color of the bruise is homogeneous, does not go 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.

In direct trauma, bruising occurs immediately after the impact. 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 with an admixture of 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 skull, 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.

Fractures of the calvaria

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 cranial vault are divided into linear (cracks), depressed (impression and depression) and comminuted.

Clinical diagnosis of closed fractures of the cranial vault, which make up about 2/3 of all its fractures, is extremely difficult. Subperiosteal and subgaleal hematomas, severe pain make palpation difficult, which should already be extremely gentle in order to avoid

displacement of a comminuted fracture and trauma to the underlying formations. The idea of ​​a possible fracture can be suggested by the history of the severity of 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 at the same time, according to the forensic In medical autopsies, about 20% of fractures remain unrecognized.

The greatest difficulty in diagnosis is represented 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 a thin apex. In addition, convoluted branches depart from the trunk, which in turn have the same branches, but thinner.

Rice. 5. X-ray signs of a fracture of the cranial vault:

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

B - a symptom of a double line (a symptom of "ice")

Linear fractures have a number of distinguishing features:

1. Symptom of transparency (linear enlightenment) - It is associated with bone rupture and is often distinct, but sometimes it can be due to a vascular pattern or contour of the cranial sutures.

split symptom - along the cracks in some sections, the line bifurcates, and then again goes single. Bifurcation occurs with through cracks, when a beam going at an angle to the fracture line can separately reflect the edges of the outer and inner plates of the arch. An illusion is created that islands of bone are gouged out along the fracture line, therefore this symptom is called the symptom of "ice". The symptom of bifurcation absolutely confirms the diagnosis of a fracture.

Zigzag symptom(lightning) - expressed by a zigzag line of enlightenment. It refers to reliable signs of a fracture, which have an absolute diagnostic value (Fig. 5).

Sometimes along with cracks there is a divergence of seams.

Treatment of patients with traumatic brain injury

The treatment of patients with traumatic brain injury is a complex and extensive set of medical measures, the choice of which in each case depends on the type, severity and progression of the injury, the stage at which therapy was started, age, comorbidities, and much more.

Assistance to victims with traumatic brain injury can be divided into three periods: assistance at the prehospital stage, treatment in a hospital (hospital stage) and aftercare in outpatient conditions (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, release the airways from vomit, retraction of the tongue, 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, they are used: analeptics (cordiamin, cytiton, lobelin), cardiac glycosides (strophanthin K, corglicon).

In an emergency, transport the patient (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 methods of treatment are used much more often, while surgical interventions are performed according to strict indications.

Patients with concussion, brain contusion, closed fractures of the cranial vault, fractures of the base of the skull, 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 concussion of the brain of the I degree, strict bed rest lasts 5-7 days, II degree - 7-10 days. With a brain contusion of I degree - 10-14 days, II degree - 2-3 weeks and III degree - at least 3-4 weeks. To determine the termination of strict bed rest, in addition to the indicated terms, the Mann-Gurevich symptom is used. If it is negative, the patient can sit up in bed, and after adaptation, get up and walk under the supervision of the staff.

Cold to the head. Apply 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 devices necessary for the treatment of patients. Exposure to head hypothermia depends on the severity of the injury. With mild injuries (concussion and brain contusion of the 1st degree), its effect is limited to 2-3 hours, and with severe injuries, the exposure lasts 7-8 hours or more, up to 1-2 days. But it should be remembered that with prolonged use of cold, every 2-3 hours a break is taken for 1 hour.

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

3. Sedatives(sodium bromide, bromcamphor, corvalol) and t ranquilizers(elenium, seduxen, tazepam).

4. Sleeping pills(phenobarbital, barbamil, etaminal sodium). Strict bed rest, the appointment of tranquilizers, sedatives and hypnotics - this is a set of measures aimed at creating rest for the damaged organ, i.e. brain. Medicines weaken external irritants, 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, decay of the destroyed brain substance, a mass of histamine-like substances (serotonin, etc.) is formed, so the appointment of antihistamines is mandatory.

Further choice of therapeutic appointments depends on the height of the patient's CSF pressure. With increased cerebrospinal fluid pressure (hypertension syndrome), treatment should be as follows: position in bed according to Fowler - with a raised head end, diet N 7 with salt and fluid restriction.

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, 40% glucose solution, 40% sodium chloride solution, 25% magnesium sulfate solution, 15% mannitol solution are used 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 8-12 ml of cerebrospinal fluid is slowly released after the lumbar puncture.

In case of hypotension syndrome, the following is prescribed: diet N 15, position in bed according to Trendelenburg - with a raised foot end. Solutions with a low concentration of salts (isotonic Ringer-Locke, 5% glucose solution) are administered intravenously. A good therapeutic effect is provided by subcutaneous injections of caffeine-sodium benzoate, 1 ml of a 10% solution, and vagosympathetic novocaine blockades.

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

In case of violation of vital functions, analeptics are administered that stimulate the respiratory center and vascular tone (cordiamin, lobeline hydrochloride, cytiton), adrenomimetic substances (adrenaline hydrochloride, norepinephrine hydrotartrate, mezaton) are used to normalize blood pressure in the whole vascular bed. The weakness of the heart muscle is stopped with cardiac glycosides (strophanthin K, corglicon).

Traumatic brain injury is often part of a polytrauma accompanied by shock and blood loss. In the complex of antishock therapy, blood and plasma-substituting solutions (rheopolyglucin, 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 with signs of brain compression. With open injuries, primary surgical treatment is performed. The wound is closed with sterile material. The hair around her 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 (furatsilin, hydrogen peroxide, rivanol) and examined. If only soft tissues are damaged, then non-viable tissues are excised. With enlarged 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 the revision of the wound, then it is necessary to carefully remove all small free-lying fragments with tweezers and examine the dura mater. In the absence of its damage, normal color, preserved ripple, the shell is not opened. The edges of the bone wound are cut with wire cutters to a width of 0.5 cm. Hemostasis is performed and the wound is sutured.

If the dura mater is damaged, i.e. there is a penetrating wound of the skull, then the primary surgical treatment is performed as described above, but with an economical excision of the edges of the shell. For a better revision of the subdural space, the wound of the dura mater is expanded. Loose bone fragments, brain detritus, 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 layered sutures are applied to the soft tissues of the integument of the skull.

Compression of the brain, regardless of the causes that caused it, should be eliminated immediately after the diagnosis is made.

With depressed closed fractures of the cranial vault, a soft tissue incision is made to the bone with the expectation to expose the fracture site. A burr hole is placed next to it, through which they try to raise the depressed fragment with a levator. If the fragments were lifted, which is very rare, and they do not move, then the operation can be completed with this, after making sure that there are no indications for an extended operation. If the fragments cannot be lifted, then a resection of the depressed area of ​​the bone is performed from the side of the burr hole. The further course of the intervention is the same as in the primary surgical treatment, but without excision in the dura mater.

When the brain is compressed by hematomas or hygroma, resection or osteoplastic surgery can be performed. The first version of the operation is that in the projection of the alleged hematoma, a search burr hole is applied. 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, an intervention is performed on the brain and membranes. The operation is completed by suturing the soft tissue, leaving a large defect in the bones of the skull. Such an operation creates a good decompression of the brain, especially when the compression of the brain is combined with severe contusion. But resection trepanation also has negative sides. After it, one more intervention is necessary to close the skull defect with a synthetic material (steractyl) or an autobone taken from the rib. If this is not done, posttrepanation syndrome will develop. Changes in intracranial pressure caused by physical stress (straining, coughing, sneezing, etc.) lead to frequent displacements of the medulla into the "window" of the skull defect. Traumatization of the brain on the edge of the burr hole causes the development of a fibrous process in this area. Adhesions are formed between the brain and the membranes, bones and integuments of the skull, which cause local and headaches, and later epileptic seizures. Osteoplastic trepanation does not leave skull defects requiring subsequent plasty. Produce a semi-oval base downward incision of the soft tissue to the bone. Five burr holes are drilled along the incision line, without separating the soft tissue flap - two at the base of the flap and three along the arc. the flap on the pedicle is turned down.The further course of the operation depends on the type of injury.After the intervention in the cranial cavity is completed, the bone flap is placed in place and the soft tissues are sutured in layers.

Control task for self-study on the topic"traumatic brain injury"

Mechanisms of traumatic brain injury.

Classification of traumatic brain injury.

List the general symptoms.

Name the local symptoms.

List the meningeal symptoms.

Name the stem symptoms.

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

How is a concussion diagnosed?

What is the diagnosis of brain injury based on?

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

Causes of brain compression.

Clinic of compression of the brain by bone fragments and foreign bodies, in contrast to brain contusion.

Clinic of cerebral compression by intracerebral and intraventricular hematomas.

Clinical presentation of cerebral compression by epi- and subdural hematomas, in contrast to cerebral contusion.

What is a subdural hygroma?

The difference between the clinic of concussion, contusion 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 injury.

Conservative treatment of acute craniocerebral injury, give a pathogenetic rationale.

Conservative treatment of brain damage in the recovery period.

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

Technique of various types of trepanation, the necessary tools.

What is posttrepanation syndrome, its treatment.

Outcomes and long-term consequences of TBI.

Traumatic brain injury - 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 clinic of TBI 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, intracerebral hematoma or brain contusion is always expressed by focal symptoms. Diagnosis of the disease can be based on the obtained anamnestic indicators, as well as during a neurological examination, X-ray, MRI or CT.

Principles of classification of traumatic brain injury

According to biomechanics, the following types of TBI are distinguished

From the point of view of biomechanics, they speak of the following types of traumatic brain injuries:

• shock-proof (when the shock wave passes from the place of collision of the head with the object through the entire brain, up to the opposite side, while 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 injury

Regarding the genesis of the lesion, craniocerebral injuries are divided into:

1. Primary (these include bruises of a focal type, axonal damage 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

According to the type of traumatic brain injury, they 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 lesions is not characteristic.
2. Combined type - characterized by the presence of damage of the extracranial type, as a result of mechanical influence.
3. Combined view - it is characterized by the combination of various types of damage (mechanical, radiation or chemical, thermal).

The nature

The severity of the disease is of three degrees: mild, moderate and severe. If we evaluate the severity of the disease on the Glasgow coma scale, then mild TBI falls under 13-15 points, moderate TBI is 9-12 points, and severe TBI is 8 points or less.

According to its symptoms, a mild degree of TBI is similar to a brain contusion in a mild form, moderate - to a moderate degree of brain contusion, while severe - to a brain contusion of a more severe degree.

According to the mechanism of occurrence of TBI

If TBI is classified according to the mechanism of its occurrence, then two categories of injuries are distinguished:

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

It should also be said that craniocerebral injuries with characteristic symptoms can be both for the first time and again.

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 remote periods. In time, each of the periods lasts differently, it all depends 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 remote period can last up to several years.

Brain concussion

A concussion is considered the most common trauma among TBIs. It accounts for more than 80% of all cases.

Diagnosis

It is not so easy to make an accurate diagnosis of a concussion the first time. 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 ask the patient in detail about how the injury was received, determine its nature, and conduct a survey of possible witnesses to this 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 is not inherent in fractures of the bones of the skull. At the same time, the index of craniocerebral pressure, as well as the biochemical composition of the cerebrospinal fluid, remain unchanged. CT or MRI is considered an accurate diagnostic method, but does not reveal intracranial spaces.

Clinical picture

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

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

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

Speaking specifically about the neurological status, it is characterized by asymmetry of mild 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 TBI, the patient feels healthy already after two weeks, but some asthenic phenomena may persist.

Treatment

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

That patient with a traumatic brain injury who is not yet conscious should be laid on his side (preferably on the right), turning his face to the ground, and bending his arms and legs at a right angle, but only if in the knee or elbow joints are not fractured. It is this position that helps the air to pass freely, reaching the lungs, and at the same time, preventing the tongue from sinking or choking on its own vomit.

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

If, after the CT and MRI, the results of the examination do not show any signs of lesions of the focal type of brain, 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 usually not prescribed. The main goal of the initial treatment is to normalize the state of the brain, restoring its functionality, as well as stopping headaches and normalizing sleep. For this, various analgesics and sedatives are used.

Forecast

In the case of a concussion and following the doctor's instructions, the process ends with recovery and the return of working capacity. After a while, all signs of concussion (depression, anxiety, irritability, loss of attention, etc.) completely disappear.

Mild brain injury

Diagnostics

If we talk about moderate brain contusion, then CT helps to detect and identify various kinds of focal changes, which include poorly located areas with low 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 state reaches several hours. At the same time, congrade, retrograde or anterograde types of amnesia have a special severity. The patient is not excluded severe vomiting and headache. In some cases, there may be a violation of important vital functions.

A moderate brain contusion is manifested, first of all, by loss of consciousness with varying duration. There is vomiting, headache, abnormalities in the cardiovascular and respiratory systems.

Other possible symptoms include:

• tachycardia;
• bradycardia;
• tachypnea (no change in breathing);
• increase in body temperature;
• the appearance of enveloped signs;
• manifestation of pyramidal signs;
• nystagmus;
• the possibility of dissociation of meningeal symptoms.

Among the most pronounced focal signs, a separate category is distinguished: various types of pupillary disorders, speech disorder, sensitivity disorder. All these signs can regress 5 weeks after the onset of 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 is not excluded. Meningeal symptoms are very common. In some cases, doctors note a skull fracture and subarachnoid hemorrhage.

Moderate brain injury

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

Diagnosis

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

In the case of a severe contusion, CT scans can reveal areas of inhomogeneously increased density, while, as a rule, there is a pronounced perifocal cerebral edema with a significant hypodense path 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 mild brain injury, then it is characterized by loss of consciousness a couple of minutes after the injury. After the victim regains consciousness, he complains of a strong 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. Very often, tachycardia and bradycardia occur in victims, and blood pressure can sometimes be elevated. As for breathing, it remains unchanged, as well as body temperature, which remains normal. Individual symptoms of a neurological nature may regress after 2 weeks.

Severe brain injury

Regarding severe brain injury, it is accompanied by loss of consciousness, which can be 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 the vital functions of a person can be noted:

• violation of the respiratory rhythm;
• increased blood pressure;
• bradyarrhythmia;
• tachyarrhythmia;
• violation of the patency of the respiratory tract;
• severe hyperthermia.

Interestingly, the focal symptoms of the affected hemisphere are often hidden behind other symptoms (gaze palsy, 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 epileptic seizures, can be expressed. It will be extremely difficult to restore the shaken functions. Very often, after recovery, patients experience residual disorders in the motor apparatus and there may be obvious mental disorders.

With a severe brain injury, the patient's condition is considered critical. For a person, a coma is inherent, lasting 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 tissues will be concentrated, they talk about certain manifestations of symptoms, such as a violation of the swallowing reflex, changes in the work of the respiratory and cardiovascular systems.

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

Often severe bruises lead to death.

Diagnostics

The diagnosis is made after evaluating 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 GM, then it is characterized, first of all, by the manifestation of a coma that arose 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 be provoked by ordinary irritations, for example, pain.

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

The most striking sign of diffuse axonal brain damage is the transformation of the patient's condition, flowing from a coma into a transient vegetative state. The onset of such a state is indicated by suddenly opening eyes, however, all kinds 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 is also observed, due to which the lateral ventricles, as well as 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 detected, 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

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

Diagnosis

With the help of CT, a biconvex or flat-convex limited zone can be detected, which is characterized by increased density, adjacent to the cranial vault or located within the boundaries of one or even two lobes. If several sources of bleeding were identified, then the zone of increased density can become even larger, differing in 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;
• skull x-ray;
• Ultrasound of the chest and abdomen;
• laboratory research;
• urine tests and consultations with various specialists.

Checkup for TBI

So, for example, examination of the body includes the detection of abrasions and bruises, identification of joint deformities and changes in the shape of the chest or abdomen. In addition, during the initial examination, nose or ear bleeding may be detected. In special cases, during examination, the specialist also detects internal bleeding occurring in the rectum or urethra. The patient may have bad breath.

skull x-ray

Using x-rays, 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 complete blood count and urine test, a biochemical blood test, a blood sugar test, and an electrolyte test. In the future, such laboratory studies should be carried out regularly.

Additional diagnostic measures

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

One of the main methods of diagnosing a patient with this diagnosis is CT. There are usually no contraindications for its implementation. However, you should be aware that with 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 localization, the number and density of hyperdense areas (or, on the contrary, hypodense ones), the location and level of displacement of the midline structures of the brain, their condition and degree of damage.

In the case of the slightest suspicion of meningitis, a lumbar puncture and a cerebrospinal fluid examination are usually prescribed to control 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. In order to determine the degree of impaired consciousness, the Glasgow coma scale is usually used, which allows you to learn about the state of speech and the ability to respond with eyes to light stimuli. Among other things, the level of focal and oculomotor disorders can also be determined.

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

Post-treatment therapy

For example, for the treatment of post-traumatic meningitis, various antimicrobials are used, which, as a rule, doctors allow for the endolumbar type of administration.

If we talk about the proper nutrition of patients with such a serious injury, then it begins 3 days after the injury. The volume of nutrition will increase gradually, and at the end of the very first week, nutrition in terms of calories should be 100% of the human body's need for it.

Speaking about the methods of nutrition, two of the most common should be distinguished: enteral and parenteral. In order to stop epileptic seizures, anticonvulsants 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 for its elimination is transcranial removal. If we talk about a subdural 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, with the bone flap 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 have postconcussion syndrome, which manifests itself in impaired cognitive functions, changes in the mood and behavior of the patient. 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 a craniocerebral 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 a conclusion regarding its influence on an individual basis. Hypoxia and arterial hypertension are considered the most unfavorable symptomatic combination in TBI.